Orthopedics

A 15-day course of oral steroids modestly improved function but not pain in patients with acute radiculopathy due to a herniated lumbar disk, according to a report published online May 19 in JAMA.

Compared with epidural steroid injections, oral steroids provide similar anti-inflammatory activity but avoid MRI, can be delivered quickly by primary care physicians, avert the risks of spinal injection, and are much cheaper. “Oral steroids are used by many community physicians, have been included in some clinical guidelines, and are noted as a treatment option by some authors,” yet no adequately powered clinical trials of the therapy have been performed until now, said Dr. Harley Goldberg of the department of physical medicine at the Kaiser Permanente Northern California Spine Care Program, San Jose, and his associates.

Their study involved 269 adults at three primary care practices who had leg pain extending below the knee in a nerve root distribution, confirmation of a herniated disk on MRI, and scores of 30 or higher on the 100-point Oswestry Disability Index (ODI). These participants were randomly assigned to receive either daily prednisone capsules (cumulative dose, 600 mg) or matching placebo in addition to usual care and were followed for 1 year.

The primary outcome measure was self-reported score on the ODI at 3 weeks. After adjustment for potential confounders, the mean score was 6.4 points higher with prednisone than with placebo, a significant but modest difference. This benefit persisted at 1-year follow-up, with a mean difference of 7.4 points between the two study groups. In addition, the active-treatment group was significantly more likely to achieve at least a 30-point or 50% improvement in ODI score at 3 weeks (RR, 1.7) and at 1 year (RR, 1.3), and showed significantly greater improvement in the physical component summary score on the Short Form 36 at 3 weeks and on the mental component summary score at 1 year, the investigators said (JAMA 2015;313:1915-23).

There were no differences between the active treatment and the placebo groups in measures of below-the-waist pain at either 3 weeks or 1 year, however, and no differences in the proportion of patients achieving 2- to 5-point improvements in pain scores on a 10-point numerical rating scale at either follow-up assessment. Most importantly, there was no significant between-group difference in the likelihood of undergoing spine surgery during the year following treatment; rates of spine surgery were 9.9% among patients who received prednisone and 9.1% among those who received placebo.

Patients who received active treatment were significantly more likely to report adverse effects (49.2%) than those who received placebo (23.9%), but these were minor and transient. No serious treatment-related adverse events occurred.

“Whether the observed improvement in function (without concomitant improvement in pain) merits use of oral steroids for patients with an acute radiculopathy is a difficult decision and, ultimately, becomes a personal one that must be weighed by individual patients and their physicians,” Dr. Goldberg and his associates said.

This study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Dr. Goldberg reported having no financial disclosures; one of his associates reported ties to the Orthopaedic Research and Education Foundation, AOSpine, Simpirica, and Intrinsic Orthopedics.

A 15-day course of oral steroids modestly improved function but not pain in patients with acute radiculopathy due to a herniated lumbar disk, according to a report published online May 19 in JAMA.

Compared with epidural steroid injections, oral steroids provide similar anti-inflammatory activity but avoid MRI, can be delivered quickly by primary care physicians, avert the risks of spinal injection, and are much cheaper. “Oral steroids are used by many community physicians, have been included in some clinical guidelines, and are noted as a treatment option by some authors,” yet no adequately powered clinical trials of the therapy have been performed until now, said Dr. Harley Goldberg of the department of physical medicine at the Kaiser Permanente Northern California Spine Care Program, San Jose, and his associates.

Their study involved 269 adults at three primary care practices who had leg pain extending below the knee in a nerve root distribution, confirmation of a herniated disk on MRI, and scores of 30 or higher on the 100-point Oswestry Disability Index (ODI). These participants were randomly assigned to receive either daily prednisone capsules (cumulative dose, 600 mg) or matching placebo in addition to usual care and were followed for 1 year.

The primary outcome measure was self-reported score on the ODI at 3 weeks. After adjustment for potential confounders, the mean score was 6.4 points higher with prednisone than with placebo, a significant but modest difference. This benefit persisted at 1-year follow-up, with a mean difference of 7.4 points between the two study groups. In addition, the active-treatment group was significantly more likely to achieve at least a 30-point or 50% improvement in ODI score at 3 weeks (RR, 1.7) and at 1 year (RR, 1.3), and showed significantly greater improvement in the physical component summary score on the Short Form 36 at 3 weeks and on the mental component summary score at 1 year, the investigators said (JAMA 2015;313:1915-23).

There were no differences between the active treatment and the placebo groups in measures of below-the-waist pain at either 3 weeks or 1 year, however, and no differences in the proportion of patients achieving 2- to 5-point improvements in pain scores on a 10-point numerical rating scale at either follow-up assessment. Most importantly, there was no significant between-group difference in the likelihood of undergoing spine surgery during the year following treatment; rates of spine surgery were 9.9% among patients who received prednisone and 9.1% among those who received placebo.

Patients who received active treatment were significantly more likely to report adverse effects (49.2%) than those who received placebo (23.9%), but these were minor and transient. No serious treatment-related adverse events occurred.

“Whether the observed improvement in function (without concomitant improvement in pain) merits use of oral steroids for patients with an acute radiculopathy is a difficult decision and, ultimately, becomes a personal one that must be weighed by individual patients and their physicians,” Dr. Goldberg and his associates said.

This study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Dr. Goldberg reported having no financial disclosures; one of his associates reported ties to the Orthopaedic Research and Education Foundation, AOSpine, Simpirica, and Intrinsic Orthopedics.

A 15-day course of oral steroids modestly improved function but not pain in patients with acute radiculopathy due to a herniated lumbar disk, according to a report published online May 19 in JAMA.

Compared with epidural steroid injections, oral steroids provide similar anti-inflammatory activity but avoid MRI, can be delivered quickly by primary care physicians, avert the risks of spinal injection, and are much cheaper. “Oral steroids are used by many community physicians, have been included in some clinical guidelines, and are noted as a treatment option by some authors,” yet no adequately powered clinical trials of the therapy have been performed until now, said Dr. Harley Goldberg of the department of physical medicine at the Kaiser Permanente Northern California Spine Care Program, San Jose, and his associates.

Their study involved 269 adults at three primary care practices who had leg pain extending below the knee in a nerve root distribution, confirmation of a herniated disk on MRI, and scores of 30 or higher on the 100-point Oswestry Disability Index (ODI). These participants were randomly assigned to receive either daily prednisone capsules (cumulative dose, 600 mg) or matching placebo in addition to usual care and were followed for 1 year.

The primary outcome measure was self-reported score on the ODI at 3 weeks. After adjustment for potential confounders, the mean score was 6.4 points higher with prednisone than with placebo, a significant but modest difference. This benefit persisted at 1-year follow-up, with a mean difference of 7.4 points between the two study groups. In addition, the active-treatment group was significantly more likely to achieve at least a 30-point or 50% improvement in ODI score at 3 weeks (RR, 1.7) and at 1 year (RR, 1.3), and showed significantly greater improvement in the physical component summary score on the Short Form 36 at 3 weeks and on the mental component summary score at 1 year, the investigators said (JAMA 2015;313:1915-23).

There were no differences between the active treatment and the placebo groups in measures of below-the-waist pain at either 3 weeks or 1 year, however, and no differences in the proportion of patients achieving 2- to 5-point improvements in pain scores on a 10-point numerical rating scale at either follow-up assessment. Most importantly, there was no significant between-group difference in the likelihood of undergoing spine surgery during the year following treatment; rates of spine surgery were 9.9% among patients who received prednisone and 9.1% among those who received placebo.

Patients who received active treatment were significantly more likely to report adverse effects (49.2%) than those who received placebo (23.9%), but these were minor and transient. No serious treatment-related adverse events occurred.

“Whether the observed improvement in function (without concomitant improvement in pain) merits use of oral steroids for patients with an acute radiculopathy is a difficult decision and, ultimately, becomes a personal one that must be weighed by individual patients and their physicians,” Dr. Goldberg and his associates said.

This study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Dr. Goldberg reported having no financial disclosures; one of his associates reported ties to the Orthopaedic Research and Education Foundation, AOSpine, Simpirica, and Intrinsic Orthopedics.

The modern age of health care has driven a national interest in quality, health care economics, and proving value. A commonly used definition for quality is value/cost. Defining the value of orthopedic residents is difficult. With changes in the delivery of health care, the implementation of the Affordable Care Act, and an increasing federal deficit, defining the value of orthopedic residents has never been more important.¹

Funding for graduate medical education (GME) has been a source of recent intense debate.^2-8 From the inception of Medicare and Medicaid services, the value of residents has been recognized, and funding has been provided for resident and fellowship education. In 2012, public tax dollars provided more than $15 billion towards GME, with more than 90% coming from the Center of Medicare and Medicaid Services (CMS).⁴ This funding was initially established to: 

• support the education of physicians

• provide well-trained physicians for future generations

• account for a disproportion of care provided to underfunded patients at teaching hospitals

• account for specialty services (eg, burn centers, trauma centers, emergency psychiatric services) that can be net revenue negative. 

The significant cost of these programs, which are almost exclusively government-funded, has been the subject of cost-cutting discussions in Congress since the Balanced Budget Act of 1997 that froze GME funding.⁹ More recently, the National Commission on Fiscal Responsibility and Reform report authored by the Bowles-Simpson Commission proposed decreases in both direct medical education (DME) and indirect medical education (IME) payments that could total $6 billion by 2015 and $60 billion by 2020.^4,7,8 The proposed cuts come on the heels of the Affordable Care Act and the projected significant increase in health care demand.¹ It is important to note that private payers do not support GME despite receiving health care provided by residents and fellows.

Despite a track record of producing well-trained and skilled physicians at the end of GME training, several reports from both the public and private sectors have identified weaknesses in the GME system. These include a mismatch between the specialty composition of physician trainees and the population needs, geographic maldistribution of the physician workforce, and a lack of fiscal transparency of GME fund use by hospitals.² A recent comprehensive report from the Institute of Medicine (IOM) entitled Graduate Medical Education that Meets the Nation’s Health Needs highlights the current issues surrounding GME funding.² The report made note of several important problems with the current GME system, including:

• The revenue impact and cost savings associated with sponsoring residents are neither tracked nor reported, and they are rarely acknowledged in analyses of GME costs.

• In 1997, Congress capped the number of Medicare-supported physician training slots. Hospitals may add residents beyond the cap but cannot receive additional Medicare payments for those trainees. The cap is equal to each hospital’s number of residents in 1996—essentially freezing the geographic distribution of Medicare-supported residencies without regard for future changes in local or regional health workforce priorities or the geography and demography of the US population.⁹

• By distributing funds directly to teaching hospitals, the Medicare payment system discourages physician training outside the hospital, in clinical settings where most health care is delivered.

• Because Medicare GME funding is formula-driven, the payments are essentially guaranteed regardless of whether the funded trainees reflect local, national, or regional health needs.

• The system’s only mechanism for ensuring accountability is the requirement that residency programs be accredited. The system does not yield useful data on program outcomes and performance.

• Despite receiving government support for their residency or fellowship training, the graduate physician has no obligation to return this government investment through service.

Some of the IOM’s proposed changes to the system include:

• Updating the GME funding to account for inflation and make GME payments based on accountable performance.

• Phasing out the current GME payment system.

• Specifying funds for “transformational” programs that promote innovation and planning for the future.

• Analyzing and redistributing GME funds based on current population needs and performance metrics.

• Increasing fiscal transparency of the CMS payments and their use by hospitals.

• Establishing a GME center within CMS for ongoing oversight.

The American Orthopaedic Association recently held a forum on GME funding for resident education.¹⁰ At that forum, departmental leaders noted the difficulty in securing additional funded resident spots from hospitals and the difficulty in proving residents’ value to the hospital administration. Some in the forum suggested that, in the future, residents may need to pay for their residency like they pay for medical school.

There is very limited published data on the financial value added by orthopedic residents. A recent study examined the service provided by a single junior resident during 2 years of primary orthopedic call.¹¹ They found that the potentially billable services provided by the resident totaled more than $79,000 per year. This only accounted for services delivered while on call every sixth night. This did not account for any surgical assisting or outpatient clinic support.¹¹ This amount is nearly twice the amount provided in DME funds to the hospital for resident support.

Although the care and service that residents deliver is obvious to orthopedic attending physicians, we must “prove” our value through continued research and reporting of services provided by residents. If we do not demonstrate our value to the funders of GME, the government, and Congress, I worry that residents who follow behind us may have to fund their own training. An additional concern is that the current shortage of orthopedic surgeons may be worsened if GME funding is decreased.¹² This shortage will be exacerbated by the aging population’s increased need for orthopedic care.¹³

As health care goes through dramatic changes, orthopedic residents and attending surgeons need to be engaged in the discussion so that we can help shape our future in a way that meets the needs of our patients and continues to allow orthopedic care to be delivered at a high level nationally.

The modern age of health care has driven a national interest in quality, health care economics, and proving value. A commonly used definition for quality is value/cost. Defining the value of orthopedic residents is difficult. With changes in the delivery of health care, the implementation of the Affordable Care Act, and an increasing federal deficit, defining the value of orthopedic residents has never been more important.¹

Funding for graduate medical education (GME) has been a source of recent intense debate.^2-8 From the inception of Medicare and Medicaid services, the value of residents has been recognized, and funding has been provided for resident and fellowship education. In 2012, public tax dollars provided more than $15 billion towards GME, with more than 90% coming from the Center of Medicare and Medicaid Services (CMS).⁴ This funding was initially established to: 

• support the education of physicians

• provide well-trained physicians for future generations

• account for a disproportion of care provided to underfunded patients at teaching hospitals

• account for specialty services (eg, burn centers, trauma centers, emergency psychiatric services) that can be net revenue negative. 

The significant cost of these programs, which are almost exclusively government-funded, has been the subject of cost-cutting discussions in Congress since the Balanced Budget Act of 1997 that froze GME funding.⁹ More recently, the National Commission on Fiscal Responsibility and Reform report authored by the Bowles-Simpson Commission proposed decreases in both direct medical education (DME) and indirect medical education (IME) payments that could total $6 billion by 2015 and $60 billion by 2020.^4,7,8 The proposed cuts come on the heels of the Affordable Care Act and the projected significant increase in health care demand.¹ It is important to note that private payers do not support GME despite receiving health care provided by residents and fellows.

Despite a track record of producing well-trained and skilled physicians at the end of GME training, several reports from both the public and private sectors have identified weaknesses in the GME system. These include a mismatch between the specialty composition of physician trainees and the population needs, geographic maldistribution of the physician workforce, and a lack of fiscal transparency of GME fund use by hospitals.² A recent comprehensive report from the Institute of Medicine (IOM) entitled Graduate Medical Education that Meets the Nation’s Health Needs highlights the current issues surrounding GME funding.² The report made note of several important problems with the current GME system, including:

• The revenue impact and cost savings associated with sponsoring residents are neither tracked nor reported, and they are rarely acknowledged in analyses of GME costs.

• In 1997, Congress capped the number of Medicare-supported physician training slots. Hospitals may add residents beyond the cap but cannot receive additional Medicare payments for those trainees. The cap is equal to each hospital’s number of residents in 1996—essentially freezing the geographic distribution of Medicare-supported residencies without regard for future changes in local or regional health workforce priorities or the geography and demography of the US population.⁹

• By distributing funds directly to teaching hospitals, the Medicare payment system discourages physician training outside the hospital, in clinical settings where most health care is delivered.

• Because Medicare GME funding is formula-driven, the payments are essentially guaranteed regardless of whether the funded trainees reflect local, national, or regional health needs.

• The system’s only mechanism for ensuring accountability is the requirement that residency programs be accredited. The system does not yield useful data on program outcomes and performance.

• Despite receiving government support for their residency or fellowship training, the graduate physician has no obligation to return this government investment through service.

Some of the IOM’s proposed changes to the system include:

• Updating the GME funding to account for inflation and make GME payments based on accountable performance.

• Phasing out the current GME payment system.

• Specifying funds for “transformational” programs that promote innovation and planning for the future.

• Analyzing and redistributing GME funds based on current population needs and performance metrics.

• Increasing fiscal transparency of the CMS payments and their use by hospitals.

• Establishing a GME center within CMS for ongoing oversight.

The American Orthopaedic Association recently held a forum on GME funding for resident education.¹⁰ At that forum, departmental leaders noted the difficulty in securing additional funded resident spots from hospitals and the difficulty in proving residents’ value to the hospital administration. Some in the forum suggested that, in the future, residents may need to pay for their residency like they pay for medical school.

There is very limited published data on the financial value added by orthopedic residents. A recent study examined the service provided by a single junior resident during 2 years of primary orthopedic call.¹¹ They found that the potentially billable services provided by the resident totaled more than $79,000 per year. This only accounted for services delivered while on call every sixth night. This did not account for any surgical assisting or outpatient clinic support.¹¹ This amount is nearly twice the amount provided in DME funds to the hospital for resident support.

Although the care and service that residents deliver is obvious to orthopedic attending physicians, we must “prove” our value through continued research and reporting of services provided by residents. If we do not demonstrate our value to the funders of GME, the government, and Congress, I worry that residents who follow behind us may have to fund their own training. An additional concern is that the current shortage of orthopedic surgeons may be worsened if GME funding is decreased.¹² This shortage will be exacerbated by the aging population’s increased need for orthopedic care.¹³

As health care goes through dramatic changes, orthopedic residents and attending surgeons need to be engaged in the discussion so that we can help shape our future in a way that meets the needs of our patients and continues to allow orthopedic care to be delivered at a high level nationally.

The modern age of health care has driven a national interest in quality, health care economics, and proving value. A commonly used definition for quality is value/cost. Defining the value of orthopedic residents is difficult. With changes in the delivery of health care, the implementation of the Affordable Care Act, and an increasing federal deficit, defining the value of orthopedic residents has never been more important.¹

Funding for graduate medical education (GME) has been a source of recent intense debate.^2-8 From the inception of Medicare and Medicaid services, the value of residents has been recognized, and funding has been provided for resident and fellowship education. In 2012, public tax dollars provided more than $15 billion towards GME, with more than 90% coming from the Center of Medicare and Medicaid Services (CMS).⁴ This funding was initially established to: 

• support the education of physicians

• provide well-trained physicians for future generations

• account for a disproportion of care provided to underfunded patients at teaching hospitals

• account for specialty services (eg, burn centers, trauma centers, emergency psychiatric services) that can be net revenue negative. 

The significant cost of these programs, which are almost exclusively government-funded, has been the subject of cost-cutting discussions in Congress since the Balanced Budget Act of 1997 that froze GME funding.⁹ More recently, the National Commission on Fiscal Responsibility and Reform report authored by the Bowles-Simpson Commission proposed decreases in both direct medical education (DME) and indirect medical education (IME) payments that could total $6 billion by 2015 and $60 billion by 2020.^4,7,8 The proposed cuts come on the heels of the Affordable Care Act and the projected significant increase in health care demand.¹ It is important to note that private payers do not support GME despite receiving health care provided by residents and fellows.

Despite a track record of producing well-trained and skilled physicians at the end of GME training, several reports from both the public and private sectors have identified weaknesses in the GME system. These include a mismatch between the specialty composition of physician trainees and the population needs, geographic maldistribution of the physician workforce, and a lack of fiscal transparency of GME fund use by hospitals.² A recent comprehensive report from the Institute of Medicine (IOM) entitled Graduate Medical Education that Meets the Nation’s Health Needs highlights the current issues surrounding GME funding.² The report made note of several important problems with the current GME system, including:

• The revenue impact and cost savings associated with sponsoring residents are neither tracked nor reported, and they are rarely acknowledged in analyses of GME costs.

• In 1997, Congress capped the number of Medicare-supported physician training slots. Hospitals may add residents beyond the cap but cannot receive additional Medicare payments for those trainees. The cap is equal to each hospital’s number of residents in 1996—essentially freezing the geographic distribution of Medicare-supported residencies without regard for future changes in local or regional health workforce priorities or the geography and demography of the US population.⁹

• By distributing funds directly to teaching hospitals, the Medicare payment system discourages physician training outside the hospital, in clinical settings where most health care is delivered.

• Because Medicare GME funding is formula-driven, the payments are essentially guaranteed regardless of whether the funded trainees reflect local, national, or regional health needs.

• The system’s only mechanism for ensuring accountability is the requirement that residency programs be accredited. The system does not yield useful data on program outcomes and performance.

• Despite receiving government support for their residency or fellowship training, the graduate physician has no obligation to return this government investment through service.

Some of the IOM’s proposed changes to the system include:

• Updating the GME funding to account for inflation and make GME payments based on accountable performance.

• Phasing out the current GME payment system.

• Specifying funds for “transformational” programs that promote innovation and planning for the future.

• Analyzing and redistributing GME funds based on current population needs and performance metrics.

• Increasing fiscal transparency of the CMS payments and their use by hospitals.

• Establishing a GME center within CMS for ongoing oversight.

The American Orthopaedic Association recently held a forum on GME funding for resident education.¹⁰ At that forum, departmental leaders noted the difficulty in securing additional funded resident spots from hospitals and the difficulty in proving residents’ value to the hospital administration. Some in the forum suggested that, in the future, residents may need to pay for their residency like they pay for medical school.

There is very limited published data on the financial value added by orthopedic residents. A recent study examined the service provided by a single junior resident during 2 years of primary orthopedic call.¹¹ They found that the potentially billable services provided by the resident totaled more than $79,000 per year. This only accounted for services delivered while on call every sixth night. This did not account for any surgical assisting or outpatient clinic support.¹¹ This amount is nearly twice the amount provided in DME funds to the hospital for resident support.

Although the care and service that residents deliver is obvious to orthopedic attending physicians, we must “prove” our value through continued research and reporting of services provided by residents. If we do not demonstrate our value to the funders of GME, the government, and Congress, I worry that residents who follow behind us may have to fund their own training. An additional concern is that the current shortage of orthopedic surgeons may be worsened if GME funding is decreased.¹² This shortage will be exacerbated by the aging population’s increased need for orthopedic care.¹³

As health care goes through dramatic changes, orthopedic residents and attending surgeons need to be engaged in the discussion so that we can help shape our future in a way that meets the needs of our patients and continues to allow orthopedic care to be delivered at a high level nationally.

Traction-pin placement is a basic orthopedic skill learned in the early years of residency training. Skeletal traction historically was used as definitive treatment for long-bone fractures, and it is still in use in countries without access to modern medical care.^1,2 In current orthopedic practice, proximal tibial and distal femoral traction pins are most commonly used to temporize femoral shaft and acetabular fractures, respectively, before definitive surgical intervention. Although traction-pin placement is common, there are complications that can cause morbidity ranging from skin irritation to death.

In this article, we report on a popliteal artery pseudoaneurysm, a unique complication related to pin placement. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 22-year-old woman with no past medical history was driving a car at 35 miles per hour when she hit a telephone pole. She was wearing a seatbelt. She was taken by ambulance for a trauma evaluation. She sustained a right posterior hip dislocation with an associated Pipkin 2 femoral head fracture (Figures 1A, 1B), a right elbow skin avulsion, and a scalp abrasion.

The patient underwent closed hip reduction under sedation, and a proximal tibial traction pin was placed (Figures 2A, 2B). At our institution, proximal tibial traction pins are placed 2 cm distal and 2 cm posterior to the tibial tubercle without the use of fluoroscopy. The skin leg is prepared and draped in sterile fashion, and a local anesthetic is used to anesthetize the skin and periosteum on the medial and lateral aspects of the leg. A 1.5-cm incision is made laterally, and soft tissue is spread laterally down to the periosteum. Then the traction pin (always the largest nonthreaded pin available) is used to sound the anterior and posterior aspects of the tibia—the goal being to end at the anterior two-thirds/posterior one-third mark. After the pin is advanced through both cortices, the place where the pin will exit the skin is noted, and another incision is made. For this patient, no complications were noted at time of pin placement.

On postinjury day 1, she was taken to the operating room for open reduction and internal fixation of the femoral head fracture through a Smith-Petersen approach. At the same time, a traction pin was removed. Routine postoperative protocols were followed. The patient was started on enoxaparin, was seen by physical therapy on postoperative day 1, and was kept non-weight-bearing on the right lower extremity. Pain was well controlled, and the patient was discharged on postoperative day 3 (postinjury day 4).

Three weeks after surgery, she returned for a scheduled follow-up with complaints of paresthesia and decreased sensation in the right lateral cutaneous femoral nerve distribution and burning pain in the toes. A stiff right ankle was noted. A night splint, amitriptyline, and additional pain medications were ordered.

The patient returned for her scheduled 6-week follow-up reporting she had not taken the enoxaparin because her pharmacy “did not have any.” Her primary care physician had given her “another blood thinner,” which she had taken orally for 1 to 2 weeks. She had complaints of right calf pain, but her hip was pain-free. There was a large amount of calf swelling and tenderness along with mild equinus contracture of the ankle. She was sent to the emergency department (ED) for Doppler ultrasound evaluation for deep venous thrombosis (DVT).

Duplex Doppler imaging of the deep venous system of the lower extremities was performed with visualization from the common femoral veins to the popliteal veins bilaterally. There was normal compressibility, respiratory phasicity, and flow with no intraluminal thrombus. A radiograph of tibia and fibula showed soft-tissue swelling and lucencies from the traction pin but no other abnormalities.

Eight weeks after surgery, the patient returned to the ED because of continuing calf pain. Given that the ultrasound findings had been negative, magnetic resonance imaging (MRI) was ordered, and orthopedic follow-up scheduled. About 10 weeks after surgery, she returned to the ED, still with calf pain, and reported having been unable to go for her MRI because of financial reasons. Physical examination revealed increased calf swelling and a new ecchymosis tracking along the tibia. Repeat ultrasound, performed from the common femoral veins through the popliteal veins, showed a right posterior calf pseudoaneurysm (8.5×4.3×5.3 cm) arising from the popliteal artery about 5 cm below the popliteal fossa. In addition, a large hematoma was seen originating in the upper posterior calf and extending inferiorly (Figure 3).

Computed tomography angiogram confirmed the ultrasound diagnosis of a large (5.6×4.8-cm) right calf pseudo­aneurysm arising possibly from a small muscular branch of the proximal tibioperoneal trunk, with a large surrounding hematoma in the posterior compartment of the proximal right calf (Figure 4). Vascular surgery was consulted, and coil embolization of the pseudoaneurysm was performed later that night in the interventional radiology suite.

After the coiling of the pseudoaneurysm, the calf swelling and pain slowly improved. At 12-week orthopedic follow-up, the patient was no longer using any pain medications, and she noted improvement in the right foot’s neuropathic symptoms. Serial casting was prescribed for the equinus contracture of the ankle. She was allowed to start weight-bearing on the right lower extremity. Radiographs at 12 weeks showed collapse of the superomedial aspect of the femoral head with surrounding sclerosis consistent with posttraumatic avascular necrosis.

At final orthopedic follow-up, about 16 weeks after surgery, the patient reported 0/10 pain. Sensation was noted as being intact throughout the right lower extremity but decreased in the tibial nerve distribution. Ankle range of motion was still limited, with 5° of dorsiflexion and 25° of plantar flexion. The hip was pain-free with flexion of 0° to 100°, 10° of internal rotation, and 20° of external rotation. Additional appointments were scheduled, but the patient did not follow up. Two years after initial injury, she returned to the ED for evaluation of rhinorrhea, and no orthopedic complaints were noted.

Discussion

Skeletal traction begins with the insertion of a wire or pin through a bone. It is extremely important to use proper technique in order to minimize the risks associated with pin insertion.³ Potential pitfalls involve the energy transferred into the bone during insertion, the incisions used to place the pin, and injury to surrounding neurovascular structures. For proximal tibial pins, standard technique dictates placing the pin in a lateral-to-medial direction 2 cm posterior to the tibial tubercle and avoiding the dense anterior cortical bone. At our institution, traction pins are placed with a power drill after the patient is given a local anesthetic or is placed under conscious sedation. Which type of anesthesia to use is based on the patient’s overall condition and on the ED attending physician’s willingness to administer conscious sedation.

The 2 most common types of tibial traction involve use of either a large Steinmann pin attached to a metal bow or a Kirschner wire (K-wire) placed under tension before traction. Which to use is the surgeon’s choice. Surgeons at our institution historically have used Steinmann pins. No studies have directly compared fine-wire and Steinmann-pin traction, but with this complication our institution is evaluating a change to tensioned wires. Compared with large Steinmann pins, fine-wire pins create less of a defect in the bone but also bend or break more easily if tension is not applied or if it fails. A fine wire with its smaller surface area may also cut more easily into osteopenic bone than a large-diameter pin would.

Proximal tibial traction typically is indicated for femoral shaft and acetabular fractures. Although the subcutaneous nature of the tibia makes for easier pin placement, the anatomy of the tibia can predispose this bone to complications. Its triangular shape can lead to intracortical rather than the preferred bicortical pin placement. Increased heat caused by intracortical placement can lead to osteonecrosis and even to damage of surrounding soft tissues. Green and Ripley⁴ found that chronic osteomyelitis typically resulted from intracortical placement of traction pins.

Injury to surrounding soft tissues, either from heat necrosis or from infection introduced through pin sites, can also have consequences. Pin-site infections increase with duration of treatment, though care seldom requires more than pin removal and antibiotics.^5,6 More-invasive infections range from cellulitis surrounding the pin site to subcutaneous abscesses. There is 1 report of a Clostridium perfringens infection leading to death only 5 days after pin placement.⁷

Neurovascular structures are at risk with any orthopedic procedure. With proximal tibial pins in pediatric patients, the peroneal nerve, the anterior tibial artery, and the proximal physis are most at risk. The deep peroneal nerve and the anterior tibial artery run together deep to the anterior compartment, which places them at highest risk with pin insertion. The peroneal and tibial arteries run deep to the deep posterior compartment along with the tibial nerve behind the posterior cortex of the tibia, which makes injury less likely.⁸

Historically, long-bone fractures were often treated with traction. Kirby and Fitts⁹ reported on 342 transfixion pins and wires used in the treatment of 233 long-bone fractures between 1943 and 1945. Of the 305 pins/wires observed over the entire treatment period (average, 6 weeks), only 12 (3.93%) developed a complication. There were 4 loose K-wires, 1 broken wire, and 1 bow failure; Steinmann pins were involved in 1 infection and 2 transient peroneal nerve palsies; and 3 Roger Anderson pins loosened. Pin-tract drainage was not included as a complication if it did not also involve localized or general signs of inflammation. The 2 peroneal nerve palsies were associated with medial-to-lateral pin insertion creating a more posterior pin path.

Pins inserted for external fixators of the tibia have injured the anterior tibial vessels and branches of the peroneal and saphenous nerves. A proximal tibial traction pin, in essence a transfixion pin, can cause similar injuries, particularly with imperfect placement (Figure 5).^3,10

A pseudoaneurysm is a pulsating, encapsulated hematoma that remains in communication with the lumen of a ruptured or injured vessel. The arterial wall itself is torn or ruptured, and the external wall of the aneurysmal sac consists of outer arterial layers, perivascular tissue, blood clot, or a layer of reactive fibrosis. This contrasts with a true aneurysm, in which all 3 arterial layers (intima, media, adventitia) remain confluent but are dilated beyond their normal diameter. Of all pseudo­aneurysms, those caused iatrogenically are the most common and are typically produced by femoral artery catheterization, accounting for 70% to 80% of the incidence.¹¹

Our patient’s injury was most likely caused by an initial error in pin placement before the pin was driven across the tibia. The typical teaching for traction-pin placement involves finding the correct starting point and then using the pin to feel the anterior and posterior surfaces of the bone (described earlier). If the pin slid posteriorly, it may have contacted the artery and caused a small tear that eventually led to the formation of the pseudoaneurysm.

The pseudoaneurysm was not the only complication in the present case. There was also the delay in diagnosis. A standard technique is used to evaluate the lower extremity venous system for DVT. The ultrasonographer starts with the probe as proximal as possible (above the inguinal ligament), ideally proximal to the saphenofemoral junction, and moves distally in 1-cm increments, checking the veins for compressibility, color, and Doppler signal. Unless advised otherwise, the ultrasonographer typically does not examine distal to the knee.^12,13 As this patient’s pseudoaneurysm was distal to the knee, it was not found on initial ultrasound, and her inability to obtain her MRI compounded the delay. The second ultrasound identified the pseudoaneurysm. The ultrasonographer examined more distally, given the contrast between the clinical diagnosis of vascular pathology and the negative Doppler study. Computed tomography angiogram confirmed the diagnosis and guided the vascular surgeons in identifying the lesion as a pseudoaneurysm, allowing it to be coiled rather than bypassed.

Duplex ultrasound is the preferred diagnostic modality for imaging pseudoaneurysms. Although our patient’s scan was performed in timely fashion, it did not image the area of pathology. Instead, this patient with multiple orthopedic injuries was scanned for DVT, the most likely cause of her lower extremity swelling. Had a pseudoaneurysm been suspected, the ultrasonographer would have been instructed to image the entire extremity and not just the area where DVT might be found.

Fortunately, despite the treatment delay, the patient recovered well from both the traumatic injuries sustained in the car crash and the likely iatrogenic pseudoaneurysm. Although traction pins are easily and frequently used, they can have complications, which are often preventable. Starting with pin placement itself, there were several opportunities for improving this patient’s care or, at a minimum, reducing the time spent in diagnosis. If the pin had been noticed sliding posteriorly during insertion, extra attention during follow-up visits could have helped identify the injury sooner. Another difficulty in diagnosis was that of obtaining the appropriate outpatient radiology studies which necessitated repeat ED visits. An additional juncture was between the patient’s multiple ED visits for similar complaints. Obtaining advanced imaging sooner could have helped in diagnosing the pseudoaneurysm earlier.

Traction-pin placement is a basic orthopedic skill learned in the early years of residency training. Skeletal traction historically was used as definitive treatment for long-bone fractures, and it is still in use in countries without access to modern medical care.^1,2 In current orthopedic practice, proximal tibial and distal femoral traction pins are most commonly used to temporize femoral shaft and acetabular fractures, respectively, before definitive surgical intervention. Although traction-pin placement is common, there are complications that can cause morbidity ranging from skin irritation to death.

In this article, we report on a popliteal artery pseudoaneurysm, a unique complication related to pin placement. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 22-year-old woman with no past medical history was driving a car at 35 miles per hour when she hit a telephone pole. She was wearing a seatbelt. She was taken by ambulance for a trauma evaluation. She sustained a right posterior hip dislocation with an associated Pipkin 2 femoral head fracture (Figures 1A, 1B), a right elbow skin avulsion, and a scalp abrasion.

The patient underwent closed hip reduction under sedation, and a proximal tibial traction pin was placed (Figures 2A, 2B). At our institution, proximal tibial traction pins are placed 2 cm distal and 2 cm posterior to the tibial tubercle without the use of fluoroscopy. The skin leg is prepared and draped in sterile fashion, and a local anesthetic is used to anesthetize the skin and periosteum on the medial and lateral aspects of the leg. A 1.5-cm incision is made laterally, and soft tissue is spread laterally down to the periosteum. Then the traction pin (always the largest nonthreaded pin available) is used to sound the anterior and posterior aspects of the tibia—the goal being to end at the anterior two-thirds/posterior one-third mark. After the pin is advanced through both cortices, the place where the pin will exit the skin is noted, and another incision is made. For this patient, no complications were noted at time of pin placement.

On postinjury day 1, she was taken to the operating room for open reduction and internal fixation of the femoral head fracture through a Smith-Petersen approach. At the same time, a traction pin was removed. Routine postoperative protocols were followed. The patient was started on enoxaparin, was seen by physical therapy on postoperative day 1, and was kept non-weight-bearing on the right lower extremity. Pain was well controlled, and the patient was discharged on postoperative day 3 (postinjury day 4).

Three weeks after surgery, she returned for a scheduled follow-up with complaints of paresthesia and decreased sensation in the right lateral cutaneous femoral nerve distribution and burning pain in the toes. A stiff right ankle was noted. A night splint, amitriptyline, and additional pain medications were ordered.

The patient returned for her scheduled 6-week follow-up reporting she had not taken the enoxaparin because her pharmacy “did not have any.” Her primary care physician had given her “another blood thinner,” which she had taken orally for 1 to 2 weeks. She had complaints of right calf pain, but her hip was pain-free. There was a large amount of calf swelling and tenderness along with mild equinus contracture of the ankle. She was sent to the emergency department (ED) for Doppler ultrasound evaluation for deep venous thrombosis (DVT).

Duplex Doppler imaging of the deep venous system of the lower extremities was performed with visualization from the common femoral veins to the popliteal veins bilaterally. There was normal compressibility, respiratory phasicity, and flow with no intraluminal thrombus. A radiograph of tibia and fibula showed soft-tissue swelling and lucencies from the traction pin but no other abnormalities.

Eight weeks after surgery, the patient returned to the ED because of continuing calf pain. Given that the ultrasound findings had been negative, magnetic resonance imaging (MRI) was ordered, and orthopedic follow-up scheduled. About 10 weeks after surgery, she returned to the ED, still with calf pain, and reported having been unable to go for her MRI because of financial reasons. Physical examination revealed increased calf swelling and a new ecchymosis tracking along the tibia. Repeat ultrasound, performed from the common femoral veins through the popliteal veins, showed a right posterior calf pseudoaneurysm (8.5×4.3×5.3 cm) arising from the popliteal artery about 5 cm below the popliteal fossa. In addition, a large hematoma was seen originating in the upper posterior calf and extending inferiorly (Figure 3).

Computed tomography angiogram confirmed the ultrasound diagnosis of a large (5.6×4.8-cm) right calf pseudo­aneurysm arising possibly from a small muscular branch of the proximal tibioperoneal trunk, with a large surrounding hematoma in the posterior compartment of the proximal right calf (Figure 4). Vascular surgery was consulted, and coil embolization of the pseudoaneurysm was performed later that night in the interventional radiology suite.

After the coiling of the pseudoaneurysm, the calf swelling and pain slowly improved. At 12-week orthopedic follow-up, the patient was no longer using any pain medications, and she noted improvement in the right foot’s neuropathic symptoms. Serial casting was prescribed for the equinus contracture of the ankle. She was allowed to start weight-bearing on the right lower extremity. Radiographs at 12 weeks showed collapse of the superomedial aspect of the femoral head with surrounding sclerosis consistent with posttraumatic avascular necrosis.

At final orthopedic follow-up, about 16 weeks after surgery, the patient reported 0/10 pain. Sensation was noted as being intact throughout the right lower extremity but decreased in the tibial nerve distribution. Ankle range of motion was still limited, with 5° of dorsiflexion and 25° of plantar flexion. The hip was pain-free with flexion of 0° to 100°, 10° of internal rotation, and 20° of external rotation. Additional appointments were scheduled, but the patient did not follow up. Two years after initial injury, she returned to the ED for evaluation of rhinorrhea, and no orthopedic complaints were noted.

Discussion

Skeletal traction begins with the insertion of a wire or pin through a bone. It is extremely important to use proper technique in order to minimize the risks associated with pin insertion.³ Potential pitfalls involve the energy transferred into the bone during insertion, the incisions used to place the pin, and injury to surrounding neurovascular structures. For proximal tibial pins, standard technique dictates placing the pin in a lateral-to-medial direction 2 cm posterior to the tibial tubercle and avoiding the dense anterior cortical bone. At our institution, traction pins are placed with a power drill after the patient is given a local anesthetic or is placed under conscious sedation. Which type of anesthesia to use is based on the patient’s overall condition and on the ED attending physician’s willingness to administer conscious sedation.

The 2 most common types of tibial traction involve use of either a large Steinmann pin attached to a metal bow or a Kirschner wire (K-wire) placed under tension before traction. Which to use is the surgeon’s choice. Surgeons at our institution historically have used Steinmann pins. No studies have directly compared fine-wire and Steinmann-pin traction, but with this complication our institution is evaluating a change to tensioned wires. Compared with large Steinmann pins, fine-wire pins create less of a defect in the bone but also bend or break more easily if tension is not applied or if it fails. A fine wire with its smaller surface area may also cut more easily into osteopenic bone than a large-diameter pin would.

Proximal tibial traction typically is indicated for femoral shaft and acetabular fractures. Although the subcutaneous nature of the tibia makes for easier pin placement, the anatomy of the tibia can predispose this bone to complications. Its triangular shape can lead to intracortical rather than the preferred bicortical pin placement. Increased heat caused by intracortical placement can lead to osteonecrosis and even to damage of surrounding soft tissues. Green and Ripley⁴ found that chronic osteomyelitis typically resulted from intracortical placement of traction pins.

Injury to surrounding soft tissues, either from heat necrosis or from infection introduced through pin sites, can also have consequences. Pin-site infections increase with duration of treatment, though care seldom requires more than pin removal and antibiotics.^5,6 More-invasive infections range from cellulitis surrounding the pin site to subcutaneous abscesses. There is 1 report of a Clostridium perfringens infection leading to death only 5 days after pin placement.⁷

Neurovascular structures are at risk with any orthopedic procedure. With proximal tibial pins in pediatric patients, the peroneal nerve, the anterior tibial artery, and the proximal physis are most at risk. The deep peroneal nerve and the anterior tibial artery run together deep to the anterior compartment, which places them at highest risk with pin insertion. The peroneal and tibial arteries run deep to the deep posterior compartment along with the tibial nerve behind the posterior cortex of the tibia, which makes injury less likely.⁸

Historically, long-bone fractures were often treated with traction. Kirby and Fitts⁹ reported on 342 transfixion pins and wires used in the treatment of 233 long-bone fractures between 1943 and 1945. Of the 305 pins/wires observed over the entire treatment period (average, 6 weeks), only 12 (3.93%) developed a complication. There were 4 loose K-wires, 1 broken wire, and 1 bow failure; Steinmann pins were involved in 1 infection and 2 transient peroneal nerve palsies; and 3 Roger Anderson pins loosened. Pin-tract drainage was not included as a complication if it did not also involve localized or general signs of inflammation. The 2 peroneal nerve palsies were associated with medial-to-lateral pin insertion creating a more posterior pin path.

Pins inserted for external fixators of the tibia have injured the anterior tibial vessels and branches of the peroneal and saphenous nerves. A proximal tibial traction pin, in essence a transfixion pin, can cause similar injuries, particularly with imperfect placement (Figure 5).^3,10

A pseudoaneurysm is a pulsating, encapsulated hematoma that remains in communication with the lumen of a ruptured or injured vessel. The arterial wall itself is torn or ruptured, and the external wall of the aneurysmal sac consists of outer arterial layers, perivascular tissue, blood clot, or a layer of reactive fibrosis. This contrasts with a true aneurysm, in which all 3 arterial layers (intima, media, adventitia) remain confluent but are dilated beyond their normal diameter. Of all pseudo­aneurysms, those caused iatrogenically are the most common and are typically produced by femoral artery catheterization, accounting for 70% to 80% of the incidence.¹¹

Our patient’s injury was most likely caused by an initial error in pin placement before the pin was driven across the tibia. The typical teaching for traction-pin placement involves finding the correct starting point and then using the pin to feel the anterior and posterior surfaces of the bone (described earlier). If the pin slid posteriorly, it may have contacted the artery and caused a small tear that eventually led to the formation of the pseudoaneurysm.

The pseudoaneurysm was not the only complication in the present case. There was also the delay in diagnosis. A standard technique is used to evaluate the lower extremity venous system for DVT. The ultrasonographer starts with the probe as proximal as possible (above the inguinal ligament), ideally proximal to the saphenofemoral junction, and moves distally in 1-cm increments, checking the veins for compressibility, color, and Doppler signal. Unless advised otherwise, the ultrasonographer typically does not examine distal to the knee.^12,13 As this patient’s pseudoaneurysm was distal to the knee, it was not found on initial ultrasound, and her inability to obtain her MRI compounded the delay. The second ultrasound identified the pseudoaneurysm. The ultrasonographer examined more distally, given the contrast between the clinical diagnosis of vascular pathology and the negative Doppler study. Computed tomography angiogram confirmed the diagnosis and guided the vascular surgeons in identifying the lesion as a pseudoaneurysm, allowing it to be coiled rather than bypassed.

Duplex ultrasound is the preferred diagnostic modality for imaging pseudoaneurysms. Although our patient’s scan was performed in timely fashion, it did not image the area of pathology. Instead, this patient with multiple orthopedic injuries was scanned for DVT, the most likely cause of her lower extremity swelling. Had a pseudoaneurysm been suspected, the ultrasonographer would have been instructed to image the entire extremity and not just the area where DVT might be found.

Fortunately, despite the treatment delay, the patient recovered well from both the traumatic injuries sustained in the car crash and the likely iatrogenic pseudoaneurysm. Although traction pins are easily and frequently used, they can have complications, which are often preventable. Starting with pin placement itself, there were several opportunities for improving this patient’s care or, at a minimum, reducing the time spent in diagnosis. If the pin had been noticed sliding posteriorly during insertion, extra attention during follow-up visits could have helped identify the injury sooner. Another difficulty in diagnosis was that of obtaining the appropriate outpatient radiology studies which necessitated repeat ED visits. An additional juncture was between the patient’s multiple ED visits for similar complaints. Obtaining advanced imaging sooner could have helped in diagnosing the pseudoaneurysm earlier.

Traction-pin placement is a basic orthopedic skill learned in the early years of residency training. Skeletal traction historically was used as definitive treatment for long-bone fractures, and it is still in use in countries without access to modern medical care.^1,2 In current orthopedic practice, proximal tibial and distal femoral traction pins are most commonly used to temporize femoral shaft and acetabular fractures, respectively, before definitive surgical intervention. Although traction-pin placement is common, there are complications that can cause morbidity ranging from skin irritation to death.

In this article, we report on a popliteal artery pseudoaneurysm, a unique complication related to pin placement. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 22-year-old woman with no past medical history was driving a car at 35 miles per hour when she hit a telephone pole. She was wearing a seatbelt. She was taken by ambulance for a trauma evaluation. She sustained a right posterior hip dislocation with an associated Pipkin 2 femoral head fracture (Figures 1A, 1B), a right elbow skin avulsion, and a scalp abrasion.

The patient underwent closed hip reduction under sedation, and a proximal tibial traction pin was placed (Figures 2A, 2B). At our institution, proximal tibial traction pins are placed 2 cm distal and 2 cm posterior to the tibial tubercle without the use of fluoroscopy. The skin leg is prepared and draped in sterile fashion, and a local anesthetic is used to anesthetize the skin and periosteum on the medial and lateral aspects of the leg. A 1.5-cm incision is made laterally, and soft tissue is spread laterally down to the periosteum. Then the traction pin (always the largest nonthreaded pin available) is used to sound the anterior and posterior aspects of the tibia—the goal being to end at the anterior two-thirds/posterior one-third mark. After the pin is advanced through both cortices, the place where the pin will exit the skin is noted, and another incision is made. For this patient, no complications were noted at time of pin placement.

On postinjury day 1, she was taken to the operating room for open reduction and internal fixation of the femoral head fracture through a Smith-Petersen approach. At the same time, a traction pin was removed. Routine postoperative protocols were followed. The patient was started on enoxaparin, was seen by physical therapy on postoperative day 1, and was kept non-weight-bearing on the right lower extremity. Pain was well controlled, and the patient was discharged on postoperative day 3 (postinjury day 4).

Three weeks after surgery, she returned for a scheduled follow-up with complaints of paresthesia and decreased sensation in the right lateral cutaneous femoral nerve distribution and burning pain in the toes. A stiff right ankle was noted. A night splint, amitriptyline, and additional pain medications were ordered.

The patient returned for her scheduled 6-week follow-up reporting she had not taken the enoxaparin because her pharmacy “did not have any.” Her primary care physician had given her “another blood thinner,” which she had taken orally for 1 to 2 weeks. She had complaints of right calf pain, but her hip was pain-free. There was a large amount of calf swelling and tenderness along with mild equinus contracture of the ankle. She was sent to the emergency department (ED) for Doppler ultrasound evaluation for deep venous thrombosis (DVT).

Duplex Doppler imaging of the deep venous system of the lower extremities was performed with visualization from the common femoral veins to the popliteal veins bilaterally. There was normal compressibility, respiratory phasicity, and flow with no intraluminal thrombus. A radiograph of tibia and fibula showed soft-tissue swelling and lucencies from the traction pin but no other abnormalities.

Eight weeks after surgery, the patient returned to the ED because of continuing calf pain. Given that the ultrasound findings had been negative, magnetic resonance imaging (MRI) was ordered, and orthopedic follow-up scheduled. About 10 weeks after surgery, she returned to the ED, still with calf pain, and reported having been unable to go for her MRI because of financial reasons. Physical examination revealed increased calf swelling and a new ecchymosis tracking along the tibia. Repeat ultrasound, performed from the common femoral veins through the popliteal veins, showed a right posterior calf pseudoaneurysm (8.5×4.3×5.3 cm) arising from the popliteal artery about 5 cm below the popliteal fossa. In addition, a large hematoma was seen originating in the upper posterior calf and extending inferiorly (Figure 3).

Computed tomography angiogram confirmed the ultrasound diagnosis of a large (5.6×4.8-cm) right calf pseudo­aneurysm arising possibly from a small muscular branch of the proximal tibioperoneal trunk, with a large surrounding hematoma in the posterior compartment of the proximal right calf (Figure 4). Vascular surgery was consulted, and coil embolization of the pseudoaneurysm was performed later that night in the interventional radiology suite.

After the coiling of the pseudoaneurysm, the calf swelling and pain slowly improved. At 12-week orthopedic follow-up, the patient was no longer using any pain medications, and she noted improvement in the right foot’s neuropathic symptoms. Serial casting was prescribed for the equinus contracture of the ankle. She was allowed to start weight-bearing on the right lower extremity. Radiographs at 12 weeks showed collapse of the superomedial aspect of the femoral head with surrounding sclerosis consistent with posttraumatic avascular necrosis.

At final orthopedic follow-up, about 16 weeks after surgery, the patient reported 0/10 pain. Sensation was noted as being intact throughout the right lower extremity but decreased in the tibial nerve distribution. Ankle range of motion was still limited, with 5° of dorsiflexion and 25° of plantar flexion. The hip was pain-free with flexion of 0° to 100°, 10° of internal rotation, and 20° of external rotation. Additional appointments were scheduled, but the patient did not follow up. Two years after initial injury, she returned to the ED for evaluation of rhinorrhea, and no orthopedic complaints were noted.

Discussion

Skeletal traction begins with the insertion of a wire or pin through a bone. It is extremely important to use proper technique in order to minimize the risks associated with pin insertion.³ Potential pitfalls involve the energy transferred into the bone during insertion, the incisions used to place the pin, and injury to surrounding neurovascular structures. For proximal tibial pins, standard technique dictates placing the pin in a lateral-to-medial direction 2 cm posterior to the tibial tubercle and avoiding the dense anterior cortical bone. At our institution, traction pins are placed with a power drill after the patient is given a local anesthetic or is placed under conscious sedation. Which type of anesthesia to use is based on the patient’s overall condition and on the ED attending physician’s willingness to administer conscious sedation.

The 2 most common types of tibial traction involve use of either a large Steinmann pin attached to a metal bow or a Kirschner wire (K-wire) placed under tension before traction. Which to use is the surgeon’s choice. Surgeons at our institution historically have used Steinmann pins. No studies have directly compared fine-wire and Steinmann-pin traction, but with this complication our institution is evaluating a change to tensioned wires. Compared with large Steinmann pins, fine-wire pins create less of a defect in the bone but also bend or break more easily if tension is not applied or if it fails. A fine wire with its smaller surface area may also cut more easily into osteopenic bone than a large-diameter pin would.

Proximal tibial traction typically is indicated for femoral shaft and acetabular fractures. Although the subcutaneous nature of the tibia makes for easier pin placement, the anatomy of the tibia can predispose this bone to complications. Its triangular shape can lead to intracortical rather than the preferred bicortical pin placement. Increased heat caused by intracortical placement can lead to osteonecrosis and even to damage of surrounding soft tissues. Green and Ripley⁴ found that chronic osteomyelitis typically resulted from intracortical placement of traction pins.

Injury to surrounding soft tissues, either from heat necrosis or from infection introduced through pin sites, can also have consequences. Pin-site infections increase with duration of treatment, though care seldom requires more than pin removal and antibiotics.^5,6 More-invasive infections range from cellulitis surrounding the pin site to subcutaneous abscesses. There is 1 report of a Clostridium perfringens infection leading to death only 5 days after pin placement.⁷

Neurovascular structures are at risk with any orthopedic procedure. With proximal tibial pins in pediatric patients, the peroneal nerve, the anterior tibial artery, and the proximal physis are most at risk. The deep peroneal nerve and the anterior tibial artery run together deep to the anterior compartment, which places them at highest risk with pin insertion. The peroneal and tibial arteries run deep to the deep posterior compartment along with the tibial nerve behind the posterior cortex of the tibia, which makes injury less likely.⁸

Historically, long-bone fractures were often treated with traction. Kirby and Fitts⁹ reported on 342 transfixion pins and wires used in the treatment of 233 long-bone fractures between 1943 and 1945. Of the 305 pins/wires observed over the entire treatment period (average, 6 weeks), only 12 (3.93%) developed a complication. There were 4 loose K-wires, 1 broken wire, and 1 bow failure; Steinmann pins were involved in 1 infection and 2 transient peroneal nerve palsies; and 3 Roger Anderson pins loosened. Pin-tract drainage was not included as a complication if it did not also involve localized or general signs of inflammation. The 2 peroneal nerve palsies were associated with medial-to-lateral pin insertion creating a more posterior pin path.

Pins inserted for external fixators of the tibia have injured the anterior tibial vessels and branches of the peroneal and saphenous nerves. A proximal tibial traction pin, in essence a transfixion pin, can cause similar injuries, particularly with imperfect placement (Figure 5).^3,10

A pseudoaneurysm is a pulsating, encapsulated hematoma that remains in communication with the lumen of a ruptured or injured vessel. The arterial wall itself is torn or ruptured, and the external wall of the aneurysmal sac consists of outer arterial layers, perivascular tissue, blood clot, or a layer of reactive fibrosis. This contrasts with a true aneurysm, in which all 3 arterial layers (intima, media, adventitia) remain confluent but are dilated beyond their normal diameter. Of all pseudo­aneurysms, those caused iatrogenically are the most common and are typically produced by femoral artery catheterization, accounting for 70% to 80% of the incidence.¹¹

Our patient’s injury was most likely caused by an initial error in pin placement before the pin was driven across the tibia. The typical teaching for traction-pin placement involves finding the correct starting point and then using the pin to feel the anterior and posterior surfaces of the bone (described earlier). If the pin slid posteriorly, it may have contacted the artery and caused a small tear that eventually led to the formation of the pseudoaneurysm.

The pseudoaneurysm was not the only complication in the present case. There was also the delay in diagnosis. A standard technique is used to evaluate the lower extremity venous system for DVT. The ultrasonographer starts with the probe as proximal as possible (above the inguinal ligament), ideally proximal to the saphenofemoral junction, and moves distally in 1-cm increments, checking the veins for compressibility, color, and Doppler signal. Unless advised otherwise, the ultrasonographer typically does not examine distal to the knee.^12,13 As this patient’s pseudoaneurysm was distal to the knee, it was not found on initial ultrasound, and her inability to obtain her MRI compounded the delay. The second ultrasound identified the pseudoaneurysm. The ultrasonographer examined more distally, given the contrast between the clinical diagnosis of vascular pathology and the negative Doppler study. Computed tomography angiogram confirmed the diagnosis and guided the vascular surgeons in identifying the lesion as a pseudoaneurysm, allowing it to be coiled rather than bypassed.

Duplex ultrasound is the preferred diagnostic modality for imaging pseudoaneurysms. Although our patient’s scan was performed in timely fashion, it did not image the area of pathology. Instead, this patient with multiple orthopedic injuries was scanned for DVT, the most likely cause of her lower extremity swelling. Had a pseudoaneurysm been suspected, the ultrasonographer would have been instructed to image the entire extremity and not just the area where DVT might be found.

Fortunately, despite the treatment delay, the patient recovered well from both the traumatic injuries sustained in the car crash and the likely iatrogenic pseudoaneurysm. Although traction pins are easily and frequently used, they can have complications, which are often preventable. Starting with pin placement itself, there were several opportunities for improving this patient’s care or, at a minimum, reducing the time spent in diagnosis. If the pin had been noticed sliding posteriorly during insertion, extra attention during follow-up visits could have helped identify the injury sooner. Another difficulty in diagnosis was that of obtaining the appropriate outpatient radiology studies which necessitated repeat ED visits. An additional juncture was between the patient’s multiple ED visits for similar complaints. Obtaining advanced imaging sooner could have helped in diagnosing the pseudoaneurysm earlier.

Reverse shoulder arthroplasty (RSA) is a treatment option for a spectrum of diseases in shoulders with rotator cuff deficiency. There are distinct morphologic changes in the scapular and glenoid anatomy in patients with chronic rotator cuff tears.¹ A muscular imbalance that occurs in the joint as a result of rotator cuff deficiency leads to morphologic changes that eliminate the compressive forces that hold the humeral head against the glenoid.² RSA effectively stabilizes the glenohumeral joint in shoulders with deficient rotator cuffs.^3,4 In early work, Grammont proposed that the glenosphere center of rotation should be medialized (concentric to the central axis of the metaglene or baseplate) and lowered.⁵ Although the medialized center of rotation in Grammont prostheses decreases shear forces and improves the deltoid lever arm, it also tends to result in mechanical impingement between the superomedial aspect of the humeral polyethylene insert and the scapular neck—so-called inferior scapular notching.^6-9

Notching, which has been reported in 50% to 96% of patients who receive a Delta III prosthesis, typically appears within the first few months after surgery but may be seen as late as 14 months after surgery.^5,10-12 Postmortem studies have shown that notching corresponds with erosion of the inferior pole of the glenoid and scapular neck, thought to be caused by the polyethylene cup of the implant.¹³ Although some studies have found that notching stabilizes after 1 year, others have shown notching progressing for up to 4 years after surgery.^11,12,14 The clinical relevance of notching continues to be controversial, but notching has been associated with poorer clinical outcomes, polyethylene wear, and local osteolysis. Component loosening has also been reported with notching of grade 3 or more.^8,10 Ultimately, there is concern that scapular notching could progress, ultimately leading to late glenoid loosening and potentially catastrophic failure.

Scapular anatomy has become an area of increased focus in rotator cuff disorders and in effects on RSA biomechanics.⁹ Recent reports have described important scapular morphology variations that suggest more individualized adjustments are needed during RSA.^9,15 In addition, some investigators have reported that development of notching appears to depend on the height and inclination of the implanted glenoid component, where an inferior position of the glenosphere leads to less impingement and better range of motion.^8,16 Simovitch and colleagues⁸ found the angle between the glenosphere and scapular neck and the craniocaudal position of the glenosphere to be highly correlated with inferior notching. They combined these 2 parameters into a predictive algorithm that provides a guideline (notching index, <35) for prevention of notching.

We conducted a study to evaluate the scapular notching index as a predictive tool and to consider other factors that may be associated with scapular notching occurring with use of Grammont reverse replacement systems. We hypothesized that patients with a notching index of less than 35 would not develop notching and that patients with an index of more than 35 would have increased incidence and severity of notching.

Materials and Methods

Patients treated with RSA for painful cuff tear arthropathy or irreparable rotator cuff tear with pseudoparesis (inability to actively elevate shoulder >90° in presence of free passive anterior elevation) were included in this retrospective review. All patients were treated between 2006 and 2010 by 1 of 2 established senior shoulder subspecialty surgeons. Patients treated with a Delta (DePuy Orthopaedics, Warsaw, Indiana) or an Aequalis (Tornier, Edina, Minnesota) reverse shoulder implant were included in the study. A standard polyethylene liner was used for all patients. These prostheses have the same neck shaft angle, 155º, as they have similar geometric designs, both based on the Grammont design—semiconstrained inverted with a fixed, lowered, medialized center of rotation. Standard instrumentation was used for all procedures. Patients were excluded if any nonstandard techniques or components were used (constrained or high-mobility liner, glenoid bone grafting). Patients who underwent revision for a previous reverse total arthroplasty, a total shoulder arthroplasty, or a hemiarthroplasty, or for treatment of acute fracture, posttraumatic deformity, or posttraumatic arthritis, were also excluded from our analyses. Minimum follow-up for study inclusion was 24 months.

All procedures were performed with the patient in the semi-beach-chair position and with use of a deltopectoral approach. The glenoid was prepared such that minimal reaming was needed to preserve the subchondral plate. The glenoid baseplate was positioned in the recommended inferior position to minimize notching and optimize functional outcomes.¹³ After surgery, all patients were managed with a simple soft immobilizer with or without a pillow with the arm at the patient’s side in internal rotation. Immediate passive mobilization was begun under the direction of physical therapists. Passive and active-assisted exercises were continued with gradual progression to independent activities of daily living at 6 weeks. Clinical evaluations were performed before and after surgery by the operating surgeon or independent research nurse. Active forward flexion, passive external rotation, strength, and visual analog scale (VAS) pain scores were reviewed and recorded. Case-specific complications were also reviewed.

Preoperative and postoperative anteroposterior radiographs were evaluated by 2 independent observers (attending surgeon, junior resident). Per standard technique, each radiograph was positioned horizontal to the scapular plane. Of the 91 patients, 66 had preoperative shoulder radiographs of acceptable quality, with complete visualization of scapular morphology. Radiographs were reviewed to measure the scapular neck angle (SNA), inferior scapular notching, prosthesis–scapular neck angle (PSNA), and peg glenoid rim distance (PGRD) (Figure 1). For the 66 patients with acceptable preoperative radiographs, SNA was determined by subtracting preoperative SNA from postoperative PSNA. Postoperative anteroposterior radiographs were used to classify degree of inferior scapular notching based on the Nerot grading scale (0-4). In addition, glenosphere overhang and glenosphere inclination were measured on postoperative radiographs.

The 91 shoulders were sorted into 2 groups based on degree of scapular notching: group 1, Nerot grade 0 (no inferior notching) and grade 1, and group 2, Nerot grades 2, 3, and 4. Group 1 had 37 patients with a size 36 glenosphere, 3 patients with size 38, and 8 patients with size 42; group 2 had 34 patients with a size 36 glenosphere, 1 patient with size 38, and 8 patients with size 42. All measurements were normalized to account for differences in glenosphere size. Groups 1 and 2 were compared on each radiographic parameter (inferior scapular notching, PSNA, PGRD, SNA).

Notching indexes were calculated ([PSNA × 0.13] + PGRD) and compared with the suggested index of 35.⁸ Simovitch and colleagues⁸ demonstrated that a notching index of more than 35 had 91% sensitivity and 88% specificity in predicting inferior notching, whereas a notching index of 35 or less avoided inferior notching 91% of the time. In this study, notching index was calculated for each patient, and then the mean values of groups 1 and 2 were compared (Table 1).

The effect of scapular notching and other individual radiographic parameters on outcomes was also evaluated with respect to forward flexion, external rotation, VAS pain score, complications, and external rotation lag sign. Mann-Whitney U test was used to test these variables; Spearman rank test was performed to determine correlation between each variable and scapular notching; logistic regression was used to explore the relationship of variables (PGRD, PSNA) as predictors of Nerot degree of inferior scapular notching, and postoperative complications; and independent-samples t test was used to determine group differences for each variable. For each investigation, the level of significance was set at P < .05. A biostatistician performed all statistical analyses using SPSS Version 19 (IBM, Armonk, New York).

Results

Our study cohort consisted of 91 shoulders. Mean follow-up was 41.8 months (range, 24.0-80.8 months). Seventy-five (82%) of the 91 shoulders developed scapular notching. Mean (SD) SNA on preoperative radiographs, used to assess preoperative scapular morphology, was 103.9° (14.5°). For all 91 shoulders, mean (SD) PSNA was 125.6° (16°), and mean (SD) PGRD was 16 (5.4) mm (Table 1). Inclination measurements were available for 86 patients. Mean (SD) inclination from 90° was 2.5° (10.3°) (range, 21°-30°). Mean (SD) SNA (postoperative PSNA minus preoperative SNA) for the 66 patients with acceptable preoperative radiographs was 24.3° (21.3°) (Table 1). Forty-eight of the 91 shoulders were placed in scapular notching group 1 (16 grade-0 shoulders, 32 grade-1 shoulders); the other 43 shoulders were placed in group 2 (33 grade-2 shoulders, 9 grade-3 shoulders, 1 grade-4 shoulder). Mean follow-up was 40 months for group 1 and 43 months for group 2.

There were no significant differences between groups 1 and 2 in SNA (102.8° vs 105.4°; P = .3), PGRD (15.4 vs 16.8 mm; P = . 47), or PSNA (125.8° vs 125.4°; P = .82) (Table 1). In addition, groups 1 and 2 had no significant differences (P > .05) in glenoid overhang and glenosphere inclination (other possible factors influencing notching).

Mean (SD) notching index was 31.8 (4.4) for group 1 and 33.1 (7.2) for group 2. These values were not significantly different (P = .29) (Table 1, Figure 2).⁸ Each was below the recommended threshold of 35 for prevention of notching (Table 1, Figure 2).

To try to understand why mean scapular notching index was low for both groups, we examined the contributing factors individually. Our cohort’s mean PGRD of 16.1 mm (15.4 and 16.8 mm for groups 1 and 2, respectively) was significantly lower than the cohort mean reported by Simovitch and colleagues⁸ (Table 2). Given that PGRD is more strongly weighted in the originally described notching index ([PSNA × 0.13] + PGRD),⁸ it was the primary driver for our notching index results, even though on average our results demonstrated a PSNA higher than that found by Simovitch and colleagues⁸ (Table 2; Figures 3, 4). Analyzing PGRD and PSNA together, we found no relationship between these variables and increased severity of inferior notching (Figure 5).

Regarding the effects of notching severity on outcomes in our study cohort, there were no significant differences between groups 1 and 2 in postoperative function, including forward flexion (123° vs 112.4°; P = .11), external rotation (18.8° vs 16.7°; P = .76), positive lag sign (P = .2), and VAS pain scores (1.2 vs 2.1; P = .15). There were also no significant differences between groups in the rate of complications (P = .92). Regression analysis determined that PSNA, PGRD, glenosphere inclination, glenosphere overhang, and implant manufacturer were not significant predictors of complications.

Discussion

RSA has provided good pain relief and restored function in patients with irreparable rotator cuff disease associated with arthritis.^5,12,17,18 Scapular notching is a complex, multifactorial process. Nevertheless, surgeons remain cautious about the implications of inferior scapular notching, which is being reported by a significant number of patients. Our cohort’s high incidence of scapular notching (82%) in the early postoperative period clearly highlights the importance of predictive models, such as the notching index.⁸ Although concerns about consequences of notching have been expressed, notching severity did not affect outcomes or increase complications in this cohort.^{5,8,11,12,17-19}

We conducted this study to examine use of a predictive tool for scapular notching, the notching index, in a large cohort of patients who underwent primary RSA. This index combines 2 well-established factors that contribute to notching—craniocaudal position and PSNA—into a predictive formula based on statistical analyses performed in a prospective cohort study.^4,5,8,12,18 In their clinical study, Simovitch and colleagues⁸ found that both craniocaudal position and PSNA were tightly coupled with inferior scapular notching, and they developed a notching index that accounts for this relationship. We hypothesized that patients with a notching index of less than the recommended 35 would not develop notching and that patients with a notching index of more than 35 would have increased incidence and severity of notching. With our cohort, the recommended index of 35 was not an appropriate threshold predictive of notching. Furthermore, the 35 threshold applied to our cohort had 89% sensitivity and 21% specificity in predicting notching. Although the sensitivity is high, and correctly predicted true instances of notching, the low specificity compromises the precision of the notching formula ([PSNA × 0.13] + PGRD).

From the formula, it can be inferred that higher PSNA values can be compensated for by decreasing PGRD and inferiorizing the glenosphere. However, this recommendation appears limited based on increasing PSNA values, as in our cohort. The previously described notching formula cannot be universally applied to all patients treated with RSA because of the complexity of this relationship and patient-specific anatomy.

 We assessed other possible anatomical and surgical factors, specific to scapular morphology, that could contribute to scapular notching. In other studies, reaming that produced an inferior tilt of the glenoid increased the likelihood of inferior notching.^8,20,21 Furthermore, we expected less inferior glenoid overhang and smaller glenosphere would predispose patients to more notching.^8,12,19 In our cohort, notching grade was not correlated with inferior tilt, glenoid overhang, or glenosphere size, which may be attributed to minimal variability in glenosphere size and a small range of glenosphere overhang.

There were limitations to this study. We examined only 2 types of RSA systems, and they had very similar Grammont designs. Other RSA designs might not have similar shortcomings with respect to inferior notching. In addition, we examined patient cases at a single time point and did not evaluate the effect of notching over time.

Overall, our results suggest that PGRD and PSNA have little effect on development of higher grade notching, particularly with use of Grammont prostheses. With newer surgical techniques, the recommendation is for inferior craniocaudal placement of the glenosphere, but this may not prevent notching with some types of patient-specific scapular morphology. Clearer surgical guidelines and techniques may help delineate the contribution of each parameter causing inferior scapular notching. Surgeons must weigh the evidence to determine how to correct patient-specific glenoid pathology and orient the glenosphere. Recent studies on bony increased-offset reverse shoulder arthroplasty (bio-RSA) techniques or newer prosthetic designs that considerably alter PSNA and the center of rotation may prevent inferior notching and provide a promising alternative to Grammont designs. Ultimately, longer follow-up is also needed to understand the clinical relevance of increased scapular notching.

Reverse shoulder arthroplasty (RSA) is a treatment option for a spectrum of diseases in shoulders with rotator cuff deficiency. There are distinct morphologic changes in the scapular and glenoid anatomy in patients with chronic rotator cuff tears.¹ A muscular imbalance that occurs in the joint as a result of rotator cuff deficiency leads to morphologic changes that eliminate the compressive forces that hold the humeral head against the glenoid.² RSA effectively stabilizes the glenohumeral joint in shoulders with deficient rotator cuffs.^3,4 In early work, Grammont proposed that the glenosphere center of rotation should be medialized (concentric to the central axis of the metaglene or baseplate) and lowered.⁵ Although the medialized center of rotation in Grammont prostheses decreases shear forces and improves the deltoid lever arm, it also tends to result in mechanical impingement between the superomedial aspect of the humeral polyethylene insert and the scapular neck—so-called inferior scapular notching.^6-9

Notching, which has been reported in 50% to 96% of patients who receive a Delta III prosthesis, typically appears within the first few months after surgery but may be seen as late as 14 months after surgery.^5,10-12 Postmortem studies have shown that notching corresponds with erosion of the inferior pole of the glenoid and scapular neck, thought to be caused by the polyethylene cup of the implant.¹³ Although some studies have found that notching stabilizes after 1 year, others have shown notching progressing for up to 4 years after surgery.^11,12,14 The clinical relevance of notching continues to be controversial, but notching has been associated with poorer clinical outcomes, polyethylene wear, and local osteolysis. Component loosening has also been reported with notching of grade 3 or more.^8,10 Ultimately, there is concern that scapular notching could progress, ultimately leading to late glenoid loosening and potentially catastrophic failure.

Scapular anatomy has become an area of increased focus in rotator cuff disorders and in effects on RSA biomechanics.⁹ Recent reports have described important scapular morphology variations that suggest more individualized adjustments are needed during RSA.^9,15 In addition, some investigators have reported that development of notching appears to depend on the height and inclination of the implanted glenoid component, where an inferior position of the glenosphere leads to less impingement and better range of motion.^8,16 Simovitch and colleagues⁸ found the angle between the glenosphere and scapular neck and the craniocaudal position of the glenosphere to be highly correlated with inferior notching. They combined these 2 parameters into a predictive algorithm that provides a guideline (notching index, <35) for prevention of notching.

We conducted a study to evaluate the scapular notching index as a predictive tool and to consider other factors that may be associated with scapular notching occurring with use of Grammont reverse replacement systems. We hypothesized that patients with a notching index of less than 35 would not develop notching and that patients with an index of more than 35 would have increased incidence and severity of notching.

Materials and Methods

Patients treated with RSA for painful cuff tear arthropathy or irreparable rotator cuff tear with pseudoparesis (inability to actively elevate shoulder >90° in presence of free passive anterior elevation) were included in this retrospective review. All patients were treated between 2006 and 2010 by 1 of 2 established senior shoulder subspecialty surgeons. Patients treated with a Delta (DePuy Orthopaedics, Warsaw, Indiana) or an Aequalis (Tornier, Edina, Minnesota) reverse shoulder implant were included in the study. A standard polyethylene liner was used for all patients. These prostheses have the same neck shaft angle, 155º, as they have similar geometric designs, both based on the Grammont design—semiconstrained inverted with a fixed, lowered, medialized center of rotation. Standard instrumentation was used for all procedures. Patients were excluded if any nonstandard techniques or components were used (constrained or high-mobility liner, glenoid bone grafting). Patients who underwent revision for a previous reverse total arthroplasty, a total shoulder arthroplasty, or a hemiarthroplasty, or for treatment of acute fracture, posttraumatic deformity, or posttraumatic arthritis, were also excluded from our analyses. Minimum follow-up for study inclusion was 24 months.

All procedures were performed with the patient in the semi-beach-chair position and with use of a deltopectoral approach. The glenoid was prepared such that minimal reaming was needed to preserve the subchondral plate. The glenoid baseplate was positioned in the recommended inferior position to minimize notching and optimize functional outcomes.¹³ After surgery, all patients were managed with a simple soft immobilizer with or without a pillow with the arm at the patient’s side in internal rotation. Immediate passive mobilization was begun under the direction of physical therapists. Passive and active-assisted exercises were continued with gradual progression to independent activities of daily living at 6 weeks. Clinical evaluations were performed before and after surgery by the operating surgeon or independent research nurse. Active forward flexion, passive external rotation, strength, and visual analog scale (VAS) pain scores were reviewed and recorded. Case-specific complications were also reviewed.

Preoperative and postoperative anteroposterior radiographs were evaluated by 2 independent observers (attending surgeon, junior resident). Per standard technique, each radiograph was positioned horizontal to the scapular plane. Of the 91 patients, 66 had preoperative shoulder radiographs of acceptable quality, with complete visualization of scapular morphology. Radiographs were reviewed to measure the scapular neck angle (SNA), inferior scapular notching, prosthesis–scapular neck angle (PSNA), and peg glenoid rim distance (PGRD) (Figure 1). For the 66 patients with acceptable preoperative radiographs, SNA was determined by subtracting preoperative SNA from postoperative PSNA. Postoperative anteroposterior radiographs were used to classify degree of inferior scapular notching based on the Nerot grading scale (0-4). In addition, glenosphere overhang and glenosphere inclination were measured on postoperative radiographs.

The 91 shoulders were sorted into 2 groups based on degree of scapular notching: group 1, Nerot grade 0 (no inferior notching) and grade 1, and group 2, Nerot grades 2, 3, and 4. Group 1 had 37 patients with a size 36 glenosphere, 3 patients with size 38, and 8 patients with size 42; group 2 had 34 patients with a size 36 glenosphere, 1 patient with size 38, and 8 patients with size 42. All measurements were normalized to account for differences in glenosphere size. Groups 1 and 2 were compared on each radiographic parameter (inferior scapular notching, PSNA, PGRD, SNA).

Notching indexes were calculated ([PSNA × 0.13] + PGRD) and compared with the suggested index of 35.⁸ Simovitch and colleagues⁸ demonstrated that a notching index of more than 35 had 91% sensitivity and 88% specificity in predicting inferior notching, whereas a notching index of 35 or less avoided inferior notching 91% of the time. In this study, notching index was calculated for each patient, and then the mean values of groups 1 and 2 were compared (Table 1).

The effect of scapular notching and other individual radiographic parameters on outcomes was also evaluated with respect to forward flexion, external rotation, VAS pain score, complications, and external rotation lag sign. Mann-Whitney U test was used to test these variables; Spearman rank test was performed to determine correlation between each variable and scapular notching; logistic regression was used to explore the relationship of variables (PGRD, PSNA) as predictors of Nerot degree of inferior scapular notching, and postoperative complications; and independent-samples t test was used to determine group differences for each variable. For each investigation, the level of significance was set at P < .05. A biostatistician performed all statistical analyses using SPSS Version 19 (IBM, Armonk, New York).

Results

Our study cohort consisted of 91 shoulders. Mean follow-up was 41.8 months (range, 24.0-80.8 months). Seventy-five (82%) of the 91 shoulders developed scapular notching. Mean (SD) SNA on preoperative radiographs, used to assess preoperative scapular morphology, was 103.9° (14.5°). For all 91 shoulders, mean (SD) PSNA was 125.6° (16°), and mean (SD) PGRD was 16 (5.4) mm (Table 1). Inclination measurements were available for 86 patients. Mean (SD) inclination from 90° was 2.5° (10.3°) (range, 21°-30°). Mean (SD) SNA (postoperative PSNA minus preoperative SNA) for the 66 patients with acceptable preoperative radiographs was 24.3° (21.3°) (Table 1). Forty-eight of the 91 shoulders were placed in scapular notching group 1 (16 grade-0 shoulders, 32 grade-1 shoulders); the other 43 shoulders were placed in group 2 (33 grade-2 shoulders, 9 grade-3 shoulders, 1 grade-4 shoulder). Mean follow-up was 40 months for group 1 and 43 months for group 2.

There were no significant differences between groups 1 and 2 in SNA (102.8° vs 105.4°; P = .3), PGRD (15.4 vs 16.8 mm; P = . 47), or PSNA (125.8° vs 125.4°; P = .82) (Table 1). In addition, groups 1 and 2 had no significant differences (P > .05) in glenoid overhang and glenosphere inclination (other possible factors influencing notching).

Mean (SD) notching index was 31.8 (4.4) for group 1 and 33.1 (7.2) for group 2. These values were not significantly different (P = .29) (Table 1, Figure 2).⁸ Each was below the recommended threshold of 35 for prevention of notching (Table 1, Figure 2).

To try to understand why mean scapular notching index was low for both groups, we examined the contributing factors individually. Our cohort’s mean PGRD of 16.1 mm (15.4 and 16.8 mm for groups 1 and 2, respectively) was significantly lower than the cohort mean reported by Simovitch and colleagues⁸ (Table 2). Given that PGRD is more strongly weighted in the originally described notching index ([PSNA × 0.13] + PGRD),⁸ it was the primary driver for our notching index results, even though on average our results demonstrated a PSNA higher than that found by Simovitch and colleagues⁸ (Table 2; Figures 3, 4). Analyzing PGRD and PSNA together, we found no relationship between these variables and increased severity of inferior notching (Figure 5).

Regarding the effects of notching severity on outcomes in our study cohort, there were no significant differences between groups 1 and 2 in postoperative function, including forward flexion (123° vs 112.4°; P = .11), external rotation (18.8° vs 16.7°; P = .76), positive lag sign (P = .2), and VAS pain scores (1.2 vs 2.1; P = .15). There were also no significant differences between groups in the rate of complications (P = .92). Regression analysis determined that PSNA, PGRD, glenosphere inclination, glenosphere overhang, and implant manufacturer were not significant predictors of complications.

Discussion

RSA has provided good pain relief and restored function in patients with irreparable rotator cuff disease associated with arthritis.^5,12,17,18 Scapular notching is a complex, multifactorial process. Nevertheless, surgeons remain cautious about the implications of inferior scapular notching, which is being reported by a significant number of patients. Our cohort’s high incidence of scapular notching (82%) in the early postoperative period clearly highlights the importance of predictive models, such as the notching index.⁸ Although concerns about consequences of notching have been expressed, notching severity did not affect outcomes or increase complications in this cohort.^{5,8,11,12,17-19}

We conducted this study to examine use of a predictive tool for scapular notching, the notching index, in a large cohort of patients who underwent primary RSA. This index combines 2 well-established factors that contribute to notching—craniocaudal position and PSNA—into a predictive formula based on statistical analyses performed in a prospective cohort study.^4,5,8,12,18 In their clinical study, Simovitch and colleagues⁸ found that both craniocaudal position and PSNA were tightly coupled with inferior scapular notching, and they developed a notching index that accounts for this relationship. We hypothesized that patients with a notching index of less than the recommended 35 would not develop notching and that patients with a notching index of more than 35 would have increased incidence and severity of notching. With our cohort, the recommended index of 35 was not an appropriate threshold predictive of notching. Furthermore, the 35 threshold applied to our cohort had 89% sensitivity and 21% specificity in predicting notching. Although the sensitivity is high, and correctly predicted true instances of notching, the low specificity compromises the precision of the notching formula ([PSNA × 0.13] + PGRD).

From the formula, it can be inferred that higher PSNA values can be compensated for by decreasing PGRD and inferiorizing the glenosphere. However, this recommendation appears limited based on increasing PSNA values, as in our cohort. The previously described notching formula cannot be universally applied to all patients treated with RSA because of the complexity of this relationship and patient-specific anatomy.

 We assessed other possible anatomical and surgical factors, specific to scapular morphology, that could contribute to scapular notching. In other studies, reaming that produced an inferior tilt of the glenoid increased the likelihood of inferior notching.^8,20,21 Furthermore, we expected less inferior glenoid overhang and smaller glenosphere would predispose patients to more notching.^8,12,19 In our cohort, notching grade was not correlated with inferior tilt, glenoid overhang, or glenosphere size, which may be attributed to minimal variability in glenosphere size and a small range of glenosphere overhang.

There were limitations to this study. We examined only 2 types of RSA systems, and they had very similar Grammont designs. Other RSA designs might not have similar shortcomings with respect to inferior notching. In addition, we examined patient cases at a single time point and did not evaluate the effect of notching over time.

Overall, our results suggest that PGRD and PSNA have little effect on development of higher grade notching, particularly with use of Grammont prostheses. With newer surgical techniques, the recommendation is for inferior craniocaudal placement of the glenosphere, but this may not prevent notching with some types of patient-specific scapular morphology. Clearer surgical guidelines and techniques may help delineate the contribution of each parameter causing inferior scapular notching. Surgeons must weigh the evidence to determine how to correct patient-specific glenoid pathology and orient the glenosphere. Recent studies on bony increased-offset reverse shoulder arthroplasty (bio-RSA) techniques or newer prosthetic designs that considerably alter PSNA and the center of rotation may prevent inferior notching and provide a promising alternative to Grammont designs. Ultimately, longer follow-up is also needed to understand the clinical relevance of increased scapular notching.

Reverse shoulder arthroplasty (RSA) is a treatment option for a spectrum of diseases in shoulders with rotator cuff deficiency. There are distinct morphologic changes in the scapular and glenoid anatomy in patients with chronic rotator cuff tears.¹ A muscular imbalance that occurs in the joint as a result of rotator cuff deficiency leads to morphologic changes that eliminate the compressive forces that hold the humeral head against the glenoid.² RSA effectively stabilizes the glenohumeral joint in shoulders with deficient rotator cuffs.^3,4 In early work, Grammont proposed that the glenosphere center of rotation should be medialized (concentric to the central axis of the metaglene or baseplate) and lowered.⁵ Although the medialized center of rotation in Grammont prostheses decreases shear forces and improves the deltoid lever arm, it also tends to result in mechanical impingement between the superomedial aspect of the humeral polyethylene insert and the scapular neck—so-called inferior scapular notching.^6-9

Notching, which has been reported in 50% to 96% of patients who receive a Delta III prosthesis, typically appears within the first few months after surgery but may be seen as late as 14 months after surgery.^5,10-12 Postmortem studies have shown that notching corresponds with erosion of the inferior pole of the glenoid and scapular neck, thought to be caused by the polyethylene cup of the implant.¹³ Although some studies have found that notching stabilizes after 1 year, others have shown notching progressing for up to 4 years after surgery.^11,12,14 The clinical relevance of notching continues to be controversial, but notching has been associated with poorer clinical outcomes, polyethylene wear, and local osteolysis. Component loosening has also been reported with notching of grade 3 or more.^8,10 Ultimately, there is concern that scapular notching could progress, ultimately leading to late glenoid loosening and potentially catastrophic failure.

Scapular anatomy has become an area of increased focus in rotator cuff disorders and in effects on RSA biomechanics.⁹ Recent reports have described important scapular morphology variations that suggest more individualized adjustments are needed during RSA.^9,15 In addition, some investigators have reported that development of notching appears to depend on the height and inclination of the implanted glenoid component, where an inferior position of the glenosphere leads to less impingement and better range of motion.^8,16 Simovitch and colleagues⁸ found the angle between the glenosphere and scapular neck and the craniocaudal position of the glenosphere to be highly correlated with inferior notching. They combined these 2 parameters into a predictive algorithm that provides a guideline (notching index, <35) for prevention of notching.

We conducted a study to evaluate the scapular notching index as a predictive tool and to consider other factors that may be associated with scapular notching occurring with use of Grammont reverse replacement systems. We hypothesized that patients with a notching index of less than 35 would not develop notching and that patients with an index of more than 35 would have increased incidence and severity of notching.

Materials and Methods

Patients treated with RSA for painful cuff tear arthropathy or irreparable rotator cuff tear with pseudoparesis (inability to actively elevate shoulder >90° in presence of free passive anterior elevation) were included in this retrospective review. All patients were treated between 2006 and 2010 by 1 of 2 established senior shoulder subspecialty surgeons. Patients treated with a Delta (DePuy Orthopaedics, Warsaw, Indiana) or an Aequalis (Tornier, Edina, Minnesota) reverse shoulder implant were included in the study. A standard polyethylene liner was used for all patients. These prostheses have the same neck shaft angle, 155º, as they have similar geometric designs, both based on the Grammont design—semiconstrained inverted with a fixed, lowered, medialized center of rotation. Standard instrumentation was used for all procedures. Patients were excluded if any nonstandard techniques or components were used (constrained or high-mobility liner, glenoid bone grafting). Patients who underwent revision for a previous reverse total arthroplasty, a total shoulder arthroplasty, or a hemiarthroplasty, or for treatment of acute fracture, posttraumatic deformity, or posttraumatic arthritis, were also excluded from our analyses. Minimum follow-up for study inclusion was 24 months.

All procedures were performed with the patient in the semi-beach-chair position and with use of a deltopectoral approach. The glenoid was prepared such that minimal reaming was needed to preserve the subchondral plate. The glenoid baseplate was positioned in the recommended inferior position to minimize notching and optimize functional outcomes.¹³ After surgery, all patients were managed with a simple soft immobilizer with or without a pillow with the arm at the patient’s side in internal rotation. Immediate passive mobilization was begun under the direction of physical therapists. Passive and active-assisted exercises were continued with gradual progression to independent activities of daily living at 6 weeks. Clinical evaluations were performed before and after surgery by the operating surgeon or independent research nurse. Active forward flexion, passive external rotation, strength, and visual analog scale (VAS) pain scores were reviewed and recorded. Case-specific complications were also reviewed.

Preoperative and postoperative anteroposterior radiographs were evaluated by 2 independent observers (attending surgeon, junior resident). Per standard technique, each radiograph was positioned horizontal to the scapular plane. Of the 91 patients, 66 had preoperative shoulder radiographs of acceptable quality, with complete visualization of scapular morphology. Radiographs were reviewed to measure the scapular neck angle (SNA), inferior scapular notching, prosthesis–scapular neck angle (PSNA), and peg glenoid rim distance (PGRD) (Figure 1). For the 66 patients with acceptable preoperative radiographs, SNA was determined by subtracting preoperative SNA from postoperative PSNA. Postoperative anteroposterior radiographs were used to classify degree of inferior scapular notching based on the Nerot grading scale (0-4). In addition, glenosphere overhang and glenosphere inclination were measured on postoperative radiographs.

The 91 shoulders were sorted into 2 groups based on degree of scapular notching: group 1, Nerot grade 0 (no inferior notching) and grade 1, and group 2, Nerot grades 2, 3, and 4. Group 1 had 37 patients with a size 36 glenosphere, 3 patients with size 38, and 8 patients with size 42; group 2 had 34 patients with a size 36 glenosphere, 1 patient with size 38, and 8 patients with size 42. All measurements were normalized to account for differences in glenosphere size. Groups 1 and 2 were compared on each radiographic parameter (inferior scapular notching, PSNA, PGRD, SNA).

Notching indexes were calculated ([PSNA × 0.13] + PGRD) and compared with the suggested index of 35.⁸ Simovitch and colleagues⁸ demonstrated that a notching index of more than 35 had 91% sensitivity and 88% specificity in predicting inferior notching, whereas a notching index of 35 or less avoided inferior notching 91% of the time. In this study, notching index was calculated for each patient, and then the mean values of groups 1 and 2 were compared (Table 1).

The effect of scapular notching and other individual radiographic parameters on outcomes was also evaluated with respect to forward flexion, external rotation, VAS pain score, complications, and external rotation lag sign. Mann-Whitney U test was used to test these variables; Spearman rank test was performed to determine correlation between each variable and scapular notching; logistic regression was used to explore the relationship of variables (PGRD, PSNA) as predictors of Nerot degree of inferior scapular notching, and postoperative complications; and independent-samples t test was used to determine group differences for each variable. For each investigation, the level of significance was set at P < .05. A biostatistician performed all statistical analyses using SPSS Version 19 (IBM, Armonk, New York).

Results

Our study cohort consisted of 91 shoulders. Mean follow-up was 41.8 months (range, 24.0-80.8 months). Seventy-five (82%) of the 91 shoulders developed scapular notching. Mean (SD) SNA on preoperative radiographs, used to assess preoperative scapular morphology, was 103.9° (14.5°). For all 91 shoulders, mean (SD) PSNA was 125.6° (16°), and mean (SD) PGRD was 16 (5.4) mm (Table 1). Inclination measurements were available for 86 patients. Mean (SD) inclination from 90° was 2.5° (10.3°) (range, 21°-30°). Mean (SD) SNA (postoperative PSNA minus preoperative SNA) for the 66 patients with acceptable preoperative radiographs was 24.3° (21.3°) (Table 1). Forty-eight of the 91 shoulders were placed in scapular notching group 1 (16 grade-0 shoulders, 32 grade-1 shoulders); the other 43 shoulders were placed in group 2 (33 grade-2 shoulders, 9 grade-3 shoulders, 1 grade-4 shoulder). Mean follow-up was 40 months for group 1 and 43 months for group 2.

There were no significant differences between groups 1 and 2 in SNA (102.8° vs 105.4°; P = .3), PGRD (15.4 vs 16.8 mm; P = . 47), or PSNA (125.8° vs 125.4°; P = .82) (Table 1). In addition, groups 1 and 2 had no significant differences (P > .05) in glenoid overhang and glenosphere inclination (other possible factors influencing notching).

Mean (SD) notching index was 31.8 (4.4) for group 1 and 33.1 (7.2) for group 2. These values were not significantly different (P = .29) (Table 1, Figure 2).⁸ Each was below the recommended threshold of 35 for prevention of notching (Table 1, Figure 2).

To try to understand why mean scapular notching index was low for both groups, we examined the contributing factors individually. Our cohort’s mean PGRD of 16.1 mm (15.4 and 16.8 mm for groups 1 and 2, respectively) was significantly lower than the cohort mean reported by Simovitch and colleagues⁸ (Table 2). Given that PGRD is more strongly weighted in the originally described notching index ([PSNA × 0.13] + PGRD),⁸ it was the primary driver for our notching index results, even though on average our results demonstrated a PSNA higher than that found by Simovitch and colleagues⁸ (Table 2; Figures 3, 4). Analyzing PGRD and PSNA together, we found no relationship between these variables and increased severity of inferior notching (Figure 5).

Regarding the effects of notching severity on outcomes in our study cohort, there were no significant differences between groups 1 and 2 in postoperative function, including forward flexion (123° vs 112.4°; P = .11), external rotation (18.8° vs 16.7°; P = .76), positive lag sign (P = .2), and VAS pain scores (1.2 vs 2.1; P = .15). There were also no significant differences between groups in the rate of complications (P = .92). Regression analysis determined that PSNA, PGRD, glenosphere inclination, glenosphere overhang, and implant manufacturer were not significant predictors of complications.

Discussion

RSA has provided good pain relief and restored function in patients with irreparable rotator cuff disease associated with arthritis.^5,12,17,18 Scapular notching is a complex, multifactorial process. Nevertheless, surgeons remain cautious about the implications of inferior scapular notching, which is being reported by a significant number of patients. Our cohort’s high incidence of scapular notching (82%) in the early postoperative period clearly highlights the importance of predictive models, such as the notching index.⁸ Although concerns about consequences of notching have been expressed, notching severity did not affect outcomes or increase complications in this cohort.^{5,8,11,12,17-19}

We conducted this study to examine use of a predictive tool for scapular notching, the notching index, in a large cohort of patients who underwent primary RSA. This index combines 2 well-established factors that contribute to notching—craniocaudal position and PSNA—into a predictive formula based on statistical analyses performed in a prospective cohort study.^4,5,8,12,18 In their clinical study, Simovitch and colleagues⁸ found that both craniocaudal position and PSNA were tightly coupled with inferior scapular notching, and they developed a notching index that accounts for this relationship. We hypothesized that patients with a notching index of less than the recommended 35 would not develop notching and that patients with a notching index of more than 35 would have increased incidence and severity of notching. With our cohort, the recommended index of 35 was not an appropriate threshold predictive of notching. Furthermore, the 35 threshold applied to our cohort had 89% sensitivity and 21% specificity in predicting notching. Although the sensitivity is high, and correctly predicted true instances of notching, the low specificity compromises the precision of the notching formula ([PSNA × 0.13] + PGRD).

From the formula, it can be inferred that higher PSNA values can be compensated for by decreasing PGRD and inferiorizing the glenosphere. However, this recommendation appears limited based on increasing PSNA values, as in our cohort. The previously described notching formula cannot be universally applied to all patients treated with RSA because of the complexity of this relationship and patient-specific anatomy.

 We assessed other possible anatomical and surgical factors, specific to scapular morphology, that could contribute to scapular notching. In other studies, reaming that produced an inferior tilt of the glenoid increased the likelihood of inferior notching.^8,20,21 Furthermore, we expected less inferior glenoid overhang and smaller glenosphere would predispose patients to more notching.^8,12,19 In our cohort, notching grade was not correlated with inferior tilt, glenoid overhang, or glenosphere size, which may be attributed to minimal variability in glenosphere size and a small range of glenosphere overhang.

There were limitations to this study. We examined only 2 types of RSA systems, and they had very similar Grammont designs. Other RSA designs might not have similar shortcomings with respect to inferior notching. In addition, we examined patient cases at a single time point and did not evaluate the effect of notching over time.

Overall, our results suggest that PGRD and PSNA have little effect on development of higher grade notching, particularly with use of Grammont prostheses. With newer surgical techniques, the recommendation is for inferior craniocaudal placement of the glenosphere, but this may not prevent notching with some types of patient-specific scapular morphology. Clearer surgical guidelines and techniques may help delineate the contribution of each parameter causing inferior scapular notching. Surgeons must weigh the evidence to determine how to correct patient-specific glenoid pathology and orient the glenosphere. Recent studies on bony increased-offset reverse shoulder arthroplasty (bio-RSA) techniques or newer prosthetic designs that considerably alter PSNA and the center of rotation may prevent inferior notching and provide a promising alternative to Grammont designs. Ultimately, longer follow-up is also needed to understand the clinical relevance of increased scapular notching.

The incidence of shoulder arthroplasty in the United States is increasing annually,^1-3 and the majority of these operations occur in older patients.^4-6 Elderly patients with cardiovascular, pulmonary, cerebral, renal, and hepatic disease are increasingly susceptible to numerous surgical complications.⁴ Myocardial infarction (MI) is a complication that occurs in 0.7% of noncardiac surgeries. This figure increases to 1.1% in patients with coronary artery disease.^7-11 Perioperative MI increases morbidity and mortality,⁸ and perioperative cardiac morbidity is the leading cause of death after anesthesia and surgery.¹² The financial effects of perioperative cardiac morbidity and mortality must also be considered. A 2009 claims analysis study estimated charges associated with a perioperative MI at $15,000 and the cost of cardiac death at $21,909.¹³

Cardiovascular complications are associated with a significant degree of morbidity and mortality in patients who undergo arthroplasty.^14-16 Although studies have elucidated 30- and 90-day morbidity and mortality rates after shoulder arthroplasty, in hip and knee arthroplasty^17-19 little has been done to determine predictors of perioperative MI in a representative database of patients. Given the increasing incidence of shoulder arthroplasty in the United States, the elective nature of this procedure, and the percentage of the US population with cardiovascular risk factors,²⁰ it is important to establish predictors of perioperative MI to ensure patients and physicians have the necessary resources to make informed decisions.

We conducted a study to examine the risk factors for perioperative MI in a large cohort of patients admitted for shoulder arthroplasty to US hospitals. We wanted to evaluate the association between perioperative MI and shoulder arthroplasty with respect to demographics, primary diagnosis, medical comorbidities, and perioperative complications. Specifically, we tested the null hypothesis that, among patients undergoing shoulder arthroplasty, and accounting for confounding variables, there would be no difference in risk factors for patients who have a perioperative MI.

Materials and Methods

This study was exempt from approval by our institutional review board. All data used in this project were deidentified before use.

Nationwide Inpatient Sample (NIS)

The Nationwide Inpatient Sample (NIS), an annual survey of hospitals, is conducted by the Healthcare Cost and Utilization Project (HCUP) and sponsored by the Agency for Healthcare Research and Quality (AHRQ). This database is the largest publicly available all-payer inpatient discharge database in the United States.²¹ Sampling 8 million hospital stays each year, NIS includes information from a representative batch of 20% of US hospitals. In 2011, 46 states and 1045 hospitals contributed information to the database, representing 97% of the US population.²² This large sample allows researchers to analyze a robust set of medical conditions and uncommon treatments. The survey, conducted each year since 1988, includes demographic, clinical, and resource use data.²³ Discharge weight files are provided by NIS to arrive at valid national estimates.

This database is particularly useful because it provides information on up to 25 medical diagnoses and 15 procedures, which are recorded with International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes. Researchers can use this database to analyze patient and hospital characteristics as well as inpatient outcomes.^24,25 Numerous studies have used NIS to address pertinent queries across the medical landscape.^22,26

Patient Selection and Analysis

We used NIS to isolate a population of 422,371 adults (≥18 years old) who underwent total shoulder arthroplasty (TSA) or hemi–shoulder arthroplasty (HSA) between January 1, 2002 and December 31, 2011. We then placed the patients in this population into 1 of 2 cohorts. The first cohort had an acute MI during the perioperative period after TSA, and the second, larger cohort did not have an acute MI after TSA. Acute MI was identified using ICD-9-CM code 410.xx. To identify a population of shoulder arthroplasty patients, we included discharges with an ICD-9-CM procedure code of 81.80 or 81.88 (both TSA) or 81.81 (HSA) in the sample. We then considered the degree to which each of 5 variables—primary diagnosis, age, sex, race, and select medical comorbidities—was predictive of in-hospital MI after TSA.

Statistical Analysis

Given the large sample used in this study, normal distribution of data was assumed. Using bivariate analysis, Pearson χ² test for categorical data, and independent-samples t test for continuous data, we compared the nonacute MI and acute MI groups. Multivariable binary logistic regression analyses allowed us to isolate the extent that primary diagnosis, age, sex, race, and medical comorbidities were predictors of acute MI after shoulder arthroplasty. Statistical significance was set at P < .05. SPSS Version 22.0 (SPSS, Chicago, Illinois) was used for all statistical analyses and data modeling.

Results

Between January 1, 2002 and December 31, 2011, an estimated total of 422,371 patients underwent shoulder arthroplasty (59.3% TSA, 40.7% HSA). Of these patients, 1174 (0.28%) had a perioperative MI, and 421,197 (99.72%) did not (Table 1). Patients with a primary diagnosis of proximal humerus fracture (33.8% vs 16.6%; P < .001) or rotator cuff arthropathy (10.1% vs 9.9%; P < .001) were more likely than patients with other diagnoses to have an in-hospital MI.

Our review of the demographics found that patients who underwent shoulder arthroplasty and had a perioperative MI were likely older (75±8.9 years vs 69±11 years; P < .001), Caucasian (94.2% vs 91.9%; P = .002), male (43.2% vs 39.7%; P = .013), in the highest median household income bracket of $63,000 or more (30.8% vs 25.6%; P < .001), and using Medicare (80.9% vs 66.3%; P < .001). They were more likely to be treated in a medical center of medium size (25.6% vs 23.7%; P = .042) or larger (61.8% vs 61.2%; P = .042). MIs occurred more often in urban environments (91.4% vs 88.5%; P = .002) and in HSA patients (55% vs 40.6%; P < .001), resulting in longer hospital  stays (9.4±7.9 days vs 2.7±2.5 days; P < .001) and higher probability of death (6.5% vs 0.1%; P < .001).

We then analyzed the 2 cohorts for medical comorbidities (Table 2). Patients in the MI cohort presented with a significantly higher incidence of congestive heart failure, previous MI, angina pectoris, chronic lung disease, hypertension, diabetes, renal failure, fluid and electrolyte disorders, pulmonary circulatory disease, coagulopathy, and deficiency anemia (P < .001) but not liver disease and obesity. Bivariate analysis of perioperative outcomes (Table 3) indicated that these patients also had a statistically higher rate of numerous other complications: pulmonary embolism (4.9% vs 0.2%; P < .001), pneumonia (15.1% vs 1.2%; P < .001), deep venous thrombosis (2.6% vs 0.2%; P < .001), cerebrovascular event (1.6% vs 0.1%; P < .001), acute renal failure (15.1% vs 1.2%; P < .001), gastrointestinal complication (1.2% vs 0.3%; P < .001), mechanical ventilation (1.2% vs 0.3%; P < .001), transfusion (33.4% vs 8.8%; P < .001), and nonroutine discharge (73.3% vs 36.0%; P < .001).

Multivariable logistic regression analysis was performed to determine independent predictors of perioperative MI after shoulder arthroplasty (Table 4). Patients with a primary diagnosis of proximal humerus fracture (odds ratio [OR], 1.38; 95% confidence interval [CI], 1.15-1.65; P < .001) were more likely than patients with a primary diagnosis of osteoarthritis to have an MI. The odds of postoperative MI increased with age (OR, 1.04 per year; 95% CI, 1.03-1.05; P < .001) and were higher in males (OR, 1.72; 95% CI, 1.52-1.96; P < .001). Compared with Caucasians, African Americans (OR, 0.19; 95% CI, 0.09-0.40; P < .001) were less likely to have an in-hospital MI after shoulder arthroplasty. After shoulder arthroplasty, the odds of MI in the perioperative period increased with each subsequent day of care (OR, 1.10; 95% CI, 1.10-1.11; P < .001).

Regarding independent comorbidities, multivariable logistic regression analysis also determined that history of congestive heart failure (OR, 4.86; 95% CI, 4.20-5.61; P < .001), angina pectoris (OR, 2.90; 95% CI, 2.02-4.17; P < .001), complicated diabetes (OR, 1.96; 95% CI, 1.49-2.57; P < .001), renal failure (OR, 1.42; 95% CI, 1.17-1.72; P < .001), fluid and electrolyte disorders (OR, 1.42; 95% CI, 1.21-1.67; P < .001), and deficiency anemia (OR, 1.62; 95% CI, 1.40-1.88; P < .001) were significant predictors of perioperative MI after shoulder arthroplasty.

Discussion

Results of other studies have elucidated 30- and 90-day mortality rates and postoperative complications after shoulder arthroplasty, but, relative to hip and knee arthroplasty,^17-19 little has been done to determine predictors of perioperative MI in a large sample of shoulder arthroplasty patients. Given the increasing rates of shoulder arthroplasty^1-3 and the demographics of this population,^4-6 it is likely that postoperative cardiovascular events will increase in frequency. We found that, in order of decreasing significance, the top 4 risk predictors for acute MI after shoulder arthroplasty were congestive heart failure, angina pectoralis, complicated diabetes mellitus, and male sex. Other pertinent risk factors included older age, Caucasian ethnicity, and a primary diagnosis of proximal humerus fracture. The rate of acute MI in patients who were older than 75 years when they underwent HSA for proximal humerus fracture was 0.80%.

Demographics

We found that patients who had an acute MI after shoulder arthroplasty were likely older, male, and Caucasian. Age and male sex are well-established risk factors for increased cardiac complications after arthroplasty.^27-29 Previous studies have indicated that the rate of cardiac events increases in arthroplasty patients older than 65 years.^19,28,29 In our study, more than 50% of the patients who had an acute perioperative MI were older than 85 years. Less explainable is the increased occurrence of acute MI in Caucasian patients and wealthy patients, given that minorities in the United States have higher rates of cardiovascular disease.³⁰ Shoulder arthroplasty is an elective procedure, more likely to be undertaken by Caucasians. Therefore, at-risk minority groups and financially challenged groups may be less likely to have this procedure.

Primary Diagnosis

In this series, patients with a primary diagnosis of proximal humerus fracture were more likely to have an in-hospital MI. This finding is consistent with previous studies indicating a higher rate of complications for proximal humerus fracture patients than for shoulder arthroplasty patients.^31,32 Given that more than 75% of patients who present with a proximal humerus fracture are older than 70 years, it would be prudent to examine operative indications after this diagnosis,³³ particularly as benefit from surgery for fractures has not been definitively demonstrated.^34-37

Comorbidities

Many of the patients in our MI cohort presented with congestive heart failure, angina pectoris, complicated diabetes, renal failure, fluid and electrolyte disorders, or deficiency anemia. This is in keeping with other studies indicating that preexisting cardiovascular morbidity increases the rate of MI after various forms of arthroplasty.^7-11 Patients in our MI cohort were also susceptible to a variety of post-MI perioperative complications, including pulmonary embolism, pneumonia, deep venous thrombosis, cerebrovascular event, acute renal failure, gastrointestinal complication, mechanical ventilation, transfusion, and nonroutine discharge, and their incidence of death was higher. These findings are consistent with reports that postoperative cardiovascular complications increase the degree of morbidity and mortality in arthroplasty patients.^14-16 It is also worth noting that the odds of MI in the perioperative period increase with each subsequent day of care. This is understandable given that patients presenting with numerous comorbidities are at increased risk for perioperative complications³⁸ resulting in hospital readmission.³⁹

The literature indicates that MI occurs as a complication in 0.7% of patients who undergo noncardiac surgery,⁷ though some series have shown it is more prevalent after arthroplasty procedures.^28,40 MI significantly increases the rate of perioperative morbidity and mortality,⁸ and perioperative cardiac morbidity is a leading cause of death after anesthesia and surgery.¹² Furthermore, the most common cause of death after lower extremity arthroplasty is cardiovascular-related.^41,42 In patients who presented for elective hip arthroplasty, cardiorespiratory disease was one of the main risk factors (with older age and male sex) shown to increase perioperative mortality.⁴³

Perioperative cardiovascular complications increase postoperative morbidity and mortality.¹² The rate of cardiovascular complications after shoulder arthroplasty ranges from 0.8% to 2.6%, and the incidence of MI hovers between 0.3% and 0.9%.^{17,19,28,40,44} A recent study in 793 patients found that, over a 30-day period, cardiovascular complications accounted for more than one-fourth of all complications.¹⁷ Singh and colleagues¹⁹ analyzed cardiopulmonary complications after primary shoulder arthroplasty in a total of 3480 patients (4019 arthroplasties) and found this group had a 90-day cardiac morbidity (MI, congestive heart failure, arrhythmia) rate of 2.6%. In that study, a Deyo-Charlson index of 1 or more was a significant independent risk factor for cardiac complications following surgery. Scores on this weighted index of 17 comorbidities are used to assess the complexities of a patient population. Given the severity of cardiovascular perioperative complications, it is important to preoperatively identify high-risk population groups and sufficiently study and optimize patients before shoulder arthroplasty.

There is much debate about the effectiveness of perioperative β-blockers in reducing perioperative cardiac morbidity and mortality.^45-48 Such a discussion is outside of the scope of this article, but it may be prudent to seek a cardiology consultation for patients presenting with risk factors for perioperative MI. β-Blockers may prove useful in reducing cardiac morbidity in high-risk patients after noncardiac surgery.^45,49

Many limitations are inherent in studies that use a nationally represented database such as NIS, which we used in this study. It is highly likely that NIS does not capture all potential postoperative complications, as this database is very large and subject to errors in data entry and clinical coding. In addition, detailed clinical information (eg, severity of certain comorbid diseases before shoulder arthroplasty, details about the intraoperative course) was not readily available for analysis. Another limitation, which may have led to an underestimate of complication rates, was our not being able to obtain information about postdischarge complications.

Despite these limitations, NIS and other databases have helped researchers answer questions about low-incidence conditions and generalize findings to a national population. In the present study, we analyzed 2 cohorts, patients with and without acute MI after shoulder arthroplasty, to determine predictors for and complications of postarthroplasty MI. We identified numerous predictors for acute MI: congestive heart failure, angina pectoris, complicated diabetes, renal failure, fluid and electrolyte disorders, and deficiency anemia prior to arthroplasty. As perioperative MI is associated with significant morbidity,^14-16 it would be wise to screen patients for such comorbid conditions, assess the severity of these conditions, and offer shoulder arthroplasty with prudence.

Conclusion

The top 4 predictors for acute MI after shoulder arthroplasty were congestive heart failure, angina pectoralis, complicated diabetes mellitus, and male sex. Other pertinent risk factors included older age, Caucasian ethnicity, and primary diagnosis of proximal humerus fracture. Surgeons and patients must be aware of predictors for adverse surgical outcomes such as perioperative MI and understand the extent to which these events increase perioperative morbidity and mortality.

The incidence of shoulder arthroplasty in the United States is increasing annually,^1-3 and the majority of these operations occur in older patients.^4-6 Elderly patients with cardiovascular, pulmonary, cerebral, renal, and hepatic disease are increasingly susceptible to numerous surgical complications.⁴ Myocardial infarction (MI) is a complication that occurs in 0.7% of noncardiac surgeries. This figure increases to 1.1% in patients with coronary artery disease.^7-11 Perioperative MI increases morbidity and mortality,⁸ and perioperative cardiac morbidity is the leading cause of death after anesthesia and surgery.¹² The financial effects of perioperative cardiac morbidity and mortality must also be considered. A 2009 claims analysis study estimated charges associated with a perioperative MI at $15,000 and the cost of cardiac death at $21,909.¹³

Cardiovascular complications are associated with a significant degree of morbidity and mortality in patients who undergo arthroplasty.^14-16 Although studies have elucidated 30- and 90-day morbidity and mortality rates after shoulder arthroplasty, in hip and knee arthroplasty^17-19 little has been done to determine predictors of perioperative MI in a representative database of patients. Given the increasing incidence of shoulder arthroplasty in the United States, the elective nature of this procedure, and the percentage of the US population with cardiovascular risk factors,²⁰ it is important to establish predictors of perioperative MI to ensure patients and physicians have the necessary resources to make informed decisions.

We conducted a study to examine the risk factors for perioperative MI in a large cohort of patients admitted for shoulder arthroplasty to US hospitals. We wanted to evaluate the association between perioperative MI and shoulder arthroplasty with respect to demographics, primary diagnosis, medical comorbidities, and perioperative complications. Specifically, we tested the null hypothesis that, among patients undergoing shoulder arthroplasty, and accounting for confounding variables, there would be no difference in risk factors for patients who have a perioperative MI.

Materials and Methods

This study was exempt from approval by our institutional review board. All data used in this project were deidentified before use.

Nationwide Inpatient Sample (NIS)

The Nationwide Inpatient Sample (NIS), an annual survey of hospitals, is conducted by the Healthcare Cost and Utilization Project (HCUP) and sponsored by the Agency for Healthcare Research and Quality (AHRQ). This database is the largest publicly available all-payer inpatient discharge database in the United States.²¹ Sampling 8 million hospital stays each year, NIS includes information from a representative batch of 20% of US hospitals. In 2011, 46 states and 1045 hospitals contributed information to the database, representing 97% of the US population.²² This large sample allows researchers to analyze a robust set of medical conditions and uncommon treatments. The survey, conducted each year since 1988, includes demographic, clinical, and resource use data.²³ Discharge weight files are provided by NIS to arrive at valid national estimates.

This database is particularly useful because it provides information on up to 25 medical diagnoses and 15 procedures, which are recorded with International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes. Researchers can use this database to analyze patient and hospital characteristics as well as inpatient outcomes.^24,25 Numerous studies have used NIS to address pertinent queries across the medical landscape.^22,26

Patient Selection and Analysis

We used NIS to isolate a population of 422,371 adults (≥18 years old) who underwent total shoulder arthroplasty (TSA) or hemi–shoulder arthroplasty (HSA) between January 1, 2002 and December 31, 2011. We then placed the patients in this population into 1 of 2 cohorts. The first cohort had an acute MI during the perioperative period after TSA, and the second, larger cohort did not have an acute MI after TSA. Acute MI was identified using ICD-9-CM code 410.xx. To identify a population of shoulder arthroplasty patients, we included discharges with an ICD-9-CM procedure code of 81.80 or 81.88 (both TSA) or 81.81 (HSA) in the sample. We then considered the degree to which each of 5 variables—primary diagnosis, age, sex, race, and select medical comorbidities—was predictive of in-hospital MI after TSA.

Statistical Analysis

Given the large sample used in this study, normal distribution of data was assumed. Using bivariate analysis, Pearson χ² test for categorical data, and independent-samples t test for continuous data, we compared the nonacute MI and acute MI groups. Multivariable binary logistic regression analyses allowed us to isolate the extent that primary diagnosis, age, sex, race, and medical comorbidities were predictors of acute MI after shoulder arthroplasty. Statistical significance was set at P < .05. SPSS Version 22.0 (SPSS, Chicago, Illinois) was used for all statistical analyses and data modeling.

Results

Between January 1, 2002 and December 31, 2011, an estimated total of 422,371 patients underwent shoulder arthroplasty (59.3% TSA, 40.7% HSA). Of these patients, 1174 (0.28%) had a perioperative MI, and 421,197 (99.72%) did not (Table 1). Patients with a primary diagnosis of proximal humerus fracture (33.8% vs 16.6%; P < .001) or rotator cuff arthropathy (10.1% vs 9.9%; P < .001) were more likely than patients with other diagnoses to have an in-hospital MI.

Our review of the demographics found that patients who underwent shoulder arthroplasty and had a perioperative MI were likely older (75±8.9 years vs 69±11 years; P < .001), Caucasian (94.2% vs 91.9%; P = .002), male (43.2% vs 39.7%; P = .013), in the highest median household income bracket of $63,000 or more (30.8% vs 25.6%; P < .001), and using Medicare (80.9% vs 66.3%; P < .001). They were more likely to be treated in a medical center of medium size (25.6% vs 23.7%; P = .042) or larger (61.8% vs 61.2%; P = .042). MIs occurred more often in urban environments (91.4% vs 88.5%; P = .002) and in HSA patients (55% vs 40.6%; P < .001), resulting in longer hospital  stays (9.4±7.9 days vs 2.7±2.5 days; P < .001) and higher probability of death (6.5% vs 0.1%; P < .001).

We then analyzed the 2 cohorts for medical comorbidities (Table 2). Patients in the MI cohort presented with a significantly higher incidence of congestive heart failure, previous MI, angina pectoris, chronic lung disease, hypertension, diabetes, renal failure, fluid and electrolyte disorders, pulmonary circulatory disease, coagulopathy, and deficiency anemia (P < .001) but not liver disease and obesity. Bivariate analysis of perioperative outcomes (Table 3) indicated that these patients also had a statistically higher rate of numerous other complications: pulmonary embolism (4.9% vs 0.2%; P < .001), pneumonia (15.1% vs 1.2%; P < .001), deep venous thrombosis (2.6% vs 0.2%; P < .001), cerebrovascular event (1.6% vs 0.1%; P < .001), acute renal failure (15.1% vs 1.2%; P < .001), gastrointestinal complication (1.2% vs 0.3%; P < .001), mechanical ventilation (1.2% vs 0.3%; P < .001), transfusion (33.4% vs 8.8%; P < .001), and nonroutine discharge (73.3% vs 36.0%; P < .001).

Multivariable logistic regression analysis was performed to determine independent predictors of perioperative MI after shoulder arthroplasty (Table 4). Patients with a primary diagnosis of proximal humerus fracture (odds ratio [OR], 1.38; 95% confidence interval [CI], 1.15-1.65; P < .001) were more likely than patients with a primary diagnosis of osteoarthritis to have an MI. The odds of postoperative MI increased with age (OR, 1.04 per year; 95% CI, 1.03-1.05; P < .001) and were higher in males (OR, 1.72; 95% CI, 1.52-1.96; P < .001). Compared with Caucasians, African Americans (OR, 0.19; 95% CI, 0.09-0.40; P < .001) were less likely to have an in-hospital MI after shoulder arthroplasty. After shoulder arthroplasty, the odds of MI in the perioperative period increased with each subsequent day of care (OR, 1.10; 95% CI, 1.10-1.11; P < .001).

Regarding independent comorbidities, multivariable logistic regression analysis also determined that history of congestive heart failure (OR, 4.86; 95% CI, 4.20-5.61; P < .001), angina pectoris (OR, 2.90; 95% CI, 2.02-4.17; P < .001), complicated diabetes (OR, 1.96; 95% CI, 1.49-2.57; P < .001), renal failure (OR, 1.42; 95% CI, 1.17-1.72; P < .001), fluid and electrolyte disorders (OR, 1.42; 95% CI, 1.21-1.67; P < .001), and deficiency anemia (OR, 1.62; 95% CI, 1.40-1.88; P < .001) were significant predictors of perioperative MI after shoulder arthroplasty.

Discussion

Results of other studies have elucidated 30- and 90-day mortality rates and postoperative complications after shoulder arthroplasty, but, relative to hip and knee arthroplasty,^17-19 little has been done to determine predictors of perioperative MI in a large sample of shoulder arthroplasty patients. Given the increasing rates of shoulder arthroplasty^1-3 and the demographics of this population,^4-6 it is likely that postoperative cardiovascular events will increase in frequency. We found that, in order of decreasing significance, the top 4 risk predictors for acute MI after shoulder arthroplasty were congestive heart failure, angina pectoralis, complicated diabetes mellitus, and male sex. Other pertinent risk factors included older age, Caucasian ethnicity, and a primary diagnosis of proximal humerus fracture. The rate of acute MI in patients who were older than 75 years when they underwent HSA for proximal humerus fracture was 0.80%.

Demographics

We found that patients who had an acute MI after shoulder arthroplasty were likely older, male, and Caucasian. Age and male sex are well-established risk factors for increased cardiac complications after arthroplasty.^27-29 Previous studies have indicated that the rate of cardiac events increases in arthroplasty patients older than 65 years.^19,28,29 In our study, more than 50% of the patients who had an acute perioperative MI were older than 85 years. Less explainable is the increased occurrence of acute MI in Caucasian patients and wealthy patients, given that minorities in the United States have higher rates of cardiovascular disease.³⁰ Shoulder arthroplasty is an elective procedure, more likely to be undertaken by Caucasians. Therefore, at-risk minority groups and financially challenged groups may be less likely to have this procedure.

Primary Diagnosis

In this series, patients with a primary diagnosis of proximal humerus fracture were more likely to have an in-hospital MI. This finding is consistent with previous studies indicating a higher rate of complications for proximal humerus fracture patients than for shoulder arthroplasty patients.^31,32 Given that more than 75% of patients who present with a proximal humerus fracture are older than 70 years, it would be prudent to examine operative indications after this diagnosis,³³ particularly as benefit from surgery for fractures has not been definitively demonstrated.^34-37

Comorbidities

Many of the patients in our MI cohort presented with congestive heart failure, angina pectoris, complicated diabetes, renal failure, fluid and electrolyte disorders, or deficiency anemia. This is in keeping with other studies indicating that preexisting cardiovascular morbidity increases the rate of MI after various forms of arthroplasty.^7-11 Patients in our MI cohort were also susceptible to a variety of post-MI perioperative complications, including pulmonary embolism, pneumonia, deep venous thrombosis, cerebrovascular event, acute renal failure, gastrointestinal complication, mechanical ventilation, transfusion, and nonroutine discharge, and their incidence of death was higher. These findings are consistent with reports that postoperative cardiovascular complications increase the degree of morbidity and mortality in arthroplasty patients.^14-16 It is also worth noting that the odds of MI in the perioperative period increase with each subsequent day of care. This is understandable given that patients presenting with numerous comorbidities are at increased risk for perioperative complications³⁸ resulting in hospital readmission.³⁹

The literature indicates that MI occurs as a complication in 0.7% of patients who undergo noncardiac surgery,⁷ though some series have shown it is more prevalent after arthroplasty procedures.^28,40 MI significantly increases the rate of perioperative morbidity and mortality,⁸ and perioperative cardiac morbidity is a leading cause of death after anesthesia and surgery.¹² Furthermore, the most common cause of death after lower extremity arthroplasty is cardiovascular-related.^41,42 In patients who presented for elective hip arthroplasty, cardiorespiratory disease was one of the main risk factors (with older age and male sex) shown to increase perioperative mortality.⁴³

Perioperative cardiovascular complications increase postoperative morbidity and mortality.¹² The rate of cardiovascular complications after shoulder arthroplasty ranges from 0.8% to 2.6%, and the incidence of MI hovers between 0.3% and 0.9%.^{17,19,28,40,44} A recent study in 793 patients found that, over a 30-day period, cardiovascular complications accounted for more than one-fourth of all complications.¹⁷ Singh and colleagues¹⁹ analyzed cardiopulmonary complications after primary shoulder arthroplasty in a total of 3480 patients (4019 arthroplasties) and found this group had a 90-day cardiac morbidity (MI, congestive heart failure, arrhythmia) rate of 2.6%. In that study, a Deyo-Charlson index of 1 or more was a significant independent risk factor for cardiac complications following surgery. Scores on this weighted index of 17 comorbidities are used to assess the complexities of a patient population. Given the severity of cardiovascular perioperative complications, it is important to preoperatively identify high-risk population groups and sufficiently study and optimize patients before shoulder arthroplasty.

There is much debate about the effectiveness of perioperative β-blockers in reducing perioperative cardiac morbidity and mortality.^45-48 Such a discussion is outside of the scope of this article, but it may be prudent to seek a cardiology consultation for patients presenting with risk factors for perioperative MI. β-Blockers may prove useful in reducing cardiac morbidity in high-risk patients after noncardiac surgery.^45,49

Many limitations are inherent in studies that use a nationally represented database such as NIS, which we used in this study. It is highly likely that NIS does not capture all potential postoperative complications, as this database is very large and subject to errors in data entry and clinical coding. In addition, detailed clinical information (eg, severity of certain comorbid diseases before shoulder arthroplasty, details about the intraoperative course) was not readily available for analysis. Another limitation, which may have led to an underestimate of complication rates, was our not being able to obtain information about postdischarge complications.

Despite these limitations, NIS and other databases have helped researchers answer questions about low-incidence conditions and generalize findings to a national population. In the present study, we analyzed 2 cohorts, patients with and without acute MI after shoulder arthroplasty, to determine predictors for and complications of postarthroplasty MI. We identified numerous predictors for acute MI: congestive heart failure, angina pectoris, complicated diabetes, renal failure, fluid and electrolyte disorders, and deficiency anemia prior to arthroplasty. As perioperative MI is associated with significant morbidity,^14-16 it would be wise to screen patients for such comorbid conditions, assess the severity of these conditions, and offer shoulder arthroplasty with prudence.

Conclusion

The top 4 predictors for acute MI after shoulder arthroplasty were congestive heart failure, angina pectoralis, complicated diabetes mellitus, and male sex. Other pertinent risk factors included older age, Caucasian ethnicity, and primary diagnosis of proximal humerus fracture. Surgeons and patients must be aware of predictors for adverse surgical outcomes such as perioperative MI and understand the extent to which these events increase perioperative morbidity and mortality.

The incidence of shoulder arthroplasty in the United States is increasing annually,^1-3 and the majority of these operations occur in older patients.^4-6 Elderly patients with cardiovascular, pulmonary, cerebral, renal, and hepatic disease are increasingly susceptible to numerous surgical complications.⁴ Myocardial infarction (MI) is a complication that occurs in 0.7% of noncardiac surgeries. This figure increases to 1.1% in patients with coronary artery disease.^7-11 Perioperative MI increases morbidity and mortality,⁸ and perioperative cardiac morbidity is the leading cause of death after anesthesia and surgery.¹² The financial effects of perioperative cardiac morbidity and mortality must also be considered. A 2009 claims analysis study estimated charges associated with a perioperative MI at $15,000 and the cost of cardiac death at $21,909.¹³

Cardiovascular complications are associated with a significant degree of morbidity and mortality in patients who undergo arthroplasty.^14-16 Although studies have elucidated 30- and 90-day morbidity and mortality rates after shoulder arthroplasty, in hip and knee arthroplasty^17-19 little has been done to determine predictors of perioperative MI in a representative database of patients. Given the increasing incidence of shoulder arthroplasty in the United States, the elective nature of this procedure, and the percentage of the US population with cardiovascular risk factors,²⁰ it is important to establish predictors of perioperative MI to ensure patients and physicians have the necessary resources to make informed decisions.

We conducted a study to examine the risk factors for perioperative MI in a large cohort of patients admitted for shoulder arthroplasty to US hospitals. We wanted to evaluate the association between perioperative MI and shoulder arthroplasty with respect to demographics, primary diagnosis, medical comorbidities, and perioperative complications. Specifically, we tested the null hypothesis that, among patients undergoing shoulder arthroplasty, and accounting for confounding variables, there would be no difference in risk factors for patients who have a perioperative MI.

Materials and Methods

This study was exempt from approval by our institutional review board. All data used in this project were deidentified before use.

Nationwide Inpatient Sample (NIS)

The Nationwide Inpatient Sample (NIS), an annual survey of hospitals, is conducted by the Healthcare Cost and Utilization Project (HCUP) and sponsored by the Agency for Healthcare Research and Quality (AHRQ). This database is the largest publicly available all-payer inpatient discharge database in the United States.²¹ Sampling 8 million hospital stays each year, NIS includes information from a representative batch of 20% of US hospitals. In 2011, 46 states and 1045 hospitals contributed information to the database, representing 97% of the US population.²² This large sample allows researchers to analyze a robust set of medical conditions and uncommon treatments. The survey, conducted each year since 1988, includes demographic, clinical, and resource use data.²³ Discharge weight files are provided by NIS to arrive at valid national estimates.

This database is particularly useful because it provides information on up to 25 medical diagnoses and 15 procedures, which are recorded with International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes. Researchers can use this database to analyze patient and hospital characteristics as well as inpatient outcomes.^24,25 Numerous studies have used NIS to address pertinent queries across the medical landscape.^22,26

Patient Selection and Analysis

We used NIS to isolate a population of 422,371 adults (≥18 years old) who underwent total shoulder arthroplasty (TSA) or hemi–shoulder arthroplasty (HSA) between January 1, 2002 and December 31, 2011. We then placed the patients in this population into 1 of 2 cohorts. The first cohort had an acute MI during the perioperative period after TSA, and the second, larger cohort did not have an acute MI after TSA. Acute MI was identified using ICD-9-CM code 410.xx. To identify a population of shoulder arthroplasty patients, we included discharges with an ICD-9-CM procedure code of 81.80 or 81.88 (both TSA) or 81.81 (HSA) in the sample. We then considered the degree to which each of 5 variables—primary diagnosis, age, sex, race, and select medical comorbidities—was predictive of in-hospital MI after TSA.

Statistical Analysis

Given the large sample used in this study, normal distribution of data was assumed. Using bivariate analysis, Pearson χ² test for categorical data, and independent-samples t test for continuous data, we compared the nonacute MI and acute MI groups. Multivariable binary logistic regression analyses allowed us to isolate the extent that primary diagnosis, age, sex, race, and medical comorbidities were predictors of acute MI after shoulder arthroplasty. Statistical significance was set at P < .05. SPSS Version 22.0 (SPSS, Chicago, Illinois) was used for all statistical analyses and data modeling.

Results

Between January 1, 2002 and December 31, 2011, an estimated total of 422,371 patients underwent shoulder arthroplasty (59.3% TSA, 40.7% HSA). Of these patients, 1174 (0.28%) had a perioperative MI, and 421,197 (99.72%) did not (Table 1). Patients with a primary diagnosis of proximal humerus fracture (33.8% vs 16.6%; P < .001) or rotator cuff arthropathy (10.1% vs 9.9%; P < .001) were more likely than patients with other diagnoses to have an in-hospital MI.

Our review of the demographics found that patients who underwent shoulder arthroplasty and had a perioperative MI were likely older (75±8.9 years vs 69±11 years; P < .001), Caucasian (94.2% vs 91.9%; P = .002), male (43.2% vs 39.7%; P = .013), in the highest median household income bracket of $63,000 or more (30.8% vs 25.6%; P < .001), and using Medicare (80.9% vs 66.3%; P < .001). They were more likely to be treated in a medical center of medium size (25.6% vs 23.7%; P = .042) or larger (61.8% vs 61.2%; P = .042). MIs occurred more often in urban environments (91.4% vs 88.5%; P = .002) and in HSA patients (55% vs 40.6%; P < .001), resulting in longer hospital  stays (9.4±7.9 days vs 2.7±2.5 days; P < .001) and higher probability of death (6.5% vs 0.1%; P < .001).

We then analyzed the 2 cohorts for medical comorbidities (Table 2). Patients in the MI cohort presented with a significantly higher incidence of congestive heart failure, previous MI, angina pectoris, chronic lung disease, hypertension, diabetes, renal failure, fluid and electrolyte disorders, pulmonary circulatory disease, coagulopathy, and deficiency anemia (P < .001) but not liver disease and obesity. Bivariate analysis of perioperative outcomes (Table 3) indicated that these patients also had a statistically higher rate of numerous other complications: pulmonary embolism (4.9% vs 0.2%; P < .001), pneumonia (15.1% vs 1.2%; P < .001), deep venous thrombosis (2.6% vs 0.2%; P < .001), cerebrovascular event (1.6% vs 0.1%; P < .001), acute renal failure (15.1% vs 1.2%; P < .001), gastrointestinal complication (1.2% vs 0.3%; P < .001), mechanical ventilation (1.2% vs 0.3%; P < .001), transfusion (33.4% vs 8.8%; P < .001), and nonroutine discharge (73.3% vs 36.0%; P < .001).

Multivariable logistic regression analysis was performed to determine independent predictors of perioperative MI after shoulder arthroplasty (Table 4). Patients with a primary diagnosis of proximal humerus fracture (odds ratio [OR], 1.38; 95% confidence interval [CI], 1.15-1.65; P < .001) were more likely than patients with a primary diagnosis of osteoarthritis to have an MI. The odds of postoperative MI increased with age (OR, 1.04 per year; 95% CI, 1.03-1.05; P < .001) and were higher in males (OR, 1.72; 95% CI, 1.52-1.96; P < .001). Compared with Caucasians, African Americans (OR, 0.19; 95% CI, 0.09-0.40; P < .001) were less likely to have an in-hospital MI after shoulder arthroplasty. After shoulder arthroplasty, the odds of MI in the perioperative period increased with each subsequent day of care (OR, 1.10; 95% CI, 1.10-1.11; P < .001).

Regarding independent comorbidities, multivariable logistic regression analysis also determined that history of congestive heart failure (OR, 4.86; 95% CI, 4.20-5.61; P < .001), angina pectoris (OR, 2.90; 95% CI, 2.02-4.17; P < .001), complicated diabetes (OR, 1.96; 95% CI, 1.49-2.57; P < .001), renal failure (OR, 1.42; 95% CI, 1.17-1.72; P < .001), fluid and electrolyte disorders (OR, 1.42; 95% CI, 1.21-1.67; P < .001), and deficiency anemia (OR, 1.62; 95% CI, 1.40-1.88; P < .001) were significant predictors of perioperative MI after shoulder arthroplasty.

Discussion

Results of other studies have elucidated 30- and 90-day mortality rates and postoperative complications after shoulder arthroplasty, but, relative to hip and knee arthroplasty,^17-19 little has been done to determine predictors of perioperative MI in a large sample of shoulder arthroplasty patients. Given the increasing rates of shoulder arthroplasty^1-3 and the demographics of this population,^4-6 it is likely that postoperative cardiovascular events will increase in frequency. We found that, in order of decreasing significance, the top 4 risk predictors for acute MI after shoulder arthroplasty were congestive heart failure, angina pectoralis, complicated diabetes mellitus, and male sex. Other pertinent risk factors included older age, Caucasian ethnicity, and a primary diagnosis of proximal humerus fracture. The rate of acute MI in patients who were older than 75 years when they underwent HSA for proximal humerus fracture was 0.80%.

Demographics

We found that patients who had an acute MI after shoulder arthroplasty were likely older, male, and Caucasian. Age and male sex are well-established risk factors for increased cardiac complications after arthroplasty.^27-29 Previous studies have indicated that the rate of cardiac events increases in arthroplasty patients older than 65 years.^19,28,29 In our study, more than 50% of the patients who had an acute perioperative MI were older than 85 years. Less explainable is the increased occurrence of acute MI in Caucasian patients and wealthy patients, given that minorities in the United States have higher rates of cardiovascular disease.³⁰ Shoulder arthroplasty is an elective procedure, more likely to be undertaken by Caucasians. Therefore, at-risk minority groups and financially challenged groups may be less likely to have this procedure.

Primary Diagnosis

In this series, patients with a primary diagnosis of proximal humerus fracture were more likely to have an in-hospital MI. This finding is consistent with previous studies indicating a higher rate of complications for proximal humerus fracture patients than for shoulder arthroplasty patients.^31,32 Given that more than 75% of patients who present with a proximal humerus fracture are older than 70 years, it would be prudent to examine operative indications after this diagnosis,³³ particularly as benefit from surgery for fractures has not been definitively demonstrated.^34-37

Comorbidities

Many of the patients in our MI cohort presented with congestive heart failure, angina pectoris, complicated diabetes, renal failure, fluid and electrolyte disorders, or deficiency anemia. This is in keeping with other studies indicating that preexisting cardiovascular morbidity increases the rate of MI after various forms of arthroplasty.^7-11 Patients in our MI cohort were also susceptible to a variety of post-MI perioperative complications, including pulmonary embolism, pneumonia, deep venous thrombosis, cerebrovascular event, acute renal failure, gastrointestinal complication, mechanical ventilation, transfusion, and nonroutine discharge, and their incidence of death was higher. These findings are consistent with reports that postoperative cardiovascular complications increase the degree of morbidity and mortality in arthroplasty patients.^14-16 It is also worth noting that the odds of MI in the perioperative period increase with each subsequent day of care. This is understandable given that patients presenting with numerous comorbidities are at increased risk for perioperative complications³⁸ resulting in hospital readmission.³⁹

The literature indicates that MI occurs as a complication in 0.7% of patients who undergo noncardiac surgery,⁷ though some series have shown it is more prevalent after arthroplasty procedures.^28,40 MI significantly increases the rate of perioperative morbidity and mortality,⁸ and perioperative cardiac morbidity is a leading cause of death after anesthesia and surgery.¹² Furthermore, the most common cause of death after lower extremity arthroplasty is cardiovascular-related.^41,42 In patients who presented for elective hip arthroplasty, cardiorespiratory disease was one of the main risk factors (with older age and male sex) shown to increase perioperative mortality.⁴³

Perioperative cardiovascular complications increase postoperative morbidity and mortality.¹² The rate of cardiovascular complications after shoulder arthroplasty ranges from 0.8% to 2.6%, and the incidence of MI hovers between 0.3% and 0.9%.^{17,19,28,40,44} A recent study in 793 patients found that, over a 30-day period, cardiovascular complications accounted for more than one-fourth of all complications.¹⁷ Singh and colleagues¹⁹ analyzed cardiopulmonary complications after primary shoulder arthroplasty in a total of 3480 patients (4019 arthroplasties) and found this group had a 90-day cardiac morbidity (MI, congestive heart failure, arrhythmia) rate of 2.6%. In that study, a Deyo-Charlson index of 1 or more was a significant independent risk factor for cardiac complications following surgery. Scores on this weighted index of 17 comorbidities are used to assess the complexities of a patient population. Given the severity of cardiovascular perioperative complications, it is important to preoperatively identify high-risk population groups and sufficiently study and optimize patients before shoulder arthroplasty.

There is much debate about the effectiveness of perioperative β-blockers in reducing perioperative cardiac morbidity and mortality.^45-48 Such a discussion is outside of the scope of this article, but it may be prudent to seek a cardiology consultation for patients presenting with risk factors for perioperative MI. β-Blockers may prove useful in reducing cardiac morbidity in high-risk patients after noncardiac surgery.^45,49

Many limitations are inherent in studies that use a nationally represented database such as NIS, which we used in this study. It is highly likely that NIS does not capture all potential postoperative complications, as this database is very large and subject to errors in data entry and clinical coding. In addition, detailed clinical information (eg, severity of certain comorbid diseases before shoulder arthroplasty, details about the intraoperative course) was not readily available for analysis. Another limitation, which may have led to an underestimate of complication rates, was our not being able to obtain information about postdischarge complications.

Despite these limitations, NIS and other databases have helped researchers answer questions about low-incidence conditions and generalize findings to a national population. In the present study, we analyzed 2 cohorts, patients with and without acute MI after shoulder arthroplasty, to determine predictors for and complications of postarthroplasty MI. We identified numerous predictors for acute MI: congestive heart failure, angina pectoris, complicated diabetes, renal failure, fluid and electrolyte disorders, and deficiency anemia prior to arthroplasty. As perioperative MI is associated with significant morbidity,^14-16 it would be wise to screen patients for such comorbid conditions, assess the severity of these conditions, and offer shoulder arthroplasty with prudence.

Conclusion

The top 4 predictors for acute MI after shoulder arthroplasty were congestive heart failure, angina pectoralis, complicated diabetes mellitus, and male sex. Other pertinent risk factors included older age, Caucasian ethnicity, and primary diagnosis of proximal humerus fracture. Surgeons and patients must be aware of predictors for adverse surgical outcomes such as perioperative MI and understand the extent to which these events increase perioperative morbidity and mortality.

Jane, age 42, presents with right knee pain that she’s had for about six months. She denies any trauma. Jane describes the pain as “vague and poorly localized” but worse with activity. She says she started a walking/running program nine months ago, when she was told she was overweight (BMI, 29). She has lost 10 pounds since then and hopes to lose more by continuing to exercise. Further review reveals that Jane has experienced increasing pain while ascending and descending stairs and that the pain is also exacerbated when she stands after prolonged sitting.

If Jane were your patient, what would you include in a physical examination, and how would you diagnose and treat her?

Knee pain is a common presentation in primary care. While traumatic knee pain is frequently addressed in the medical literature, little has been written about chronic nontraumatic nonarthritic knee pain such as Jane’s. Thus, while physical exam tests often lead to the correct diagnosis for traumatic knee pain, there is limited information on the use of such tests to determine the etiology of chronic knee pain.

This review was developed to fill that gap. The pages that follow contain general guidance on the diagnosis and treatment of chronic nontraumatic knee pain. The conditions are presented anatomically—anterior, lateral, medial, or posterior—with common etiologies, history and physical exam findings, and diagnosis and treatment options for each (see Table, page 28).^1-31

ANTERIOR KNEE PAIN
Patellofemoral pain syndrome (PFPS)
The most common cause of anterior knee pain, PFPS is a complex entity with an etiology that has not been well described.² The quadriceps tendon, medial and lateral retinacula, iliotibial band (ITB), vastus medialis and lateralis, and the insertion of the patellar tendon on the anterior tibial tubercle all play a role in proper tracking of the patellofemoral joint; an imbalance in any of these forces leads to abnormal patellar tracking over the femoral condyles, and pain ensues. PFPS can also be secondary to joint overload, in which excessive physical activity (eg, running, lunges, or squats) overloads the patellofemoral joint and causes pain.

Risk factors for PFPS include strength imbalances in the quadriceps, hamstring, and hip muscle groups, and increased training, such as running longer distances.^4,32 A recent review showed no relationship between an increased quadriceps (Q)-angle and PFPS, so that is no longer considered a major risk factor.⁵

Diagnosis. PFPS is a diagnosis of exclusion and is primarily based on history and physical exam. Anterior knee pain that is exacerbated when seated for long periods of time (the “theater sign”) or by descending stairs is a classic indication of PFPS.¹ Patients may complain of knee stiffness or “giving out” secondary to sharp knee pain and a sensation of popping or crepitus in the joint. Swelling is not a common finding.²

A recent meta-analysis revealed limited evidence for the use of any specific physical exam tests to diagnose PFPS. But pain during squatting and pain with a patellar tilt test were most consistent with a diagnosis of PFPS. (The patellar tilt test involves lifting the lateral edge of the patella superiorly while the patient lies supine with knee extended; pain with < 20° of lift suggests a tight lateral retinaculum). Conversely, the absence of pain during squatting or the absence of lateral retinacular pain helps rule it out.2 A physical exam of the cruciate and collateral ligaments should be performed in a patient with a history of instability. Radiography is not needed for a diagnosis but may be considered if examination reveals an effusion, the patient is 50 or older, or no improvement occurs after eight to 12 weeks of treatment.³³

Treatment. The most effective and strongly supported treatment for PFPS is a six-week physiotherapy program focusing on strengthening the quadriceps and hip muscles and stretching the quadriceps, ITB, hamstrings, and hip flexors.^4,5 There is limited information about the use of NSAIDs, but they can be considered for short-term management.²

Patellar taping and bracing have shown some promise as adjunct therapies for PFPS, although the data for both are nonconclusive. There is a paucity of prospective randomized trials of patellar bracing, and a 2012 Cochrane review found limited evidence of its efficacy.³⁴ But a 2014 meta-analysis revealed moderate evidence in support of patellar taping early on to help decrease pain,⁶ and a recent review suggests that it can be helpful in both the short and long term.⁷

Taping or bracing may be useful when combined with a tailored physical therapy program. Evidence for treatments such as biofeedback, chiropractic manipulation, and orthotics is limited, and they should be used only as adjunctive therapy.⁴

When you examine Jane, you find no swelling of the affected knee. You perform the tilt test, which elicits pain. Squatting causes some pain, as well. You diagnose PFPS and provide a referral for six weeks of physiotherapy.

Patellofemoral instability (PFI)
PFI occurs when the patella disengages completely from the trochlear groove.¹¹ PFI’s etiology also relates to the complexity of the patellofemoral joint. Here, too, stability of the joint is achieved with a combination of soft-tissue and bony restraints. At full extension and early flexion of the knee, however, the mechanisms of stability are limited, resulting in increased instability. Other associated factors include Q-angle, lateral pull from a tight ITB, and opposing forces from the vastus lateralis and vastus medialis obliquus (VMO).^8-10

Risk factors for PFI. The most common predisposing factors for PFI are trochlear dysplasia, patella alta, and lateralization of the tibial tuberosity or patella.^10,11 Older patients, predominately women, have an increased risk for PFI.⁹ Patients usually have a history of patellar subluxation or dislocation in their youth, with approximately 17% of those who had a first dislocation experiencing a recurrence.⁹ A family history of PFI is common, as well.¹⁰

Diagnosis. Patients with PFI often present with nonspecific anterior knee pain secondary to recurrent dislocation.¹³ Notable exam findings include
• A positive J sign (noted if the patella suddenly shifts medially during early knee flexion or laterally during full extension)
• Decreased quadriceps (specifically VMO) and hamstring strength and flexibility
• Patellar hypermobility, which should be no more than a quarter to a half of the patellar diameter bilaterally
• Pain during a patellar tilt test

• A positive patellar apprehension test.10 (With the patient lying with the knee flexed to 20°, place thumbs on the medial patella and push laterally; the patient will straighten leg with pain or “apprehension” prior to patellar dislocation.)

Plain radiography should be ordered in all cases to assess for osseous trauma/deformity and to help guide surgical consideration. MRI can provide additional information when significant soft-tissue damage is suspected or the patient does not improve with conservative therapy.^8,11

Treatment. A recent Cochrane review showed that conservative treatment (VMO strengthening, bracing, and proprioceptive therapy) prevented future dislocations more effectively than surgical intervention.¹¹ However, surgery is indicated when obvious predisposing anatomic conditions (osteochondral fracture, intra-articular deformity, or a major tear of a medial soft-tissue stabilizer) are clearly shown on imaging.^8,11

Patellar tendinopathy
An overuse injury often called “jumper’s knee” because it is associated with high-intensity jumping sports (eg, volleyball and basketball), patellar tendinopathy is an insertional tendinopathy with pain most commonly at the proximal patellar tendon.¹⁰ The pathology of the injury, though poorly understood, is believed to result from an impaired healing response to microtears.^12,14

Diagnosis. Patients with patellar tendinopathy typically present with anterior suprapatellar pain aggravated by activity. Classically, the pain can occur in any of four phases¹²
1. Pain isolated after activity
2. Pain that occurs during activity but does not impede activity
3. Pain that occurs both during and after the activity and interferes with competition
4. A complete tendon disruption.

Examination should include an assessment of the patellar tendon for localized thickening, nodularity, crepitus, and focal suprapatellar tenderness. The muscle tendon function should be evaluated by assessing knee mobility and strength of the quads via straight-leg raise, decline squat, or single-leg squats.¹² The Victorian Institute of Sport Assessment (VISA) questionnaire can be used to quantify the symptoms and to help track the patient’s progress throughout therapy.³¹ There are no proven special tests or radiologic studies to aid in the diagnosis of patellar tendinopathy,¹⁴ but MRI can be used for further evaluation when findings are equivocal.³⁵

Treatment. A wide range of options, from eccentric training (eg, three sets of 15 repetitions performed twice a day for 12 weeks) and physical therapy to platelet-rich plasma (PRP) injections, sclerosing injections, and surgery, are available for the treatment of patellar tendinopathy.^13-15 While no specific data have proven the superiority of any one therapy, expert consensus recommends eccentric exercise as initial therapy, performed for 12 weeks.^14,15

It’s also interesting to note that a recently published study showed that three weekly PRP injections helped 75% of patients—all of whom failed to respond to four months of eccentric therapy—return to their presymptom activity level within 90 days.¹⁶ Corticosteroid injections should not be used to treat patellar tendinopathy due to the risk for tendon rupture.¹⁵ Orthopedic referral for surgical intervention should be considered for patients who fail to respond after three to six months of conservative therapy.¹⁴

Next: Lateral knee pain >>

LATERAL KNEE PAIN
Iliotibial band syndrome (ITBS)
A common source of lateral knee pain, ITBS is found particularly in runners, cyclists, and endurance athletes.^17-19,36,37 The exact pathophysiology behind this diagnosis is debatable, but the most accepted etiology is inflammation generated from microtrauma to the soft tissues with inadequate healing time, resulting in persistent inflammation. ITBS is often associated with excessive overall running mileage, a sudden increase in mileage, or an abrupt change in training.^18,37

Diagnosis. Patients often complain of persistent nontraumatic lateral knee pain that worsens with repetitive knee flexion (eg, running or cycling).^17-19,37 A physical exam will often reveal pain over the lateral femoral condyle and a positive Noble’s test (see Figure 1, page 30). A positive Ober’s test (see Figure 2, page 32) is suggestive of ITBS, as well. The sensitivity and specificity of these tests are not well established, but in patients performing repetitive knee flexion activities with subjective lateral knee pain, pain over the lateral femoral condyle and a positive Ober’s and/or Noble’s test suggest an ITBS diagnosis.¹⁸ Imaging is not indicated initially, but MRI should be used in refractory cases to rule out other etiologies.^17,19

Treatment. First-line therapy for ITBS is conservative,^17-19,36,37 often involving a combination of techniques such as refraining from the activity that triggers the pain, NSAIDs, activity modification to reduce the strain over the ITB, myofascial release via foam rollers, and physical therapy focused on stretching the ITB, tensor fasciae latae, and gluteus medius while strengthening the gluteus medius and core muscles.¹⁷ No single program has been shown to be better than another. 

Corticosteroid injections are second-line therapy and have been shown to improve pain compared with placebo up to two weeks postinjection.^17,19 When symptoms persist for more than six months despite conservative treatment, surgical intervention may be indicated.^18,19 Patients who experience temporary pain relief with corticosteroid injections often respond best to surgery.³⁶

MEDIAL KNEE PAIN
Medial plica syndrome
Because of its anatomic location, the medial plica—which can be palpated in up to 84% of the population²⁰—is susceptible to impingement by the medial femoral condyle or the patellofemoral joint. Trauma with repetitive knee movement leads to inflammation and thickening of the plica, resulting in medial plica syndrome.^20,38 Initial inflammation may be triggered by blunt trauma, a sudden increase in activity, or transient synovitis.²²

Diagnosis. Medial plica syndrome is a challenging diagnosis. Patients generally have nonspecific complaints of aching medial knee pain, locking, and catching similar to complaints of a medial meniscal injury.²⁰

Evaluation should include the mediopatellar plica test, which is performed with the patient lying supine with the knee fully extended. Pressure is placed over the inferomedial patellofemoral joint, creating an impingement of the medial plica between the finger and the medial femoral condyle. Elimination or marked diminishing of pain with knee flexion to 90° is considered a positive test.²¹

A recent systematic review found this test to be more diagnostically accurate than an MRI (sensitivity of the test is 90% and specificity is 89%, vs 77% and 58%, respectively, for MRI) for detection of medial plica syndrome. Ultrasound is almost as accurate, with a sensitivity of 90% and specificity of 83%.³⁹

Treatment of medial plica syndrome centers on physiotherapy and quadriceps strengthening,²⁰ augmented with NSAIDs. Intra-articular corticosteroid injections are considered second-line treatment.^20,22 An orthopedics referral is indicated to consider arthroscopic plica removal for refractory cases.^20,22

Pes anserine bursitis
The anserine bursal complex, located approximately 5 cm distal to the medial joint line, is formed by the combined insertion of the sartorius, gracilis, and semitendinosus tendons,³⁹ but the exact mechanism of pain is not well understood. Whether the pathophysiology is from an insertional tendonitis or overt bursitis is unknown, and no studies have focused on prevalence or risk factors. What is known is that overweight individuals and women with a wide pelvis seem to have a greater predilection and those with pes planus, diabetes, or knee osteoarthritis are at increased risk.²³

Diagnosis. Medial knee pain reproduced on palpation of the anatomic site of insertion of the pes anserine tendon complex supports a diagnosis of pes anserine bursitis, with or without edema. Radiologic studies are not needed but may be helpful if significant bony pathology is suspected. Ultrasound, CT, and MRI are not recommended.²³

Treatment. Resting the affected knee, cryotherapy, NSAIDs, and use of a pillow at night to relieve direct bursal pressure are recommended.³³ Weight loss in obese patients, treatment of pes planus, and control of diabetes may be helpful, as well. Although the literature is limited and dated, corticosteroid injection has been found to reduce the pain and may be considered as second-line treatment.^24-26

POSTERIOR KNEE PAIN
Popliteal (Baker’s) cyst
The popliteal fossa contains six of the numerous bursa of the knee; the bursa beneath the medial head of the gastrocnemius muscle and the semimembranosus tendon is most commonly involved in the formation of a popliteal cyst.⁴⁰ It is postulated that increased intra-articular pressure forces fluid into the bursa, leading to expansion and pain. This can be idiopathic or secondary to internal derangement or trauma to the knee.⁴¹ Older age, a remote history of knee trauma, or a coexisting joint disease such as osteoarthritis, meniscal pathology, or rheumatoid arthritis are significant risk factors for popliteal cysts.²⁷

Diagnosis. Most popliteal cysts are asymptomatic in adults and discovered incidentally after routine imaging to evaluate other knee pathology. However, symptomatic popliteal cysts present as a palpable mass in the popliteal fossa, resulting in pain and limited range of motion.

During the physical exam with the patient lying supine, a medial popliteal mass that is most prominent with the knee fully extended is common. A positive Foucher’s sign (the painful mass is palpated posteriorly in the popliteal fossa with the knee fully extended; pain is relieved and/or the mass reduced in size with knee flexion to 45°) suggests a diagnosis of popliteal cyst.^27,28

Radiologic studies are generally not needed to diagnose a popliteal cyst. However, if diagnostic uncertainty remains after the history and physical exam, plain knee radiographs and ultrasound should be obtained. This combination provides complementary information and helps rule out a fracture, arthritis, and thrombosis as the cause of the pain.²⁷ MRI is helpful if the diagnosis is still in doubt or if patients are suspected of having significant internal derangement leading to cyst formation. Arthrography or CT is generally not needed.^27,41

Treatment. As popliteal cysts are often associated with other knee pathology, management of the underlying condition often leads to cyst regression. Keeping the knee in flexion can decrease the available space and assist in pain control in the acute phase.²⁷ Cold packs and NSAIDs can also be used initially. Cyst aspiration and intra-articular corticosteroid injection have been shown to be effective for cysts that do not respond to this conservative approach.²⁷ However, addressing and managing the underlying knee pathology (eg, osteoarthritis, meniscal pathology, or rheumatoid arthritis) will prevent popliteal cysts from recurring.

Continue for when the problem is painful knee effusion >>

WHEN THE PROBLEM IS PAINFUL KNEE EFFUSION
Nontraumatic knee effusion can be the primary source of knee pain or the result of underlying pathology. It is mentioned here because clinical suspicion is paramount to diagnosis of a septic joint—a serious cause of painful knee effusion that warrants prompt treatment.

As in other causes of knee pain, a detailed history of the character of the pain is essential. Septic arthritis and crystalline disease (gout, pseudogout) should be suspected in patients without a history of trauma who cannot bear weight. Systemic complaints point to an infection and, with the exception of a possible low-grade fever, are not typically seen in crystalline disease. Notable findings include an erythematous, hot, swollen knee and pain with both active and passive movement. 

Plain radiographs of the knee should be ordered to rule out significant trauma or arthritis as the etiology. It is important to perform joint aspiration with synovial fluid analysis. Fluid analysis should include a white blood cell (WBC) count with differential, Gram stain and cultures, and polarized light microscopy (not readily available in an outpatient setting).²⁹

Synovial fluid analysis characteristics suggestive of a septic joint include turbid quality, WBC > 50,000/mL, an elevated protein content, and a low glucose concentration.³⁰ Gram stain and culture will help identify the infectious agent. Orthopedic referral should not be delayed in patients with a suspected infectious joint. Corticosteroids should not be injected during aspiration if infection is being ruled out.

When Jane returns for a follow-up visit eight weeks later, she states that the knee pain has resolved and that she has returned to running. She has lost an additional eight pounds and continues to diet. And, at the advice of her physical therapist, she is continuing her physiotherapy regimen at home to prevent a recurrence of PFPS.

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