Alternative splicing enables resistance to CTL019

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CTL019

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New research has provided an explanation for resistance to CTL019, a CD19 chimeric antigen receptor (CAR) T-cell therapy.

Investigators analyzed samples from children with B-cell acute lymphoblastic leukemia (B-ALL) and found evidence to suggest that CTL019 resistance can be caused by CD19 splicing alterations.

These alterations prompt the loss of certain parts of the CD19 protein that are recognized by the CAR T cells.

The team described this work in Cancer Discovery.

They noted that 10% to 20% of B-ALL patients treated with CD19-directed immunotherapy may experience relapse.

“Some of them can be successfully retreated, but, in others, a more pernicious kind of leukemia may emerge, which no longer responds to CTL019,” said study author Andrei Thomas-Tikhonenko, PhD, of the University of Pennsylvania in Philadelphia.

“In some cases, resistance is accompanied by the disappearance of the target CD19 protein from the cell surface . . . . Our goal was to figure out how the CD19 protein manages to vanish and whether it is gone for good or whether it could, under certain circumstances, be coaxed back.”

“Our initial finding from this study was that, in most cases, the CD19 genetic code was not irretrievably lost. We also discovered that the CD19 protein was still being made, but as a shorter version, which escapes detection by the immune system.”

To understand the mechanism of CTL019 resistance, Dr Thomas-Tikhonenko and his colleagues studied multiple tumor samples from 4 children with B-ALL. The samples were collected before the patients were treated with CTL019 and/or after they developed resistance to the therapy.

The investigators found that, in some cases, 1 copy of the gene coding for CD19 (located on chromosome 16) was deleted, and the other copy was damaged as a result of mutations in coding areas of the CD19 gene, most frequently in exon 2.

However, the team also discovered alternatively spliced CD19 messenger RNA species in which exons 2, 5, and 6 were frequently skipped, making mutations in exon 2 largely irrelevant.

Subsequent investigation revealed that deletion of exons 5 and 6 resulted in premature termination of CD19.

Deletion of exon 2 resulted in the production of a modified version of CD19, which was more stable than its standard version. The shortened protein was functional and could perform many of the tasks that CD19 is known to handle, but it cannot be targeted by CTL019.

The importance of exon skipping in CTL019 resistance cannot be overstated, Dr Thomas-Tikhonenko said.

“Without exons 5 and 6, the CD19 protein has no way of being retained on the cell surface,” he explained. “The case of missing exon 2 is more complex. Although the resultant protein can make it to the cell surface, albeit not very efficiently, it can no longer be recognized by CTL019.”

He and his colleagues believe this research can inform future use of CTL019 and immunotherapy in general.

“[A]lternative splicing could be a potent, built-in mechanism of resistance, and it might be better to target proteins that, unlike CD19, are not prone to exon skipping,” Dr Thomas-Tikhonenko said.

“[In addition,] it might be important to preselect patients for CTL019 and similar therapies and make sure that the alternatively spliced CD19 variants are not already present in their leukemias. If they are, resistance could develop very quickly.”

Designing new immunotherapeutics that can recognize the shortened version of CD19 is another approach to overcoming CTL019 resistance, he added.

He and his colleagues noted that this study was limited by the relatively small number of samples analyzed, which might have prevented the investigators from identifying additional mechanisms of resistance.

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CTL019

Photo from Penn Medicine

New research has provided an explanation for resistance to CTL019, a CD19 chimeric antigen receptor (CAR) T-cell therapy.

Investigators analyzed samples from children with B-cell acute lymphoblastic leukemia (B-ALL) and found evidence to suggest that CTL019 resistance can be caused by CD19 splicing alterations.

These alterations prompt the loss of certain parts of the CD19 protein that are recognized by the CAR T cells.

The team described this work in Cancer Discovery.

They noted that 10% to 20% of B-ALL patients treated with CD19-directed immunotherapy may experience relapse.

“Some of them can be successfully retreated, but, in others, a more pernicious kind of leukemia may emerge, which no longer responds to CTL019,” said study author Andrei Thomas-Tikhonenko, PhD, of the University of Pennsylvania in Philadelphia.

“In some cases, resistance is accompanied by the disappearance of the target CD19 protein from the cell surface . . . . Our goal was to figure out how the CD19 protein manages to vanish and whether it is gone for good or whether it could, under certain circumstances, be coaxed back.”

“Our initial finding from this study was that, in most cases, the CD19 genetic code was not irretrievably lost. We also discovered that the CD19 protein was still being made, but as a shorter version, which escapes detection by the immune system.”

To understand the mechanism of CTL019 resistance, Dr Thomas-Tikhonenko and his colleagues studied multiple tumor samples from 4 children with B-ALL. The samples were collected before the patients were treated with CTL019 and/or after they developed resistance to the therapy.

The investigators found that, in some cases, 1 copy of the gene coding for CD19 (located on chromosome 16) was deleted, and the other copy was damaged as a result of mutations in coding areas of the CD19 gene, most frequently in exon 2.

However, the team also discovered alternatively spliced CD19 messenger RNA species in which exons 2, 5, and 6 were frequently skipped, making mutations in exon 2 largely irrelevant.

Subsequent investigation revealed that deletion of exons 5 and 6 resulted in premature termination of CD19.

Deletion of exon 2 resulted in the production of a modified version of CD19, which was more stable than its standard version. The shortened protein was functional and could perform many of the tasks that CD19 is known to handle, but it cannot be targeted by CTL019.

The importance of exon skipping in CTL019 resistance cannot be overstated, Dr Thomas-Tikhonenko said.

“Without exons 5 and 6, the CD19 protein has no way of being retained on the cell surface,” he explained. “The case of missing exon 2 is more complex. Although the resultant protein can make it to the cell surface, albeit not very efficiently, it can no longer be recognized by CTL019.”

He and his colleagues believe this research can inform future use of CTL019 and immunotherapy in general.

“[A]lternative splicing could be a potent, built-in mechanism of resistance, and it might be better to target proteins that, unlike CD19, are not prone to exon skipping,” Dr Thomas-Tikhonenko said.

“[In addition,] it might be important to preselect patients for CTL019 and similar therapies and make sure that the alternatively spliced CD19 variants are not already present in their leukemias. If they are, resistance could develop very quickly.”

Designing new immunotherapeutics that can recognize the shortened version of CD19 is another approach to overcoming CTL019 resistance, he added.

He and his colleagues noted that this study was limited by the relatively small number of samples analyzed, which might have prevented the investigators from identifying additional mechanisms of resistance.

CTL019

Photo from Penn Medicine

New research has provided an explanation for resistance to CTL019, a CD19 chimeric antigen receptor (CAR) T-cell therapy.

Investigators analyzed samples from children with B-cell acute lymphoblastic leukemia (B-ALL) and found evidence to suggest that CTL019 resistance can be caused by CD19 splicing alterations.

These alterations prompt the loss of certain parts of the CD19 protein that are recognized by the CAR T cells.

The team described this work in Cancer Discovery.

They noted that 10% to 20% of B-ALL patients treated with CD19-directed immunotherapy may experience relapse.

“Some of them can be successfully retreated, but, in others, a more pernicious kind of leukemia may emerge, which no longer responds to CTL019,” said study author Andrei Thomas-Tikhonenko, PhD, of the University of Pennsylvania in Philadelphia.

“In some cases, resistance is accompanied by the disappearance of the target CD19 protein from the cell surface . . . . Our goal was to figure out how the CD19 protein manages to vanish and whether it is gone for good or whether it could, under certain circumstances, be coaxed back.”

“Our initial finding from this study was that, in most cases, the CD19 genetic code was not irretrievably lost. We also discovered that the CD19 protein was still being made, but as a shorter version, which escapes detection by the immune system.”

To understand the mechanism of CTL019 resistance, Dr Thomas-Tikhonenko and his colleagues studied multiple tumor samples from 4 children with B-ALL. The samples were collected before the patients were treated with CTL019 and/or after they developed resistance to the therapy.

The investigators found that, in some cases, 1 copy of the gene coding for CD19 (located on chromosome 16) was deleted, and the other copy was damaged as a result of mutations in coding areas of the CD19 gene, most frequently in exon 2.

However, the team also discovered alternatively spliced CD19 messenger RNA species in which exons 2, 5, and 6 were frequently skipped, making mutations in exon 2 largely irrelevant.

Subsequent investigation revealed that deletion of exons 5 and 6 resulted in premature termination of CD19.

Deletion of exon 2 resulted in the production of a modified version of CD19, which was more stable than its standard version. The shortened protein was functional and could perform many of the tasks that CD19 is known to handle, but it cannot be targeted by CTL019.

The importance of exon skipping in CTL019 resistance cannot be overstated, Dr Thomas-Tikhonenko said.

“Without exons 5 and 6, the CD19 protein has no way of being retained on the cell surface,” he explained. “The case of missing exon 2 is more complex. Although the resultant protein can make it to the cell surface, albeit not very efficiently, it can no longer be recognized by CTL019.”

He and his colleagues believe this research can inform future use of CTL019 and immunotherapy in general.

“[A]lternative splicing could be a potent, built-in mechanism of resistance, and it might be better to target proteins that, unlike CD19, are not prone to exon skipping,” Dr Thomas-Tikhonenko said.

“[In addition,] it might be important to preselect patients for CTL019 and similar therapies and make sure that the alternatively spliced CD19 variants are not already present in their leukemias. If they are, resistance could develop very quickly.”

Designing new immunotherapeutics that can recognize the shortened version of CD19 is another approach to overcoming CTL019 resistance, he added.

He and his colleagues noted that this study was limited by the relatively small number of samples analyzed, which might have prevented the investigators from identifying additional mechanisms of resistance.

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Drug can block malaria transmission, studies show

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Plasmodium sporozoite

Image by Ute Frevert

and Margaret Shear

PHILADELPHIA—A drug used to treat multiple tropical diseases can also inhibit malaria transmission, according to a pair of studies presented at the ASTMH 64th Annual Meeting.

One study suggests the drug, ivermectin, can reduce the transmission of malaria caused by Plasmodium falciparum, the most prevalent malaria parasite in Africa.

The other study indicates that ivermectin can block the transmission of Plasmodium vivax parasites, which are common in Southeast Asia.

Kevin Kobylinski, PhD, of the Armed Forces Research Institute of Medical Sciences in Bangkok, Thailand, presented results of the P vivax study as abstract 1283.

And Brian D. Foy, PhD, of Colorado State University in Fort Collins, presented results of the P falciparum trial as abstract LB-5237.

P falciparum malaria

Dr Foy and his colleagues are assessing the ability of ivermectin to block malaria transmission in 4 villages in Burkina Faso, Africa.

Lab studies have shown that when mosquitoes feed on the blood of people who have taken ivermectin, it interferes with the mosquitoes’ ability to transmit malaria parasites to humans. Sometimes, it kills the mosquitoes outright, but, more often, it weakens them and interferes with their digestive system so they eventually die in the harsh conditions of nature.

“Even if the mosquitoes don’t get enough ivermectin to directly kill them, we think a sublethal dose should be sufficiently toxic to reduce malaria transmission,” Dr Foy said.

But he noted that because the goal is to interrupt malaria transmission, the drug must be taken by a majority of the people in a town or village, who then pass it along to the mosquitoes.

For the last few months, most of the population in the 4 villages in Burkina Faso has been receiving a single dose of ivermectin every 3 weeks. Individuals who are not eligible to take the drug include children less than 90 cm tall, pregnant women, and newly breastfeeding women.

The measure of success is a reduction in malaria incidence among children younger than 5, most of whom will not actually take the drug. But this is the age group most at risk of serious illness and death from the disease.

Thus far, the researchers have observed a roughly 16% reduction in childhood malaria episodes.

“These are preliminary results, but we expect to see further reductions in malaria fevers as we continue with the trial, which is occurring during the rainy season when malaria transmission typically peaks,” Dr Foy said.

“The drop in malaria fevers we’re seeing with the ivermectin treatment is in addition to whatever is being achieved with insecticide-treated bednets, which are in widespread use in all of the villages participating in the study.”

P vivax malaria

Dr Kobylinski and his colleagues found that ivermectin can affect P vivax parasites as well. The researchers tested the drug’s potential to block malaria transmission by feeding blood meals containing ivermectin and P vivax parasites to Anopheles dirus mosquitoes, the predominant malaria vector in Southeast Asia.

Ivermectin effectively killed A dirus mosquitoes, and it inhibited the ability of any surviving mosquitoes to develop P vivax parasites.

Dr Kobylinski noted that malaria experts are considering combining ivermectin with other medications in mass drug administration (MDA) campaigns that would seek to stop the spread of drug-resistant parasites in Southeast Asia by eliminating malaria from the entire region.

He said ivermectin could help increase compliance with an MDA strategy in places like Thailand, where drug-resistant malaria is spreading but overall malaria infection rates are relatively low.

 

 

“There is a lot of interest in launching MDA campaigns to fight drug-resistant malaria in Southeast Asia, but it can be hard to convince someone to take malaria medications if they don’t have an active malaria infection,” Dr Kobylinski said.

“But if you put ivermectin into the mix, that could improve participation because many people recognize the benefits of taking ivermectin for more common problems, like scabies.”

About ivermectin

Over the last 3 decades, more than 1 billion doses of ivermectin have been distributed in Africa and Latin America in MDA campaigns that have reduced the burden of lymphatic filariasis, which causes elephantiasis, and onchocerciasis, the disease that causes river blindness.

Ivermectin can also kill several types of debilitating intestinal worms known as soil-transmitted helminths.

Earlier this month, the Nobel Prize in Physiology or Medicine was awarded to a pair of researchers who isolated the precursor of ivermectin, avermectin, from an organism discovered in a single soil sample collected in Japan in the 1970s.

Publications
Topics

Plasmodium sporozoite

Image by Ute Frevert

and Margaret Shear

PHILADELPHIA—A drug used to treat multiple tropical diseases can also inhibit malaria transmission, according to a pair of studies presented at the ASTMH 64th Annual Meeting.

One study suggests the drug, ivermectin, can reduce the transmission of malaria caused by Plasmodium falciparum, the most prevalent malaria parasite in Africa.

The other study indicates that ivermectin can block the transmission of Plasmodium vivax parasites, which are common in Southeast Asia.

Kevin Kobylinski, PhD, of the Armed Forces Research Institute of Medical Sciences in Bangkok, Thailand, presented results of the P vivax study as abstract 1283.

And Brian D. Foy, PhD, of Colorado State University in Fort Collins, presented results of the P falciparum trial as abstract LB-5237.

P falciparum malaria

Dr Foy and his colleagues are assessing the ability of ivermectin to block malaria transmission in 4 villages in Burkina Faso, Africa.

Lab studies have shown that when mosquitoes feed on the blood of people who have taken ivermectin, it interferes with the mosquitoes’ ability to transmit malaria parasites to humans. Sometimes, it kills the mosquitoes outright, but, more often, it weakens them and interferes with their digestive system so they eventually die in the harsh conditions of nature.

“Even if the mosquitoes don’t get enough ivermectin to directly kill them, we think a sublethal dose should be sufficiently toxic to reduce malaria transmission,” Dr Foy said.

But he noted that because the goal is to interrupt malaria transmission, the drug must be taken by a majority of the people in a town or village, who then pass it along to the mosquitoes.

For the last few months, most of the population in the 4 villages in Burkina Faso has been receiving a single dose of ivermectin every 3 weeks. Individuals who are not eligible to take the drug include children less than 90 cm tall, pregnant women, and newly breastfeeding women.

The measure of success is a reduction in malaria incidence among children younger than 5, most of whom will not actually take the drug. But this is the age group most at risk of serious illness and death from the disease.

Thus far, the researchers have observed a roughly 16% reduction in childhood malaria episodes.

“These are preliminary results, but we expect to see further reductions in malaria fevers as we continue with the trial, which is occurring during the rainy season when malaria transmission typically peaks,” Dr Foy said.

“The drop in malaria fevers we’re seeing with the ivermectin treatment is in addition to whatever is being achieved with insecticide-treated bednets, which are in widespread use in all of the villages participating in the study.”

P vivax malaria

Dr Kobylinski and his colleagues found that ivermectin can affect P vivax parasites as well. The researchers tested the drug’s potential to block malaria transmission by feeding blood meals containing ivermectin and P vivax parasites to Anopheles dirus mosquitoes, the predominant malaria vector in Southeast Asia.

Ivermectin effectively killed A dirus mosquitoes, and it inhibited the ability of any surviving mosquitoes to develop P vivax parasites.

Dr Kobylinski noted that malaria experts are considering combining ivermectin with other medications in mass drug administration (MDA) campaigns that would seek to stop the spread of drug-resistant parasites in Southeast Asia by eliminating malaria from the entire region.

He said ivermectin could help increase compliance with an MDA strategy in places like Thailand, where drug-resistant malaria is spreading but overall malaria infection rates are relatively low.

 

 

“There is a lot of interest in launching MDA campaigns to fight drug-resistant malaria in Southeast Asia, but it can be hard to convince someone to take malaria medications if they don’t have an active malaria infection,” Dr Kobylinski said.

“But if you put ivermectin into the mix, that could improve participation because many people recognize the benefits of taking ivermectin for more common problems, like scabies.”

About ivermectin

Over the last 3 decades, more than 1 billion doses of ivermectin have been distributed in Africa and Latin America in MDA campaigns that have reduced the burden of lymphatic filariasis, which causes elephantiasis, and onchocerciasis, the disease that causes river blindness.

Ivermectin can also kill several types of debilitating intestinal worms known as soil-transmitted helminths.

Earlier this month, the Nobel Prize in Physiology or Medicine was awarded to a pair of researchers who isolated the precursor of ivermectin, avermectin, from an organism discovered in a single soil sample collected in Japan in the 1970s.

Plasmodium sporozoite

Image by Ute Frevert

and Margaret Shear

PHILADELPHIA—A drug used to treat multiple tropical diseases can also inhibit malaria transmission, according to a pair of studies presented at the ASTMH 64th Annual Meeting.

One study suggests the drug, ivermectin, can reduce the transmission of malaria caused by Plasmodium falciparum, the most prevalent malaria parasite in Africa.

The other study indicates that ivermectin can block the transmission of Plasmodium vivax parasites, which are common in Southeast Asia.

Kevin Kobylinski, PhD, of the Armed Forces Research Institute of Medical Sciences in Bangkok, Thailand, presented results of the P vivax study as abstract 1283.

And Brian D. Foy, PhD, of Colorado State University in Fort Collins, presented results of the P falciparum trial as abstract LB-5237.

P falciparum malaria

Dr Foy and his colleagues are assessing the ability of ivermectin to block malaria transmission in 4 villages in Burkina Faso, Africa.

Lab studies have shown that when mosquitoes feed on the blood of people who have taken ivermectin, it interferes with the mosquitoes’ ability to transmit malaria parasites to humans. Sometimes, it kills the mosquitoes outright, but, more often, it weakens them and interferes with their digestive system so they eventually die in the harsh conditions of nature.

“Even if the mosquitoes don’t get enough ivermectin to directly kill them, we think a sublethal dose should be sufficiently toxic to reduce malaria transmission,” Dr Foy said.

But he noted that because the goal is to interrupt malaria transmission, the drug must be taken by a majority of the people in a town or village, who then pass it along to the mosquitoes.

For the last few months, most of the population in the 4 villages in Burkina Faso has been receiving a single dose of ivermectin every 3 weeks. Individuals who are not eligible to take the drug include children less than 90 cm tall, pregnant women, and newly breastfeeding women.

The measure of success is a reduction in malaria incidence among children younger than 5, most of whom will not actually take the drug. But this is the age group most at risk of serious illness and death from the disease.

Thus far, the researchers have observed a roughly 16% reduction in childhood malaria episodes.

“These are preliminary results, but we expect to see further reductions in malaria fevers as we continue with the trial, which is occurring during the rainy season when malaria transmission typically peaks,” Dr Foy said.

“The drop in malaria fevers we’re seeing with the ivermectin treatment is in addition to whatever is being achieved with insecticide-treated bednets, which are in widespread use in all of the villages participating in the study.”

P vivax malaria

Dr Kobylinski and his colleagues found that ivermectin can affect P vivax parasites as well. The researchers tested the drug’s potential to block malaria transmission by feeding blood meals containing ivermectin and P vivax parasites to Anopheles dirus mosquitoes, the predominant malaria vector in Southeast Asia.

Ivermectin effectively killed A dirus mosquitoes, and it inhibited the ability of any surviving mosquitoes to develop P vivax parasites.

Dr Kobylinski noted that malaria experts are considering combining ivermectin with other medications in mass drug administration (MDA) campaigns that would seek to stop the spread of drug-resistant parasites in Southeast Asia by eliminating malaria from the entire region.

He said ivermectin could help increase compliance with an MDA strategy in places like Thailand, where drug-resistant malaria is spreading but overall malaria infection rates are relatively low.

 

 

“There is a lot of interest in launching MDA campaigns to fight drug-resistant malaria in Southeast Asia, but it can be hard to convince someone to take malaria medications if they don’t have an active malaria infection,” Dr Kobylinski said.

“But if you put ivermectin into the mix, that could improve participation because many people recognize the benefits of taking ivermectin for more common problems, like scabies.”

About ivermectin

Over the last 3 decades, more than 1 billion doses of ivermectin have been distributed in Africa and Latin America in MDA campaigns that have reduced the burden of lymphatic filariasis, which causes elephantiasis, and onchocerciasis, the disease that causes river blindness.

Ivermectin can also kill several types of debilitating intestinal worms known as soil-transmitted helminths.

Earlier this month, the Nobel Prize in Physiology or Medicine was awarded to a pair of researchers who isolated the precursor of ivermectin, avermectin, from an organism discovered in a single soil sample collected in Japan in the 1970s.

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Acute Multiple Flexor Tendon Injury and Carpal Tunnel Syndrome After Open Distal Radius Fracture

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Acute Multiple Flexor Tendon Injury and Carpal Tunnel Syndrome After Open Distal Radius Fracture

The literature on extensor tendon rupture and even chronic flexor tendon rupture after volar plating and distal radius fracture malunion is ubiquitous. However, acute and subacute flexor tendon ruptures caused by distal radius fractures have been reported only in limited case reports. These rare injuries may involve multiple tendons and are associated with high-energy mechanisms. This case report details the involvement of multiple flexor tendon injuries associated with a Gustilo-Anderson type II distal radius fracture and the development of acute carpal tunnel syndrome (CTS) after a motor vehicle collision. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

The patient is a 46-year-old woman who was involved in a motor vehicle collision. She was triaged as a trauma patient via Advanced Trauma Life Support protocol, and treated with antibiotic and tetanus prophylaxis. Radiographs showed an open, comminuted, displaced intra-articular distal radius fracture on the right side (Figures 1A, 1B). The fracture was closed reduced and splinted in the emergency department (Figures 2A, 2B). On initial examination, the patient had diffuse paresthesias in the digits that were most pronounced in the median nerve distribution. Motor examination was limited secondary to pain; however, she demonstrated gentle flexion and extension of the digits. The hand was well perfused, and a palpable radial pulse was present. 

 

After clearance was obtained, she was taken urgently to the operating room. The wound was volar and transverse, approximately 2 cm in length, and approximately 4 cm proximal to the wrist crease. The wound was extended proximally and distally for a standard volar (Henry) approach. The flexor carpi radialis tendon was found to be partially lacerated, comprising 60% of the tendon. The fracture was readily identified because the deep fascia and the pronator quadratus were disrupted. No deep tendon lacerations were identified. The median nerve was found to be in continuity. After satisfactory débridement of the fracture and the wound, reduction and fixation was achieved with a volar locking plate and a single Kirschner wire. The flexor carpi radialis tendon was repaired with a modified Kessler stitch and epitenon repair. The wound was closed primarily in layers (Figures 3A, 3B).

The patient’s immediate postoperative neurologic examination was compromised secondary to the patient having a supraclavicular nerve block for anesthesia. Regional anesthesia was chosen because the patient’s pulmonologist recommended avoiding general anesthesia owing to her history of severe asthma that frequently required corticosteroid treatment. Once the block wore off, she complained of persistent paresthesias in all digits but most pronounced in the median nerve distribution. She was able to flex the interphalangeal joint to the index finger but could not flex the interphalangeal joint to the thumb. Over the course of the night, she was also noted to have worsening pain out of proportion to her injury.

As the paresthesias became denser in the median nerve distribution, she was diagnosed with acute CTS and was taken urgently back to the operating room under general anesthesia. After releasing the carpal tunnel through a separate incision, the original wound was reopened and explored. The median nerve was again visualized and found to be in continuity. All 4 tendons to both the flexor digitorum superficialis and flexor digitorum profundus were identified. The flexor pollicis longus (FPL) was not visualized in the wound. The distal portion of the FPL was retracted in the thumb tendon sheath and retrieved blindly with a tendon passer. The proximal portion was retracted to the mid-forearm. The laceration occurred distal to the musculotendinous junction. The tendon was repaired with a modified Kessler stitch as well as a box suture, resulting in 4 core strands across the tendon. The hand and the wrist were splinted in a thumb spica cast, and the patient was started on a modified Duran protocol 1 week after surgery. Median nerve function improved postoperatively. 

Discussion

The rupture of the extensor pollicis longus tendon in nondisplaced distal radius fractures is not uncommon, but occurs in fewer than 5% of nondisplaced distal radius fractures.1 Although less common, chronic complications with flexor tendon rupture after distal radius fracture are well described.1-6 Flexor tendon rupture after distal radius malunion or volar plating is a known complication and is thought to be the result of attritional tendon wear because the flexors rub against protruding bone or plate;3,4,7 however, the initial tendon injury may play a role in those tendons that rupture more quickly.3 When secondary to volar plating, the rupture typically occurs within 1 year of injury,7 but, in both plating and malunion, it has been characterized as a late complication up to 10 years and even 20 years after injury.3,4 Similar to other reports, this rupture was encountered during a volar wrist approach. It has been suggested that, as the incidence of volar plating rises, more acute flexor tendon injuries may be diagnosed because of anatomic exposure,2 but this has not been reported in the literature. 

 

 

Acute and subacute flexor tendon ruptures are rarely reported in the literature. To our knowledge, there are only 2 other reports of acute flexor tendon rupture2,5 after a distal radius fracture, neither of which involved the FPL. These cases, which involved ruptures of the flexor digitorum superficialis and flexor carpi radialis, were thought to be the result of tendon laceration by a volar bone spike. There is also one report of subacute FPL and flexor digitorum profundus rupture approximately 4 weeks after closed reduction of a distal radius fracture.6 Although sparse, the literature regarding flexor tendon rupture and distal radius fractures suggests that involvement of the flexor digitorum superficialis and the flexor digitorum profundus tendons is most common and that the rupture typically occurs in 1 to 4 months.1

We report a rare case of 2 acute flexor tendon lacerations after a Gustilo-Anderson type II open distal radius fracture, likely caused by the volar spike of bone that created the open injury. This case also was complicated by the development of acute CTS. 

To our knowledge, despite a rate of acute CTS reported as high as 5.4% in operatively treated distal radius fractures, there are no established associations between acute CTS and flexor tendon rupture in the setting of distal radius fracture.8,9 In a 2008 retrospective case–control study by Dyer and colleagues,8 fracture translation is the most important risk factor for the development of acute CTS associated with fracture of the distal radius. Although not statistically significant, ipsilateral upper extremity trauma, higher-energy injuries, younger age, and male sex were also associated with the development of acute CTS. Open injuries occurred in only 3 of 50 cases of acute CTS.8

In agreement with published reports, the probability and the timing of tendon rupture are likely related to the severity of the deforming forces applied during the initial insult rather than the resultant stresses.1 Clinicians should have a high suspicion of acute CTS and possible tendon injuries after a high-energy injury with a significantly displaced open distal radius fracture and median nerve paresthesias. A thoughtful and complete preoperative examination of the flexor tendons may prevent the need for reoperation. Concerns for flexor injury and acute CTS should be elevated with the observation of a disrupted pronator. For patients with a volarly displaced fragment after fracture reduction, this concern should be even more elevated.9 Preoperative median nerve symptoms in the setting of the severely displaced fracture should necessitate an acute carpal tunnel release. If 1 flexor tendon is injured, the surgeon should remember that multiple flexor tendons may be involved. We recommend that any injured tendons be repaired primarily, if possible, and the patient started on appropriate rehabilitation.

References

1.    Ashall G. Flexor pollicis longus rupture after fracture of the distal radius. Injury. 1991;22(2):153-155.

2.    Dimatteo L, Wolf JM. Flexor carpi radialis tendon rupture as a complication of a closed distal radius fracture: a case report. J Hand Surg Am. 2007;32(6):818-820.

3.    Kato N, Nemoto K, Arino H, Ichikawa T, Fujikawa K. Ruptures of flexor tendons at the wrist as a complication of fracture of the distal radius. Scand J Plast Reconstr Surg Hand Surg. 2002;36(4):245-248.

4.    Monda MK, Ellis A, Karmani S. Late rupture of flexor pollicis longus tendon 10 years after volar buttress plate fixation of a distal radius fracture: a case report. Acta Orthop Belg. 2010;76(4):549-551.

5.    Southmayd WW, Millender LH, Nalebuff EA. Rupture of the flexor tendons of the index finger after Colles’ fracture. Case report. J Bone Joint Surg Am. 1975;57(4):562-563.

6.    Wong FY, Pho RW. Median nerve compression, with tendon ruptures, after Colles’ fracture. J Hand Surg Br. 1984;9(2):139-141.

7.    Woon CYL, Lee JYL, Ng SW, Teoh LC. Late rupture of flexor pollicis longus tendon after volar distal radius plating: a case report and review of the literature. Inj Extra. 2007;38(7):235-238.

8.    Dyer G, Lozano-Calderon S, Gannon C, Baratz M, Ring D. Predictors of acute carpal tunnel syndrome associated with fracture of the distal radius. J Hand Surg Am. 2008;33(8):1309-1313.

9.    Paley D, McMurtry RY. Median nerve compression by volarly displaced fragments of the distal radius. Clin Orthop Relat Res. 1987;(215):139-147.

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Author and Disclosure Information

John Erickson, MD, Brian Culp, MD, Stephen Kayiaros, MD, and James Monica, MD

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

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The American Journal of Orthopedics - 44(11)
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american journal of orthopedics, AJO, case report and literature review, case report, literature review, flexor tendon injury, injury, tendon, carpal tunnel syndrome, open distal radius fracture, fracture management, fracture, trauma, hand, fingers, CTS, erickson, culp, kayiaros, monica
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John Erickson, MD, Brian Culp, MD, Stephen Kayiaros, MD, and James Monica, MD

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John Erickson, MD, Brian Culp, MD, Stephen Kayiaros, MD, and James Monica, MD

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The literature on extensor tendon rupture and even chronic flexor tendon rupture after volar plating and distal radius fracture malunion is ubiquitous. However, acute and subacute flexor tendon ruptures caused by distal radius fractures have been reported only in limited case reports. These rare injuries may involve multiple tendons and are associated with high-energy mechanisms. This case report details the involvement of multiple flexor tendon injuries associated with a Gustilo-Anderson type II distal radius fracture and the development of acute carpal tunnel syndrome (CTS) after a motor vehicle collision. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

The patient is a 46-year-old woman who was involved in a motor vehicle collision. She was triaged as a trauma patient via Advanced Trauma Life Support protocol, and treated with antibiotic and tetanus prophylaxis. Radiographs showed an open, comminuted, displaced intra-articular distal radius fracture on the right side (Figures 1A, 1B). The fracture was closed reduced and splinted in the emergency department (Figures 2A, 2B). On initial examination, the patient had diffuse paresthesias in the digits that were most pronounced in the median nerve distribution. Motor examination was limited secondary to pain; however, she demonstrated gentle flexion and extension of the digits. The hand was well perfused, and a palpable radial pulse was present. 

 

After clearance was obtained, she was taken urgently to the operating room. The wound was volar and transverse, approximately 2 cm in length, and approximately 4 cm proximal to the wrist crease. The wound was extended proximally and distally for a standard volar (Henry) approach. The flexor carpi radialis tendon was found to be partially lacerated, comprising 60% of the tendon. The fracture was readily identified because the deep fascia and the pronator quadratus were disrupted. No deep tendon lacerations were identified. The median nerve was found to be in continuity. After satisfactory débridement of the fracture and the wound, reduction and fixation was achieved with a volar locking plate and a single Kirschner wire. The flexor carpi radialis tendon was repaired with a modified Kessler stitch and epitenon repair. The wound was closed primarily in layers (Figures 3A, 3B).

The patient’s immediate postoperative neurologic examination was compromised secondary to the patient having a supraclavicular nerve block for anesthesia. Regional anesthesia was chosen because the patient’s pulmonologist recommended avoiding general anesthesia owing to her history of severe asthma that frequently required corticosteroid treatment. Once the block wore off, she complained of persistent paresthesias in all digits but most pronounced in the median nerve distribution. She was able to flex the interphalangeal joint to the index finger but could not flex the interphalangeal joint to the thumb. Over the course of the night, she was also noted to have worsening pain out of proportion to her injury.

As the paresthesias became denser in the median nerve distribution, she was diagnosed with acute CTS and was taken urgently back to the operating room under general anesthesia. After releasing the carpal tunnel through a separate incision, the original wound was reopened and explored. The median nerve was again visualized and found to be in continuity. All 4 tendons to both the flexor digitorum superficialis and flexor digitorum profundus were identified. The flexor pollicis longus (FPL) was not visualized in the wound. The distal portion of the FPL was retracted in the thumb tendon sheath and retrieved blindly with a tendon passer. The proximal portion was retracted to the mid-forearm. The laceration occurred distal to the musculotendinous junction. The tendon was repaired with a modified Kessler stitch as well as a box suture, resulting in 4 core strands across the tendon. The hand and the wrist were splinted in a thumb spica cast, and the patient was started on a modified Duran protocol 1 week after surgery. Median nerve function improved postoperatively. 

Discussion

The rupture of the extensor pollicis longus tendon in nondisplaced distal radius fractures is not uncommon, but occurs in fewer than 5% of nondisplaced distal radius fractures.1 Although less common, chronic complications with flexor tendon rupture after distal radius fracture are well described.1-6 Flexor tendon rupture after distal radius malunion or volar plating is a known complication and is thought to be the result of attritional tendon wear because the flexors rub against protruding bone or plate;3,4,7 however, the initial tendon injury may play a role in those tendons that rupture more quickly.3 When secondary to volar plating, the rupture typically occurs within 1 year of injury,7 but, in both plating and malunion, it has been characterized as a late complication up to 10 years and even 20 years after injury.3,4 Similar to other reports, this rupture was encountered during a volar wrist approach. It has been suggested that, as the incidence of volar plating rises, more acute flexor tendon injuries may be diagnosed because of anatomic exposure,2 but this has not been reported in the literature. 

 

 

Acute and subacute flexor tendon ruptures are rarely reported in the literature. To our knowledge, there are only 2 other reports of acute flexor tendon rupture2,5 after a distal radius fracture, neither of which involved the FPL. These cases, which involved ruptures of the flexor digitorum superficialis and flexor carpi radialis, were thought to be the result of tendon laceration by a volar bone spike. There is also one report of subacute FPL and flexor digitorum profundus rupture approximately 4 weeks after closed reduction of a distal radius fracture.6 Although sparse, the literature regarding flexor tendon rupture and distal radius fractures suggests that involvement of the flexor digitorum superficialis and the flexor digitorum profundus tendons is most common and that the rupture typically occurs in 1 to 4 months.1

We report a rare case of 2 acute flexor tendon lacerations after a Gustilo-Anderson type II open distal radius fracture, likely caused by the volar spike of bone that created the open injury. This case also was complicated by the development of acute CTS. 

To our knowledge, despite a rate of acute CTS reported as high as 5.4% in operatively treated distal radius fractures, there are no established associations between acute CTS and flexor tendon rupture in the setting of distal radius fracture.8,9 In a 2008 retrospective case–control study by Dyer and colleagues,8 fracture translation is the most important risk factor for the development of acute CTS associated with fracture of the distal radius. Although not statistically significant, ipsilateral upper extremity trauma, higher-energy injuries, younger age, and male sex were also associated with the development of acute CTS. Open injuries occurred in only 3 of 50 cases of acute CTS.8

In agreement with published reports, the probability and the timing of tendon rupture are likely related to the severity of the deforming forces applied during the initial insult rather than the resultant stresses.1 Clinicians should have a high suspicion of acute CTS and possible tendon injuries after a high-energy injury with a significantly displaced open distal radius fracture and median nerve paresthesias. A thoughtful and complete preoperative examination of the flexor tendons may prevent the need for reoperation. Concerns for flexor injury and acute CTS should be elevated with the observation of a disrupted pronator. For patients with a volarly displaced fragment after fracture reduction, this concern should be even more elevated.9 Preoperative median nerve symptoms in the setting of the severely displaced fracture should necessitate an acute carpal tunnel release. If 1 flexor tendon is injured, the surgeon should remember that multiple flexor tendons may be involved. We recommend that any injured tendons be repaired primarily, if possible, and the patient started on appropriate rehabilitation.

The literature on extensor tendon rupture and even chronic flexor tendon rupture after volar plating and distal radius fracture malunion is ubiquitous. However, acute and subacute flexor tendon ruptures caused by distal radius fractures have been reported only in limited case reports. These rare injuries may involve multiple tendons and are associated with high-energy mechanisms. This case report details the involvement of multiple flexor tendon injuries associated with a Gustilo-Anderson type II distal radius fracture and the development of acute carpal tunnel syndrome (CTS) after a motor vehicle collision. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

The patient is a 46-year-old woman who was involved in a motor vehicle collision. She was triaged as a trauma patient via Advanced Trauma Life Support protocol, and treated with antibiotic and tetanus prophylaxis. Radiographs showed an open, comminuted, displaced intra-articular distal radius fracture on the right side (Figures 1A, 1B). The fracture was closed reduced and splinted in the emergency department (Figures 2A, 2B). On initial examination, the patient had diffuse paresthesias in the digits that were most pronounced in the median nerve distribution. Motor examination was limited secondary to pain; however, she demonstrated gentle flexion and extension of the digits. The hand was well perfused, and a palpable radial pulse was present. 

 

After clearance was obtained, she was taken urgently to the operating room. The wound was volar and transverse, approximately 2 cm in length, and approximately 4 cm proximal to the wrist crease. The wound was extended proximally and distally for a standard volar (Henry) approach. The flexor carpi radialis tendon was found to be partially lacerated, comprising 60% of the tendon. The fracture was readily identified because the deep fascia and the pronator quadratus were disrupted. No deep tendon lacerations were identified. The median nerve was found to be in continuity. After satisfactory débridement of the fracture and the wound, reduction and fixation was achieved with a volar locking plate and a single Kirschner wire. The flexor carpi radialis tendon was repaired with a modified Kessler stitch and epitenon repair. The wound was closed primarily in layers (Figures 3A, 3B).

The patient’s immediate postoperative neurologic examination was compromised secondary to the patient having a supraclavicular nerve block for anesthesia. Regional anesthesia was chosen because the patient’s pulmonologist recommended avoiding general anesthesia owing to her history of severe asthma that frequently required corticosteroid treatment. Once the block wore off, she complained of persistent paresthesias in all digits but most pronounced in the median nerve distribution. She was able to flex the interphalangeal joint to the index finger but could not flex the interphalangeal joint to the thumb. Over the course of the night, she was also noted to have worsening pain out of proportion to her injury.

As the paresthesias became denser in the median nerve distribution, she was diagnosed with acute CTS and was taken urgently back to the operating room under general anesthesia. After releasing the carpal tunnel through a separate incision, the original wound was reopened and explored. The median nerve was again visualized and found to be in continuity. All 4 tendons to both the flexor digitorum superficialis and flexor digitorum profundus were identified. The flexor pollicis longus (FPL) was not visualized in the wound. The distal portion of the FPL was retracted in the thumb tendon sheath and retrieved blindly with a tendon passer. The proximal portion was retracted to the mid-forearm. The laceration occurred distal to the musculotendinous junction. The tendon was repaired with a modified Kessler stitch as well as a box suture, resulting in 4 core strands across the tendon. The hand and the wrist were splinted in a thumb spica cast, and the patient was started on a modified Duran protocol 1 week after surgery. Median nerve function improved postoperatively. 

Discussion

The rupture of the extensor pollicis longus tendon in nondisplaced distal radius fractures is not uncommon, but occurs in fewer than 5% of nondisplaced distal radius fractures.1 Although less common, chronic complications with flexor tendon rupture after distal radius fracture are well described.1-6 Flexor tendon rupture after distal radius malunion or volar plating is a known complication and is thought to be the result of attritional tendon wear because the flexors rub against protruding bone or plate;3,4,7 however, the initial tendon injury may play a role in those tendons that rupture more quickly.3 When secondary to volar plating, the rupture typically occurs within 1 year of injury,7 but, in both plating and malunion, it has been characterized as a late complication up to 10 years and even 20 years after injury.3,4 Similar to other reports, this rupture was encountered during a volar wrist approach. It has been suggested that, as the incidence of volar plating rises, more acute flexor tendon injuries may be diagnosed because of anatomic exposure,2 but this has not been reported in the literature. 

 

 

Acute and subacute flexor tendon ruptures are rarely reported in the literature. To our knowledge, there are only 2 other reports of acute flexor tendon rupture2,5 after a distal radius fracture, neither of which involved the FPL. These cases, which involved ruptures of the flexor digitorum superficialis and flexor carpi radialis, were thought to be the result of tendon laceration by a volar bone spike. There is also one report of subacute FPL and flexor digitorum profundus rupture approximately 4 weeks after closed reduction of a distal radius fracture.6 Although sparse, the literature regarding flexor tendon rupture and distal radius fractures suggests that involvement of the flexor digitorum superficialis and the flexor digitorum profundus tendons is most common and that the rupture typically occurs in 1 to 4 months.1

We report a rare case of 2 acute flexor tendon lacerations after a Gustilo-Anderson type II open distal radius fracture, likely caused by the volar spike of bone that created the open injury. This case also was complicated by the development of acute CTS. 

To our knowledge, despite a rate of acute CTS reported as high as 5.4% in operatively treated distal radius fractures, there are no established associations between acute CTS and flexor tendon rupture in the setting of distal radius fracture.8,9 In a 2008 retrospective case–control study by Dyer and colleagues,8 fracture translation is the most important risk factor for the development of acute CTS associated with fracture of the distal radius. Although not statistically significant, ipsilateral upper extremity trauma, higher-energy injuries, younger age, and male sex were also associated with the development of acute CTS. Open injuries occurred in only 3 of 50 cases of acute CTS.8

In agreement with published reports, the probability and the timing of tendon rupture are likely related to the severity of the deforming forces applied during the initial insult rather than the resultant stresses.1 Clinicians should have a high suspicion of acute CTS and possible tendon injuries after a high-energy injury with a significantly displaced open distal radius fracture and median nerve paresthesias. A thoughtful and complete preoperative examination of the flexor tendons may prevent the need for reoperation. Concerns for flexor injury and acute CTS should be elevated with the observation of a disrupted pronator. For patients with a volarly displaced fragment after fracture reduction, this concern should be even more elevated.9 Preoperative median nerve symptoms in the setting of the severely displaced fracture should necessitate an acute carpal tunnel release. If 1 flexor tendon is injured, the surgeon should remember that multiple flexor tendons may be involved. We recommend that any injured tendons be repaired primarily, if possible, and the patient started on appropriate rehabilitation.

References

1.    Ashall G. Flexor pollicis longus rupture after fracture of the distal radius. Injury. 1991;22(2):153-155.

2.    Dimatteo L, Wolf JM. Flexor carpi radialis tendon rupture as a complication of a closed distal radius fracture: a case report. J Hand Surg Am. 2007;32(6):818-820.

3.    Kato N, Nemoto K, Arino H, Ichikawa T, Fujikawa K. Ruptures of flexor tendons at the wrist as a complication of fracture of the distal radius. Scand J Plast Reconstr Surg Hand Surg. 2002;36(4):245-248.

4.    Monda MK, Ellis A, Karmani S. Late rupture of flexor pollicis longus tendon 10 years after volar buttress plate fixation of a distal radius fracture: a case report. Acta Orthop Belg. 2010;76(4):549-551.

5.    Southmayd WW, Millender LH, Nalebuff EA. Rupture of the flexor tendons of the index finger after Colles’ fracture. Case report. J Bone Joint Surg Am. 1975;57(4):562-563.

6.    Wong FY, Pho RW. Median nerve compression, with tendon ruptures, after Colles’ fracture. J Hand Surg Br. 1984;9(2):139-141.

7.    Woon CYL, Lee JYL, Ng SW, Teoh LC. Late rupture of flexor pollicis longus tendon after volar distal radius plating: a case report and review of the literature. Inj Extra. 2007;38(7):235-238.

8.    Dyer G, Lozano-Calderon S, Gannon C, Baratz M, Ring D. Predictors of acute carpal tunnel syndrome associated with fracture of the distal radius. J Hand Surg Am. 2008;33(8):1309-1313.

9.    Paley D, McMurtry RY. Median nerve compression by volarly displaced fragments of the distal radius. Clin Orthop Relat Res. 1987;(215):139-147.

References

1.    Ashall G. Flexor pollicis longus rupture after fracture of the distal radius. Injury. 1991;22(2):153-155.

2.    Dimatteo L, Wolf JM. Flexor carpi radialis tendon rupture as a complication of a closed distal radius fracture: a case report. J Hand Surg Am. 2007;32(6):818-820.

3.    Kato N, Nemoto K, Arino H, Ichikawa T, Fujikawa K. Ruptures of flexor tendons at the wrist as a complication of fracture of the distal radius. Scand J Plast Reconstr Surg Hand Surg. 2002;36(4):245-248.

4.    Monda MK, Ellis A, Karmani S. Late rupture of flexor pollicis longus tendon 10 years after volar buttress plate fixation of a distal radius fracture: a case report. Acta Orthop Belg. 2010;76(4):549-551.

5.    Southmayd WW, Millender LH, Nalebuff EA. Rupture of the flexor tendons of the index finger after Colles’ fracture. Case report. J Bone Joint Surg Am. 1975;57(4):562-563.

6.    Wong FY, Pho RW. Median nerve compression, with tendon ruptures, after Colles’ fracture. J Hand Surg Br. 1984;9(2):139-141.

7.    Woon CYL, Lee JYL, Ng SW, Teoh LC. Late rupture of flexor pollicis longus tendon after volar distal radius plating: a case report and review of the literature. Inj Extra. 2007;38(7):235-238.

8.    Dyer G, Lozano-Calderon S, Gannon C, Baratz M, Ring D. Predictors of acute carpal tunnel syndrome associated with fracture of the distal radius. J Hand Surg Am. 2008;33(8):1309-1313.

9.    Paley D, McMurtry RY. Median nerve compression by volarly displaced fragments of the distal radius. Clin Orthop Relat Res. 1987;(215):139-147.

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The American Journal of Orthopedics - 44(11)
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Acute Multiple Flexor Tendon Injury and Carpal Tunnel Syndrome After Open Distal Radius Fracture
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american journal of orthopedics, AJO, case report and literature review, case report, literature review, flexor tendon injury, injury, tendon, carpal tunnel syndrome, open distal radius fracture, fracture management, fracture, trauma, hand, fingers, CTS, erickson, culp, kayiaros, monica
Legacy Keywords
american journal of orthopedics, AJO, case report and literature review, case report, literature review, flexor tendon injury, injury, tendon, carpal tunnel syndrome, open distal radius fracture, fracture management, fracture, trauma, hand, fingers, CTS, erickson, culp, kayiaros, monica
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Medicaid Insurance Is Associated With Larger Curves in Patients Who Require Scoliosis Surgery

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Medicaid Insurance Is Associated With Larger Curves in Patients Who Require Scoliosis Surgery

Rising health care costs have led many health insurers to limit benefits, which may be a problem for children in need of specialty care. Uninsured children have poorer access to specialty care than insured children. Children with public health coverage have better access to specialty care than uninsured children but inferior access compared with privately insured children.1,2 It is well documented that children with government insurance have limited access to orthopedic care for fractures, ligamentous knee injuries, and other injuries.1,3-5 Adolescent idiopathic scoliosis (AIS) differs from many other conditions managed by pediatric orthopedists, as it may be progressive, with management becoming increasingly more complex as the curve magnitude increases.6 The ability to access care earlier in the disease process may allow for earlier nonoperative interventions, such as bracing. For patients who require spinal fusion, earlier diagnosis and referral to a specialist could potentially result in shorter fusions and preserve distal motion segments. The ability to access the health care system in a timely fashion would therefore be of utmost importance for patients with scoliosis.

The literature on AIS is lacking in studies focused on care access based on insurance coverage and the potential impact that this may have on curve progression.7-9 We conducted a study to determine whether there is a difference between patients with and without private insurance who present to a busy urban pediatric orthopedic practice for management of scoliosis that eventually resulted in surgical treatment.

Materials and Methods

After obtaining institutional review board approval for this study, we retrospectively reviewed the medical records of patients (age, 10-18 years) who underwent posterior spinal fusion (PSF) for newly diagnosed AIS between 2008 and 2012. We excluded patients treated with growing spine instrumentation (growing rods), patients younger than 10 years or older than 18 years at presentation, and patients without adequate radiographs or clinical data, including insurance status. To focus on newly diagnosed scoliosis, we also excluded patients who had been seen for second opinions or whose scoliosis had been managed elsewhere in the past. Patients with syndromic, neuromuscular, or congenital scoliosis were also excluded.

Medical records were checked to ascertain time from initial evaluation to decision for surgery, time from recommendation for surgery until actual procedure, and insurance status. Distance traveled was figured from patients’ home addresses. Cobb angles were calculated from initial preoperative and final preoperative posteroanterior (PA) radiographs. Curves as seen on PA, lateral, and maximal effort, supine bending thoracic and lumbar radiographs from the initial preoperative visit were classified using the system of Lenke and colleagues.10 Hospital records were queried to determine number of levels fused at surgery, number of implants placed, and length of stay. Patients were evaluated without prior screening of insurance status and without prior consultation with referring physicians. Surgical procedures were scheduled on a first-come, first-served basis without preference for insurance status.

Results

We identified 135 consecutive patients with newly diagnosed AIS treated with PSF by our group between January 2008 and December 2012 (Table 1). Sixty-one percent had private insurance; 39% had Medicaid. There was no difference in age or ASA (American Society of Anesthesiologists) score between groups. Mean (SD) Cobb angle at initial presentation was 47.5° (14.3°) (range, 18.0°-86.0°) for the private insurance group and 57.2° (15.7°) (range, 23.0°-95.0°) for the Medicaid group (P < .0001). At time of surgery, mean (SD) Cobb angles were 54.6° (11.7°) and 60.6° (13.9°) for the private insurance and Medicaid groups, respectively (P = .008). There was no difference in curve types (Lenke and colleagues10 classification) between groups (Table 2, P = .83). Medicaid patients traveled a shorter mean (SD) distance for care, 56.3 (57.0) miles, versus 73.7 (66.7) miles (P = .05). There was no statistical difference (P = .14) in mean (SD) surgical wait time from surgery recommendation to actual surgery, 103.1 (62.4) days and 128.8 (137.5) days for the private insurance and Medicaid groups, respectively. The difference between patient groups in mean (SD) number of levels fused did not reach statistical significance (P = .16), 10.3 (2.2) levels for the Medicaid group and 9.7 (2.3) levels for the private insurance group. Mean (SD) estimated blood loss was higher for Medicaid patients, 445.7 (415.9) mL versus 335.1 (271.5) mL (P = .06), though there was no difference in use of posterior column osteotomies between groups. There was no difference (P = .11) in mean (SD) length of hospital stay between Medicaid patients, 2.6 (0.8) days, and private insurance patients, 2.4 (0.5) days.

 

 

 

Discussion

According to an extensive body of literature, patients with government insurance have limited access to specialty care.1,11,12 Medicaid-insured children in need of orthopedic care are no exception. Sabharwal and colleagues13 examined a database of pediatric fracture cases and found that 52% of the privately insured patients and 22% of the publicly insured patients received orthopedic care (P = .013).13 When Pierce and colleagues14 called 42 orthopedic practices regarding a fictitious 14-year-old patient with an anterior cruciate ligament tear, 38 offered an appointment within 2 weeks to a privately insured patient, and 6 offered such an appointment to a publicly insured patient. Skaggs and colleagues4 surveyed 230 orthopedic practices nationally and found that Medicaid-insured children had limited access to orthopedic care; 41 practices (18%) would not see a child with Medicaid under any circumstances. Using a fictitious case of a 10-year-old boy with a forearm fracture, Iobst and colleagues3 tried making an appointment at 100 orthopedic offices. Eight gave an appointment within 1 week to a Medicaid-insured patient, and 36 gave an appointment to a privately insured patient.3

There are few data regarding insurance status and scoliosis care in children. Spinal deformity differs from simple fractures and ligamentous injuries, as timely care may result in a less invasive treatment (bracing) if the curvature is caught early. Goldstein and colleagues9 recently evaluated 642 patients who presented for scoliosis evaluation over a 10-year period. There was no difference in curve magnitudes between patients with and without Medicaid insurance. Thirty-two percent of these patients were evaluated for a second opinion, and the authors chose not to subdivide patients on the basis of curve severity and treatment needed, noting only no difference between groups. There was no discussion of the potential difference between patients with and without private insurance with respect to surgically versus nonsurgically treated curves. We wanted to focus specifically on patients who required surgical intervention, as our experience has been that many patients with government insurance present with either very mild scoliosis (10°) or very large curves that were not identified because of lack of primary care access or inadequate school screening. Although summing these 2 groups would result in a similar average, they would represent a different cohort than patients with curves along a bell curve. Furthermore, it is the group of patients who would require surgical intervention that is so critical to identify early in order to intervene.

Our data suggest a difference in presenting curves between patients with and without private insurance. The approximately 10° difference between patient groups in this study could potentially represent the difference between bracing and surgery. Furthermore, Miyanji and colleagues6 evaluated the relationship between Cobb angle and health care consumption and correlated larger curve magnitudes with more levels fused, longer surgeries, and higher rates of transfusion. Specifically, every 10° increase in curve magnitude resulted in 7.8 more minutes of operative time, 0.3 extra levels fused, and 1.5 times increased risk for requiring a blood transfusion.

Cho and Egorova15 recently evaluated insurance status with respect to surgical outcomes using a national inpatient database and found that 42.4% of surgeries for AIS in children with Medicaid had fusions involving 9 or more levels, whereas only 33.6% of privately insured patients had fusions of 9 or more levels. There was no difference in osteotomy or reoperation for pseudarthrosis between groups, but there was a slightly higher rate of infectious (1.1% vs 0.6%) and hemorrhagic (2.5% vs 1.7%) complications in the Medicaid group. Hospital stay was longer in patients with Medicaid, though complications were not different between groups.

The mean difference in the magnitude of the curves treated in our study was not more than 10° between patients with and without Medicaid, perhaps explaining the lack of a statistically significant difference in number of levels fused between groups. Although the groups were similar with respect to the percentage requiring posterior column spinal osteotomies, we noted a difference in estimated blood loss between groups, likely explained by the fact that a junior surgeon was added just before initiation of the study period, potentially skewing the estimated blood loss as this surgeon gained experience. Payer status has been correlated to length of hospital stay in children with scoliosis. Vitale and colleagues8 reviewed the effect of payer status on surgical outcomes in 3606 scoliosis patients from a statewide database in California and concluded that, compared with patients having all other payment sources, Medicaid patients had higher odds for complications and longer hospital stay. Our hospital has adopted a highly coordinated care pathway that allows for discharge on postoperative day 2, likely explaining the lack of any difference in postoperative stay.16

 

 

The disparity in curve magnitudes among patients with and without private insurance is striking and probably multifactorial. Very likely, the combination of schools with limited screening programs within urban or rural school systems,17 restricted access to pediatricians,18,19 and longer waits to see orthopedic specialists20 all contribute to this disparity. It should be noted that school screening is mandatory in our state. This discrepancy may be related to a previously established tendency in minority populations toward waiting longer to seek care and refusing surgical recommendations, though we were unable to query socioeconomic factors such as race and household income.21,22 It is clearly important to increase access to care for underinsured patients with scoliosis. A comprehensive approach, including providing better education in the schools, establishing communication with referring primary care providers, and increasing access through more physicians or physician extenders, is likely needed. Orthopedists should perhaps treat scoliosis evaluation with the same sense of urgency given to minor fractures, and primary care providers should try to ensure that appropriate referrals for scoliosis are made. Also curious was the shorter travel distance for Medicaid patients versus private insurance patients in this study. We hypothesize this is related to our urban location and its large Medicaid population.

Our study had several limitations. Our electronic medical records (EMR) system does not store data related to the time a patient calls for an initial appointment, limiting our ability to determine how long patients waited for their initial consultation. Furthermore, the decision to undergo surgery is multifactorial and cannot be simplified into time from initial recommendation to surgery, as some patients delay surgery because of school or other obligations. These data should be reasonably consistent over time, as patients seen in the early spring in both groups may delay surgery until the summer, and those diagnosed in June may prefer earlier surgery.

Summary

Children with AIS are at risk for curve progression. Therefore, delays in providing timely care may result in worsening scoliosis. Compared with private insurance patients, Medicaid patients presented with larger curve magnitudes. Further study is needed to better delineate ways to improve care access for patients with scoliosis in communities with larger Medicaid populations.

References

1.    Skaggs DL. Less access to care for children with Medicaid. Orthopedics. 2003;26(12):1184, 1186.

2.    Skinner AC, Mayer ML. Effects of insurance status on children’s access to specialty care: a systematic review of the literature. BMC Health Serv Res. 2007;7:194.

3.    Iobst C, King W, Baitner A, Tidwell M, Swirsky S, Skaggs DL. Access to care for children with fractures. J Pediatr Orthop. 2010;30(3):244-247.

4.    Skaggs DL, Lehmann CL, Rice C, et al. Access to orthopaedic care for children with Medicaid versus private insurance: results of a national survey. J Pediatr Orthop. 2006;26(3):400-404.

5.    Skaggs DL, Oda JE, Lerman L, et al. Insurance status and delay in orthotic treatment in children. J Pediatr Orthop. 2007;27(1):94-97.

6.    Miyanji F, Slobogean GP, Samdani AF, et al. Is larger scoliosis curve magnitude associated with increased perioperative health-care resource utilization? A multicenter analysis of 325 adolescent idiopathic scoliosis curves. J Bone Joint Surg Am. 2012;94(9):809-813.

7.    Nuno M, Drazin DG, Acosta FL Jr. Differences in treatments and outcomes for idiopathic scoliosis patients treated in the United States from 1998 to 2007: impact of socioeconomic variables and ethnicity. Spine J. 2013;13(2):116-123.

8.    Vitale MA, Arons RR, Hyman JE, Skaggs DL, Roye DP, Vitale MG. The contribution of hospital volume, payer status, and other factors on the surgical outcomes of scoliosis patients: a review of 3,606 cases in the state of California. J Pediatr Orthop. 2005;25(3):393-399.

9.    Goldstein RY, Joiner ER, Skaggs DL. Insurance status does not predict curve magnitude in adolescent idiopathic scoliosis at first presentation to an orthopaedic surgeon. J Pediatr Orthop. 2015;35(1):39-42.

10.  Lenke LG, Betz RR, Harms J, et al. Adolescent idiopathic scoliosis: a new classification to determine extent of spinal arthrodesis. J Bone Joint Surg Am. 2001;83(8):1169-1181.

11.  Alosh H, Riley LH 3rd, Skolasky RL. Insurance status, geography, race, and ethnicity as predictors of anterior cervical spine surgery rates and in-hospital mortality: an examination of United States trends from 1992 to 2005. Spine. 2009;34(18):1956-1962.

12.  Newacheck PW, Hughes DC, Hung YY, Wong S, Stoddard JJ. The unmet health needs of America’s children. Pediatrics. 2000;105(4 pt 2):989-997.

13.  Sabharwal S, Zhao C, McClemens E, Kaufmann A. Pediatric orthopaedic patients presenting to a university emergency department after visiting another emergency department: demographics and health insurance status. J Pediatr Orthop. 2007;27(6):690-694.

14.  Pierce TR, Mehlman CT, Tamai J, Skaggs DL. Access to care for the adolescent anterior cruciate ligament patient with Medicaid versus private insurance. J Pediatr Orthop. 2012;32(3):245-248.

15.  Cho SK, Egorova NN. The association between insurance status and complications, length of stay, and costs for pediatric idiopathic scoliosis. Spine. 2015;40(4):247-256.

16.  Fletcher ND, Shourbaji N, Mitchell PM, Oswald TS, Devito DP, Bruce RW Jr. Clinical and economic implications of early discharge following posterior spinal fusion for adolescent idiopathic scoliosis. J Child Orthop. 2014;8(3):257-263.

17.  Kasper MJ, Robbins L, Root L, Peterson MG, Allegrante JP. A musculoskeletal outreach screening, treatment, and education program for urban minority children. Arthritis Care Res. 1993;6(3):126-133.

18.  Berman S, Dolins J, Tang SF, Yudkowsky B. Factors that influence the willingness of private primary care pediatricians to accept more Medicaid patients. Pediatrics. 2002;110(2 pt 1):239-248.

19.  Sommers BD. Protecting low-income children’s access to care: are physician visits associated with reduced patient dropout from Medicaid and the Children’s Health Insurance Program? Pediatrics. 2006;118(1):e36-e42.

20.  Bisgaier J, Polsky D, Rhodes KV. Academic medical centers and equity in specialty care access for children. Arch Pediatr Adolesc Med. 2012;166(4):304-310.

21.  Sedlis SP, Fisher VJ, Tice D, Esposito R, Madmon L, Steinberg EH. Racial differences in performance of invasive cardiac procedures in a Department of Veterans Affairs medical center. J Clin Epidemiol. 1997;50(8):899-901.

22.  Mitchell JB, McCormack LA. Time trends in late-stage diagnosis of cervical cancer. Differences by race/ethnicity and income. Med Care. 1997;35(12):1220-1224.

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Nicholas D. Fletcher, MD, David E. Lazarus, MD, Mihir J. Desai, MD, Nick N. Patel, MD, and Robert W. Bruce Jr., MD

Authors’ Disclosure Statement: Dr. Fletcher reports he is a consultant for Orthopaediatrics, Biomet, and Medtronic and receives research support from the Susan Harrison Foundation. The other authors report no actual or potential conflict of interest in relation to this article.

Issue
The American Journal of Orthopedics - 44(11)
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E454-E457
Legacy Keywords
american journal of orthopedics, AJO, online exclusive, original study, study, medicaid, insurance, scoliosis, surgery, adolescent, adolescent idiopathic scoliosis, AIS, spine, posterior spinal fusion, PSF, fletcher, lazarus, desai, patel, bruce
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Nicholas D. Fletcher, MD, David E. Lazarus, MD, Mihir J. Desai, MD, Nick N. Patel, MD, and Robert W. Bruce Jr., MD

Authors’ Disclosure Statement: Dr. Fletcher reports he is a consultant for Orthopaediatrics, Biomet, and Medtronic and receives research support from the Susan Harrison Foundation. The other authors report no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

Nicholas D. Fletcher, MD, David E. Lazarus, MD, Mihir J. Desai, MD, Nick N. Patel, MD, and Robert W. Bruce Jr., MD

Authors’ Disclosure Statement: Dr. Fletcher reports he is a consultant for Orthopaediatrics, Biomet, and Medtronic and receives research support from the Susan Harrison Foundation. The other authors report no actual or potential conflict of interest in relation to this article.

Article PDF
Article PDF

Rising health care costs have led many health insurers to limit benefits, which may be a problem for children in need of specialty care. Uninsured children have poorer access to specialty care than insured children. Children with public health coverage have better access to specialty care than uninsured children but inferior access compared with privately insured children.1,2 It is well documented that children with government insurance have limited access to orthopedic care for fractures, ligamentous knee injuries, and other injuries.1,3-5 Adolescent idiopathic scoliosis (AIS) differs from many other conditions managed by pediatric orthopedists, as it may be progressive, with management becoming increasingly more complex as the curve magnitude increases.6 The ability to access care earlier in the disease process may allow for earlier nonoperative interventions, such as bracing. For patients who require spinal fusion, earlier diagnosis and referral to a specialist could potentially result in shorter fusions and preserve distal motion segments. The ability to access the health care system in a timely fashion would therefore be of utmost importance for patients with scoliosis.

The literature on AIS is lacking in studies focused on care access based on insurance coverage and the potential impact that this may have on curve progression.7-9 We conducted a study to determine whether there is a difference between patients with and without private insurance who present to a busy urban pediatric orthopedic practice for management of scoliosis that eventually resulted in surgical treatment.

Materials and Methods

After obtaining institutional review board approval for this study, we retrospectively reviewed the medical records of patients (age, 10-18 years) who underwent posterior spinal fusion (PSF) for newly diagnosed AIS between 2008 and 2012. We excluded patients treated with growing spine instrumentation (growing rods), patients younger than 10 years or older than 18 years at presentation, and patients without adequate radiographs or clinical data, including insurance status. To focus on newly diagnosed scoliosis, we also excluded patients who had been seen for second opinions or whose scoliosis had been managed elsewhere in the past. Patients with syndromic, neuromuscular, or congenital scoliosis were also excluded.

Medical records were checked to ascertain time from initial evaluation to decision for surgery, time from recommendation for surgery until actual procedure, and insurance status. Distance traveled was figured from patients’ home addresses. Cobb angles were calculated from initial preoperative and final preoperative posteroanterior (PA) radiographs. Curves as seen on PA, lateral, and maximal effort, supine bending thoracic and lumbar radiographs from the initial preoperative visit were classified using the system of Lenke and colleagues.10 Hospital records were queried to determine number of levels fused at surgery, number of implants placed, and length of stay. Patients were evaluated without prior screening of insurance status and without prior consultation with referring physicians. Surgical procedures were scheduled on a first-come, first-served basis without preference for insurance status.

Results

We identified 135 consecutive patients with newly diagnosed AIS treated with PSF by our group between January 2008 and December 2012 (Table 1). Sixty-one percent had private insurance; 39% had Medicaid. There was no difference in age or ASA (American Society of Anesthesiologists) score between groups. Mean (SD) Cobb angle at initial presentation was 47.5° (14.3°) (range, 18.0°-86.0°) for the private insurance group and 57.2° (15.7°) (range, 23.0°-95.0°) for the Medicaid group (P < .0001). At time of surgery, mean (SD) Cobb angles were 54.6° (11.7°) and 60.6° (13.9°) for the private insurance and Medicaid groups, respectively (P = .008). There was no difference in curve types (Lenke and colleagues10 classification) between groups (Table 2, P = .83). Medicaid patients traveled a shorter mean (SD) distance for care, 56.3 (57.0) miles, versus 73.7 (66.7) miles (P = .05). There was no statistical difference (P = .14) in mean (SD) surgical wait time from surgery recommendation to actual surgery, 103.1 (62.4) days and 128.8 (137.5) days for the private insurance and Medicaid groups, respectively. The difference between patient groups in mean (SD) number of levels fused did not reach statistical significance (P = .16), 10.3 (2.2) levels for the Medicaid group and 9.7 (2.3) levels for the private insurance group. Mean (SD) estimated blood loss was higher for Medicaid patients, 445.7 (415.9) mL versus 335.1 (271.5) mL (P = .06), though there was no difference in use of posterior column osteotomies between groups. There was no difference (P = .11) in mean (SD) length of hospital stay between Medicaid patients, 2.6 (0.8) days, and private insurance patients, 2.4 (0.5) days.

 

 

 

Discussion

According to an extensive body of literature, patients with government insurance have limited access to specialty care.1,11,12 Medicaid-insured children in need of orthopedic care are no exception. Sabharwal and colleagues13 examined a database of pediatric fracture cases and found that 52% of the privately insured patients and 22% of the publicly insured patients received orthopedic care (P = .013).13 When Pierce and colleagues14 called 42 orthopedic practices regarding a fictitious 14-year-old patient with an anterior cruciate ligament tear, 38 offered an appointment within 2 weeks to a privately insured patient, and 6 offered such an appointment to a publicly insured patient. Skaggs and colleagues4 surveyed 230 orthopedic practices nationally and found that Medicaid-insured children had limited access to orthopedic care; 41 practices (18%) would not see a child with Medicaid under any circumstances. Using a fictitious case of a 10-year-old boy with a forearm fracture, Iobst and colleagues3 tried making an appointment at 100 orthopedic offices. Eight gave an appointment within 1 week to a Medicaid-insured patient, and 36 gave an appointment to a privately insured patient.3

There are few data regarding insurance status and scoliosis care in children. Spinal deformity differs from simple fractures and ligamentous injuries, as timely care may result in a less invasive treatment (bracing) if the curvature is caught early. Goldstein and colleagues9 recently evaluated 642 patients who presented for scoliosis evaluation over a 10-year period. There was no difference in curve magnitudes between patients with and without Medicaid insurance. Thirty-two percent of these patients were evaluated for a second opinion, and the authors chose not to subdivide patients on the basis of curve severity and treatment needed, noting only no difference between groups. There was no discussion of the potential difference between patients with and without private insurance with respect to surgically versus nonsurgically treated curves. We wanted to focus specifically on patients who required surgical intervention, as our experience has been that many patients with government insurance present with either very mild scoliosis (10°) or very large curves that were not identified because of lack of primary care access or inadequate school screening. Although summing these 2 groups would result in a similar average, they would represent a different cohort than patients with curves along a bell curve. Furthermore, it is the group of patients who would require surgical intervention that is so critical to identify early in order to intervene.

Our data suggest a difference in presenting curves between patients with and without private insurance. The approximately 10° difference between patient groups in this study could potentially represent the difference between bracing and surgery. Furthermore, Miyanji and colleagues6 evaluated the relationship between Cobb angle and health care consumption and correlated larger curve magnitudes with more levels fused, longer surgeries, and higher rates of transfusion. Specifically, every 10° increase in curve magnitude resulted in 7.8 more minutes of operative time, 0.3 extra levels fused, and 1.5 times increased risk for requiring a blood transfusion.

Cho and Egorova15 recently evaluated insurance status with respect to surgical outcomes using a national inpatient database and found that 42.4% of surgeries for AIS in children with Medicaid had fusions involving 9 or more levels, whereas only 33.6% of privately insured patients had fusions of 9 or more levels. There was no difference in osteotomy or reoperation for pseudarthrosis between groups, but there was a slightly higher rate of infectious (1.1% vs 0.6%) and hemorrhagic (2.5% vs 1.7%) complications in the Medicaid group. Hospital stay was longer in patients with Medicaid, though complications were not different between groups.

The mean difference in the magnitude of the curves treated in our study was not more than 10° between patients with and without Medicaid, perhaps explaining the lack of a statistically significant difference in number of levels fused between groups. Although the groups were similar with respect to the percentage requiring posterior column spinal osteotomies, we noted a difference in estimated blood loss between groups, likely explained by the fact that a junior surgeon was added just before initiation of the study period, potentially skewing the estimated blood loss as this surgeon gained experience. Payer status has been correlated to length of hospital stay in children with scoliosis. Vitale and colleagues8 reviewed the effect of payer status on surgical outcomes in 3606 scoliosis patients from a statewide database in California and concluded that, compared with patients having all other payment sources, Medicaid patients had higher odds for complications and longer hospital stay. Our hospital has adopted a highly coordinated care pathway that allows for discharge on postoperative day 2, likely explaining the lack of any difference in postoperative stay.16

 

 

The disparity in curve magnitudes among patients with and without private insurance is striking and probably multifactorial. Very likely, the combination of schools with limited screening programs within urban or rural school systems,17 restricted access to pediatricians,18,19 and longer waits to see orthopedic specialists20 all contribute to this disparity. It should be noted that school screening is mandatory in our state. This discrepancy may be related to a previously established tendency in minority populations toward waiting longer to seek care and refusing surgical recommendations, though we were unable to query socioeconomic factors such as race and household income.21,22 It is clearly important to increase access to care for underinsured patients with scoliosis. A comprehensive approach, including providing better education in the schools, establishing communication with referring primary care providers, and increasing access through more physicians or physician extenders, is likely needed. Orthopedists should perhaps treat scoliosis evaluation with the same sense of urgency given to minor fractures, and primary care providers should try to ensure that appropriate referrals for scoliosis are made. Also curious was the shorter travel distance for Medicaid patients versus private insurance patients in this study. We hypothesize this is related to our urban location and its large Medicaid population.

Our study had several limitations. Our electronic medical records (EMR) system does not store data related to the time a patient calls for an initial appointment, limiting our ability to determine how long patients waited for their initial consultation. Furthermore, the decision to undergo surgery is multifactorial and cannot be simplified into time from initial recommendation to surgery, as some patients delay surgery because of school or other obligations. These data should be reasonably consistent over time, as patients seen in the early spring in both groups may delay surgery until the summer, and those diagnosed in June may prefer earlier surgery.

Summary

Children with AIS are at risk for curve progression. Therefore, delays in providing timely care may result in worsening scoliosis. Compared with private insurance patients, Medicaid patients presented with larger curve magnitudes. Further study is needed to better delineate ways to improve care access for patients with scoliosis in communities with larger Medicaid populations.

Rising health care costs have led many health insurers to limit benefits, which may be a problem for children in need of specialty care. Uninsured children have poorer access to specialty care than insured children. Children with public health coverage have better access to specialty care than uninsured children but inferior access compared with privately insured children.1,2 It is well documented that children with government insurance have limited access to orthopedic care for fractures, ligamentous knee injuries, and other injuries.1,3-5 Adolescent idiopathic scoliosis (AIS) differs from many other conditions managed by pediatric orthopedists, as it may be progressive, with management becoming increasingly more complex as the curve magnitude increases.6 The ability to access care earlier in the disease process may allow for earlier nonoperative interventions, such as bracing. For patients who require spinal fusion, earlier diagnosis and referral to a specialist could potentially result in shorter fusions and preserve distal motion segments. The ability to access the health care system in a timely fashion would therefore be of utmost importance for patients with scoliosis.

The literature on AIS is lacking in studies focused on care access based on insurance coverage and the potential impact that this may have on curve progression.7-9 We conducted a study to determine whether there is a difference between patients with and without private insurance who present to a busy urban pediatric orthopedic practice for management of scoliosis that eventually resulted in surgical treatment.

Materials and Methods

After obtaining institutional review board approval for this study, we retrospectively reviewed the medical records of patients (age, 10-18 years) who underwent posterior spinal fusion (PSF) for newly diagnosed AIS between 2008 and 2012. We excluded patients treated with growing spine instrumentation (growing rods), patients younger than 10 years or older than 18 years at presentation, and patients without adequate radiographs or clinical data, including insurance status. To focus on newly diagnosed scoliosis, we also excluded patients who had been seen for second opinions or whose scoliosis had been managed elsewhere in the past. Patients with syndromic, neuromuscular, or congenital scoliosis were also excluded.

Medical records were checked to ascertain time from initial evaluation to decision for surgery, time from recommendation for surgery until actual procedure, and insurance status. Distance traveled was figured from patients’ home addresses. Cobb angles were calculated from initial preoperative and final preoperative posteroanterior (PA) radiographs. Curves as seen on PA, lateral, and maximal effort, supine bending thoracic and lumbar radiographs from the initial preoperative visit were classified using the system of Lenke and colleagues.10 Hospital records were queried to determine number of levels fused at surgery, number of implants placed, and length of stay. Patients were evaluated without prior screening of insurance status and without prior consultation with referring physicians. Surgical procedures were scheduled on a first-come, first-served basis without preference for insurance status.

Results

We identified 135 consecutive patients with newly diagnosed AIS treated with PSF by our group between January 2008 and December 2012 (Table 1). Sixty-one percent had private insurance; 39% had Medicaid. There was no difference in age or ASA (American Society of Anesthesiologists) score between groups. Mean (SD) Cobb angle at initial presentation was 47.5° (14.3°) (range, 18.0°-86.0°) for the private insurance group and 57.2° (15.7°) (range, 23.0°-95.0°) for the Medicaid group (P < .0001). At time of surgery, mean (SD) Cobb angles were 54.6° (11.7°) and 60.6° (13.9°) for the private insurance and Medicaid groups, respectively (P = .008). There was no difference in curve types (Lenke and colleagues10 classification) between groups (Table 2, P = .83). Medicaid patients traveled a shorter mean (SD) distance for care, 56.3 (57.0) miles, versus 73.7 (66.7) miles (P = .05). There was no statistical difference (P = .14) in mean (SD) surgical wait time from surgery recommendation to actual surgery, 103.1 (62.4) days and 128.8 (137.5) days for the private insurance and Medicaid groups, respectively. The difference between patient groups in mean (SD) number of levels fused did not reach statistical significance (P = .16), 10.3 (2.2) levels for the Medicaid group and 9.7 (2.3) levels for the private insurance group. Mean (SD) estimated blood loss was higher for Medicaid patients, 445.7 (415.9) mL versus 335.1 (271.5) mL (P = .06), though there was no difference in use of posterior column osteotomies between groups. There was no difference (P = .11) in mean (SD) length of hospital stay between Medicaid patients, 2.6 (0.8) days, and private insurance patients, 2.4 (0.5) days.

 

 

 

Discussion

According to an extensive body of literature, patients with government insurance have limited access to specialty care.1,11,12 Medicaid-insured children in need of orthopedic care are no exception. Sabharwal and colleagues13 examined a database of pediatric fracture cases and found that 52% of the privately insured patients and 22% of the publicly insured patients received orthopedic care (P = .013).13 When Pierce and colleagues14 called 42 orthopedic practices regarding a fictitious 14-year-old patient with an anterior cruciate ligament tear, 38 offered an appointment within 2 weeks to a privately insured patient, and 6 offered such an appointment to a publicly insured patient. Skaggs and colleagues4 surveyed 230 orthopedic practices nationally and found that Medicaid-insured children had limited access to orthopedic care; 41 practices (18%) would not see a child with Medicaid under any circumstances. Using a fictitious case of a 10-year-old boy with a forearm fracture, Iobst and colleagues3 tried making an appointment at 100 orthopedic offices. Eight gave an appointment within 1 week to a Medicaid-insured patient, and 36 gave an appointment to a privately insured patient.3

There are few data regarding insurance status and scoliosis care in children. Spinal deformity differs from simple fractures and ligamentous injuries, as timely care may result in a less invasive treatment (bracing) if the curvature is caught early. Goldstein and colleagues9 recently evaluated 642 patients who presented for scoliosis evaluation over a 10-year period. There was no difference in curve magnitudes between patients with and without Medicaid insurance. Thirty-two percent of these patients were evaluated for a second opinion, and the authors chose not to subdivide patients on the basis of curve severity and treatment needed, noting only no difference between groups. There was no discussion of the potential difference between patients with and without private insurance with respect to surgically versus nonsurgically treated curves. We wanted to focus specifically on patients who required surgical intervention, as our experience has been that many patients with government insurance present with either very mild scoliosis (10°) or very large curves that were not identified because of lack of primary care access or inadequate school screening. Although summing these 2 groups would result in a similar average, they would represent a different cohort than patients with curves along a bell curve. Furthermore, it is the group of patients who would require surgical intervention that is so critical to identify early in order to intervene.

Our data suggest a difference in presenting curves between patients with and without private insurance. The approximately 10° difference between patient groups in this study could potentially represent the difference between bracing and surgery. Furthermore, Miyanji and colleagues6 evaluated the relationship between Cobb angle and health care consumption and correlated larger curve magnitudes with more levels fused, longer surgeries, and higher rates of transfusion. Specifically, every 10° increase in curve magnitude resulted in 7.8 more minutes of operative time, 0.3 extra levels fused, and 1.5 times increased risk for requiring a blood transfusion.

Cho and Egorova15 recently evaluated insurance status with respect to surgical outcomes using a national inpatient database and found that 42.4% of surgeries for AIS in children with Medicaid had fusions involving 9 or more levels, whereas only 33.6% of privately insured patients had fusions of 9 or more levels. There was no difference in osteotomy or reoperation for pseudarthrosis between groups, but there was a slightly higher rate of infectious (1.1% vs 0.6%) and hemorrhagic (2.5% vs 1.7%) complications in the Medicaid group. Hospital stay was longer in patients with Medicaid, though complications were not different between groups.

The mean difference in the magnitude of the curves treated in our study was not more than 10° between patients with and without Medicaid, perhaps explaining the lack of a statistically significant difference in number of levels fused between groups. Although the groups were similar with respect to the percentage requiring posterior column spinal osteotomies, we noted a difference in estimated blood loss between groups, likely explained by the fact that a junior surgeon was added just before initiation of the study period, potentially skewing the estimated blood loss as this surgeon gained experience. Payer status has been correlated to length of hospital stay in children with scoliosis. Vitale and colleagues8 reviewed the effect of payer status on surgical outcomes in 3606 scoliosis patients from a statewide database in California and concluded that, compared with patients having all other payment sources, Medicaid patients had higher odds for complications and longer hospital stay. Our hospital has adopted a highly coordinated care pathway that allows for discharge on postoperative day 2, likely explaining the lack of any difference in postoperative stay.16

 

 

The disparity in curve magnitudes among patients with and without private insurance is striking and probably multifactorial. Very likely, the combination of schools with limited screening programs within urban or rural school systems,17 restricted access to pediatricians,18,19 and longer waits to see orthopedic specialists20 all contribute to this disparity. It should be noted that school screening is mandatory in our state. This discrepancy may be related to a previously established tendency in minority populations toward waiting longer to seek care and refusing surgical recommendations, though we were unable to query socioeconomic factors such as race and household income.21,22 It is clearly important to increase access to care for underinsured patients with scoliosis. A comprehensive approach, including providing better education in the schools, establishing communication with referring primary care providers, and increasing access through more physicians or physician extenders, is likely needed. Orthopedists should perhaps treat scoliosis evaluation with the same sense of urgency given to minor fractures, and primary care providers should try to ensure that appropriate referrals for scoliosis are made. Also curious was the shorter travel distance for Medicaid patients versus private insurance patients in this study. We hypothesize this is related to our urban location and its large Medicaid population.

Our study had several limitations. Our electronic medical records (EMR) system does not store data related to the time a patient calls for an initial appointment, limiting our ability to determine how long patients waited for their initial consultation. Furthermore, the decision to undergo surgery is multifactorial and cannot be simplified into time from initial recommendation to surgery, as some patients delay surgery because of school or other obligations. These data should be reasonably consistent over time, as patients seen in the early spring in both groups may delay surgery until the summer, and those diagnosed in June may prefer earlier surgery.

Summary

Children with AIS are at risk for curve progression. Therefore, delays in providing timely care may result in worsening scoliosis. Compared with private insurance patients, Medicaid patients presented with larger curve magnitudes. Further study is needed to better delineate ways to improve care access for patients with scoliosis in communities with larger Medicaid populations.

References

1.    Skaggs DL. Less access to care for children with Medicaid. Orthopedics. 2003;26(12):1184, 1186.

2.    Skinner AC, Mayer ML. Effects of insurance status on children’s access to specialty care: a systematic review of the literature. BMC Health Serv Res. 2007;7:194.

3.    Iobst C, King W, Baitner A, Tidwell M, Swirsky S, Skaggs DL. Access to care for children with fractures. J Pediatr Orthop. 2010;30(3):244-247.

4.    Skaggs DL, Lehmann CL, Rice C, et al. Access to orthopaedic care for children with Medicaid versus private insurance: results of a national survey. J Pediatr Orthop. 2006;26(3):400-404.

5.    Skaggs DL, Oda JE, Lerman L, et al. Insurance status and delay in orthotic treatment in children. J Pediatr Orthop. 2007;27(1):94-97.

6.    Miyanji F, Slobogean GP, Samdani AF, et al. Is larger scoliosis curve magnitude associated with increased perioperative health-care resource utilization? A multicenter analysis of 325 adolescent idiopathic scoliosis curves. J Bone Joint Surg Am. 2012;94(9):809-813.

7.    Nuno M, Drazin DG, Acosta FL Jr. Differences in treatments and outcomes for idiopathic scoliosis patients treated in the United States from 1998 to 2007: impact of socioeconomic variables and ethnicity. Spine J. 2013;13(2):116-123.

8.    Vitale MA, Arons RR, Hyman JE, Skaggs DL, Roye DP, Vitale MG. The contribution of hospital volume, payer status, and other factors on the surgical outcomes of scoliosis patients: a review of 3,606 cases in the state of California. J Pediatr Orthop. 2005;25(3):393-399.

9.    Goldstein RY, Joiner ER, Skaggs DL. Insurance status does not predict curve magnitude in adolescent idiopathic scoliosis at first presentation to an orthopaedic surgeon. J Pediatr Orthop. 2015;35(1):39-42.

10.  Lenke LG, Betz RR, Harms J, et al. Adolescent idiopathic scoliosis: a new classification to determine extent of spinal arthrodesis. J Bone Joint Surg Am. 2001;83(8):1169-1181.

11.  Alosh H, Riley LH 3rd, Skolasky RL. Insurance status, geography, race, and ethnicity as predictors of anterior cervical spine surgery rates and in-hospital mortality: an examination of United States trends from 1992 to 2005. Spine. 2009;34(18):1956-1962.

12.  Newacheck PW, Hughes DC, Hung YY, Wong S, Stoddard JJ. The unmet health needs of America’s children. Pediatrics. 2000;105(4 pt 2):989-997.

13.  Sabharwal S, Zhao C, McClemens E, Kaufmann A. Pediatric orthopaedic patients presenting to a university emergency department after visiting another emergency department: demographics and health insurance status. J Pediatr Orthop. 2007;27(6):690-694.

14.  Pierce TR, Mehlman CT, Tamai J, Skaggs DL. Access to care for the adolescent anterior cruciate ligament patient with Medicaid versus private insurance. J Pediatr Orthop. 2012;32(3):245-248.

15.  Cho SK, Egorova NN. The association between insurance status and complications, length of stay, and costs for pediatric idiopathic scoliosis. Spine. 2015;40(4):247-256.

16.  Fletcher ND, Shourbaji N, Mitchell PM, Oswald TS, Devito DP, Bruce RW Jr. Clinical and economic implications of early discharge following posterior spinal fusion for adolescent idiopathic scoliosis. J Child Orthop. 2014;8(3):257-263.

17.  Kasper MJ, Robbins L, Root L, Peterson MG, Allegrante JP. A musculoskeletal outreach screening, treatment, and education program for urban minority children. Arthritis Care Res. 1993;6(3):126-133.

18.  Berman S, Dolins J, Tang SF, Yudkowsky B. Factors that influence the willingness of private primary care pediatricians to accept more Medicaid patients. Pediatrics. 2002;110(2 pt 1):239-248.

19.  Sommers BD. Protecting low-income children’s access to care: are physician visits associated with reduced patient dropout from Medicaid and the Children’s Health Insurance Program? Pediatrics. 2006;118(1):e36-e42.

20.  Bisgaier J, Polsky D, Rhodes KV. Academic medical centers and equity in specialty care access for children. Arch Pediatr Adolesc Med. 2012;166(4):304-310.

21.  Sedlis SP, Fisher VJ, Tice D, Esposito R, Madmon L, Steinberg EH. Racial differences in performance of invasive cardiac procedures in a Department of Veterans Affairs medical center. J Clin Epidemiol. 1997;50(8):899-901.

22.  Mitchell JB, McCormack LA. Time trends in late-stage diagnosis of cervical cancer. Differences by race/ethnicity and income. Med Care. 1997;35(12):1220-1224.

References

1.    Skaggs DL. Less access to care for children with Medicaid. Orthopedics. 2003;26(12):1184, 1186.

2.    Skinner AC, Mayer ML. Effects of insurance status on children’s access to specialty care: a systematic review of the literature. BMC Health Serv Res. 2007;7:194.

3.    Iobst C, King W, Baitner A, Tidwell M, Swirsky S, Skaggs DL. Access to care for children with fractures. J Pediatr Orthop. 2010;30(3):244-247.

4.    Skaggs DL, Lehmann CL, Rice C, et al. Access to orthopaedic care for children with Medicaid versus private insurance: results of a national survey. J Pediatr Orthop. 2006;26(3):400-404.

5.    Skaggs DL, Oda JE, Lerman L, et al. Insurance status and delay in orthotic treatment in children. J Pediatr Orthop. 2007;27(1):94-97.

6.    Miyanji F, Slobogean GP, Samdani AF, et al. Is larger scoliosis curve magnitude associated with increased perioperative health-care resource utilization? A multicenter analysis of 325 adolescent idiopathic scoliosis curves. J Bone Joint Surg Am. 2012;94(9):809-813.

7.    Nuno M, Drazin DG, Acosta FL Jr. Differences in treatments and outcomes for idiopathic scoliosis patients treated in the United States from 1998 to 2007: impact of socioeconomic variables and ethnicity. Spine J. 2013;13(2):116-123.

8.    Vitale MA, Arons RR, Hyman JE, Skaggs DL, Roye DP, Vitale MG. The contribution of hospital volume, payer status, and other factors on the surgical outcomes of scoliosis patients: a review of 3,606 cases in the state of California. J Pediatr Orthop. 2005;25(3):393-399.

9.    Goldstein RY, Joiner ER, Skaggs DL. Insurance status does not predict curve magnitude in adolescent idiopathic scoliosis at first presentation to an orthopaedic surgeon. J Pediatr Orthop. 2015;35(1):39-42.

10.  Lenke LG, Betz RR, Harms J, et al. Adolescent idiopathic scoliosis: a new classification to determine extent of spinal arthrodesis. J Bone Joint Surg Am. 2001;83(8):1169-1181.

11.  Alosh H, Riley LH 3rd, Skolasky RL. Insurance status, geography, race, and ethnicity as predictors of anterior cervical spine surgery rates and in-hospital mortality: an examination of United States trends from 1992 to 2005. Spine. 2009;34(18):1956-1962.

12.  Newacheck PW, Hughes DC, Hung YY, Wong S, Stoddard JJ. The unmet health needs of America’s children. Pediatrics. 2000;105(4 pt 2):989-997.

13.  Sabharwal S, Zhao C, McClemens E, Kaufmann A. Pediatric orthopaedic patients presenting to a university emergency department after visiting another emergency department: demographics and health insurance status. J Pediatr Orthop. 2007;27(6):690-694.

14.  Pierce TR, Mehlman CT, Tamai J, Skaggs DL. Access to care for the adolescent anterior cruciate ligament patient with Medicaid versus private insurance. J Pediatr Orthop. 2012;32(3):245-248.

15.  Cho SK, Egorova NN. The association between insurance status and complications, length of stay, and costs for pediatric idiopathic scoliosis. Spine. 2015;40(4):247-256.

16.  Fletcher ND, Shourbaji N, Mitchell PM, Oswald TS, Devito DP, Bruce RW Jr. Clinical and economic implications of early discharge following posterior spinal fusion for adolescent idiopathic scoliosis. J Child Orthop. 2014;8(3):257-263.

17.  Kasper MJ, Robbins L, Root L, Peterson MG, Allegrante JP. A musculoskeletal outreach screening, treatment, and education program for urban minority children. Arthritis Care Res. 1993;6(3):126-133.

18.  Berman S, Dolins J, Tang SF, Yudkowsky B. Factors that influence the willingness of private primary care pediatricians to accept more Medicaid patients. Pediatrics. 2002;110(2 pt 1):239-248.

19.  Sommers BD. Protecting low-income children’s access to care: are physician visits associated with reduced patient dropout from Medicaid and the Children’s Health Insurance Program? Pediatrics. 2006;118(1):e36-e42.

20.  Bisgaier J, Polsky D, Rhodes KV. Academic medical centers and equity in specialty care access for children. Arch Pediatr Adolesc Med. 2012;166(4):304-310.

21.  Sedlis SP, Fisher VJ, Tice D, Esposito R, Madmon L, Steinberg EH. Racial differences in performance of invasive cardiac procedures in a Department of Veterans Affairs medical center. J Clin Epidemiol. 1997;50(8):899-901.

22.  Mitchell JB, McCormack LA. Time trends in late-stage diagnosis of cervical cancer. Differences by race/ethnicity and income. Med Care. 1997;35(12):1220-1224.

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Risk Factors for Discharge to Rehabilitation Among Hip Fracture Patients

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Risk Factors for Discharge to Rehabilitation Among Hip Fracture Patients

Length of stay (LOS) is a significant driver of costs after hip fracture surgery.1-3 Multiple studies have identified factors associated with increased LOS in hip fracture patients. These factors include admission time, delay to surgery, presence of comorbidities, and older age.4-9

One significant and potentially modifiable factor affecting LOS is delayed transfer to a rehabilitation center after surgery.8-11 Although patients after orthopedic surgeries require additional rehabilitation services or subacute care directly attributable to their injuries, specialized rehabilitation centers may not always have beds readily available.6-11 Studies have shown that delays in transfer to skilled nursing facilities or rehabilitation centers are highly common among orthopedic patients.8 It is therefore imperative that orthopedists have a mechanism for predicting and identifying which patients require rehabilitation services early in the postoperative period. Identifying risk factors and stratifying patients who are most likely to require rehabilitation would facilitate the early transfer of these patients and thereby directly decrease LOS and hospitalization-related costs.

In this article, we report results from prospective, national, multicenter data to identify commonly measured risk factors for discharge to rehabilitation facilities for hip fracture patients. Through multivariate analysis of ACS-NSQIP (American College of Surgeons National Surgical Quality Improvement Program) data, we determined which risk factors significantly predispose patients to discharge to rehabilitation centers versus discharge home. Knowledge of these risk factors allows the practicing orthopedist to be better equipped to identify patients who require additional rehabilitation early in the postoperative course. By mobilizing case managers and social workers to help avoid delays in the transfers of these identified patients, LOS-associated costs may ultimately decrease.

Materials and Methods

After obtaining institutional review board approval for this study from the Office of Research at Vanderbilt University, we prospectively collected 2011 discharge data from the ACS-NSQIP database (these data are unavailable for earlier years). All patients who underwent hip fracture surgery in 2011 were identified by CPT (Current Procedural Terminology) codes. Cases of patients with unknown discharge information and of those who died during their hospitalizations were excluded from analysis. For the remaining patients, discharge information as categorized by ACS-NSQIP included skilled care (eg, subacute hospital, skilled nursing home), unskilled facility (eg, nursing home, assisted facility), separate acute care, and rehabilitation. All other patients were discharged home without additional assistance or to the previous home where they received chronic care, assisted living, or unskilled aid. Patients were dichotomized according to whether they were discharged home or to one of the rehabilitation facilities mentioned.

To determine which risk factors significantly contributed to a patient’s discharge to rehabilitation, we ran univariate analyses using Fisher exact tests for categorical variables and Student t tests for continuous variables on multiple patient factors, including demographics, preoperative comorbidities, and operative factors. Demographics included age and sex. Preoperative comorbidities included 32 conditions: diabetes mellitus, active smoking status, current alcohol use, dyspnea, history of chronic obstructive pulmonary disease, history of congestive heart failure, hypertension requiring medication, history of esophageal varices, history of myocardial infarction, current renal failure, current dialysis dependence, steroid use, recent weight loss, existing bleeding disorder, transfusion before discharge, presence of central nervous system tumor, recent chemotherapy, recent radiation therapy, previous percutaneous coronary intervention, previous percutaneous coronary stenting, history of angina, peripheral vascular disease, cerebrovascular accidents, recent surgery (within 30 days), rest pain, impaired sensorium, history of transient ischemic attacks, current hemiplegia status, current paraplegia status, current quadriplegia status, current ascites, hypertension, and disseminated cancer. Operative factors included wound infection, DNR (do not resuscitate) status, ventilator support, anesthesia type, wound class, ASA (American Society of Anesthesiologists) class, and operative time.

For the univariate analyses, significance was set at P < .05. Demographics, preoperative comorbidities, and operative factors that were significantly associated with discharge to a rehabilitation facility in the univariate analysis were selected as covariates for a multivariate analysis. We incorporated a binary logistic regression to analyze which of these significant risk factors are correlated with a patient’s discharge to a rehabilitation facility after hip fracture surgery.

Results

A total of 4974 patients undergoing surgery for hip fractures in 2011 were identified. Of these patients, 4815 had complete information on discharge location and were included in the analysis.

Table 1 lists the results of the univariate analysis comparing demographics, preoperative comorbidities, and operative factors between the home and rehabilitation groups. Both age (P < .001) and sex (P = .012) were significantly different between groups; the rehabilitation group was older by about 10 years and included significantly more females. In addition to demographic factors, 16 preoperative comorbidities, and 5 surgical factors were significantly associated with discharge to rehabilitation.

 

 

Surgery type significantly affected discharge to rehabilitation (Figure). Patients who were undergoing open plating of a femoral neck fracture or intramedullary nailing of an intertrochanteric, peritrochanteric, or subtrochanteric femoral fracture constituted 30% of all patients discharged to rehabilitation centers. In contrast, patients undergoing percutaneous skeletal fixation of a proximal femoral fracture constituted only 5.5% of all patients discharged to rehabilitation. Based on surgery type, we broke down discharge location further, into categories of skilled nursing facility, unskilled facility (not patient’s previous home), separate acute-care facility, dedicated rehabilitation center, and home. Of all 4815 patients combined, 2102 (43.6%) were discharged to a skilled nursing facility, 31 (0.6%) to an unskilled facility (not home), 106 (2.2%) to separate acute care, 1312 (27.2%) to a dedicated rehabilitation center, and 950 (19.7%) home.

Table 2 lists the significant results from the multivariate logistical analysis comparing discharge to a rehabilitation center and discharge home after controlling for the significant risk factors (Table 1). Current diabetes, history of dyspnea, previous myocardial infarction, history of ischemic attacks, current bleeding disorder, transfusion during hospitalization, previous percutaneous cardiac stenting, chemotherapy, past cerebrovascular accident, presence of cancer, surgery type based on CPT code, history of chronic obstructive pulmonary disease or congestive heart failure, current smoking status, and operative time longer than 90 minutes were not significantly correlated with discharge to rehabilitation in the multivariate analysis. All significant factors were associated with higher odds of discharge to rehabilitation except for DNR status. DNR patients were 2.04 times more likely (95% CI, 1.49-2.78; P < .001) to be discharged home than to rehabilitation centers.

Applying these adjusted odds ratios, we see that an elderly woman (age, >65 years) who underwent general anesthesia with an ASA class higher than 2 was 17.63 times more likely than a patient without these risk factors to be discharged to rehabilitation. If this patient were also dialysis-dependent, she would be 61.52 times more likely than a similar patient without dialysis needs to be discharged to rehabilitation.

Even when controlling for all significant and nonsignificant variables in multivariate logistical analysis, age over 65 years (β = 1.05; P < .001), female sex (β = 1.76; P = .004), dialysis dependence (β = 12.98; P = .036), hypertension requiring medication (β = 1.53; P = .032), and ASA class higher than 2 (β = 1.98; P = .001) were found to be significant risk factors for discharge to rehabilitation.

Discussion

This study was the first to investigate the issue of which patient risk factors allow the practicing orthopedist to identify patients who require rehabilitation after hip fracture surgery. Through our multivariate analysis, which controlled for demographics, comorbidities, and operative factors, we found that older age, female sex, history of percutaneous coronary intervention, dialysis dependence, general anesthesia, and ASA class higher than 2 significantly increased the odds of discharge to a rehabilitation center versus home.

Using our study’s results, we can create a risk stratification model for patients and thereby a means of targeting patients who need rehabilitation and starting the process of finding a rehabilitation bed early in the postoperative course. Our study’s variables are easily measured metrics that may be collected in any hospital setting. Especially for hip fracture patients, early planning and discharge to the appropriate rehabilitation center are important in decreasing LOS and associated hospitalization costs. According to one report,3 about 85% of all hip fracture costs are directly related to LOS, given the unnecessarily long rehabilitation periods in hospitals. Hollingworth and colleagues2 compared costs for patients who remained in the hospital with costs for those discharged with rehabilitation services. Overall costs were significantly lower for patients discharged home with rehabilitation. The authors concluded that 40% of hip fracture patients may be suitable for early discharge.2 In an analysis of Medicare payments for hip fracture treatment, hospital costs including LOS accounted for 60% of all payments.12 The results of these 2 studies suggest that the overall driver of hip fracture costs is prolonged LOS and that, if patients are discharged to rehabilitation, then overall costs may be lowered through a direct reduction in hospital LOS. Given that hip fractures account for almost 350,000 hospital admissions in the United States each year, and using our institution’s average hospital charge per day ($4500), about $1.6 billion may be saved if each patient’s LOS decreased by 1 day.13 Although multiple factors affect LOS, discharge planning is under orthopedists’ direct control. Therefore, early identification of patients who will require rehabilitation may help reduce LOS-associated costs in our health care system.

 

 

The patient variables that were significantly associated with discharge to rehabilitation are also associated with increased morbidity and mortality in hip fracture patients, according to the literature,14-20 which provides some external validation of using these risk factors as predictors for rehabilitation. A patient with one of these risk factors may require rehabilitation, given that rehabilitation services are specifically linked to lower morbidity and mortality rates among hip fracture patients. For example, patients with dialysis needs were 3.49 times more likely to be discharged to a rehabilitation center in our study. In a 2000 study by Coco and Rush,16 hip fracture patients on dialysis had a 1-year mortality rate 2.5 times higher than that of patients who were not dialysis-dependent. In 2010, Cameron and colleagues17 found that cardiovascular disease was associated with a 2.68 times higher risk of mortality in hip fracture patients. Similarly in our study, both hypertension and history of percutaneous coronary intervention were associated with discharge to rehabilitation. We found higher odds of discharge to rehabilitation with higher ASA classes, which mirror results from a study by Michel and colleagues,15 who found that higher (vs lower) preoperative ASA classes were associated with higher 1-year mortality in hip fracture patients. Interestingly, DNR status was associated with higher odds of discharge home, which may reflect patients’ desires to forgo noninvasive or lifesaving procedures that may be performed at rehabilitation facilities. Although general anesthesia predisposed patients to discharge to a rehabilitation center, multiple studies have found no association between anesthesia type and postoperative mortality rates for hip fracture patients.18,19 Last, Marcantonio and colleagues20 found delirium specifically had a higher odds ratio for discharge, but our univariate analysis did not find a significant association between impaired sensorium and discharge location. Given the correlation of our risk factors with increased morbidity and mortality in the literature, our study’s results provide the initial groundwork for creating a risk calculator that orthopedists can use to predict discharge to rehabilitation.

Our study had some limitations. Although we analyzed a large number of demographics, preoperative comorbidities, and surgical factors, our univariate analysis was limited to information in the ACS-NSQIP database. We did not incorporate other clinically relevant factors (eg, social factors, including patients’ support networks) that may influence discharge decisions. Furthermore, ACS-NSQIP records patient data only up to 30 days after surgery. Discharge information for the time after that was missing for a subset of hip fracture patients, and these patients had to be excluded, potentially skewing our data. ACS-NSQIP also does not collect cost data for patients based on hospitalization or LOS, so we could not determine whether patients discharged to rehabilitation incurred higher costs because of longer hospitalizations.

Nevertheless, our study identified significant patient and operative variables that are associated with discharge to a rehabilitation center. By identifying hip fracture patients with these risk factors early and mobilizing the appropriate resources, practicing orthopedists should be better equipped to help facilitate the discharge of patients to the appropriate location after surgery. Validation of these risk factors should be prospectively determined with an analysis of LOS and cost implications. Use of a risk calculator may in fact result in decreased LOS and hospital-related costs. Furthermore, using these risk factors in a prospective patient cohort would help validate their use and determine whether there is clinical correlation. The orthopedists in our institution are becoming more aware of these risk factors, but validation is necessary.

References

1.    Garcia AE, Bonnaig JV, Yoneda ZT, et al. Patient variables which may predict length of stay and hospital costs in elderly patients with hip fracture. J Orthop Trauma. 2012;26(11):620-623.

2.    Hollingworth W, Todd C, Parker M, Roberts JA, Williams R. Cost analysis of early discharge after hip fracture. BMJ. 1993;307(6909):903-906.

3.    Sund R, Riihimäki J, Mäkelä M, et al. Modeling the length of the care episode after hip fracture: does the type of fracture matter? Scand J Surg. 2009;98(3):169-174.

4.    Fox KM, Magaziner J, Hebel JR, Kenzora JE, Kashner TM. Intertrochanteric versus femoral neck hip fractures: differential characteristics, treatment, and sequelae. J Gerontol A Biol Sci Med Sci. 1999;54(12):M635-M640.

5.    Foss NB, Palm H, Krasheninnikoff M, Kehlet H, Gebuhr P. Impact of surgical complications on length of stay after hip fracture surgery. Injury. 2007;38(7):780-784.

6.    Lefaivre KA, Macadam SA, Davidson DJ, Gandhi R, Chan H, Broekhuyse HM. Length of stay, mortality, morbidity and delay to surgery in hip fractures. J Bone Joint Surg Br. 2009;91(7):922-927.

7.    Clague JE, Craddock E, Andrew G, Horan MA, Pendleton N. Predictors of outcome following hip fracture. Admission time predicts length of stay and in-hospital mortality. Injury. 2002;33(1):1-6.

8.    Parker MJ, Todd CJ, Palmer CR, et al. Inter-hospital variations in length of hospital stay following hip fracture. Age Ageing. 1998;27(31):333-337.

9.    Brasel KJ, Rasmussen J, Cauley C, Weigelt JA. Reasons for delayed discharge of trauma patients. J Surg Res. 2002;107(2):223-226.

10.  Bonar SK, Tinetti ME, Speechley M, Cooney LM. Factors associated with short- versus long-term skilled nursing facility placement among community-living hip fracture patients. J Am Geriatr Soc. 1990;38(10):1139-1144.

11.  Bentler SE, Liu L, Obrizan M, et al. The aftermath of hip fracture: discharge placement, functional status change, and mortality. Am J Epidemiol. 2009;170(10):1290-1299.

12.  Birkmeyer JD, Gust C, Baser O, Dimick JB, Sutherland JM, Skinner JS. Medicare payments for common inpatient procedures: implications for episode-based payment bundling. Health Serv Res. 2010;45(6 pt 1):1783-1795.

13.  American Academy of Orthopaedic Surgeons. Burden of Musculoskeletal Diseases in the United States: Prevalence, Societal and Economic Cost. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2008.

14.  Maciejewski ML, Radcliff A, Henderson WG, et al. Determinants of postsurgical discharge setting for male hip fracture patients. J Rehabil Res Dev. 2013;50(9):1267-1276.

15.  Michel JP, Klopfenstein C, Hoffmeyer P, Stern R, Grab B. Hip fracture surgery: is the pre-operative American Society of Anesthesiologists (ASA) score a predictor of functional outcome? Aging Clin Exp Res. 2002;14(5):389-394.

16.  Coco M, Rush H. Increased incidence of hip fractures in dialysis patients with low serum parathyroid hormone. Am J Kidney Dis. 2000;36(6):1115-1121.

17.  Cameron ID, Chen JS, March LM, et al. Hip fracture causes excess mortality owing to cardiovascular and infectious disease in institutionalized older people: a prospective 5-year study. J Bone Miner Res. 2010;25(4):866-872.

18.  White SM, Moppett IK, Griffiths R. Outcome by mode of anaesthesia for hip fracture surgery. An observational audit of 65 535 patients in a national dataset. Anaesthesia. 2014;69(3):224-230.

19.  Le-Wendling L, Bihorac A, Baslanti TO, et al. Regional anesthesia as compared with general anesthesia for surgery in geriatric patients with hip fracture: does it decrease morbidity, mortality, and health care costs? Results of a single-centered study. Pain Med. 2012;13(7):948-956.

20.  Marcantonio ER, Flacker JM, Michaels M, Resnick NM. Delirium is independently associated with poor functional recovery after hip fracture. J Am Geriatr Soc. 2000;48(6):618-624.

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Vasanth Sathiyakumar, MD, Rachel Thakore, BS, Sarah E. Greenberg, BA, Ashley C. Dodd, BS, William Obremskey, MD, MPH, and Manish K. Sethi, MD

Authors’ Disclosure Statement: Dr. Obremskey previously consulted for Biometrics, gave expert testimony in legal matters, and was committee chair of the Orthopaedic Trauma Association and the Southeastern Fracture Consortium; he has received a grant from the US Department of Defense. The other authors report no actual or potential conflict of interest in relation to this article.

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Authors’ Disclosure Statement: Dr. Obremskey previously consulted for Biometrics, gave expert testimony in legal matters, and was committee chair of the Orthopaedic Trauma Association and the Southeastern Fracture Consortium; he has received a grant from the US Department of Defense. The other authors report no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

Vasanth Sathiyakumar, MD, Rachel Thakore, BS, Sarah E. Greenberg, BA, Ashley C. Dodd, BS, William Obremskey, MD, MPH, and Manish K. Sethi, MD

Authors’ Disclosure Statement: Dr. Obremskey previously consulted for Biometrics, gave expert testimony in legal matters, and was committee chair of the Orthopaedic Trauma Association and the Southeastern Fracture Consortium; he has received a grant from the US Department of Defense. The other authors report no actual or potential conflict of interest in relation to this article.

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Length of stay (LOS) is a significant driver of costs after hip fracture surgery.1-3 Multiple studies have identified factors associated with increased LOS in hip fracture patients. These factors include admission time, delay to surgery, presence of comorbidities, and older age.4-9

One significant and potentially modifiable factor affecting LOS is delayed transfer to a rehabilitation center after surgery.8-11 Although patients after orthopedic surgeries require additional rehabilitation services or subacute care directly attributable to their injuries, specialized rehabilitation centers may not always have beds readily available.6-11 Studies have shown that delays in transfer to skilled nursing facilities or rehabilitation centers are highly common among orthopedic patients.8 It is therefore imperative that orthopedists have a mechanism for predicting and identifying which patients require rehabilitation services early in the postoperative period. Identifying risk factors and stratifying patients who are most likely to require rehabilitation would facilitate the early transfer of these patients and thereby directly decrease LOS and hospitalization-related costs.

In this article, we report results from prospective, national, multicenter data to identify commonly measured risk factors for discharge to rehabilitation facilities for hip fracture patients. Through multivariate analysis of ACS-NSQIP (American College of Surgeons National Surgical Quality Improvement Program) data, we determined which risk factors significantly predispose patients to discharge to rehabilitation centers versus discharge home. Knowledge of these risk factors allows the practicing orthopedist to be better equipped to identify patients who require additional rehabilitation early in the postoperative course. By mobilizing case managers and social workers to help avoid delays in the transfers of these identified patients, LOS-associated costs may ultimately decrease.

Materials and Methods

After obtaining institutional review board approval for this study from the Office of Research at Vanderbilt University, we prospectively collected 2011 discharge data from the ACS-NSQIP database (these data are unavailable for earlier years). All patients who underwent hip fracture surgery in 2011 were identified by CPT (Current Procedural Terminology) codes. Cases of patients with unknown discharge information and of those who died during their hospitalizations were excluded from analysis. For the remaining patients, discharge information as categorized by ACS-NSQIP included skilled care (eg, subacute hospital, skilled nursing home), unskilled facility (eg, nursing home, assisted facility), separate acute care, and rehabilitation. All other patients were discharged home without additional assistance or to the previous home where they received chronic care, assisted living, or unskilled aid. Patients were dichotomized according to whether they were discharged home or to one of the rehabilitation facilities mentioned.

To determine which risk factors significantly contributed to a patient’s discharge to rehabilitation, we ran univariate analyses using Fisher exact tests for categorical variables and Student t tests for continuous variables on multiple patient factors, including demographics, preoperative comorbidities, and operative factors. Demographics included age and sex. Preoperative comorbidities included 32 conditions: diabetes mellitus, active smoking status, current alcohol use, dyspnea, history of chronic obstructive pulmonary disease, history of congestive heart failure, hypertension requiring medication, history of esophageal varices, history of myocardial infarction, current renal failure, current dialysis dependence, steroid use, recent weight loss, existing bleeding disorder, transfusion before discharge, presence of central nervous system tumor, recent chemotherapy, recent radiation therapy, previous percutaneous coronary intervention, previous percutaneous coronary stenting, history of angina, peripheral vascular disease, cerebrovascular accidents, recent surgery (within 30 days), rest pain, impaired sensorium, history of transient ischemic attacks, current hemiplegia status, current paraplegia status, current quadriplegia status, current ascites, hypertension, and disseminated cancer. Operative factors included wound infection, DNR (do not resuscitate) status, ventilator support, anesthesia type, wound class, ASA (American Society of Anesthesiologists) class, and operative time.

For the univariate analyses, significance was set at P < .05. Demographics, preoperative comorbidities, and operative factors that were significantly associated with discharge to a rehabilitation facility in the univariate analysis were selected as covariates for a multivariate analysis. We incorporated a binary logistic regression to analyze which of these significant risk factors are correlated with a patient’s discharge to a rehabilitation facility after hip fracture surgery.

Results

A total of 4974 patients undergoing surgery for hip fractures in 2011 were identified. Of these patients, 4815 had complete information on discharge location and were included in the analysis.

Table 1 lists the results of the univariate analysis comparing demographics, preoperative comorbidities, and operative factors between the home and rehabilitation groups. Both age (P < .001) and sex (P = .012) were significantly different between groups; the rehabilitation group was older by about 10 years and included significantly more females. In addition to demographic factors, 16 preoperative comorbidities, and 5 surgical factors were significantly associated with discharge to rehabilitation.

 

 

Surgery type significantly affected discharge to rehabilitation (Figure). Patients who were undergoing open plating of a femoral neck fracture or intramedullary nailing of an intertrochanteric, peritrochanteric, or subtrochanteric femoral fracture constituted 30% of all patients discharged to rehabilitation centers. In contrast, patients undergoing percutaneous skeletal fixation of a proximal femoral fracture constituted only 5.5% of all patients discharged to rehabilitation. Based on surgery type, we broke down discharge location further, into categories of skilled nursing facility, unskilled facility (not patient’s previous home), separate acute-care facility, dedicated rehabilitation center, and home. Of all 4815 patients combined, 2102 (43.6%) were discharged to a skilled nursing facility, 31 (0.6%) to an unskilled facility (not home), 106 (2.2%) to separate acute care, 1312 (27.2%) to a dedicated rehabilitation center, and 950 (19.7%) home.

Table 2 lists the significant results from the multivariate logistical analysis comparing discharge to a rehabilitation center and discharge home after controlling for the significant risk factors (Table 1). Current diabetes, history of dyspnea, previous myocardial infarction, history of ischemic attacks, current bleeding disorder, transfusion during hospitalization, previous percutaneous cardiac stenting, chemotherapy, past cerebrovascular accident, presence of cancer, surgery type based on CPT code, history of chronic obstructive pulmonary disease or congestive heart failure, current smoking status, and operative time longer than 90 minutes were not significantly correlated with discharge to rehabilitation in the multivariate analysis. All significant factors were associated with higher odds of discharge to rehabilitation except for DNR status. DNR patients were 2.04 times more likely (95% CI, 1.49-2.78; P < .001) to be discharged home than to rehabilitation centers.

Applying these adjusted odds ratios, we see that an elderly woman (age, >65 years) who underwent general anesthesia with an ASA class higher than 2 was 17.63 times more likely than a patient without these risk factors to be discharged to rehabilitation. If this patient were also dialysis-dependent, she would be 61.52 times more likely than a similar patient without dialysis needs to be discharged to rehabilitation.

Even when controlling for all significant and nonsignificant variables in multivariate logistical analysis, age over 65 years (β = 1.05; P < .001), female sex (β = 1.76; P = .004), dialysis dependence (β = 12.98; P = .036), hypertension requiring medication (β = 1.53; P = .032), and ASA class higher than 2 (β = 1.98; P = .001) were found to be significant risk factors for discharge to rehabilitation.

Discussion

This study was the first to investigate the issue of which patient risk factors allow the practicing orthopedist to identify patients who require rehabilitation after hip fracture surgery. Through our multivariate analysis, which controlled for demographics, comorbidities, and operative factors, we found that older age, female sex, history of percutaneous coronary intervention, dialysis dependence, general anesthesia, and ASA class higher than 2 significantly increased the odds of discharge to a rehabilitation center versus home.

Using our study’s results, we can create a risk stratification model for patients and thereby a means of targeting patients who need rehabilitation and starting the process of finding a rehabilitation bed early in the postoperative course. Our study’s variables are easily measured metrics that may be collected in any hospital setting. Especially for hip fracture patients, early planning and discharge to the appropriate rehabilitation center are important in decreasing LOS and associated hospitalization costs. According to one report,3 about 85% of all hip fracture costs are directly related to LOS, given the unnecessarily long rehabilitation periods in hospitals. Hollingworth and colleagues2 compared costs for patients who remained in the hospital with costs for those discharged with rehabilitation services. Overall costs were significantly lower for patients discharged home with rehabilitation. The authors concluded that 40% of hip fracture patients may be suitable for early discharge.2 In an analysis of Medicare payments for hip fracture treatment, hospital costs including LOS accounted for 60% of all payments.12 The results of these 2 studies suggest that the overall driver of hip fracture costs is prolonged LOS and that, if patients are discharged to rehabilitation, then overall costs may be lowered through a direct reduction in hospital LOS. Given that hip fractures account for almost 350,000 hospital admissions in the United States each year, and using our institution’s average hospital charge per day ($4500), about $1.6 billion may be saved if each patient’s LOS decreased by 1 day.13 Although multiple factors affect LOS, discharge planning is under orthopedists’ direct control. Therefore, early identification of patients who will require rehabilitation may help reduce LOS-associated costs in our health care system.

 

 

The patient variables that were significantly associated with discharge to rehabilitation are also associated with increased morbidity and mortality in hip fracture patients, according to the literature,14-20 which provides some external validation of using these risk factors as predictors for rehabilitation. A patient with one of these risk factors may require rehabilitation, given that rehabilitation services are specifically linked to lower morbidity and mortality rates among hip fracture patients. For example, patients with dialysis needs were 3.49 times more likely to be discharged to a rehabilitation center in our study. In a 2000 study by Coco and Rush,16 hip fracture patients on dialysis had a 1-year mortality rate 2.5 times higher than that of patients who were not dialysis-dependent. In 2010, Cameron and colleagues17 found that cardiovascular disease was associated with a 2.68 times higher risk of mortality in hip fracture patients. Similarly in our study, both hypertension and history of percutaneous coronary intervention were associated with discharge to rehabilitation. We found higher odds of discharge to rehabilitation with higher ASA classes, which mirror results from a study by Michel and colleagues,15 who found that higher (vs lower) preoperative ASA classes were associated with higher 1-year mortality in hip fracture patients. Interestingly, DNR status was associated with higher odds of discharge home, which may reflect patients’ desires to forgo noninvasive or lifesaving procedures that may be performed at rehabilitation facilities. Although general anesthesia predisposed patients to discharge to a rehabilitation center, multiple studies have found no association between anesthesia type and postoperative mortality rates for hip fracture patients.18,19 Last, Marcantonio and colleagues20 found delirium specifically had a higher odds ratio for discharge, but our univariate analysis did not find a significant association between impaired sensorium and discharge location. Given the correlation of our risk factors with increased morbidity and mortality in the literature, our study’s results provide the initial groundwork for creating a risk calculator that orthopedists can use to predict discharge to rehabilitation.

Our study had some limitations. Although we analyzed a large number of demographics, preoperative comorbidities, and surgical factors, our univariate analysis was limited to information in the ACS-NSQIP database. We did not incorporate other clinically relevant factors (eg, social factors, including patients’ support networks) that may influence discharge decisions. Furthermore, ACS-NSQIP records patient data only up to 30 days after surgery. Discharge information for the time after that was missing for a subset of hip fracture patients, and these patients had to be excluded, potentially skewing our data. ACS-NSQIP also does not collect cost data for patients based on hospitalization or LOS, so we could not determine whether patients discharged to rehabilitation incurred higher costs because of longer hospitalizations.

Nevertheless, our study identified significant patient and operative variables that are associated with discharge to a rehabilitation center. By identifying hip fracture patients with these risk factors early and mobilizing the appropriate resources, practicing orthopedists should be better equipped to help facilitate the discharge of patients to the appropriate location after surgery. Validation of these risk factors should be prospectively determined with an analysis of LOS and cost implications. Use of a risk calculator may in fact result in decreased LOS and hospital-related costs. Furthermore, using these risk factors in a prospective patient cohort would help validate their use and determine whether there is clinical correlation. The orthopedists in our institution are becoming more aware of these risk factors, but validation is necessary.

Length of stay (LOS) is a significant driver of costs after hip fracture surgery.1-3 Multiple studies have identified factors associated with increased LOS in hip fracture patients. These factors include admission time, delay to surgery, presence of comorbidities, and older age.4-9

One significant and potentially modifiable factor affecting LOS is delayed transfer to a rehabilitation center after surgery.8-11 Although patients after orthopedic surgeries require additional rehabilitation services or subacute care directly attributable to their injuries, specialized rehabilitation centers may not always have beds readily available.6-11 Studies have shown that delays in transfer to skilled nursing facilities or rehabilitation centers are highly common among orthopedic patients.8 It is therefore imperative that orthopedists have a mechanism for predicting and identifying which patients require rehabilitation services early in the postoperative period. Identifying risk factors and stratifying patients who are most likely to require rehabilitation would facilitate the early transfer of these patients and thereby directly decrease LOS and hospitalization-related costs.

In this article, we report results from prospective, national, multicenter data to identify commonly measured risk factors for discharge to rehabilitation facilities for hip fracture patients. Through multivariate analysis of ACS-NSQIP (American College of Surgeons National Surgical Quality Improvement Program) data, we determined which risk factors significantly predispose patients to discharge to rehabilitation centers versus discharge home. Knowledge of these risk factors allows the practicing orthopedist to be better equipped to identify patients who require additional rehabilitation early in the postoperative course. By mobilizing case managers and social workers to help avoid delays in the transfers of these identified patients, LOS-associated costs may ultimately decrease.

Materials and Methods

After obtaining institutional review board approval for this study from the Office of Research at Vanderbilt University, we prospectively collected 2011 discharge data from the ACS-NSQIP database (these data are unavailable for earlier years). All patients who underwent hip fracture surgery in 2011 were identified by CPT (Current Procedural Terminology) codes. Cases of patients with unknown discharge information and of those who died during their hospitalizations were excluded from analysis. For the remaining patients, discharge information as categorized by ACS-NSQIP included skilled care (eg, subacute hospital, skilled nursing home), unskilled facility (eg, nursing home, assisted facility), separate acute care, and rehabilitation. All other patients were discharged home without additional assistance or to the previous home where they received chronic care, assisted living, or unskilled aid. Patients were dichotomized according to whether they were discharged home or to one of the rehabilitation facilities mentioned.

To determine which risk factors significantly contributed to a patient’s discharge to rehabilitation, we ran univariate analyses using Fisher exact tests for categorical variables and Student t tests for continuous variables on multiple patient factors, including demographics, preoperative comorbidities, and operative factors. Demographics included age and sex. Preoperative comorbidities included 32 conditions: diabetes mellitus, active smoking status, current alcohol use, dyspnea, history of chronic obstructive pulmonary disease, history of congestive heart failure, hypertension requiring medication, history of esophageal varices, history of myocardial infarction, current renal failure, current dialysis dependence, steroid use, recent weight loss, existing bleeding disorder, transfusion before discharge, presence of central nervous system tumor, recent chemotherapy, recent radiation therapy, previous percutaneous coronary intervention, previous percutaneous coronary stenting, history of angina, peripheral vascular disease, cerebrovascular accidents, recent surgery (within 30 days), rest pain, impaired sensorium, history of transient ischemic attacks, current hemiplegia status, current paraplegia status, current quadriplegia status, current ascites, hypertension, and disseminated cancer. Operative factors included wound infection, DNR (do not resuscitate) status, ventilator support, anesthesia type, wound class, ASA (American Society of Anesthesiologists) class, and operative time.

For the univariate analyses, significance was set at P < .05. Demographics, preoperative comorbidities, and operative factors that were significantly associated with discharge to a rehabilitation facility in the univariate analysis were selected as covariates for a multivariate analysis. We incorporated a binary logistic regression to analyze which of these significant risk factors are correlated with a patient’s discharge to a rehabilitation facility after hip fracture surgery.

Results

A total of 4974 patients undergoing surgery for hip fractures in 2011 were identified. Of these patients, 4815 had complete information on discharge location and were included in the analysis.

Table 1 lists the results of the univariate analysis comparing demographics, preoperative comorbidities, and operative factors between the home and rehabilitation groups. Both age (P < .001) and sex (P = .012) were significantly different between groups; the rehabilitation group was older by about 10 years and included significantly more females. In addition to demographic factors, 16 preoperative comorbidities, and 5 surgical factors were significantly associated with discharge to rehabilitation.

 

 

Surgery type significantly affected discharge to rehabilitation (Figure). Patients who were undergoing open plating of a femoral neck fracture or intramedullary nailing of an intertrochanteric, peritrochanteric, or subtrochanteric femoral fracture constituted 30% of all patients discharged to rehabilitation centers. In contrast, patients undergoing percutaneous skeletal fixation of a proximal femoral fracture constituted only 5.5% of all patients discharged to rehabilitation. Based on surgery type, we broke down discharge location further, into categories of skilled nursing facility, unskilled facility (not patient’s previous home), separate acute-care facility, dedicated rehabilitation center, and home. Of all 4815 patients combined, 2102 (43.6%) were discharged to a skilled nursing facility, 31 (0.6%) to an unskilled facility (not home), 106 (2.2%) to separate acute care, 1312 (27.2%) to a dedicated rehabilitation center, and 950 (19.7%) home.

Table 2 lists the significant results from the multivariate logistical analysis comparing discharge to a rehabilitation center and discharge home after controlling for the significant risk factors (Table 1). Current diabetes, history of dyspnea, previous myocardial infarction, history of ischemic attacks, current bleeding disorder, transfusion during hospitalization, previous percutaneous cardiac stenting, chemotherapy, past cerebrovascular accident, presence of cancer, surgery type based on CPT code, history of chronic obstructive pulmonary disease or congestive heart failure, current smoking status, and operative time longer than 90 minutes were not significantly correlated with discharge to rehabilitation in the multivariate analysis. All significant factors were associated with higher odds of discharge to rehabilitation except for DNR status. DNR patients were 2.04 times more likely (95% CI, 1.49-2.78; P < .001) to be discharged home than to rehabilitation centers.

Applying these adjusted odds ratios, we see that an elderly woman (age, >65 years) who underwent general anesthesia with an ASA class higher than 2 was 17.63 times more likely than a patient without these risk factors to be discharged to rehabilitation. If this patient were also dialysis-dependent, she would be 61.52 times more likely than a similar patient without dialysis needs to be discharged to rehabilitation.

Even when controlling for all significant and nonsignificant variables in multivariate logistical analysis, age over 65 years (β = 1.05; P < .001), female sex (β = 1.76; P = .004), dialysis dependence (β = 12.98; P = .036), hypertension requiring medication (β = 1.53; P = .032), and ASA class higher than 2 (β = 1.98; P = .001) were found to be significant risk factors for discharge to rehabilitation.

Discussion

This study was the first to investigate the issue of which patient risk factors allow the practicing orthopedist to identify patients who require rehabilitation after hip fracture surgery. Through our multivariate analysis, which controlled for demographics, comorbidities, and operative factors, we found that older age, female sex, history of percutaneous coronary intervention, dialysis dependence, general anesthesia, and ASA class higher than 2 significantly increased the odds of discharge to a rehabilitation center versus home.

Using our study’s results, we can create a risk stratification model for patients and thereby a means of targeting patients who need rehabilitation and starting the process of finding a rehabilitation bed early in the postoperative course. Our study’s variables are easily measured metrics that may be collected in any hospital setting. Especially for hip fracture patients, early planning and discharge to the appropriate rehabilitation center are important in decreasing LOS and associated hospitalization costs. According to one report,3 about 85% of all hip fracture costs are directly related to LOS, given the unnecessarily long rehabilitation periods in hospitals. Hollingworth and colleagues2 compared costs for patients who remained in the hospital with costs for those discharged with rehabilitation services. Overall costs were significantly lower for patients discharged home with rehabilitation. The authors concluded that 40% of hip fracture patients may be suitable for early discharge.2 In an analysis of Medicare payments for hip fracture treatment, hospital costs including LOS accounted for 60% of all payments.12 The results of these 2 studies suggest that the overall driver of hip fracture costs is prolonged LOS and that, if patients are discharged to rehabilitation, then overall costs may be lowered through a direct reduction in hospital LOS. Given that hip fractures account for almost 350,000 hospital admissions in the United States each year, and using our institution’s average hospital charge per day ($4500), about $1.6 billion may be saved if each patient’s LOS decreased by 1 day.13 Although multiple factors affect LOS, discharge planning is under orthopedists’ direct control. Therefore, early identification of patients who will require rehabilitation may help reduce LOS-associated costs in our health care system.

 

 

The patient variables that were significantly associated with discharge to rehabilitation are also associated with increased morbidity and mortality in hip fracture patients, according to the literature,14-20 which provides some external validation of using these risk factors as predictors for rehabilitation. A patient with one of these risk factors may require rehabilitation, given that rehabilitation services are specifically linked to lower morbidity and mortality rates among hip fracture patients. For example, patients with dialysis needs were 3.49 times more likely to be discharged to a rehabilitation center in our study. In a 2000 study by Coco and Rush,16 hip fracture patients on dialysis had a 1-year mortality rate 2.5 times higher than that of patients who were not dialysis-dependent. In 2010, Cameron and colleagues17 found that cardiovascular disease was associated with a 2.68 times higher risk of mortality in hip fracture patients. Similarly in our study, both hypertension and history of percutaneous coronary intervention were associated with discharge to rehabilitation. We found higher odds of discharge to rehabilitation with higher ASA classes, which mirror results from a study by Michel and colleagues,15 who found that higher (vs lower) preoperative ASA classes were associated with higher 1-year mortality in hip fracture patients. Interestingly, DNR status was associated with higher odds of discharge home, which may reflect patients’ desires to forgo noninvasive or lifesaving procedures that may be performed at rehabilitation facilities. Although general anesthesia predisposed patients to discharge to a rehabilitation center, multiple studies have found no association between anesthesia type and postoperative mortality rates for hip fracture patients.18,19 Last, Marcantonio and colleagues20 found delirium specifically had a higher odds ratio for discharge, but our univariate analysis did not find a significant association between impaired sensorium and discharge location. Given the correlation of our risk factors with increased morbidity and mortality in the literature, our study’s results provide the initial groundwork for creating a risk calculator that orthopedists can use to predict discharge to rehabilitation.

Our study had some limitations. Although we analyzed a large number of demographics, preoperative comorbidities, and surgical factors, our univariate analysis was limited to information in the ACS-NSQIP database. We did not incorporate other clinically relevant factors (eg, social factors, including patients’ support networks) that may influence discharge decisions. Furthermore, ACS-NSQIP records patient data only up to 30 days after surgery. Discharge information for the time after that was missing for a subset of hip fracture patients, and these patients had to be excluded, potentially skewing our data. ACS-NSQIP also does not collect cost data for patients based on hospitalization or LOS, so we could not determine whether patients discharged to rehabilitation incurred higher costs because of longer hospitalizations.

Nevertheless, our study identified significant patient and operative variables that are associated with discharge to a rehabilitation center. By identifying hip fracture patients with these risk factors early and mobilizing the appropriate resources, practicing orthopedists should be better equipped to help facilitate the discharge of patients to the appropriate location after surgery. Validation of these risk factors should be prospectively determined with an analysis of LOS and cost implications. Use of a risk calculator may in fact result in decreased LOS and hospital-related costs. Furthermore, using these risk factors in a prospective patient cohort would help validate their use and determine whether there is clinical correlation. The orthopedists in our institution are becoming more aware of these risk factors, but validation is necessary.

References

1.    Garcia AE, Bonnaig JV, Yoneda ZT, et al. Patient variables which may predict length of stay and hospital costs in elderly patients with hip fracture. J Orthop Trauma. 2012;26(11):620-623.

2.    Hollingworth W, Todd C, Parker M, Roberts JA, Williams R. Cost analysis of early discharge after hip fracture. BMJ. 1993;307(6909):903-906.

3.    Sund R, Riihimäki J, Mäkelä M, et al. Modeling the length of the care episode after hip fracture: does the type of fracture matter? Scand J Surg. 2009;98(3):169-174.

4.    Fox KM, Magaziner J, Hebel JR, Kenzora JE, Kashner TM. Intertrochanteric versus femoral neck hip fractures: differential characteristics, treatment, and sequelae. J Gerontol A Biol Sci Med Sci. 1999;54(12):M635-M640.

5.    Foss NB, Palm H, Krasheninnikoff M, Kehlet H, Gebuhr P. Impact of surgical complications on length of stay after hip fracture surgery. Injury. 2007;38(7):780-784.

6.    Lefaivre KA, Macadam SA, Davidson DJ, Gandhi R, Chan H, Broekhuyse HM. Length of stay, mortality, morbidity and delay to surgery in hip fractures. J Bone Joint Surg Br. 2009;91(7):922-927.

7.    Clague JE, Craddock E, Andrew G, Horan MA, Pendleton N. Predictors of outcome following hip fracture. Admission time predicts length of stay and in-hospital mortality. Injury. 2002;33(1):1-6.

8.    Parker MJ, Todd CJ, Palmer CR, et al. Inter-hospital variations in length of hospital stay following hip fracture. Age Ageing. 1998;27(31):333-337.

9.    Brasel KJ, Rasmussen J, Cauley C, Weigelt JA. Reasons for delayed discharge of trauma patients. J Surg Res. 2002;107(2):223-226.

10.  Bonar SK, Tinetti ME, Speechley M, Cooney LM. Factors associated with short- versus long-term skilled nursing facility placement among community-living hip fracture patients. J Am Geriatr Soc. 1990;38(10):1139-1144.

11.  Bentler SE, Liu L, Obrizan M, et al. The aftermath of hip fracture: discharge placement, functional status change, and mortality. Am J Epidemiol. 2009;170(10):1290-1299.

12.  Birkmeyer JD, Gust C, Baser O, Dimick JB, Sutherland JM, Skinner JS. Medicare payments for common inpatient procedures: implications for episode-based payment bundling. Health Serv Res. 2010;45(6 pt 1):1783-1795.

13.  American Academy of Orthopaedic Surgeons. Burden of Musculoskeletal Diseases in the United States: Prevalence, Societal and Economic Cost. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2008.

14.  Maciejewski ML, Radcliff A, Henderson WG, et al. Determinants of postsurgical discharge setting for male hip fracture patients. J Rehabil Res Dev. 2013;50(9):1267-1276.

15.  Michel JP, Klopfenstein C, Hoffmeyer P, Stern R, Grab B. Hip fracture surgery: is the pre-operative American Society of Anesthesiologists (ASA) score a predictor of functional outcome? Aging Clin Exp Res. 2002;14(5):389-394.

16.  Coco M, Rush H. Increased incidence of hip fractures in dialysis patients with low serum parathyroid hormone. Am J Kidney Dis. 2000;36(6):1115-1121.

17.  Cameron ID, Chen JS, March LM, et al. Hip fracture causes excess mortality owing to cardiovascular and infectious disease in institutionalized older people: a prospective 5-year study. J Bone Miner Res. 2010;25(4):866-872.

18.  White SM, Moppett IK, Griffiths R. Outcome by mode of anaesthesia for hip fracture surgery. An observational audit of 65 535 patients in a national dataset. Anaesthesia. 2014;69(3):224-230.

19.  Le-Wendling L, Bihorac A, Baslanti TO, et al. Regional anesthesia as compared with general anesthesia for surgery in geriatric patients with hip fracture: does it decrease morbidity, mortality, and health care costs? Results of a single-centered study. Pain Med. 2012;13(7):948-956.

20.  Marcantonio ER, Flacker JM, Michaels M, Resnick NM. Delirium is independently associated with poor functional recovery after hip fracture. J Am Geriatr Soc. 2000;48(6):618-624.

References

1.    Garcia AE, Bonnaig JV, Yoneda ZT, et al. Patient variables which may predict length of stay and hospital costs in elderly patients with hip fracture. J Orthop Trauma. 2012;26(11):620-623.

2.    Hollingworth W, Todd C, Parker M, Roberts JA, Williams R. Cost analysis of early discharge after hip fracture. BMJ. 1993;307(6909):903-906.

3.    Sund R, Riihimäki J, Mäkelä M, et al. Modeling the length of the care episode after hip fracture: does the type of fracture matter? Scand J Surg. 2009;98(3):169-174.

4.    Fox KM, Magaziner J, Hebel JR, Kenzora JE, Kashner TM. Intertrochanteric versus femoral neck hip fractures: differential characteristics, treatment, and sequelae. J Gerontol A Biol Sci Med Sci. 1999;54(12):M635-M640.

5.    Foss NB, Palm H, Krasheninnikoff M, Kehlet H, Gebuhr P. Impact of surgical complications on length of stay after hip fracture surgery. Injury. 2007;38(7):780-784.

6.    Lefaivre KA, Macadam SA, Davidson DJ, Gandhi R, Chan H, Broekhuyse HM. Length of stay, mortality, morbidity and delay to surgery in hip fractures. J Bone Joint Surg Br. 2009;91(7):922-927.

7.    Clague JE, Craddock E, Andrew G, Horan MA, Pendleton N. Predictors of outcome following hip fracture. Admission time predicts length of stay and in-hospital mortality. Injury. 2002;33(1):1-6.

8.    Parker MJ, Todd CJ, Palmer CR, et al. Inter-hospital variations in length of hospital stay following hip fracture. Age Ageing. 1998;27(31):333-337.

9.    Brasel KJ, Rasmussen J, Cauley C, Weigelt JA. Reasons for delayed discharge of trauma patients. J Surg Res. 2002;107(2):223-226.

10.  Bonar SK, Tinetti ME, Speechley M, Cooney LM. Factors associated with short- versus long-term skilled nursing facility placement among community-living hip fracture patients. J Am Geriatr Soc. 1990;38(10):1139-1144.

11.  Bentler SE, Liu L, Obrizan M, et al. The aftermath of hip fracture: discharge placement, functional status change, and mortality. Am J Epidemiol. 2009;170(10):1290-1299.

12.  Birkmeyer JD, Gust C, Baser O, Dimick JB, Sutherland JM, Skinner JS. Medicare payments for common inpatient procedures: implications for episode-based payment bundling. Health Serv Res. 2010;45(6 pt 1):1783-1795.

13.  American Academy of Orthopaedic Surgeons. Burden of Musculoskeletal Diseases in the United States: Prevalence, Societal and Economic Cost. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2008.

14.  Maciejewski ML, Radcliff A, Henderson WG, et al. Determinants of postsurgical discharge setting for male hip fracture patients. J Rehabil Res Dev. 2013;50(9):1267-1276.

15.  Michel JP, Klopfenstein C, Hoffmeyer P, Stern R, Grab B. Hip fracture surgery: is the pre-operative American Society of Anesthesiologists (ASA) score a predictor of functional outcome? Aging Clin Exp Res. 2002;14(5):389-394.

16.  Coco M, Rush H. Increased incidence of hip fractures in dialysis patients with low serum parathyroid hormone. Am J Kidney Dis. 2000;36(6):1115-1121.

17.  Cameron ID, Chen JS, March LM, et al. Hip fracture causes excess mortality owing to cardiovascular and infectious disease in institutionalized older people: a prospective 5-year study. J Bone Miner Res. 2010;25(4):866-872.

18.  White SM, Moppett IK, Griffiths R. Outcome by mode of anaesthesia for hip fracture surgery. An observational audit of 65 535 patients in a national dataset. Anaesthesia. 2014;69(3):224-230.

19.  Le-Wendling L, Bihorac A, Baslanti TO, et al. Regional anesthesia as compared with general anesthesia for surgery in geriatric patients with hip fracture: does it decrease morbidity, mortality, and health care costs? Results of a single-centered study. Pain Med. 2012;13(7):948-956.

20.  Marcantonio ER, Flacker JM, Michaels M, Resnick NM. Delirium is independently associated with poor functional recovery after hip fracture. J Am Geriatr Soc. 2000;48(6):618-624.

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Reinforcing a Spica Cast With a Fiberglass Bar

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Reinforcing a Spica Cast With a Fiberglass Bar

Femur fractures (Orthopaedic Trauma Association classes 31, 32, 33)1 are common childhood injuries, occurring at a rate of 19 per 100,000 children in the United States.2 Peak occurrence is bimodal at ages 2 and 17 years. The most common mechanism of injury in children under 6 years is a fall, and hip spica casting is the preferred treatment modality in this group.3-5

A bar connecting the legs of the spica cast has been shown to facilitate patient transport5 and significantly decrease mechanical failure of the spica cast.6 This bar often consists of a broom handle or pipe that must be cut to size during the case and subsequently incorporated into the cast—tasks that are often inconvenient and time-consuming for on-call or emergency department staff unfamiliar with orthopedic tools.

In this article, we review a spica cast application that incorporates a low-cost, lightweight technique for fabricating a connecting bar from existing fiberglass casting material. The Institutional Review Board at Connecticut Children’s Medical Center approved this work.

Technique of Double-Leg Spica Casting With Fiberglass Bar

A spica casting table (Orthopedic Systems) with a well-padded post is placed on the operating room table and adjusted to the length of the patient from perineum to just below the shoulders. With the patient under general anesthesia, folded towels are used to provide 2 to 4 cm of padding on the anterior torso, atop which a waterproof pantaloon is applied. The patient is transferred to the spica table, and the patient’s arms are gently secured to the casting table with cast padding or tape in an abducted position at the shoulders. A surgeon controls the legs by holding the feet with the long fingers just above the heels, the index fingers on the anterior ankle, and the thumbs on the soles of the feet. Cast padding is wrapped from the nipple line to the supramalleolar region on each leg. The bony prominences of the malleoli, patella, fibular head, femoral condyles, iliac crests, and coccyx are well padded.

Fiberglass is then rolled without compression onto the patient, beginning with the torso and perineal areas. The injured leg is wrapped to its final length above the malleoli while the uninjured leg is kept free. Maintaining the position of the injured leg with simultaneous molding at the fracture site, typically to promote valgus, allows fracture reduction. The fracture position is then checked under image intensification. For femur fractures, hip abduction and flexion are set to 45° and 90°, respectively, while knee flexion is between 50° and 90°. The uninjured leg is then wrapped with fiberglass. Additional strips of fiberglass can be used to reinforce weak junctional regions between the torso and the legs, posteriorly over the “intern’s triangle” and anteriorly along the hip crease.

A connecting fiberglass bar is then created using a fiberglass roll once the cast is hardened. A 2-inch fiberglass roll is wrapped around one leg to secure its position (Figure 1A) and then rolled around the second limb (Figure 1B). Fiberglass is then pulled taut and rolled around the bridge that has been created in order to thicken the bar (Figure 2). The roll is again brought around the closest limb, wrapped back across the bridge to the other limb, and rolled out to its full length. Last, the legs are abducted 1 to 2 cm to tension the bar (Figure 3). Although this does not produce enough movement to cause a crease and a resultant ulcer, careful inspection of common pressure points (eg, popliteal fossa) should be performed after the cast is complete.

The chest towels are removed, and the final cast is inspected clinically and fluoroscopically at the fracture site before extubation. The cast is trimmed as needed to ensure room for perineal care, as well as full ankle flexion and extension without impingement. Cast edges are further petaled with plastic tape (Hy-Tape International) to provide padding and prevent the waterproof lining from tearing.

Postoperative care involves overnight observation and caregiver practice in perineal care. Frequent rotation from supine to prone is encouraged. Nurses confirm car-seat fit before discharge. If needed, radiographs are obtained 7 to 10 days later to help with wedging adjustment. The cast is removed in the clinic when adequate callus is appreciated on subsequent radiographs.

Case Series

Our experience with this technique in 16 unilateral femur fractures has been favorable (Table). Patient age ranged from 5 months to 3 years. Mean pretreatment angulation was 13° varus and 11° procurvatum. The majority of fractures were femoral shaft fractures; 1 was proximal, 2 distal.

 

 

All fractures united without cast revision. Mean cast time was 4.5 weeks (range, 16 days–6 weeks). Immediate postoperative alignment was 2.5° varus (range, 11° valgus to 16° varus) and 7° procurvatum (range, 1° recurvatum to 22° procurvatum). Mean shortening was 1.5 cm (range, 0-2.7 cm). Final alignment was 1° valgus (range, 9° valgus to 12° varus) and 5° procurvatum (range, 0° to 22°). Mean follow-up was 8 months. There were no cases of skin maceration or cast failure. No casts precluded use of a spica car-seat. Figure 4 shows a typical case with a midshaft fracture treated with closed reduction and casting for 4 weeks with good remodeling at final follow-up, 19 months after injury.

Discussion

Although single-leg walking spica casts have been shown to safely treat low-energy femur fractures in children 1 to 6 years old,7 length-unstable femur fractures, bilateral femur fractures, and patients with hip dysplasia continue to be managed with a double-leg hip spica construct. Cast integrity remains fundamental to the control of most fractures and prevention of cast-related complications, such as skin maceration and ulceration. Surgeons typically use spica cast reinforcement schemes—such as cast augments of the torso–limb junction, with multiple layers of casting material or incorporation of a connecting bar between the legs, typically constructed by overwrapping a wooden dowel in casting material—to improve the mechanical stability of casts.6 The present technique of creating a connecting bar from fiberglass casting material significantly simplifies the standard wooden dowel approach and provided excellent results in our treatment group in terms of cast integrity and fracture alignment. In addition, at our institution, a roll of fiberglass costs $2.10, whereas a wooden dowel costs $3 to $10 and can be difficult to locate if not frequently used. Other tube-shaped materials, such as the disposable material used to package implants and tubes, carry an even lower cost. However, we have found that a single fiberglass roll is most readily available and easiest to apply.

Although proper spica cast application remains important in managing pediatric trauma, it lacks a good technical description in the literature. In this technical report, we have presented our standard spica cast application method, which minimizes the range of cast complications that have been reported, from minor skin irritation to superior mesenteric artery syndrome. Two salient technical highlights are use of waterproof pantaloon liners and cast petaling, which we have found almost eliminate the morbidity of potential skin complications, reported to occur at a rate of 28%.8 In addition, we forgo applying the cast on the injured leg in segments. Application of a short-leg cast on the injured leg to allow traction on the leg during cast application is of dubious utility and may be potentially harmful, with described complications of peroneal nerve palsy and compartment syndrome.9-11 Further, it is important to use an abdominal spacer (eg, a stack of towels) under the cast padding to create room for abdominal expansion and minimize pressure thought to induce superior mesenteric artery syndrome. Plastic or rubber abdominal spacers have also been described.12,13 Last, leg position is important for reduction and maintenance of the fracture, as well as patient care. Literature advocates minimizing hip abduction to just that needed for perineal care and maximizing hip flexion and knee extension to optimize car-seat fit and safety.14

Conclusion

Construction of a spica cast lower limb connecting bar from readily available fiberglass casting material allows a facile and rapid addition to the mechanical stability of a spica cast in the treatment of pediatric femur fractures. The technique is low-cost and obviates the need for additional extraneous materials.

References

1.    Slongo TF, Audigé L; AO Pediatric Classification Group. Fracture and dislocation classification compendium for children: the AO Pediatric Comprehensive Classification of Long Bone Fractures (PCCF). J Orthop Trauma. 2007;21(10):S135-S160.

2.    Hinton RY, Lincoln A, Crockett MM, Sponseller P, Smith G. Fractures of the femoral shaft in children. Incidence, mechanisms, and sociodemographic risk factors. J Bone Joint Surg Am. 1999;81(4):500-509.

3.    Campbell WC, Canale ST, Beaty JH, eds. Campbell’s Operative Orthopaedics. 11th ed. Philadelphia, PA: Mosby Elsevier; 2008.

4.    Lovell WW, Winter RB, Morrissy RT, Weinstein SL. Lovell and Winter’s Pediatric Orthopaedics. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.

5.    Green NE, Swiontkowski MF, eds. Skeletal Trauma in Children. 4th ed. Philadelphia, PA: Elsevier Health Sciences; 2009.

6.    Hosalkar HS, Jones S, Chowdhury M, Chatoo M, Hill RA. Connecting bar for hip spica reinforcement: does it help? J Pediatr Orthop B. 2003;12(2):100-102.

7.    Flynn JM, Garner MR, Jones KJ, et al. The treatment of low-energy femoral shaft fractures: a prospective study comparing the “walking spica” with the traditional spica cast. J Bone Joint Surg Am. 2011;93(23):2196-2202.

8.    DiFazio R, Vessey J, Zurakowski D, Hresko MT, Matheney T. Incidence of skin complications and associated charges in children treated with hip spica casts for femur fractures. J Pediatr Orthop. 2011;31(1):17-22.

9.    Weiss AP, Schenck RC Jr, Sponseller PD, Thompson JD. Peroneal nerve palsy after early cast application for femoral fractures in children. J Pediatr Orthop. 1992;12(1):25-28.

10. Mubarak SJ, Frick S, Sink E, Rathjen K, Noonan KJ. Volkmann contracture and compartment syndromes after femur fractures in children treated with 90/90 spica casts. J Pediatr Orthop. 2006;26(5):567-572.

11. Large TM, Frick SL. Compartment syndrome of the leg after treatment of a femoral fracture with an early sitting spica cast. A report of two cases. J Bone Joint Surg Am. 2003;85(11):2207-2210.

12. Sharma S, Azzopardi T. Reduction of abdominal pressure for prophylaxis of the mesenteric artery syndrome (cast syndrome) in a hip spica—a simple technique. Ann R Coll Surg Engl. 2006;88(3):317.

13. Kiter E, Demirkan F, Kiliç BA, Erkula G. A new technique for creating an abdominal window in a hip spica cast. J Orthop Trauma. 2003;17(6):442-443.

14. Zielinski J, Oliver G, Sybesma J, Walter N, Atkinson P. Casting technique and restraint choice influence child safety during transport of body casted children subjected to a simulated frontal MVA. J Trauma. 2009;66(6):1653-1665.

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Sonia Chaudhry, MD, Kevin Kang, MD, and Mark C. Lee, MD

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

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Sonia Chaudhry, MD, Kevin Kang, MD, and Mark C. Lee, MD

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

Author and Disclosure Information

Sonia Chaudhry, MD, Kevin Kang, MD, and Mark C. Lee, MD

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

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Femur fractures (Orthopaedic Trauma Association classes 31, 32, 33)1 are common childhood injuries, occurring at a rate of 19 per 100,000 children in the United States.2 Peak occurrence is bimodal at ages 2 and 17 years. The most common mechanism of injury in children under 6 years is a fall, and hip spica casting is the preferred treatment modality in this group.3-5

A bar connecting the legs of the spica cast has been shown to facilitate patient transport5 and significantly decrease mechanical failure of the spica cast.6 This bar often consists of a broom handle or pipe that must be cut to size during the case and subsequently incorporated into the cast—tasks that are often inconvenient and time-consuming for on-call or emergency department staff unfamiliar with orthopedic tools.

In this article, we review a spica cast application that incorporates a low-cost, lightweight technique for fabricating a connecting bar from existing fiberglass casting material. The Institutional Review Board at Connecticut Children’s Medical Center approved this work.

Technique of Double-Leg Spica Casting With Fiberglass Bar

A spica casting table (Orthopedic Systems) with a well-padded post is placed on the operating room table and adjusted to the length of the patient from perineum to just below the shoulders. With the patient under general anesthesia, folded towels are used to provide 2 to 4 cm of padding on the anterior torso, atop which a waterproof pantaloon is applied. The patient is transferred to the spica table, and the patient’s arms are gently secured to the casting table with cast padding or tape in an abducted position at the shoulders. A surgeon controls the legs by holding the feet with the long fingers just above the heels, the index fingers on the anterior ankle, and the thumbs on the soles of the feet. Cast padding is wrapped from the nipple line to the supramalleolar region on each leg. The bony prominences of the malleoli, patella, fibular head, femoral condyles, iliac crests, and coccyx are well padded.

Fiberglass is then rolled without compression onto the patient, beginning with the torso and perineal areas. The injured leg is wrapped to its final length above the malleoli while the uninjured leg is kept free. Maintaining the position of the injured leg with simultaneous molding at the fracture site, typically to promote valgus, allows fracture reduction. The fracture position is then checked under image intensification. For femur fractures, hip abduction and flexion are set to 45° and 90°, respectively, while knee flexion is between 50° and 90°. The uninjured leg is then wrapped with fiberglass. Additional strips of fiberglass can be used to reinforce weak junctional regions between the torso and the legs, posteriorly over the “intern’s triangle” and anteriorly along the hip crease.

A connecting fiberglass bar is then created using a fiberglass roll once the cast is hardened. A 2-inch fiberglass roll is wrapped around one leg to secure its position (Figure 1A) and then rolled around the second limb (Figure 1B). Fiberglass is then pulled taut and rolled around the bridge that has been created in order to thicken the bar (Figure 2). The roll is again brought around the closest limb, wrapped back across the bridge to the other limb, and rolled out to its full length. Last, the legs are abducted 1 to 2 cm to tension the bar (Figure 3). Although this does not produce enough movement to cause a crease and a resultant ulcer, careful inspection of common pressure points (eg, popliteal fossa) should be performed after the cast is complete.

The chest towels are removed, and the final cast is inspected clinically and fluoroscopically at the fracture site before extubation. The cast is trimmed as needed to ensure room for perineal care, as well as full ankle flexion and extension without impingement. Cast edges are further petaled with plastic tape (Hy-Tape International) to provide padding and prevent the waterproof lining from tearing.

Postoperative care involves overnight observation and caregiver practice in perineal care. Frequent rotation from supine to prone is encouraged. Nurses confirm car-seat fit before discharge. If needed, radiographs are obtained 7 to 10 days later to help with wedging adjustment. The cast is removed in the clinic when adequate callus is appreciated on subsequent radiographs.

Case Series

Our experience with this technique in 16 unilateral femur fractures has been favorable (Table). Patient age ranged from 5 months to 3 years. Mean pretreatment angulation was 13° varus and 11° procurvatum. The majority of fractures were femoral shaft fractures; 1 was proximal, 2 distal.

 

 

All fractures united without cast revision. Mean cast time was 4.5 weeks (range, 16 days–6 weeks). Immediate postoperative alignment was 2.5° varus (range, 11° valgus to 16° varus) and 7° procurvatum (range, 1° recurvatum to 22° procurvatum). Mean shortening was 1.5 cm (range, 0-2.7 cm). Final alignment was 1° valgus (range, 9° valgus to 12° varus) and 5° procurvatum (range, 0° to 22°). Mean follow-up was 8 months. There were no cases of skin maceration or cast failure. No casts precluded use of a spica car-seat. Figure 4 shows a typical case with a midshaft fracture treated with closed reduction and casting for 4 weeks with good remodeling at final follow-up, 19 months after injury.

Discussion

Although single-leg walking spica casts have been shown to safely treat low-energy femur fractures in children 1 to 6 years old,7 length-unstable femur fractures, bilateral femur fractures, and patients with hip dysplasia continue to be managed with a double-leg hip spica construct. Cast integrity remains fundamental to the control of most fractures and prevention of cast-related complications, such as skin maceration and ulceration. Surgeons typically use spica cast reinforcement schemes—such as cast augments of the torso–limb junction, with multiple layers of casting material or incorporation of a connecting bar between the legs, typically constructed by overwrapping a wooden dowel in casting material—to improve the mechanical stability of casts.6 The present technique of creating a connecting bar from fiberglass casting material significantly simplifies the standard wooden dowel approach and provided excellent results in our treatment group in terms of cast integrity and fracture alignment. In addition, at our institution, a roll of fiberglass costs $2.10, whereas a wooden dowel costs $3 to $10 and can be difficult to locate if not frequently used. Other tube-shaped materials, such as the disposable material used to package implants and tubes, carry an even lower cost. However, we have found that a single fiberglass roll is most readily available and easiest to apply.

Although proper spica cast application remains important in managing pediatric trauma, it lacks a good technical description in the literature. In this technical report, we have presented our standard spica cast application method, which minimizes the range of cast complications that have been reported, from minor skin irritation to superior mesenteric artery syndrome. Two salient technical highlights are use of waterproof pantaloon liners and cast petaling, which we have found almost eliminate the morbidity of potential skin complications, reported to occur at a rate of 28%.8 In addition, we forgo applying the cast on the injured leg in segments. Application of a short-leg cast on the injured leg to allow traction on the leg during cast application is of dubious utility and may be potentially harmful, with described complications of peroneal nerve palsy and compartment syndrome.9-11 Further, it is important to use an abdominal spacer (eg, a stack of towels) under the cast padding to create room for abdominal expansion and minimize pressure thought to induce superior mesenteric artery syndrome. Plastic or rubber abdominal spacers have also been described.12,13 Last, leg position is important for reduction and maintenance of the fracture, as well as patient care. Literature advocates minimizing hip abduction to just that needed for perineal care and maximizing hip flexion and knee extension to optimize car-seat fit and safety.14

Conclusion

Construction of a spica cast lower limb connecting bar from readily available fiberglass casting material allows a facile and rapid addition to the mechanical stability of a spica cast in the treatment of pediatric femur fractures. The technique is low-cost and obviates the need for additional extraneous materials.

Femur fractures (Orthopaedic Trauma Association classes 31, 32, 33)1 are common childhood injuries, occurring at a rate of 19 per 100,000 children in the United States.2 Peak occurrence is bimodal at ages 2 and 17 years. The most common mechanism of injury in children under 6 years is a fall, and hip spica casting is the preferred treatment modality in this group.3-5

A bar connecting the legs of the spica cast has been shown to facilitate patient transport5 and significantly decrease mechanical failure of the spica cast.6 This bar often consists of a broom handle or pipe that must be cut to size during the case and subsequently incorporated into the cast—tasks that are often inconvenient and time-consuming for on-call or emergency department staff unfamiliar with orthopedic tools.

In this article, we review a spica cast application that incorporates a low-cost, lightweight technique for fabricating a connecting bar from existing fiberglass casting material. The Institutional Review Board at Connecticut Children’s Medical Center approved this work.

Technique of Double-Leg Spica Casting With Fiberglass Bar

A spica casting table (Orthopedic Systems) with a well-padded post is placed on the operating room table and adjusted to the length of the patient from perineum to just below the shoulders. With the patient under general anesthesia, folded towels are used to provide 2 to 4 cm of padding on the anterior torso, atop which a waterproof pantaloon is applied. The patient is transferred to the spica table, and the patient’s arms are gently secured to the casting table with cast padding or tape in an abducted position at the shoulders. A surgeon controls the legs by holding the feet with the long fingers just above the heels, the index fingers on the anterior ankle, and the thumbs on the soles of the feet. Cast padding is wrapped from the nipple line to the supramalleolar region on each leg. The bony prominences of the malleoli, patella, fibular head, femoral condyles, iliac crests, and coccyx are well padded.

Fiberglass is then rolled without compression onto the patient, beginning with the torso and perineal areas. The injured leg is wrapped to its final length above the malleoli while the uninjured leg is kept free. Maintaining the position of the injured leg with simultaneous molding at the fracture site, typically to promote valgus, allows fracture reduction. The fracture position is then checked under image intensification. For femur fractures, hip abduction and flexion are set to 45° and 90°, respectively, while knee flexion is between 50° and 90°. The uninjured leg is then wrapped with fiberglass. Additional strips of fiberglass can be used to reinforce weak junctional regions between the torso and the legs, posteriorly over the “intern’s triangle” and anteriorly along the hip crease.

A connecting fiberglass bar is then created using a fiberglass roll once the cast is hardened. A 2-inch fiberglass roll is wrapped around one leg to secure its position (Figure 1A) and then rolled around the second limb (Figure 1B). Fiberglass is then pulled taut and rolled around the bridge that has been created in order to thicken the bar (Figure 2). The roll is again brought around the closest limb, wrapped back across the bridge to the other limb, and rolled out to its full length. Last, the legs are abducted 1 to 2 cm to tension the bar (Figure 3). Although this does not produce enough movement to cause a crease and a resultant ulcer, careful inspection of common pressure points (eg, popliteal fossa) should be performed after the cast is complete.

The chest towels are removed, and the final cast is inspected clinically and fluoroscopically at the fracture site before extubation. The cast is trimmed as needed to ensure room for perineal care, as well as full ankle flexion and extension without impingement. Cast edges are further petaled with plastic tape (Hy-Tape International) to provide padding and prevent the waterproof lining from tearing.

Postoperative care involves overnight observation and caregiver practice in perineal care. Frequent rotation from supine to prone is encouraged. Nurses confirm car-seat fit before discharge. If needed, radiographs are obtained 7 to 10 days later to help with wedging adjustment. The cast is removed in the clinic when adequate callus is appreciated on subsequent radiographs.

Case Series

Our experience with this technique in 16 unilateral femur fractures has been favorable (Table). Patient age ranged from 5 months to 3 years. Mean pretreatment angulation was 13° varus and 11° procurvatum. The majority of fractures were femoral shaft fractures; 1 was proximal, 2 distal.

 

 

All fractures united without cast revision. Mean cast time was 4.5 weeks (range, 16 days–6 weeks). Immediate postoperative alignment was 2.5° varus (range, 11° valgus to 16° varus) and 7° procurvatum (range, 1° recurvatum to 22° procurvatum). Mean shortening was 1.5 cm (range, 0-2.7 cm). Final alignment was 1° valgus (range, 9° valgus to 12° varus) and 5° procurvatum (range, 0° to 22°). Mean follow-up was 8 months. There were no cases of skin maceration or cast failure. No casts precluded use of a spica car-seat. Figure 4 shows a typical case with a midshaft fracture treated with closed reduction and casting for 4 weeks with good remodeling at final follow-up, 19 months after injury.

Discussion

Although single-leg walking spica casts have been shown to safely treat low-energy femur fractures in children 1 to 6 years old,7 length-unstable femur fractures, bilateral femur fractures, and patients with hip dysplasia continue to be managed with a double-leg hip spica construct. Cast integrity remains fundamental to the control of most fractures and prevention of cast-related complications, such as skin maceration and ulceration. Surgeons typically use spica cast reinforcement schemes—such as cast augments of the torso–limb junction, with multiple layers of casting material or incorporation of a connecting bar between the legs, typically constructed by overwrapping a wooden dowel in casting material—to improve the mechanical stability of casts.6 The present technique of creating a connecting bar from fiberglass casting material significantly simplifies the standard wooden dowel approach and provided excellent results in our treatment group in terms of cast integrity and fracture alignment. In addition, at our institution, a roll of fiberglass costs $2.10, whereas a wooden dowel costs $3 to $10 and can be difficult to locate if not frequently used. Other tube-shaped materials, such as the disposable material used to package implants and tubes, carry an even lower cost. However, we have found that a single fiberglass roll is most readily available and easiest to apply.

Although proper spica cast application remains important in managing pediatric trauma, it lacks a good technical description in the literature. In this technical report, we have presented our standard spica cast application method, which minimizes the range of cast complications that have been reported, from minor skin irritation to superior mesenteric artery syndrome. Two salient technical highlights are use of waterproof pantaloon liners and cast petaling, which we have found almost eliminate the morbidity of potential skin complications, reported to occur at a rate of 28%.8 In addition, we forgo applying the cast on the injured leg in segments. Application of a short-leg cast on the injured leg to allow traction on the leg during cast application is of dubious utility and may be potentially harmful, with described complications of peroneal nerve palsy and compartment syndrome.9-11 Further, it is important to use an abdominal spacer (eg, a stack of towels) under the cast padding to create room for abdominal expansion and minimize pressure thought to induce superior mesenteric artery syndrome. Plastic or rubber abdominal spacers have also been described.12,13 Last, leg position is important for reduction and maintenance of the fracture, as well as patient care. Literature advocates minimizing hip abduction to just that needed for perineal care and maximizing hip flexion and knee extension to optimize car-seat fit and safety.14

Conclusion

Construction of a spica cast lower limb connecting bar from readily available fiberglass casting material allows a facile and rapid addition to the mechanical stability of a spica cast in the treatment of pediatric femur fractures. The technique is low-cost and obviates the need for additional extraneous materials.

References

1.    Slongo TF, Audigé L; AO Pediatric Classification Group. Fracture and dislocation classification compendium for children: the AO Pediatric Comprehensive Classification of Long Bone Fractures (PCCF). J Orthop Trauma. 2007;21(10):S135-S160.

2.    Hinton RY, Lincoln A, Crockett MM, Sponseller P, Smith G. Fractures of the femoral shaft in children. Incidence, mechanisms, and sociodemographic risk factors. J Bone Joint Surg Am. 1999;81(4):500-509.

3.    Campbell WC, Canale ST, Beaty JH, eds. Campbell’s Operative Orthopaedics. 11th ed. Philadelphia, PA: Mosby Elsevier; 2008.

4.    Lovell WW, Winter RB, Morrissy RT, Weinstein SL. Lovell and Winter’s Pediatric Orthopaedics. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.

5.    Green NE, Swiontkowski MF, eds. Skeletal Trauma in Children. 4th ed. Philadelphia, PA: Elsevier Health Sciences; 2009.

6.    Hosalkar HS, Jones S, Chowdhury M, Chatoo M, Hill RA. Connecting bar for hip spica reinforcement: does it help? J Pediatr Orthop B. 2003;12(2):100-102.

7.    Flynn JM, Garner MR, Jones KJ, et al. The treatment of low-energy femoral shaft fractures: a prospective study comparing the “walking spica” with the traditional spica cast. J Bone Joint Surg Am. 2011;93(23):2196-2202.

8.    DiFazio R, Vessey J, Zurakowski D, Hresko MT, Matheney T. Incidence of skin complications and associated charges in children treated with hip spica casts for femur fractures. J Pediatr Orthop. 2011;31(1):17-22.

9.    Weiss AP, Schenck RC Jr, Sponseller PD, Thompson JD. Peroneal nerve palsy after early cast application for femoral fractures in children. J Pediatr Orthop. 1992;12(1):25-28.

10. Mubarak SJ, Frick S, Sink E, Rathjen K, Noonan KJ. Volkmann contracture and compartment syndromes after femur fractures in children treated with 90/90 spica casts. J Pediatr Orthop. 2006;26(5):567-572.

11. Large TM, Frick SL. Compartment syndrome of the leg after treatment of a femoral fracture with an early sitting spica cast. A report of two cases. J Bone Joint Surg Am. 2003;85(11):2207-2210.

12. Sharma S, Azzopardi T. Reduction of abdominal pressure for prophylaxis of the mesenteric artery syndrome (cast syndrome) in a hip spica—a simple technique. Ann R Coll Surg Engl. 2006;88(3):317.

13. Kiter E, Demirkan F, Kiliç BA, Erkula G. A new technique for creating an abdominal window in a hip spica cast. J Orthop Trauma. 2003;17(6):442-443.

14. Zielinski J, Oliver G, Sybesma J, Walter N, Atkinson P. Casting technique and restraint choice influence child safety during transport of body casted children subjected to a simulated frontal MVA. J Trauma. 2009;66(6):1653-1665.

References

1.    Slongo TF, Audigé L; AO Pediatric Classification Group. Fracture and dislocation classification compendium for children: the AO Pediatric Comprehensive Classification of Long Bone Fractures (PCCF). J Orthop Trauma. 2007;21(10):S135-S160.

2.    Hinton RY, Lincoln A, Crockett MM, Sponseller P, Smith G. Fractures of the femoral shaft in children. Incidence, mechanisms, and sociodemographic risk factors. J Bone Joint Surg Am. 1999;81(4):500-509.

3.    Campbell WC, Canale ST, Beaty JH, eds. Campbell’s Operative Orthopaedics. 11th ed. Philadelphia, PA: Mosby Elsevier; 2008.

4.    Lovell WW, Winter RB, Morrissy RT, Weinstein SL. Lovell and Winter’s Pediatric Orthopaedics. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.

5.    Green NE, Swiontkowski MF, eds. Skeletal Trauma in Children. 4th ed. Philadelphia, PA: Elsevier Health Sciences; 2009.

6.    Hosalkar HS, Jones S, Chowdhury M, Chatoo M, Hill RA. Connecting bar for hip spica reinforcement: does it help? J Pediatr Orthop B. 2003;12(2):100-102.

7.    Flynn JM, Garner MR, Jones KJ, et al. The treatment of low-energy femoral shaft fractures: a prospective study comparing the “walking spica” with the traditional spica cast. J Bone Joint Surg Am. 2011;93(23):2196-2202.

8.    DiFazio R, Vessey J, Zurakowski D, Hresko MT, Matheney T. Incidence of skin complications and associated charges in children treated with hip spica casts for femur fractures. J Pediatr Orthop. 2011;31(1):17-22.

9.    Weiss AP, Schenck RC Jr, Sponseller PD, Thompson JD. Peroneal nerve palsy after early cast application for femoral fractures in children. J Pediatr Orthop. 1992;12(1):25-28.

10. Mubarak SJ, Frick S, Sink E, Rathjen K, Noonan KJ. Volkmann contracture and compartment syndromes after femur fractures in children treated with 90/90 spica casts. J Pediatr Orthop. 2006;26(5):567-572.

11. Large TM, Frick SL. Compartment syndrome of the leg after treatment of a femoral fracture with an early sitting spica cast. A report of two cases. J Bone Joint Surg Am. 2003;85(11):2207-2210.

12. Sharma S, Azzopardi T. Reduction of abdominal pressure for prophylaxis of the mesenteric artery syndrome (cast syndrome) in a hip spica—a simple technique. Ann R Coll Surg Engl. 2006;88(3):317.

13. Kiter E, Demirkan F, Kiliç BA, Erkula G. A new technique for creating an abdominal window in a hip spica cast. J Orthop Trauma. 2003;17(6):442-443.

14. Zielinski J, Oliver G, Sybesma J, Walter N, Atkinson P. Casting technique and restraint choice influence child safety during transport of body casted children subjected to a simulated frontal MVA. J Trauma. 2009;66(6):1653-1665.

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Collagenase Enzymatic Fasciotomy for Dupuytren Contracture in Patients on Chronic Immunosuppression

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Collagenase Enzymatic Fasciotomy for Dupuytren Contracture in Patients on Chronic Immunosuppression

The incidence of Dupuytren disease increases with advancing age,1 as do the medical comorbidities of patients seeking treatment for disabling hand contractures. For patients with significant comorbidities, open surgical fasciectomy, the current standard of treatment for Dupuytren disease,2,3 may be associated with increased perioperative risks.

Collagenase enzymatic fasciotomy has become an accepted nonsurgical treatment alternative to traditional fasciectomy or surgical fasciotomy for significant digital contractures caused by Dupuytren disease.4-6 Clostridium histolyticum collagenase (CHC) is a foreign protein, made up of 2 collagenases isolated from the bacteria C histolyticum.7 The collagenases are zinc-dependent matrix metalloproteinases that cleave the triple helical structure of collagen molecules.8 Also known as Xiaflex (Auxilium Pharmaceuticals), CHC was approved by the US Food and Drug Administration (FDA) in February 2010 for use in patients with Dupuytren contractures.

 Enzymatic rupture is safe and efficacious at midterm follow-up and offers the theoretical advantage of avoiding palmar and digital fasciectomy and the associated risks of surgical-site infection and wound-healing complications.6 The risks of surgical wound complications are magnified in immunosuppressed patients, particularly those on chronic steroid therapy; wound-healing complication rates may be increased 2 to 5 times compared with controls.9 In a pooled literature review, wound-healing complications were reported after 22.9% of open primary fasciectomies, with infection occurring in 2.4%.10 A nonsurgical alternative is therefore particularly appealing for a patient cohort that may be at higher risk for a frequently described complication of surgery for Dupuytren contracture.

The exclusion criteria in the trials for FDA approval were extensive and included breast-feeding, pregnancy, bleeding disorder, recent stroke, use of tetracycline derivative within 14 days before start of study, use of anticoagulant within 7 days before start of study, allergy to collagenase, and chronic muscular, neurologic, or neuromuscular disorder affecting the hands.6 Safety and efficacy of collagenase in patients requiring chronic immunosuppressive therapy for medical comorbidities have not been previously documented. Furthermore, although skin tears were reported in 11% of patients after manual cord rupture in the CORD (Collagenase Option for the Reduction of Dupuytren’s) I trial,6 the likelihood of deep and superficial infection and delayed wound healing has not been quantitated.

In this article, we report on outcomes of 13 collagenase enzymatic fasciotomies performed in 8 patients who were on chronic immunosuppressive therapy.

Methods

Institutional review board approval was obtained at both academic hand surgery institutions. We retrospectively reviewed prospectively collected clinical data within our 2 centers’ databases of patients with Dupuytren disease. Eight patients on chronic immunosuppressive therapies treated with collagenase for metacarpophalangeal (MP) or proximal interphalangeal (PIP) joint contractures between February 2010 and December 2011 were identified. Three of these patients received collagenase injections into 2 or more separate Dupuytren cords at different encounters, resulting in a total of 13 individual collagenase enzymatic fasciotomies.

Collagenase injections were administered following CORD I trial protocol,6 except we injected Dupuytren cords crossing the PIP joint using a lateral approach to minimize risk of flexor tendon rupture. Manipulation of the treated joint was performed between 24 and 48 hours after collagenase injection under local anesthesia with 3 mL of 1% mepivacaine or lidocaine without epinephrine. After manipulation and cord rupture, patients were placed in a hand-based extension splint to wear at night for up to 3 months. Patients were followed at 1 and 12 months.

Results

Patients’ baseline characteristics are summarized in Table 1. Four patients were maintained on chronic prednisone therapy, 3 on methotrexate, and 1 on azathioprine. Therapy duration, medication dose, and diagnoses requiring immunosuppressant therapy varied among patients.

Outcomes and adverse events are summarized in Table 2. Mean number of joint contractures per hand treated was 2.8 (MP, 1.4; PIP, 1.4). However, not all joints met the intervention criteria. Of the 13 joints treated, 7 were MP joints, and 6 were PIP joints. Mean preinjection contracture of the treated joints was 53.0° (range, 20°-90°). Twelve of the 13 joint contractures improved. At mean follow-up of 6.7 months (range, 1-22 months), mean magnitude of contracture improved to 12.9° (range, 0°-45°). Mean MP joint contracture improved from 42.0° to 4.2° (range, 0°-10°), and mean PIP joint contracture improved from 65.8° to 21.7° (range, 0°-45°).

All 13 collagenase injections were well tolerated, and there were no systemic reactions. Injection-site pain was common. Mild injection-site bruising and edema were reported in all cases. Enzymatic fasciotomy was performed in all patients, and immediate improvement in contracture after manipulation 24 to 48 hours after injection was recorded.

Three of the 13 injections were complicated by skin tears during manipulation and cord rupture. All 3 skin tears were treated with local wound care, which included use of povidone-iodine and wet-to-dry dressings. There was no evidence of subsequent superficial or deep, local or regional infection. In 2 cases, the wound healed within 1 week; in the third case, wound healing was present by 2 weeks. Once the wounds showed early re-epithelialization, hand-based extension splinting in a position of comfort was used at night for up to 3 months after injection. Two of the 13 injections were complicated by small blood blisters. These were treated with observation and resolved spontaneously.

 

 

Discussion

Collagenase enzymatic fasciotomy appeared to be a safe and efficacious alternative to surgical treatment of Dupuytren contractures in this cohort of patients maintained on chronic immunosuppressive agents. MP contractures responded more substantially than PIP contractures did, as expected.6 No previously undescribed adverse outcomes were noted in these 8 patients on chronic immunosuppressive therapy beyond those reported in the CORD I trial. Three (23%) of the 13 collagenase injections in our series were complicated by skin tears after manipulation. Skins tears were reported in 22 (11%) of 204 patients after manual cord rupture in the CORD I trial.6 Given the limited numbers in this series, it remains unclear if chronic immunosuppression truly increases the risk of skin tears in this subset of patients. Other common treatment-related adverse events seen in the CORD I trial—injection-site hemorrhage (37%), pruritis (11%) and lymphadenopathy (10%)—were not seen after the 13 injections in our case series. We are prospectively following all patients with Dupuytren disease, and this is an area of ongoing research at our centers.

The immunosuppressive actions of prednisone, azathioprine, and methotrexate are well documented. Prednisone is a glucocorticoid, converted in the liver to prednisolone, which suppresses inflammation and immune responses by regulation of gene expression. Its immunosuppressive actions are multifactorial, relating to inhibition of lymphocytes, neutrophils, and monocytes. These effects are dose- and time-dependent11 and may become evident in patients receiving low doses over prolonged periods. Skin atrophy12 and delayed wound healing9 are side effects of long-term prednisone use. Skin atrophy may make the prednisone-treated patient more susceptible to skin tears after collagenase injection and manipulation. Azathioprine inhibits purine synthesis, which is especially important in the proliferation of immune cells.13 It has been shown to inhibit both cellular immunity at low doses and humoral immunity at higher doses.14 Methotrexate inhibits lymphocyte folic acid metabolism. The immunosuppressive properties of low-dose methotrexate have been linked to the induction of apoptosis in activated T cells.15

A more complex process in immunosuppressed patients is the immunogenicity of injected collagenase. As CHC in current use is a mixture of 2 foreign proteins, an immunologic response is expected in the host after injection. It has been shown that, after 3 injections of CHC into Dupuytren cords, 100% of patients developed antibodies to both enzymes in their serum.6 More than 85% demonstrated anti-CHC antibodies after a single injection. However, no patients showed signs of anaphylaxis or allergic reaction, and there was no correlation between serum levels of anti-CHC and adverse events. It has been hypothesized that there is a potential for cross-reactivity of the anti-CHC antibodies with human matrix metalloproteinases, causing enzymatic dysfunction within the host.16 This has yet to be reported clinically, and Xiaflex is currently under postmarketing surveillance. Immunocompromised people, with suppressed humoral and cellular immune responses, may produce less of an antibody response to the foreign CHC proteins. Whether this conclusively leads to a change in the side effect profile of the medication in these individuals is beyond the scope of this article. However, we identified no new side effects in this small but higher risk cohort. The issue should be continually monitored as collagenase is used in wider clinical settings.

Collagenase enzymatic fasciotomy is a new nonsurgical therapeutic option for Dupuytren disease. Indications and guidelines for use continue to evolve. This case series highlights the use of collagenase in 8 patients who were on long-term immunosuppressive therapy. This study has the limitations inherent to retrospective analyses. It is difficult to generalize results across broader immunosuppressed populations. A larger cohort, with long-term follow-up assessing recurrence of contracture, is needed to make definitive conclusions about use of collagenase in this challenging subset of patients. Based on our observations in this limited cohort, it appears appropriate to pursue further studies on use of collagenase enzymatic fasciotomy. A randomized, prospective or case–control series comparing surgical fasciectomy with enzymatic fasciotomy would yield further meaningful data. As more patients seek nonsurgical treatment for Dupuytren disease, its safety and efficacy in select cohorts of patients should continue to be evaluated.

References

1.    Loos B, Puschkin V, Horch RE. 50 years experience with Dupuytren’s contracture in the Erlangen University Hospital—a retrospective analysis of 2919 operated hands from 1956 to 2006. BMC Musculoskelet Disord. 2007;8:60.

2.    Coert JH, Nérin JP, Meek MF. Results of partial fasciectomy for Dupuytren disease in 261 consecutive patients. Ann Plast Surg. 2006;57(1):13-17.

3.    Sennwald GR. Fasciectomy for treatment of Dupuytren’s disease and early complications. J Hand Surg Am. 1990;15(5):755-761.

4.    Badalamente MA, Hurst LC. Enzyme injection as nonsurgical treatment of Dupuytren’s disease. J Hand Surg Am. 2000;25(4):629-636.

5.      Badalamente MA, Hurst LC, Hentz VR. Collagen as a clinical target: nonoperative treatment of Dupuytren’s disease. J Hand Surg Am. 2002;27(5):788-798.

6.    Hurst LC, Badalamente MA, Hentz VR, et al; CORD I Study Group. Injectable collagenase Clostridium histolyticum for Dupuytren’s contracture. N Engl J Med. 2009;361(10):968-979.

7.    Mookhtiar KA, Van Wart HE. Clostridium histolyticum collagenases: a new look at some old enzymes. Matrix Suppl. 1992;1:116-126.

8.    Watanabe K. Collagenolytic proteases from bacteria. Appl Microbiol Biotechnol. 2004;63(5):520-526.

9.    Wang AS, Armstrong EJ, Armstrong AW. Corticosteroids and wound healing: clinical considerations in the perioperative period. Am J Surg. 2013;206(3):410-417.

10. Denkler K. Surgical complications associated with fasciectomy for Dupuytren’s disease: a 20-year review of the English literature. Eplasty. 2010;10:e15.

11. Stuck AE, Minder CE, Frey FJ. Risk of infectious complications in patients taking glucocorticosteroids. Rev Infect Dis. 1989;11(6):954-963.

12. Oikarinen A, Autio P. New aspects of the mechanism of corticosteroid-induced dermal atrophy. Clin Exp Dermatol. 1991;16(6):416-419.

13. Makinodan T, Santos GW, Quinn RP. Immunosuppressive drugs. Pharmacol Rev. 1970;22(2):189-247.

14. Röllinghoff M, Schrader J, Wagner H. Effect of azathioprine and cytosine arabinoside on humoral and cellular immunity in vitro. Clin Exp Immunol. 1973;15(2):261-269.

15. Genestier L, Paillot R, Fournel S, Ferraro C, Miossec P, Revillard JP. Immunosuppressive properties of methotrexate: apoptosis and clonal deletion of activated peripheral T cells. J Clin Invest. 1998;102(2):322-328.

16. Desai SS, Hentz VR. Collagenase Clostridium histolyticum for Dupuytren’s contracture. Expert Opin Biol Ther. 2010;10(9):1395-1404.

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Michael J. Waters, BMBS, B. Physio, Mark R. Belsky, MD, Philip E. Blazar, MD, Matthew I. Leibman, MD, and David E. Ruchelsman, MD

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

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american journal of orthopedics, AJO, original study, study, collagenase enzymatic fasciotomy, dupuytren contracture, chronic immunosuppression, hand, dupuytren, disease, therapy, therapies, joints, waters, belsky, blazar, leibman, ruchelsman
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Michael J. Waters, BMBS, B. Physio, Mark R. Belsky, MD, Philip E. Blazar, MD, Matthew I. Leibman, MD, and David E. Ruchelsman, MD

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Author and Disclosure Information

Michael J. Waters, BMBS, B. Physio, Mark R. Belsky, MD, Philip E. Blazar, MD, Matthew I. Leibman, MD, and David E. Ruchelsman, MD

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

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The incidence of Dupuytren disease increases with advancing age,1 as do the medical comorbidities of patients seeking treatment for disabling hand contractures. For patients with significant comorbidities, open surgical fasciectomy, the current standard of treatment for Dupuytren disease,2,3 may be associated with increased perioperative risks.

Collagenase enzymatic fasciotomy has become an accepted nonsurgical treatment alternative to traditional fasciectomy or surgical fasciotomy for significant digital contractures caused by Dupuytren disease.4-6 Clostridium histolyticum collagenase (CHC) is a foreign protein, made up of 2 collagenases isolated from the bacteria C histolyticum.7 The collagenases are zinc-dependent matrix metalloproteinases that cleave the triple helical structure of collagen molecules.8 Also known as Xiaflex (Auxilium Pharmaceuticals), CHC was approved by the US Food and Drug Administration (FDA) in February 2010 for use in patients with Dupuytren contractures.

 Enzymatic rupture is safe and efficacious at midterm follow-up and offers the theoretical advantage of avoiding palmar and digital fasciectomy and the associated risks of surgical-site infection and wound-healing complications.6 The risks of surgical wound complications are magnified in immunosuppressed patients, particularly those on chronic steroid therapy; wound-healing complication rates may be increased 2 to 5 times compared with controls.9 In a pooled literature review, wound-healing complications were reported after 22.9% of open primary fasciectomies, with infection occurring in 2.4%.10 A nonsurgical alternative is therefore particularly appealing for a patient cohort that may be at higher risk for a frequently described complication of surgery for Dupuytren contracture.

The exclusion criteria in the trials for FDA approval were extensive and included breast-feeding, pregnancy, bleeding disorder, recent stroke, use of tetracycline derivative within 14 days before start of study, use of anticoagulant within 7 days before start of study, allergy to collagenase, and chronic muscular, neurologic, or neuromuscular disorder affecting the hands.6 Safety and efficacy of collagenase in patients requiring chronic immunosuppressive therapy for medical comorbidities have not been previously documented. Furthermore, although skin tears were reported in 11% of patients after manual cord rupture in the CORD (Collagenase Option for the Reduction of Dupuytren’s) I trial,6 the likelihood of deep and superficial infection and delayed wound healing has not been quantitated.

In this article, we report on outcomes of 13 collagenase enzymatic fasciotomies performed in 8 patients who were on chronic immunosuppressive therapy.

Methods

Institutional review board approval was obtained at both academic hand surgery institutions. We retrospectively reviewed prospectively collected clinical data within our 2 centers’ databases of patients with Dupuytren disease. Eight patients on chronic immunosuppressive therapies treated with collagenase for metacarpophalangeal (MP) or proximal interphalangeal (PIP) joint contractures between February 2010 and December 2011 were identified. Three of these patients received collagenase injections into 2 or more separate Dupuytren cords at different encounters, resulting in a total of 13 individual collagenase enzymatic fasciotomies.

Collagenase injections were administered following CORD I trial protocol,6 except we injected Dupuytren cords crossing the PIP joint using a lateral approach to minimize risk of flexor tendon rupture. Manipulation of the treated joint was performed between 24 and 48 hours after collagenase injection under local anesthesia with 3 mL of 1% mepivacaine or lidocaine without epinephrine. After manipulation and cord rupture, patients were placed in a hand-based extension splint to wear at night for up to 3 months. Patients were followed at 1 and 12 months.

Results

Patients’ baseline characteristics are summarized in Table 1. Four patients were maintained on chronic prednisone therapy, 3 on methotrexate, and 1 on azathioprine. Therapy duration, medication dose, and diagnoses requiring immunosuppressant therapy varied among patients.

Outcomes and adverse events are summarized in Table 2. Mean number of joint contractures per hand treated was 2.8 (MP, 1.4; PIP, 1.4). However, not all joints met the intervention criteria. Of the 13 joints treated, 7 were MP joints, and 6 were PIP joints. Mean preinjection contracture of the treated joints was 53.0° (range, 20°-90°). Twelve of the 13 joint contractures improved. At mean follow-up of 6.7 months (range, 1-22 months), mean magnitude of contracture improved to 12.9° (range, 0°-45°). Mean MP joint contracture improved from 42.0° to 4.2° (range, 0°-10°), and mean PIP joint contracture improved from 65.8° to 21.7° (range, 0°-45°).

All 13 collagenase injections were well tolerated, and there were no systemic reactions. Injection-site pain was common. Mild injection-site bruising and edema were reported in all cases. Enzymatic fasciotomy was performed in all patients, and immediate improvement in contracture after manipulation 24 to 48 hours after injection was recorded.

Three of the 13 injections were complicated by skin tears during manipulation and cord rupture. All 3 skin tears were treated with local wound care, which included use of povidone-iodine and wet-to-dry dressings. There was no evidence of subsequent superficial or deep, local or regional infection. In 2 cases, the wound healed within 1 week; in the third case, wound healing was present by 2 weeks. Once the wounds showed early re-epithelialization, hand-based extension splinting in a position of comfort was used at night for up to 3 months after injection. Two of the 13 injections were complicated by small blood blisters. These were treated with observation and resolved spontaneously.

 

 

Discussion

Collagenase enzymatic fasciotomy appeared to be a safe and efficacious alternative to surgical treatment of Dupuytren contractures in this cohort of patients maintained on chronic immunosuppressive agents. MP contractures responded more substantially than PIP contractures did, as expected.6 No previously undescribed adverse outcomes were noted in these 8 patients on chronic immunosuppressive therapy beyond those reported in the CORD I trial. Three (23%) of the 13 collagenase injections in our series were complicated by skin tears after manipulation. Skins tears were reported in 22 (11%) of 204 patients after manual cord rupture in the CORD I trial.6 Given the limited numbers in this series, it remains unclear if chronic immunosuppression truly increases the risk of skin tears in this subset of patients. Other common treatment-related adverse events seen in the CORD I trial—injection-site hemorrhage (37%), pruritis (11%) and lymphadenopathy (10%)—were not seen after the 13 injections in our case series. We are prospectively following all patients with Dupuytren disease, and this is an area of ongoing research at our centers.

The immunosuppressive actions of prednisone, azathioprine, and methotrexate are well documented. Prednisone is a glucocorticoid, converted in the liver to prednisolone, which suppresses inflammation and immune responses by regulation of gene expression. Its immunosuppressive actions are multifactorial, relating to inhibition of lymphocytes, neutrophils, and monocytes. These effects are dose- and time-dependent11 and may become evident in patients receiving low doses over prolonged periods. Skin atrophy12 and delayed wound healing9 are side effects of long-term prednisone use. Skin atrophy may make the prednisone-treated patient more susceptible to skin tears after collagenase injection and manipulation. Azathioprine inhibits purine synthesis, which is especially important in the proliferation of immune cells.13 It has been shown to inhibit both cellular immunity at low doses and humoral immunity at higher doses.14 Methotrexate inhibits lymphocyte folic acid metabolism. The immunosuppressive properties of low-dose methotrexate have been linked to the induction of apoptosis in activated T cells.15

A more complex process in immunosuppressed patients is the immunogenicity of injected collagenase. As CHC in current use is a mixture of 2 foreign proteins, an immunologic response is expected in the host after injection. It has been shown that, after 3 injections of CHC into Dupuytren cords, 100% of patients developed antibodies to both enzymes in their serum.6 More than 85% demonstrated anti-CHC antibodies after a single injection. However, no patients showed signs of anaphylaxis or allergic reaction, and there was no correlation between serum levels of anti-CHC and adverse events. It has been hypothesized that there is a potential for cross-reactivity of the anti-CHC antibodies with human matrix metalloproteinases, causing enzymatic dysfunction within the host.16 This has yet to be reported clinically, and Xiaflex is currently under postmarketing surveillance. Immunocompromised people, with suppressed humoral and cellular immune responses, may produce less of an antibody response to the foreign CHC proteins. Whether this conclusively leads to a change in the side effect profile of the medication in these individuals is beyond the scope of this article. However, we identified no new side effects in this small but higher risk cohort. The issue should be continually monitored as collagenase is used in wider clinical settings.

Collagenase enzymatic fasciotomy is a new nonsurgical therapeutic option for Dupuytren disease. Indications and guidelines for use continue to evolve. This case series highlights the use of collagenase in 8 patients who were on long-term immunosuppressive therapy. This study has the limitations inherent to retrospective analyses. It is difficult to generalize results across broader immunosuppressed populations. A larger cohort, with long-term follow-up assessing recurrence of contracture, is needed to make definitive conclusions about use of collagenase in this challenging subset of patients. Based on our observations in this limited cohort, it appears appropriate to pursue further studies on use of collagenase enzymatic fasciotomy. A randomized, prospective or case–control series comparing surgical fasciectomy with enzymatic fasciotomy would yield further meaningful data. As more patients seek nonsurgical treatment for Dupuytren disease, its safety and efficacy in select cohorts of patients should continue to be evaluated.

The incidence of Dupuytren disease increases with advancing age,1 as do the medical comorbidities of patients seeking treatment for disabling hand contractures. For patients with significant comorbidities, open surgical fasciectomy, the current standard of treatment for Dupuytren disease,2,3 may be associated with increased perioperative risks.

Collagenase enzymatic fasciotomy has become an accepted nonsurgical treatment alternative to traditional fasciectomy or surgical fasciotomy for significant digital contractures caused by Dupuytren disease.4-6 Clostridium histolyticum collagenase (CHC) is a foreign protein, made up of 2 collagenases isolated from the bacteria C histolyticum.7 The collagenases are zinc-dependent matrix metalloproteinases that cleave the triple helical structure of collagen molecules.8 Also known as Xiaflex (Auxilium Pharmaceuticals), CHC was approved by the US Food and Drug Administration (FDA) in February 2010 for use in patients with Dupuytren contractures.

 Enzymatic rupture is safe and efficacious at midterm follow-up and offers the theoretical advantage of avoiding palmar and digital fasciectomy and the associated risks of surgical-site infection and wound-healing complications.6 The risks of surgical wound complications are magnified in immunosuppressed patients, particularly those on chronic steroid therapy; wound-healing complication rates may be increased 2 to 5 times compared with controls.9 In a pooled literature review, wound-healing complications were reported after 22.9% of open primary fasciectomies, with infection occurring in 2.4%.10 A nonsurgical alternative is therefore particularly appealing for a patient cohort that may be at higher risk for a frequently described complication of surgery for Dupuytren contracture.

The exclusion criteria in the trials for FDA approval were extensive and included breast-feeding, pregnancy, bleeding disorder, recent stroke, use of tetracycline derivative within 14 days before start of study, use of anticoagulant within 7 days before start of study, allergy to collagenase, and chronic muscular, neurologic, or neuromuscular disorder affecting the hands.6 Safety and efficacy of collagenase in patients requiring chronic immunosuppressive therapy for medical comorbidities have not been previously documented. Furthermore, although skin tears were reported in 11% of patients after manual cord rupture in the CORD (Collagenase Option for the Reduction of Dupuytren’s) I trial,6 the likelihood of deep and superficial infection and delayed wound healing has not been quantitated.

In this article, we report on outcomes of 13 collagenase enzymatic fasciotomies performed in 8 patients who were on chronic immunosuppressive therapy.

Methods

Institutional review board approval was obtained at both academic hand surgery institutions. We retrospectively reviewed prospectively collected clinical data within our 2 centers’ databases of patients with Dupuytren disease. Eight patients on chronic immunosuppressive therapies treated with collagenase for metacarpophalangeal (MP) or proximal interphalangeal (PIP) joint contractures between February 2010 and December 2011 were identified. Three of these patients received collagenase injections into 2 or more separate Dupuytren cords at different encounters, resulting in a total of 13 individual collagenase enzymatic fasciotomies.

Collagenase injections were administered following CORD I trial protocol,6 except we injected Dupuytren cords crossing the PIP joint using a lateral approach to minimize risk of flexor tendon rupture. Manipulation of the treated joint was performed between 24 and 48 hours after collagenase injection under local anesthesia with 3 mL of 1% mepivacaine or lidocaine without epinephrine. After manipulation and cord rupture, patients were placed in a hand-based extension splint to wear at night for up to 3 months. Patients were followed at 1 and 12 months.

Results

Patients’ baseline characteristics are summarized in Table 1. Four patients were maintained on chronic prednisone therapy, 3 on methotrexate, and 1 on azathioprine. Therapy duration, medication dose, and diagnoses requiring immunosuppressant therapy varied among patients.

Outcomes and adverse events are summarized in Table 2. Mean number of joint contractures per hand treated was 2.8 (MP, 1.4; PIP, 1.4). However, not all joints met the intervention criteria. Of the 13 joints treated, 7 were MP joints, and 6 were PIP joints. Mean preinjection contracture of the treated joints was 53.0° (range, 20°-90°). Twelve of the 13 joint contractures improved. At mean follow-up of 6.7 months (range, 1-22 months), mean magnitude of contracture improved to 12.9° (range, 0°-45°). Mean MP joint contracture improved from 42.0° to 4.2° (range, 0°-10°), and mean PIP joint contracture improved from 65.8° to 21.7° (range, 0°-45°).

All 13 collagenase injections were well tolerated, and there were no systemic reactions. Injection-site pain was common. Mild injection-site bruising and edema were reported in all cases. Enzymatic fasciotomy was performed in all patients, and immediate improvement in contracture after manipulation 24 to 48 hours after injection was recorded.

Three of the 13 injections were complicated by skin tears during manipulation and cord rupture. All 3 skin tears were treated with local wound care, which included use of povidone-iodine and wet-to-dry dressings. There was no evidence of subsequent superficial or deep, local or regional infection. In 2 cases, the wound healed within 1 week; in the third case, wound healing was present by 2 weeks. Once the wounds showed early re-epithelialization, hand-based extension splinting in a position of comfort was used at night for up to 3 months after injection. Two of the 13 injections were complicated by small blood blisters. These were treated with observation and resolved spontaneously.

 

 

Discussion

Collagenase enzymatic fasciotomy appeared to be a safe and efficacious alternative to surgical treatment of Dupuytren contractures in this cohort of patients maintained on chronic immunosuppressive agents. MP contractures responded more substantially than PIP contractures did, as expected.6 No previously undescribed adverse outcomes were noted in these 8 patients on chronic immunosuppressive therapy beyond those reported in the CORD I trial. Three (23%) of the 13 collagenase injections in our series were complicated by skin tears after manipulation. Skins tears were reported in 22 (11%) of 204 patients after manual cord rupture in the CORD I trial.6 Given the limited numbers in this series, it remains unclear if chronic immunosuppression truly increases the risk of skin tears in this subset of patients. Other common treatment-related adverse events seen in the CORD I trial—injection-site hemorrhage (37%), pruritis (11%) and lymphadenopathy (10%)—were not seen after the 13 injections in our case series. We are prospectively following all patients with Dupuytren disease, and this is an area of ongoing research at our centers.

The immunosuppressive actions of prednisone, azathioprine, and methotrexate are well documented. Prednisone is a glucocorticoid, converted in the liver to prednisolone, which suppresses inflammation and immune responses by regulation of gene expression. Its immunosuppressive actions are multifactorial, relating to inhibition of lymphocytes, neutrophils, and monocytes. These effects are dose- and time-dependent11 and may become evident in patients receiving low doses over prolonged periods. Skin atrophy12 and delayed wound healing9 are side effects of long-term prednisone use. Skin atrophy may make the prednisone-treated patient more susceptible to skin tears after collagenase injection and manipulation. Azathioprine inhibits purine synthesis, which is especially important in the proliferation of immune cells.13 It has been shown to inhibit both cellular immunity at low doses and humoral immunity at higher doses.14 Methotrexate inhibits lymphocyte folic acid metabolism. The immunosuppressive properties of low-dose methotrexate have been linked to the induction of apoptosis in activated T cells.15

A more complex process in immunosuppressed patients is the immunogenicity of injected collagenase. As CHC in current use is a mixture of 2 foreign proteins, an immunologic response is expected in the host after injection. It has been shown that, after 3 injections of CHC into Dupuytren cords, 100% of patients developed antibodies to both enzymes in their serum.6 More than 85% demonstrated anti-CHC antibodies after a single injection. However, no patients showed signs of anaphylaxis or allergic reaction, and there was no correlation between serum levels of anti-CHC and adverse events. It has been hypothesized that there is a potential for cross-reactivity of the anti-CHC antibodies with human matrix metalloproteinases, causing enzymatic dysfunction within the host.16 This has yet to be reported clinically, and Xiaflex is currently under postmarketing surveillance. Immunocompromised people, with suppressed humoral and cellular immune responses, may produce less of an antibody response to the foreign CHC proteins. Whether this conclusively leads to a change in the side effect profile of the medication in these individuals is beyond the scope of this article. However, we identified no new side effects in this small but higher risk cohort. The issue should be continually monitored as collagenase is used in wider clinical settings.

Collagenase enzymatic fasciotomy is a new nonsurgical therapeutic option for Dupuytren disease. Indications and guidelines for use continue to evolve. This case series highlights the use of collagenase in 8 patients who were on long-term immunosuppressive therapy. This study has the limitations inherent to retrospective analyses. It is difficult to generalize results across broader immunosuppressed populations. A larger cohort, with long-term follow-up assessing recurrence of contracture, is needed to make definitive conclusions about use of collagenase in this challenging subset of patients. Based on our observations in this limited cohort, it appears appropriate to pursue further studies on use of collagenase enzymatic fasciotomy. A randomized, prospective or case–control series comparing surgical fasciectomy with enzymatic fasciotomy would yield further meaningful data. As more patients seek nonsurgical treatment for Dupuytren disease, its safety and efficacy in select cohorts of patients should continue to be evaluated.

References

1.    Loos B, Puschkin V, Horch RE. 50 years experience with Dupuytren’s contracture in the Erlangen University Hospital—a retrospective analysis of 2919 operated hands from 1956 to 2006. BMC Musculoskelet Disord. 2007;8:60.

2.    Coert JH, Nérin JP, Meek MF. Results of partial fasciectomy for Dupuytren disease in 261 consecutive patients. Ann Plast Surg. 2006;57(1):13-17.

3.    Sennwald GR. Fasciectomy for treatment of Dupuytren’s disease and early complications. J Hand Surg Am. 1990;15(5):755-761.

4.    Badalamente MA, Hurst LC. Enzyme injection as nonsurgical treatment of Dupuytren’s disease. J Hand Surg Am. 2000;25(4):629-636.

5.      Badalamente MA, Hurst LC, Hentz VR. Collagen as a clinical target: nonoperative treatment of Dupuytren’s disease. J Hand Surg Am. 2002;27(5):788-798.

6.    Hurst LC, Badalamente MA, Hentz VR, et al; CORD I Study Group. Injectable collagenase Clostridium histolyticum for Dupuytren’s contracture. N Engl J Med. 2009;361(10):968-979.

7.    Mookhtiar KA, Van Wart HE. Clostridium histolyticum collagenases: a new look at some old enzymes. Matrix Suppl. 1992;1:116-126.

8.    Watanabe K. Collagenolytic proteases from bacteria. Appl Microbiol Biotechnol. 2004;63(5):520-526.

9.    Wang AS, Armstrong EJ, Armstrong AW. Corticosteroids and wound healing: clinical considerations in the perioperative period. Am J Surg. 2013;206(3):410-417.

10. Denkler K. Surgical complications associated with fasciectomy for Dupuytren’s disease: a 20-year review of the English literature. Eplasty. 2010;10:e15.

11. Stuck AE, Minder CE, Frey FJ. Risk of infectious complications in patients taking glucocorticosteroids. Rev Infect Dis. 1989;11(6):954-963.

12. Oikarinen A, Autio P. New aspects of the mechanism of corticosteroid-induced dermal atrophy. Clin Exp Dermatol. 1991;16(6):416-419.

13. Makinodan T, Santos GW, Quinn RP. Immunosuppressive drugs. Pharmacol Rev. 1970;22(2):189-247.

14. Röllinghoff M, Schrader J, Wagner H. Effect of azathioprine and cytosine arabinoside on humoral and cellular immunity in vitro. Clin Exp Immunol. 1973;15(2):261-269.

15. Genestier L, Paillot R, Fournel S, Ferraro C, Miossec P, Revillard JP. Immunosuppressive properties of methotrexate: apoptosis and clonal deletion of activated peripheral T cells. J Clin Invest. 1998;102(2):322-328.

16. Desai SS, Hentz VR. Collagenase Clostridium histolyticum for Dupuytren’s contracture. Expert Opin Biol Ther. 2010;10(9):1395-1404.

References

1.    Loos B, Puschkin V, Horch RE. 50 years experience with Dupuytren’s contracture in the Erlangen University Hospital—a retrospective analysis of 2919 operated hands from 1956 to 2006. BMC Musculoskelet Disord. 2007;8:60.

2.    Coert JH, Nérin JP, Meek MF. Results of partial fasciectomy for Dupuytren disease in 261 consecutive patients. Ann Plast Surg. 2006;57(1):13-17.

3.    Sennwald GR. Fasciectomy for treatment of Dupuytren’s disease and early complications. J Hand Surg Am. 1990;15(5):755-761.

4.    Badalamente MA, Hurst LC. Enzyme injection as nonsurgical treatment of Dupuytren’s disease. J Hand Surg Am. 2000;25(4):629-636.

5.      Badalamente MA, Hurst LC, Hentz VR. Collagen as a clinical target: nonoperative treatment of Dupuytren’s disease. J Hand Surg Am. 2002;27(5):788-798.

6.    Hurst LC, Badalamente MA, Hentz VR, et al; CORD I Study Group. Injectable collagenase Clostridium histolyticum for Dupuytren’s contracture. N Engl J Med. 2009;361(10):968-979.

7.    Mookhtiar KA, Van Wart HE. Clostridium histolyticum collagenases: a new look at some old enzymes. Matrix Suppl. 1992;1:116-126.

8.    Watanabe K. Collagenolytic proteases from bacteria. Appl Microbiol Biotechnol. 2004;63(5):520-526.

9.    Wang AS, Armstrong EJ, Armstrong AW. Corticosteroids and wound healing: clinical considerations in the perioperative period. Am J Surg. 2013;206(3):410-417.

10. Denkler K. Surgical complications associated with fasciectomy for Dupuytren’s disease: a 20-year review of the English literature. Eplasty. 2010;10:e15.

11. Stuck AE, Minder CE, Frey FJ. Risk of infectious complications in patients taking glucocorticosteroids. Rev Infect Dis. 1989;11(6):954-963.

12. Oikarinen A, Autio P. New aspects of the mechanism of corticosteroid-induced dermal atrophy. Clin Exp Dermatol. 1991;16(6):416-419.

13. Makinodan T, Santos GW, Quinn RP. Immunosuppressive drugs. Pharmacol Rev. 1970;22(2):189-247.

14. Röllinghoff M, Schrader J, Wagner H. Effect of azathioprine and cytosine arabinoside on humoral and cellular immunity in vitro. Clin Exp Immunol. 1973;15(2):261-269.

15. Genestier L, Paillot R, Fournel S, Ferraro C, Miossec P, Revillard JP. Immunosuppressive properties of methotrexate: apoptosis and clonal deletion of activated peripheral T cells. J Clin Invest. 1998;102(2):322-328.

16. Desai SS, Hentz VR. Collagenase Clostridium histolyticum for Dupuytren’s contracture. Expert Opin Biol Ther. 2010;10(9):1395-1404.

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The American Journal of Orthopedics - 44(11)
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Collagenase Enzymatic Fasciotomy for Dupuytren Contracture in Patients on Chronic Immunosuppression
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american journal of orthopedics, AJO, original study, study, collagenase enzymatic fasciotomy, dupuytren contracture, chronic immunosuppression, hand, dupuytren, disease, therapy, therapies, joints, waters, belsky, blazar, leibman, ruchelsman
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american journal of orthopedics, AJO, original study, study, collagenase enzymatic fasciotomy, dupuytren contracture, chronic immunosuppression, hand, dupuytren, disease, therapy, therapies, joints, waters, belsky, blazar, leibman, ruchelsman
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Open Carpal Tunnel Release With Use of a Nasal Turbinate Speculum

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Open Carpal Tunnel Release With Use of a Nasal Turbinate Speculum

Carpal tunnel syndrome (CTS) is a disorder characterized by entrapment of the median nerve at the wrist, which may lead to symptoms of pain, paresthesia, and, ultimately, thenar muscle atrophy. Surgical intervention is indicated with persistent or progressive symptoms despite nonoperative management. Timely surgical decompression aims to halt progression of this disorder and prevent permanent peripheral nerve injury.

Carpal tunnel release (CTR) is the most common hand and wrist surgery in the United States, with about 400,000 operations performed annually.1,2 Several methods of decompressing the carpal tunnel have been described.3 These include standard open CTR (OCTR), mini-open approaches, and various endoscopic techniques. OCTR was initially described by Sir James Learmonth in 1933,4 and it remains the gold-standard surgical treatment for patients with symptomatic CTS. Uniform excellent results with high patient satisfaction and low complication rates have been reported in several series.5-9 Common to all techniques is complete proximal-to-distal division of the transverse carpal ligament (TCL). Magnetic resonance imaging studies have shown that TCL transection and the resulting diastasis between the radial and ulnar leaflets cause a significant increase in the volume of the carpal tunnel, leading to decreased pressure.10,11

Endoscopic CTR (ECTR) techniques were developed in an effort to reduce complications, scar sensitivity, and pillar pain and facilitate more rapid return to work.12-17 Outcome studies have demonstrated that both open and endoscopic releases yield patient-reported subjective improvements over preoperative symptoms.18-22 A randomized, controlled trial by Trumble and colleagues23 in 2002 found that ECTR led to improved patient outcomes in the early postoperative period (first 3 months), though differences in outcomes were reduced at final follow-up. More recently (2007), a Cochrane review of 33 trials concluded there was no strong evidence favoring use of alternative techniques over OCTR.3 Further, OCTR has been found to be technically less demanding and associated with decreased complications and costs.24

Indications

The benefit of median nerve decompression at the wrist for CTS is clear.6,7 Indications for surgery in patients with CTS include persistent symptoms despite nonoperative treatment, objective sensory disturbance or motor weakness, and thenar atrophy. Symptomatic response to corticosteroid injection is predictive of success after carpal tunnel surgery.25 More than 87% of patients who gain symptomatic relief from corticosteroid injection have an excellent surgical outcome.

Technique

OCTR allows direct visualization of the TCL and the distal volar forearm fascia (DVFF) and evaluation for the presence of anomalous branching patterns of the median nerve. OCTR traditionally was performed through a 4- to 5-cm longitudinal incision extending from the wrist crease proximally to the Kaplan cardinal line distally. The mini-open technique is identical with the exception of incision length. We routinely use a 2.5- to 3-cm incision. Regardless of incision length, each OCTR should proceed through the same reproducible steps.

We perform OCTR under tourniquet control. Choice of anesthesia is surgeon and patient preference. We prefer local anesthesia with conscious sedation. After conscious sedation is administered, we infiltrate the carpal tunnel and surrounding subcutaneous tissue with 10 mL of a 50:50 mixture of 0.5% bupivacaine and 1% lidocaine without epinephrine.

A 2.5- to 3-cm longitudinal incision is made along the axis of the radial border of the ring finger from the Kaplan cardinal line26 and extending about 3 cm proximally toward the wrist flexion crease ulnar to the palmaris longus if present (Figure 1).

After the skin is incised longitudinally, the subcutaneous fat is mobilized and cutaneous sensory branches identified and protected. The underlying superficial palmar fascia is incised in line with the skin incision. The underlying midportion of the TCL is now visualized.

Transverse Carpal Ligament Release

Occasionally, the investing fascia along the ulnar edge of the thenar musculature is mobilized radialward (if the thenar musculature is well developed) to visualize the proximal limb of the TCL. Injury to any anomalous motor branch of the median nerve is avoided by directly visualizing and then incising the TCL (Figure 2). The TCL is incised along its ulnar border just radial to the hook of hamate from distal to proximal in line with the radial border of the ring finger. Staying near the ulnar attachment of the TCL keeps the plane of ligament division farther away from the median nerve and its recurrent motor branches. Although the ulnar neurovascular bundle typically resides ulnar to the hook of hamate in the canal of Guyon, the surgeon must be aware that it can be located radial to the hook in some instances.27,28 In the elderly, the ulnar artery may be tortuous and enter the field and require retraction. The TCL is incised distally until the sentinel fat pad, which marks the superficial palmar arterial arch, is visualized. This bed of adipose tissue marks the distal edge of the TCL.29

 

 

Proximally, subcutaneous tissues above the proximal limb of the TCL and DVFF are mobilized to about 2 cm proximal to the wrist flexion crease to create a plane for the fine long nasal turbinate speculum. The nasal turbinate speculum is then inserted into this plane above the proximal limb of the TCL and DVFF (Figure 3). Once inserted to the level of the confluence of the TCL and the DVFF, the speculum is opened.

Topside visualization is now encountered with the ulnar neurovascular bundle protected by the ulnar blade of the speculum. A long-handle scalpel is used to incise the TCL and the DVFF under direct visualization from proximal to distal in line with the previously completed distal release (Figure 4). As the nasal turbinate speculum is stretching the TCL and putting it under tension, the TCL can be heard splitting as it is being incised. Once the TCL and the DVFF are divided, the speculum is slowly closed and removed. Wide diastasis of the radial and ulnar leaflets of the TCL and the DVFF is directly visualized. Complete decompression of the median nerve from the distal forearm fascia to the superficial palmar arch is confirmed.

Adhesions between the undersurface of the radial leaflet and the flexor tendons and median nerve are mobilized. The median nerve is assessed for “hourglass” morphology or atrophy. The flexor tendons can be swept radialward with a free elevator to inspect the floor of the carpal tunnel. Flexor tenosynovectomy is not routinely performed. The incision is closed with interrupted simple sutures using 4-0 nylon.

Study Results

This study was conducted at Hand Surgery PC, Newton-Wellesley Hospital, Tufts University School of Medicine. Over a 10-month interval, 101 consecutive mini-OCTRs (63 right hands, 38 left hands) were performed with this proximal release modification in 88 patients (51 females, 37 males) by Dr. Ruchelsman and Dr. Belsky (Table). CTRs performed in the setting of wrist and/or carpal trauma were excluded. Mean age was 62.8 years. Mean follow-up was 11.3 weeks (~3 months). For isolated cases of CTR, mean tourniquet time was 16 minutes. CTS symptoms were relieved in all patients with a high degree of satisfaction as measured with history and examination findings at follow-up visits. There were no major complications (eg, infection, neural or vascular damage, severe residual pain). Four patients reported minor residual numbness in the fingers at latest follow-up but nevertheless had major improvement over preoperative baseline. These 4 patients had preoperative electromyograms or nerve conduction studies documenting the extent of their disease. There was 1 case of minor wound complication. Three weeks after surgery, the patient had a 1-cm wound opening, which closed with local wound care. The patient did not develop any drainage, infection, bleeding, or neurologic symptoms.

Discussion

Open release of the TCL—the gold standard of surgical treatment for CTS—produces reliable symptom relief in the vast majority of patients.25,30 Given that the most common complication of carpal tunnel surgery is incomplete release of the TCL,31,32 this technique, which uses a nasal turbinate speculum to better visualize the median nerve, could potentially reduce the reoperation rate. The nasal turbinate speculum allows the surgeon to see the confluence of the TCL and the DVFF. In addition, as the complete release can be visualized, there is minimal chance of injury.

The 2007 Cochrane review3 found no strong evidence supporting replacing OCTR with endoscopic techniques. Previous investigators have questioned the utility of ECTR given that it is higher in cost and more resource-intensive than OCTR1,33,34 and is associated with higher rates of certain complications.5,22,35-37 A 2004 meta-analysis of 13 randomized, controlled trials found a higher rate of reversible nerve damage with an odds ratio of 3.1 for ECTR versus OCTR.35 A more recent (2006) review of more than 80 studies found transient neurapraxias in 1.45% of ECTR cases and 0.25% of OCTR cases.5 The same study reported overall complication rates (reversible and major neurovascular structural injuries) of 0.74% for OCTR and 1.63% for ECTR (P < .005). Another limitation of ECTR is that endoscopic techniques require a higher degree of surgical skill, which makes teaching residents and fellows more challenging.

The novel nasal turbinate speculum technique presented here is easily reproducible and allows first-time surgeons to visualize all important structures. Given that this technique does not require an endoscope or an endoscope-viewing tower, it is likely more cost-effective and requires less time for turnover between cases. Patients obtain good relief of their CTS symptoms with this technique, and most return to their daily activities within weeks after operation.

References

1.    Ono S, Clapham PJ, Chung KC. Optimal management of carpal tunnel syndrome. Int J Gen Med. 2010;3(4):255-261.

2.    Concannon MJ, Brownfield ML, Puckett CL. The incidence of recurrence after endoscopic carpal tunnel release. Plast Reconstr Surg. 2000;105(5):1662-1665.

3.    Scholten RJ, Mink van der Molen A, Uitdehaag BM, Bouter LM, de Vet HC. Surgical treatment options for carpal tunnel syndrome. Cochrane Database Syst Rev. 2007;(4):CD003905.

4.    In memoriam Sir James Learmonth, K.C.V.O., C.B.E., hon. F.R.C.S. (1895-1967). Ann R Coll Surg Engl. 1967;41(5):438-439.

5.    Benson LS, Bare AA, Nagle DJ, Harder VS, Williams CS, Visotsky JL. Complications of endoscopic and open carpal tunnel release. Arthroscopy. 2006;22(9):919-924, 924.e1-e2.

6.    Jarvik JG, Comstock BA, Kliot M, et al. Surgery versus non-surgical therapy for carpal tunnel syndrome: a randomised parallel-group trial. Lancet. 2009;374(9695):1074-1081.

7.    Verdugo RJ, Salinas RA, Castillo JL, et al. Surgical versus non-surgical treatment for carpal tunnel syndrome. Cochrane Database Syst Rev. 2008;(4):CD001552.

8.    Garland H, Langworth EP, Taverner D, et al. Surgical treatment for the carpal tunnel syndrome. Lancet. 1964;1(7343):1129-1130.

9.    Gerritsen AA, de Vet HC, Scholten RJ, et al. Splinting vs surgery in the treatment of carpal tunnel syndrome: a randomized controlled trial. JAMA. 2002;288(10):1245-1251.

10.  Gelberman RH, Hergenroeder PT, Hargens AR, et al. The carpal tunnel syndrome. A study of carpal canal pressures. J Bone Joint Surg Am. 1981;63(3):380-383.

11.  Sucher BM. Myofascial manipulative release of carpal tunnel syndrome: documentation with magnetic resonance imaging. J Am Osteopath Assoc. 1993;93(12):1273-1278.

12.  Pereira EE, Miranda DA, Sere I, et al. Endoscopic release of the carpal tunnel: a 2-portal-modified technique. Tech Hand Up Extrem Surg. 2010;14(4):263-265.

13.  Louis DS, Greene TL, Noellert RC. Complications of carpal tunnel surgery. J Neurosurg. 1985;62(3):352-356.

14.  Mirza MA, King ET Jr, Tanveer S. Palmar uniportal extrabursal endoscopic carpal tunnel release. Arthroscopy. 1995;11(1):82-90.

15.  Brown MG, Keyser B, Rothenberg ES. Endoscopic carpal tunnel release. J Hand Surg Am. 1992;17(6):1009-1011.

16.  Agee JM, McCarroll HR Jr, Tortosa RD, et al. Endoscopic release of the carpal tunnel: a randomized prospective multicenter study. J Hand Surg Am. 1992;17(6):987-995.

17.  Okutsu I, Ninomiya S, Takatori Y, et al. Endoscopic management of carpal tunnel syndrome. Arthroscopy. 1989;5(1):11-18.

18.  Ghaly RF, Saban KL, Haley DA, et al. Endoscopic carpal tunnel release surgery: report of patient satisfaction. Neurol Res. 2000;22(6):551-555.

19.  Lee WP, Plancher KD, Strickland JW. Carpal tunnel release with a small palmar incision. Hand Clin. 1996;12(2):271-284.

20.  Biyani A, Downes EM. An open twin incision technique of carpal tunnel decompression with reduced incidence of scar tenderness. J Hand Surg Br. 1993;18(3):331-334.

21.  Brown RA, Gelberman RH, Seiler JG 3rd, et al. Carpal tunnel release. A prospective, randomized assessment of open and endoscopic methods. J Bone Joint Surg Am. 1993;75(9):1265-1275.

22.  Chow JC. Endoscopic release of the carpal ligament for carpal tunnel syndrome: 22-month clinical result. Arthroscopy. 1990;6(4):288-296.

23.  Trumble TE, Diao E, Abrams RA, et al. Single-portal endoscopic carpal tunnel release compared with open release: a prospective, randomized trial. J Bone Joint Surg Am. 2002;84(7):1107-1115.

24.  Gerritsen AA, Uitdehaag BM, van Geldere D, et al. Systematic review of randomized clinical trials of surgical treatment for carpal tunnel syndrome. Br J Surg. 2001;88(10):1285-1295.

25.  Edgell SE, McCabe SJ, Breidenbach WC, et al. Predicting the outcome of carpal tunnel release. J Hand Surg Am. 2003;28(2):255-261.

26.  Vella JC, Hartigan BJ, Stern PJ. Kaplan’s cardinal line. J Hand Surg Am. 2006;31(6):912-918.

27.  Kwon JY, Kim JY, Hong JT, et al. Position change of the neurovascular structures around the carpal tunnel with dynamic wrist motion. J Korean Neurosurg Soc. 2011;50(4):377-380.

28.  Netscher D, Polsen C, Thornby J, et al. Anatomic delineation of the ulnar nerve and ulnar artery in relation to the carpal tunnel by axial magnetic resonance imaging scanning. J Hand Surg Am. 1996;21(2):273-276.

29.  Madhav TJ, To P, Stern PJ. The palmar fat pad is a reliable intraoperative landmark during carpal tunnel release. J Hand Surg Am. 2009;34(7):1204-1209.

30.  Kulick MI, Gordillo G, Javidi T, et al. Long-term analysis of patients having surgical treatment for carpal tunnel syndrome. J Hand Surg Am. 1986;11(1):59-66.

31.  Bland JD. Treatment of carpal tunnel syndrome. Muscle Nerve. 2007;36(2):167-171.

32.  MacDonald RI, Lichtman DM, Hanlon JJ, et al. Complications of surgical release for carpal tunnel syndrome. J Hand Surg Am. 1978;3(1):70-76.

33.  Atroshi I, Larsson GU, Ornstein E, Hofer M, Johnsson R, Ranstam J. Outcomes of endoscopic surgery compared with open surgery for carpal tunnel syndrome among employed patients: randomised controlled trial. BMJ. 2006;332(7556):1473.

34.  Ferdinand RD, MacLean JG. Endoscopic versus open carpal tunnel release in bilateral carpal tunnel syndrome. A prospective, randomised, blinded assessment. J Bone Joint Surg Br. 2002;84(3):375-379.

35.  Thoma A, Veltri K, Haines T, et al. A meta-analysis of randomized controlled trials comparing endoscopic and open carpal tunnel decompression. Plast Reconstr Surg. 2004;114(5):1137-1146.

36.  Murphy RX Jr, Jennings JF, Wukich DK. Major neurovascular complications of endoscopic carpal tunnel release. J Hand Surg Am. 1994;19(1):114-118.

37.  Palmer DH, Paulson JC, Lane-Larsen CL, et al. Endoscopic carpal tunnel release: a comparison of two techniques with open release. Arthroscopy. 1993;9(5):498-508.

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Raghuveer C. Muppavarapu, MD, Sean S. Rajaee, MD, David E. Ruchelsman, MD, and Mark R. Belsky, MD

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

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The American Journal of Orthopedics - 44(11)
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495-498
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american journal of orthopedics, AJO, orthopedic technologies and techniques, technology, technique, carpal tunnel release, carpal, nasal turbinate speculum, transverse carpal ligament, TCL, nerve, injury, CTR, wrist, ligament, muppavarapu, rajaee, ruchelsman, belsky
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Raghuveer C. Muppavarapu, MD, Sean S. Rajaee, MD, David E. Ruchelsman, MD, and Mark R. Belsky, MD

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

Author and Disclosure Information

Raghuveer C. Muppavarapu, MD, Sean S. Rajaee, MD, David E. Ruchelsman, MD, and Mark R. Belsky, MD

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

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Article PDF

Carpal tunnel syndrome (CTS) is a disorder characterized by entrapment of the median nerve at the wrist, which may lead to symptoms of pain, paresthesia, and, ultimately, thenar muscle atrophy. Surgical intervention is indicated with persistent or progressive symptoms despite nonoperative management. Timely surgical decompression aims to halt progression of this disorder and prevent permanent peripheral nerve injury.

Carpal tunnel release (CTR) is the most common hand and wrist surgery in the United States, with about 400,000 operations performed annually.1,2 Several methods of decompressing the carpal tunnel have been described.3 These include standard open CTR (OCTR), mini-open approaches, and various endoscopic techniques. OCTR was initially described by Sir James Learmonth in 1933,4 and it remains the gold-standard surgical treatment for patients with symptomatic CTS. Uniform excellent results with high patient satisfaction and low complication rates have been reported in several series.5-9 Common to all techniques is complete proximal-to-distal division of the transverse carpal ligament (TCL). Magnetic resonance imaging studies have shown that TCL transection and the resulting diastasis between the radial and ulnar leaflets cause a significant increase in the volume of the carpal tunnel, leading to decreased pressure.10,11

Endoscopic CTR (ECTR) techniques were developed in an effort to reduce complications, scar sensitivity, and pillar pain and facilitate more rapid return to work.12-17 Outcome studies have demonstrated that both open and endoscopic releases yield patient-reported subjective improvements over preoperative symptoms.18-22 A randomized, controlled trial by Trumble and colleagues23 in 2002 found that ECTR led to improved patient outcomes in the early postoperative period (first 3 months), though differences in outcomes were reduced at final follow-up. More recently (2007), a Cochrane review of 33 trials concluded there was no strong evidence favoring use of alternative techniques over OCTR.3 Further, OCTR has been found to be technically less demanding and associated with decreased complications and costs.24

Indications

The benefit of median nerve decompression at the wrist for CTS is clear.6,7 Indications for surgery in patients with CTS include persistent symptoms despite nonoperative treatment, objective sensory disturbance or motor weakness, and thenar atrophy. Symptomatic response to corticosteroid injection is predictive of success after carpal tunnel surgery.25 More than 87% of patients who gain symptomatic relief from corticosteroid injection have an excellent surgical outcome.

Technique

OCTR allows direct visualization of the TCL and the distal volar forearm fascia (DVFF) and evaluation for the presence of anomalous branching patterns of the median nerve. OCTR traditionally was performed through a 4- to 5-cm longitudinal incision extending from the wrist crease proximally to the Kaplan cardinal line distally. The mini-open technique is identical with the exception of incision length. We routinely use a 2.5- to 3-cm incision. Regardless of incision length, each OCTR should proceed through the same reproducible steps.

We perform OCTR under tourniquet control. Choice of anesthesia is surgeon and patient preference. We prefer local anesthesia with conscious sedation. After conscious sedation is administered, we infiltrate the carpal tunnel and surrounding subcutaneous tissue with 10 mL of a 50:50 mixture of 0.5% bupivacaine and 1% lidocaine without epinephrine.

A 2.5- to 3-cm longitudinal incision is made along the axis of the radial border of the ring finger from the Kaplan cardinal line26 and extending about 3 cm proximally toward the wrist flexion crease ulnar to the palmaris longus if present (Figure 1).

After the skin is incised longitudinally, the subcutaneous fat is mobilized and cutaneous sensory branches identified and protected. The underlying superficial palmar fascia is incised in line with the skin incision. The underlying midportion of the TCL is now visualized.

Transverse Carpal Ligament Release

Occasionally, the investing fascia along the ulnar edge of the thenar musculature is mobilized radialward (if the thenar musculature is well developed) to visualize the proximal limb of the TCL. Injury to any anomalous motor branch of the median nerve is avoided by directly visualizing and then incising the TCL (Figure 2). The TCL is incised along its ulnar border just radial to the hook of hamate from distal to proximal in line with the radial border of the ring finger. Staying near the ulnar attachment of the TCL keeps the plane of ligament division farther away from the median nerve and its recurrent motor branches. Although the ulnar neurovascular bundle typically resides ulnar to the hook of hamate in the canal of Guyon, the surgeon must be aware that it can be located radial to the hook in some instances.27,28 In the elderly, the ulnar artery may be tortuous and enter the field and require retraction. The TCL is incised distally until the sentinel fat pad, which marks the superficial palmar arterial arch, is visualized. This bed of adipose tissue marks the distal edge of the TCL.29

 

 

Proximally, subcutaneous tissues above the proximal limb of the TCL and DVFF are mobilized to about 2 cm proximal to the wrist flexion crease to create a plane for the fine long nasal turbinate speculum. The nasal turbinate speculum is then inserted into this plane above the proximal limb of the TCL and DVFF (Figure 3). Once inserted to the level of the confluence of the TCL and the DVFF, the speculum is opened.

Topside visualization is now encountered with the ulnar neurovascular bundle protected by the ulnar blade of the speculum. A long-handle scalpel is used to incise the TCL and the DVFF under direct visualization from proximal to distal in line with the previously completed distal release (Figure 4). As the nasal turbinate speculum is stretching the TCL and putting it under tension, the TCL can be heard splitting as it is being incised. Once the TCL and the DVFF are divided, the speculum is slowly closed and removed. Wide diastasis of the radial and ulnar leaflets of the TCL and the DVFF is directly visualized. Complete decompression of the median nerve from the distal forearm fascia to the superficial palmar arch is confirmed.

Adhesions between the undersurface of the radial leaflet and the flexor tendons and median nerve are mobilized. The median nerve is assessed for “hourglass” morphology or atrophy. The flexor tendons can be swept radialward with a free elevator to inspect the floor of the carpal tunnel. Flexor tenosynovectomy is not routinely performed. The incision is closed with interrupted simple sutures using 4-0 nylon.

Study Results

This study was conducted at Hand Surgery PC, Newton-Wellesley Hospital, Tufts University School of Medicine. Over a 10-month interval, 101 consecutive mini-OCTRs (63 right hands, 38 left hands) were performed with this proximal release modification in 88 patients (51 females, 37 males) by Dr. Ruchelsman and Dr. Belsky (Table). CTRs performed in the setting of wrist and/or carpal trauma were excluded. Mean age was 62.8 years. Mean follow-up was 11.3 weeks (~3 months). For isolated cases of CTR, mean tourniquet time was 16 minutes. CTS symptoms were relieved in all patients with a high degree of satisfaction as measured with history and examination findings at follow-up visits. There were no major complications (eg, infection, neural or vascular damage, severe residual pain). Four patients reported minor residual numbness in the fingers at latest follow-up but nevertheless had major improvement over preoperative baseline. These 4 patients had preoperative electromyograms or nerve conduction studies documenting the extent of their disease. There was 1 case of minor wound complication. Three weeks after surgery, the patient had a 1-cm wound opening, which closed with local wound care. The patient did not develop any drainage, infection, bleeding, or neurologic symptoms.

Discussion

Open release of the TCL—the gold standard of surgical treatment for CTS—produces reliable symptom relief in the vast majority of patients.25,30 Given that the most common complication of carpal tunnel surgery is incomplete release of the TCL,31,32 this technique, which uses a nasal turbinate speculum to better visualize the median nerve, could potentially reduce the reoperation rate. The nasal turbinate speculum allows the surgeon to see the confluence of the TCL and the DVFF. In addition, as the complete release can be visualized, there is minimal chance of injury.

The 2007 Cochrane review3 found no strong evidence supporting replacing OCTR with endoscopic techniques. Previous investigators have questioned the utility of ECTR given that it is higher in cost and more resource-intensive than OCTR1,33,34 and is associated with higher rates of certain complications.5,22,35-37 A 2004 meta-analysis of 13 randomized, controlled trials found a higher rate of reversible nerve damage with an odds ratio of 3.1 for ECTR versus OCTR.35 A more recent (2006) review of more than 80 studies found transient neurapraxias in 1.45% of ECTR cases and 0.25% of OCTR cases.5 The same study reported overall complication rates (reversible and major neurovascular structural injuries) of 0.74% for OCTR and 1.63% for ECTR (P < .005). Another limitation of ECTR is that endoscopic techniques require a higher degree of surgical skill, which makes teaching residents and fellows more challenging.

The novel nasal turbinate speculum technique presented here is easily reproducible and allows first-time surgeons to visualize all important structures. Given that this technique does not require an endoscope or an endoscope-viewing tower, it is likely more cost-effective and requires less time for turnover between cases. Patients obtain good relief of their CTS symptoms with this technique, and most return to their daily activities within weeks after operation.

Carpal tunnel syndrome (CTS) is a disorder characterized by entrapment of the median nerve at the wrist, which may lead to symptoms of pain, paresthesia, and, ultimately, thenar muscle atrophy. Surgical intervention is indicated with persistent or progressive symptoms despite nonoperative management. Timely surgical decompression aims to halt progression of this disorder and prevent permanent peripheral nerve injury.

Carpal tunnel release (CTR) is the most common hand and wrist surgery in the United States, with about 400,000 operations performed annually.1,2 Several methods of decompressing the carpal tunnel have been described.3 These include standard open CTR (OCTR), mini-open approaches, and various endoscopic techniques. OCTR was initially described by Sir James Learmonth in 1933,4 and it remains the gold-standard surgical treatment for patients with symptomatic CTS. Uniform excellent results with high patient satisfaction and low complication rates have been reported in several series.5-9 Common to all techniques is complete proximal-to-distal division of the transverse carpal ligament (TCL). Magnetic resonance imaging studies have shown that TCL transection and the resulting diastasis between the radial and ulnar leaflets cause a significant increase in the volume of the carpal tunnel, leading to decreased pressure.10,11

Endoscopic CTR (ECTR) techniques were developed in an effort to reduce complications, scar sensitivity, and pillar pain and facilitate more rapid return to work.12-17 Outcome studies have demonstrated that both open and endoscopic releases yield patient-reported subjective improvements over preoperative symptoms.18-22 A randomized, controlled trial by Trumble and colleagues23 in 2002 found that ECTR led to improved patient outcomes in the early postoperative period (first 3 months), though differences in outcomes were reduced at final follow-up. More recently (2007), a Cochrane review of 33 trials concluded there was no strong evidence favoring use of alternative techniques over OCTR.3 Further, OCTR has been found to be technically less demanding and associated with decreased complications and costs.24

Indications

The benefit of median nerve decompression at the wrist for CTS is clear.6,7 Indications for surgery in patients with CTS include persistent symptoms despite nonoperative treatment, objective sensory disturbance or motor weakness, and thenar atrophy. Symptomatic response to corticosteroid injection is predictive of success after carpal tunnel surgery.25 More than 87% of patients who gain symptomatic relief from corticosteroid injection have an excellent surgical outcome.

Technique

OCTR allows direct visualization of the TCL and the distal volar forearm fascia (DVFF) and evaluation for the presence of anomalous branching patterns of the median nerve. OCTR traditionally was performed through a 4- to 5-cm longitudinal incision extending from the wrist crease proximally to the Kaplan cardinal line distally. The mini-open technique is identical with the exception of incision length. We routinely use a 2.5- to 3-cm incision. Regardless of incision length, each OCTR should proceed through the same reproducible steps.

We perform OCTR under tourniquet control. Choice of anesthesia is surgeon and patient preference. We prefer local anesthesia with conscious sedation. After conscious sedation is administered, we infiltrate the carpal tunnel and surrounding subcutaneous tissue with 10 mL of a 50:50 mixture of 0.5% bupivacaine and 1% lidocaine without epinephrine.

A 2.5- to 3-cm longitudinal incision is made along the axis of the radial border of the ring finger from the Kaplan cardinal line26 and extending about 3 cm proximally toward the wrist flexion crease ulnar to the palmaris longus if present (Figure 1).

After the skin is incised longitudinally, the subcutaneous fat is mobilized and cutaneous sensory branches identified and protected. The underlying superficial palmar fascia is incised in line with the skin incision. The underlying midportion of the TCL is now visualized.

Transverse Carpal Ligament Release

Occasionally, the investing fascia along the ulnar edge of the thenar musculature is mobilized radialward (if the thenar musculature is well developed) to visualize the proximal limb of the TCL. Injury to any anomalous motor branch of the median nerve is avoided by directly visualizing and then incising the TCL (Figure 2). The TCL is incised along its ulnar border just radial to the hook of hamate from distal to proximal in line with the radial border of the ring finger. Staying near the ulnar attachment of the TCL keeps the plane of ligament division farther away from the median nerve and its recurrent motor branches. Although the ulnar neurovascular bundle typically resides ulnar to the hook of hamate in the canal of Guyon, the surgeon must be aware that it can be located radial to the hook in some instances.27,28 In the elderly, the ulnar artery may be tortuous and enter the field and require retraction. The TCL is incised distally until the sentinel fat pad, which marks the superficial palmar arterial arch, is visualized. This bed of adipose tissue marks the distal edge of the TCL.29

 

 

Proximally, subcutaneous tissues above the proximal limb of the TCL and DVFF are mobilized to about 2 cm proximal to the wrist flexion crease to create a plane for the fine long nasal turbinate speculum. The nasal turbinate speculum is then inserted into this plane above the proximal limb of the TCL and DVFF (Figure 3). Once inserted to the level of the confluence of the TCL and the DVFF, the speculum is opened.

Topside visualization is now encountered with the ulnar neurovascular bundle protected by the ulnar blade of the speculum. A long-handle scalpel is used to incise the TCL and the DVFF under direct visualization from proximal to distal in line with the previously completed distal release (Figure 4). As the nasal turbinate speculum is stretching the TCL and putting it under tension, the TCL can be heard splitting as it is being incised. Once the TCL and the DVFF are divided, the speculum is slowly closed and removed. Wide diastasis of the radial and ulnar leaflets of the TCL and the DVFF is directly visualized. Complete decompression of the median nerve from the distal forearm fascia to the superficial palmar arch is confirmed.

Adhesions between the undersurface of the radial leaflet and the flexor tendons and median nerve are mobilized. The median nerve is assessed for “hourglass” morphology or atrophy. The flexor tendons can be swept radialward with a free elevator to inspect the floor of the carpal tunnel. Flexor tenosynovectomy is not routinely performed. The incision is closed with interrupted simple sutures using 4-0 nylon.

Study Results

This study was conducted at Hand Surgery PC, Newton-Wellesley Hospital, Tufts University School of Medicine. Over a 10-month interval, 101 consecutive mini-OCTRs (63 right hands, 38 left hands) were performed with this proximal release modification in 88 patients (51 females, 37 males) by Dr. Ruchelsman and Dr. Belsky (Table). CTRs performed in the setting of wrist and/or carpal trauma were excluded. Mean age was 62.8 years. Mean follow-up was 11.3 weeks (~3 months). For isolated cases of CTR, mean tourniquet time was 16 minutes. CTS symptoms were relieved in all patients with a high degree of satisfaction as measured with history and examination findings at follow-up visits. There were no major complications (eg, infection, neural or vascular damage, severe residual pain). Four patients reported minor residual numbness in the fingers at latest follow-up but nevertheless had major improvement over preoperative baseline. These 4 patients had preoperative electromyograms or nerve conduction studies documenting the extent of their disease. There was 1 case of minor wound complication. Three weeks after surgery, the patient had a 1-cm wound opening, which closed with local wound care. The patient did not develop any drainage, infection, bleeding, or neurologic symptoms.

Discussion

Open release of the TCL—the gold standard of surgical treatment for CTS—produces reliable symptom relief in the vast majority of patients.25,30 Given that the most common complication of carpal tunnel surgery is incomplete release of the TCL,31,32 this technique, which uses a nasal turbinate speculum to better visualize the median nerve, could potentially reduce the reoperation rate. The nasal turbinate speculum allows the surgeon to see the confluence of the TCL and the DVFF. In addition, as the complete release can be visualized, there is minimal chance of injury.

The 2007 Cochrane review3 found no strong evidence supporting replacing OCTR with endoscopic techniques. Previous investigators have questioned the utility of ECTR given that it is higher in cost and more resource-intensive than OCTR1,33,34 and is associated with higher rates of certain complications.5,22,35-37 A 2004 meta-analysis of 13 randomized, controlled trials found a higher rate of reversible nerve damage with an odds ratio of 3.1 for ECTR versus OCTR.35 A more recent (2006) review of more than 80 studies found transient neurapraxias in 1.45% of ECTR cases and 0.25% of OCTR cases.5 The same study reported overall complication rates (reversible and major neurovascular structural injuries) of 0.74% for OCTR and 1.63% for ECTR (P < .005). Another limitation of ECTR is that endoscopic techniques require a higher degree of surgical skill, which makes teaching residents and fellows more challenging.

The novel nasal turbinate speculum technique presented here is easily reproducible and allows first-time surgeons to visualize all important structures. Given that this technique does not require an endoscope or an endoscope-viewing tower, it is likely more cost-effective and requires less time for turnover between cases. Patients obtain good relief of their CTS symptoms with this technique, and most return to their daily activities within weeks after operation.

References

1.    Ono S, Clapham PJ, Chung KC. Optimal management of carpal tunnel syndrome. Int J Gen Med. 2010;3(4):255-261.

2.    Concannon MJ, Brownfield ML, Puckett CL. The incidence of recurrence after endoscopic carpal tunnel release. Plast Reconstr Surg. 2000;105(5):1662-1665.

3.    Scholten RJ, Mink van der Molen A, Uitdehaag BM, Bouter LM, de Vet HC. Surgical treatment options for carpal tunnel syndrome. Cochrane Database Syst Rev. 2007;(4):CD003905.

4.    In memoriam Sir James Learmonth, K.C.V.O., C.B.E., hon. F.R.C.S. (1895-1967). Ann R Coll Surg Engl. 1967;41(5):438-439.

5.    Benson LS, Bare AA, Nagle DJ, Harder VS, Williams CS, Visotsky JL. Complications of endoscopic and open carpal tunnel release. Arthroscopy. 2006;22(9):919-924, 924.e1-e2.

6.    Jarvik JG, Comstock BA, Kliot M, et al. Surgery versus non-surgical therapy for carpal tunnel syndrome: a randomised parallel-group trial. Lancet. 2009;374(9695):1074-1081.

7.    Verdugo RJ, Salinas RA, Castillo JL, et al. Surgical versus non-surgical treatment for carpal tunnel syndrome. Cochrane Database Syst Rev. 2008;(4):CD001552.

8.    Garland H, Langworth EP, Taverner D, et al. Surgical treatment for the carpal tunnel syndrome. Lancet. 1964;1(7343):1129-1130.

9.    Gerritsen AA, de Vet HC, Scholten RJ, et al. Splinting vs surgery in the treatment of carpal tunnel syndrome: a randomized controlled trial. JAMA. 2002;288(10):1245-1251.

10.  Gelberman RH, Hergenroeder PT, Hargens AR, et al. The carpal tunnel syndrome. A study of carpal canal pressures. J Bone Joint Surg Am. 1981;63(3):380-383.

11.  Sucher BM. Myofascial manipulative release of carpal tunnel syndrome: documentation with magnetic resonance imaging. J Am Osteopath Assoc. 1993;93(12):1273-1278.

12.  Pereira EE, Miranda DA, Sere I, et al. Endoscopic release of the carpal tunnel: a 2-portal-modified technique. Tech Hand Up Extrem Surg. 2010;14(4):263-265.

13.  Louis DS, Greene TL, Noellert RC. Complications of carpal tunnel surgery. J Neurosurg. 1985;62(3):352-356.

14.  Mirza MA, King ET Jr, Tanveer S. Palmar uniportal extrabursal endoscopic carpal tunnel release. Arthroscopy. 1995;11(1):82-90.

15.  Brown MG, Keyser B, Rothenberg ES. Endoscopic carpal tunnel release. J Hand Surg Am. 1992;17(6):1009-1011.

16.  Agee JM, McCarroll HR Jr, Tortosa RD, et al. Endoscopic release of the carpal tunnel: a randomized prospective multicenter study. J Hand Surg Am. 1992;17(6):987-995.

17.  Okutsu I, Ninomiya S, Takatori Y, et al. Endoscopic management of carpal tunnel syndrome. Arthroscopy. 1989;5(1):11-18.

18.  Ghaly RF, Saban KL, Haley DA, et al. Endoscopic carpal tunnel release surgery: report of patient satisfaction. Neurol Res. 2000;22(6):551-555.

19.  Lee WP, Plancher KD, Strickland JW. Carpal tunnel release with a small palmar incision. Hand Clin. 1996;12(2):271-284.

20.  Biyani A, Downes EM. An open twin incision technique of carpal tunnel decompression with reduced incidence of scar tenderness. J Hand Surg Br. 1993;18(3):331-334.

21.  Brown RA, Gelberman RH, Seiler JG 3rd, et al. Carpal tunnel release. A prospective, randomized assessment of open and endoscopic methods. J Bone Joint Surg Am. 1993;75(9):1265-1275.

22.  Chow JC. Endoscopic release of the carpal ligament for carpal tunnel syndrome: 22-month clinical result. Arthroscopy. 1990;6(4):288-296.

23.  Trumble TE, Diao E, Abrams RA, et al. Single-portal endoscopic carpal tunnel release compared with open release: a prospective, randomized trial. J Bone Joint Surg Am. 2002;84(7):1107-1115.

24.  Gerritsen AA, Uitdehaag BM, van Geldere D, et al. Systematic review of randomized clinical trials of surgical treatment for carpal tunnel syndrome. Br J Surg. 2001;88(10):1285-1295.

25.  Edgell SE, McCabe SJ, Breidenbach WC, et al. Predicting the outcome of carpal tunnel release. J Hand Surg Am. 2003;28(2):255-261.

26.  Vella JC, Hartigan BJ, Stern PJ. Kaplan’s cardinal line. J Hand Surg Am. 2006;31(6):912-918.

27.  Kwon JY, Kim JY, Hong JT, et al. Position change of the neurovascular structures around the carpal tunnel with dynamic wrist motion. J Korean Neurosurg Soc. 2011;50(4):377-380.

28.  Netscher D, Polsen C, Thornby J, et al. Anatomic delineation of the ulnar nerve and ulnar artery in relation to the carpal tunnel by axial magnetic resonance imaging scanning. J Hand Surg Am. 1996;21(2):273-276.

29.  Madhav TJ, To P, Stern PJ. The palmar fat pad is a reliable intraoperative landmark during carpal tunnel release. J Hand Surg Am. 2009;34(7):1204-1209.

30.  Kulick MI, Gordillo G, Javidi T, et al. Long-term analysis of patients having surgical treatment for carpal tunnel syndrome. J Hand Surg Am. 1986;11(1):59-66.

31.  Bland JD. Treatment of carpal tunnel syndrome. Muscle Nerve. 2007;36(2):167-171.

32.  MacDonald RI, Lichtman DM, Hanlon JJ, et al. Complications of surgical release for carpal tunnel syndrome. J Hand Surg Am. 1978;3(1):70-76.

33.  Atroshi I, Larsson GU, Ornstein E, Hofer M, Johnsson R, Ranstam J. Outcomes of endoscopic surgery compared with open surgery for carpal tunnel syndrome among employed patients: randomised controlled trial. BMJ. 2006;332(7556):1473.

34.  Ferdinand RD, MacLean JG. Endoscopic versus open carpal tunnel release in bilateral carpal tunnel syndrome. A prospective, randomised, blinded assessment. J Bone Joint Surg Br. 2002;84(3):375-379.

35.  Thoma A, Veltri K, Haines T, et al. A meta-analysis of randomized controlled trials comparing endoscopic and open carpal tunnel decompression. Plast Reconstr Surg. 2004;114(5):1137-1146.

36.  Murphy RX Jr, Jennings JF, Wukich DK. Major neurovascular complications of endoscopic carpal tunnel release. J Hand Surg Am. 1994;19(1):114-118.

37.  Palmer DH, Paulson JC, Lane-Larsen CL, et al. Endoscopic carpal tunnel release: a comparison of two techniques with open release. Arthroscopy. 1993;9(5):498-508.

References

1.    Ono S, Clapham PJ, Chung KC. Optimal management of carpal tunnel syndrome. Int J Gen Med. 2010;3(4):255-261.

2.    Concannon MJ, Brownfield ML, Puckett CL. The incidence of recurrence after endoscopic carpal tunnel release. Plast Reconstr Surg. 2000;105(5):1662-1665.

3.    Scholten RJ, Mink van der Molen A, Uitdehaag BM, Bouter LM, de Vet HC. Surgical treatment options for carpal tunnel syndrome. Cochrane Database Syst Rev. 2007;(4):CD003905.

4.    In memoriam Sir James Learmonth, K.C.V.O., C.B.E., hon. F.R.C.S. (1895-1967). Ann R Coll Surg Engl. 1967;41(5):438-439.

5.    Benson LS, Bare AA, Nagle DJ, Harder VS, Williams CS, Visotsky JL. Complications of endoscopic and open carpal tunnel release. Arthroscopy. 2006;22(9):919-924, 924.e1-e2.

6.    Jarvik JG, Comstock BA, Kliot M, et al. Surgery versus non-surgical therapy for carpal tunnel syndrome: a randomised parallel-group trial. Lancet. 2009;374(9695):1074-1081.

7.    Verdugo RJ, Salinas RA, Castillo JL, et al. Surgical versus non-surgical treatment for carpal tunnel syndrome. Cochrane Database Syst Rev. 2008;(4):CD001552.

8.    Garland H, Langworth EP, Taverner D, et al. Surgical treatment for the carpal tunnel syndrome. Lancet. 1964;1(7343):1129-1130.

9.    Gerritsen AA, de Vet HC, Scholten RJ, et al. Splinting vs surgery in the treatment of carpal tunnel syndrome: a randomized controlled trial. JAMA. 2002;288(10):1245-1251.

10.  Gelberman RH, Hergenroeder PT, Hargens AR, et al. The carpal tunnel syndrome. A study of carpal canal pressures. J Bone Joint Surg Am. 1981;63(3):380-383.

11.  Sucher BM. Myofascial manipulative release of carpal tunnel syndrome: documentation with magnetic resonance imaging. J Am Osteopath Assoc. 1993;93(12):1273-1278.

12.  Pereira EE, Miranda DA, Sere I, et al. Endoscopic release of the carpal tunnel: a 2-portal-modified technique. Tech Hand Up Extrem Surg. 2010;14(4):263-265.

13.  Louis DS, Greene TL, Noellert RC. Complications of carpal tunnel surgery. J Neurosurg. 1985;62(3):352-356.

14.  Mirza MA, King ET Jr, Tanveer S. Palmar uniportal extrabursal endoscopic carpal tunnel release. Arthroscopy. 1995;11(1):82-90.

15.  Brown MG, Keyser B, Rothenberg ES. Endoscopic carpal tunnel release. J Hand Surg Am. 1992;17(6):1009-1011.

16.  Agee JM, McCarroll HR Jr, Tortosa RD, et al. Endoscopic release of the carpal tunnel: a randomized prospective multicenter study. J Hand Surg Am. 1992;17(6):987-995.

17.  Okutsu I, Ninomiya S, Takatori Y, et al. Endoscopic management of carpal tunnel syndrome. Arthroscopy. 1989;5(1):11-18.

18.  Ghaly RF, Saban KL, Haley DA, et al. Endoscopic carpal tunnel release surgery: report of patient satisfaction. Neurol Res. 2000;22(6):551-555.

19.  Lee WP, Plancher KD, Strickland JW. Carpal tunnel release with a small palmar incision. Hand Clin. 1996;12(2):271-284.

20.  Biyani A, Downes EM. An open twin incision technique of carpal tunnel decompression with reduced incidence of scar tenderness. J Hand Surg Br. 1993;18(3):331-334.

21.  Brown RA, Gelberman RH, Seiler JG 3rd, et al. Carpal tunnel release. A prospective, randomized assessment of open and endoscopic methods. J Bone Joint Surg Am. 1993;75(9):1265-1275.

22.  Chow JC. Endoscopic release of the carpal ligament for carpal tunnel syndrome: 22-month clinical result. Arthroscopy. 1990;6(4):288-296.

23.  Trumble TE, Diao E, Abrams RA, et al. Single-portal endoscopic carpal tunnel release compared with open release: a prospective, randomized trial. J Bone Joint Surg Am. 2002;84(7):1107-1115.

24.  Gerritsen AA, Uitdehaag BM, van Geldere D, et al. Systematic review of randomized clinical trials of surgical treatment for carpal tunnel syndrome. Br J Surg. 2001;88(10):1285-1295.

25.  Edgell SE, McCabe SJ, Breidenbach WC, et al. Predicting the outcome of carpal tunnel release. J Hand Surg Am. 2003;28(2):255-261.

26.  Vella JC, Hartigan BJ, Stern PJ. Kaplan’s cardinal line. J Hand Surg Am. 2006;31(6):912-918.

27.  Kwon JY, Kim JY, Hong JT, et al. Position change of the neurovascular structures around the carpal tunnel with dynamic wrist motion. J Korean Neurosurg Soc. 2011;50(4):377-380.

28.  Netscher D, Polsen C, Thornby J, et al. Anatomic delineation of the ulnar nerve and ulnar artery in relation to the carpal tunnel by axial magnetic resonance imaging scanning. J Hand Surg Am. 1996;21(2):273-276.

29.  Madhav TJ, To P, Stern PJ. The palmar fat pad is a reliable intraoperative landmark during carpal tunnel release. J Hand Surg Am. 2009;34(7):1204-1209.

30.  Kulick MI, Gordillo G, Javidi T, et al. Long-term analysis of patients having surgical treatment for carpal tunnel syndrome. J Hand Surg Am. 1986;11(1):59-66.

31.  Bland JD. Treatment of carpal tunnel syndrome. Muscle Nerve. 2007;36(2):167-171.

32.  MacDonald RI, Lichtman DM, Hanlon JJ, et al. Complications of surgical release for carpal tunnel syndrome. J Hand Surg Am. 1978;3(1):70-76.

33.  Atroshi I, Larsson GU, Ornstein E, Hofer M, Johnsson R, Ranstam J. Outcomes of endoscopic surgery compared with open surgery for carpal tunnel syndrome among employed patients: randomised controlled trial. BMJ. 2006;332(7556):1473.

34.  Ferdinand RD, MacLean JG. Endoscopic versus open carpal tunnel release in bilateral carpal tunnel syndrome. A prospective, randomised, blinded assessment. J Bone Joint Surg Br. 2002;84(3):375-379.

35.  Thoma A, Veltri K, Haines T, et al. A meta-analysis of randomized controlled trials comparing endoscopic and open carpal tunnel decompression. Plast Reconstr Surg. 2004;114(5):1137-1146.

36.  Murphy RX Jr, Jennings JF, Wukich DK. Major neurovascular complications of endoscopic carpal tunnel release. J Hand Surg Am. 1994;19(1):114-118.

37.  Palmer DH, Paulson JC, Lane-Larsen CL, et al. Endoscopic carpal tunnel release: a comparison of two techniques with open release. Arthroscopy. 1993;9(5):498-508.

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Excision of Symptomatic Spinous Process Nonunion in Adolescent Athletes

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Fractures of the spinous process of the lower cervical spine or upper thoracic spine are frequently referred to as clay-shoveler’s fractures. Originally reported by Hall1 in 1940, these fractures were described in workers in Australia who dug drains in clay soil and threw the clay overhead with long shovels. Occasionally, the mud would not release from the shovel, causing excess force to be transmitted to the supraspinous ligaments and resulting in a forceful avulsion fracture of one or multiple spinous processes. The few reports following the earliest description in the literature frequently describe the mechanism of injury as being athletic in nature.2-4 The forceful contraction of the paraspinal and trapezius muscles on the supraspinous ligaments and the resultant attachment to the spinous processes make this a not uncommon injury during athletics, especially with a flexed position of the neck and shoulders. The resultant fracture or apophyseal avulsion is painful and often necessitates a visit to the physician, with plain films, computed tomography (CT) scans, or magnetic resonance imaging (MRI) confirming the diagnosis.5

Treatment of these fractures has not been well described, but frequently a period of rest followed by physical therapy will allow a return to activity. We present a series of adolescent athletes who developed nonunion of the fracture of the T1 spinous process with continued symptoms, despite rest and conservative therapy, and who underwent surgical excision of the ununited fragment.

Materials and Methods

We obtained institutional review board permission for this study and searched the surgical database between 2006 and 2013 for patients who had undergone resection of a spinous process nonunion. We collected demographic data on the patients, evaluated the radiographic studies, and reviewed operative reports and follow-up patient data.

Results

Dr. Hedequist operated on 3 patients with a spinous process nonunion over the study time period. The average age of the patients was 14 years; the location of the spinous process fracture was the T1 vertebra in all patients. Two patients sustained the injury while playing hockey and 1 during wrestling. The average duration of symptoms prior to operation was 10 months; all patients had seen physicians without a diagnosis prior to evaluation at out institution. All patients had a trial of physical therapy before surgery, and all had been unable to return to sport after injury secondary to pain.

Examination of all patients revealed pain directly over the fracture site and accentuated by forward flexion of the neck and shoulders. Evaluation of injury plain films revealed a fracture fragment in 2 patients (Figure 1). All 3 patients underwent MRI and CT scans confirming the diagnosis. MRI confirmed areas of increased signal at the tip of the T1 spinous process, with inflammation in the supraspinous ligament directly at that region (Figure 2). The CT scans confirmed the presence of a bony fragment correlating with the tip of the T1 spinous process (Figure 3).

   

Surgery was performed under general endotracheal anesthesia via a midline incision over the affected area down to the spinous process. The supraspinous ligament was opened revealing an easily identified and definable ununited ossicle, which was removed without taking down the interspinous ligament. All 3 nonunions were noted to be atrophic with no evidence of surrounding inflammatory tissue or bursa. The residual end of the spinous process was smoothed down with a rongeur. Standard closure was performed. There were no surgical complications.

All patients had complete relief of pain at follow-up; 1 patient returned to full sports activity at 6 weeks and the other 2 returned to full sports activity at 3 months. There was no loss of cervical motion or trapezial strength at follow-up. All patients voiced satisfaction with the decision for surgical intervention.

Discussion

Clay-shoveler’s fracture is an injury well known to orthopedists. This fracture is thought to be caused by a forceful contraction of the thoracic paraspinal and trapezial muscles, causing an avulsion fracture with pain and frequently a “pop” experienced by the patient.1 Usually considered self-limiting injuries, treatment involves a period of rest and activity modification with occasional physical therapy. Return to sports has been reported with occasional pain but with patient satisfaction.3,5,6

Our series of patients represent a group of adolescent athletes who sustained spinous process fractures of the T1 vertebra and, despite a significant period of rest and activity modification, were unable to return to sports given their pain. The examination of these patients revealed focal tenderness at the tip of the spinous process. The diagnosis is made clinically, with radiographic studies confirming the diagnosis. In our series of patients, MRI was the original modality used to confirm injury to the area, with hyperintensity seen in the area of the supraspinous ligament and tip of the spinous process. CT confirmed the nonunion and presence of an ossicle in all patients. Surgical exposure of that area easily exposed the ununited ossicle, which was removed in all patients.

 

 

To our knowledge, this is the first report in the literature describing surgical excision of an ununited spinous process fracture in adolescent athletes. The original descriptive case series by Hall1 states “in the minds of surgeons who have seen many of these cases that early operative removal of the fragments is the proper routine treatment.” Since that original series, we have not found articles in the literature that support surgical removal; however, persistent symptoms after fracture are described.5 It is not surprising that these patients developed pain at the site of the fracture given the forces acting in that area. The trapezial and paraspinal muscles acting on that area are forceful and repetitive during activities, especially sports. All our patients had pain with attempts at activity and all had had a significant period of rest. In a recent article, this injury was described in adolescents without the patients having clear relief of symptoms despite a period of inactivity.5 While physical therapy is therapeutic in some patients experiencing pain, it can be a source of aggravation due to neck and shoulder motion and muscle contraction. It is not surprising that therapy would not help in most cases, as neck and shoulder motion and muscle contraction are the sources of continuing discomfort.

Clinical practice suggests that most patients with spinous process fractures will become pain-free; however, that is not universal. This series demonstrates that a small subset of patients with this injury will continue to have significant symptoms despite a period of rest. In those patients who desire a pain-free return to sports, we recommend consideration of surgical excision after confirmation of nonunion with radiographic studies. The inherent risks of surgical treatment are minimal with this procedure, and the benefits include return to pain-free sports activity, with the resultant physical and psychosocial benefits for adolescent athletes.

References

1.    Hall RDM. Clay-shoveler’s fracture. J Bone Joint Surg Am. 1940;22(1):63-75.

2.    Herrick RT. Clay-shoveler’s fracture in power-lifting. A case report. Am J Sports Med. 1981;9(1):29-30.

3.    Hetsroni I, Mann G, Dolev E, Morgenstern D, Nyska M. Clay shoveler’s fracture in a volleyball player. Phys Sportsmed. 2005;33(7):38-42.

4.    Kaloostian PE, Kim JE, Calabresi PA, Bydon A, Witham T. Clay-shoveler’s fracture during indoor rock climbing. Orthopedics. 2013;36(3):e381-e383.

5.    Yamaguchi KT Jr, Myung KS, Alonso MA, Skaggs DL. Clay-shoveler’s fracture equivalent in children. Spine. 2012;37(26):e1672-e1675.

6.    Kang DH, Lee SH. Multiple spinous process fractures of the thoracic vertebrae (clay-shoveler’s fracture) in a beginning golfer: a case report. Spine. 2009;34(15):e534-e537.

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Fractures of the spinous process of the lower cervical spine or upper thoracic spine are frequently referred to as clay-shoveler’s fractures. Originally reported by Hall1 in 1940, these fractures were described in workers in Australia who dug drains in clay soil and threw the clay overhead with long shovels. Occasionally, the mud would not release from the shovel, causing excess force to be transmitted to the supraspinous ligaments and resulting in a forceful avulsion fracture of one or multiple spinous processes. The few reports following the earliest description in the literature frequently describe the mechanism of injury as being athletic in nature.2-4 The forceful contraction of the paraspinal and trapezius muscles on the supraspinous ligaments and the resultant attachment to the spinous processes make this a not uncommon injury during athletics, especially with a flexed position of the neck and shoulders. The resultant fracture or apophyseal avulsion is painful and often necessitates a visit to the physician, with plain films, computed tomography (CT) scans, or magnetic resonance imaging (MRI) confirming the diagnosis.5

Treatment of these fractures has not been well described, but frequently a period of rest followed by physical therapy will allow a return to activity. We present a series of adolescent athletes who developed nonunion of the fracture of the T1 spinous process with continued symptoms, despite rest and conservative therapy, and who underwent surgical excision of the ununited fragment.

Materials and Methods

We obtained institutional review board permission for this study and searched the surgical database between 2006 and 2013 for patients who had undergone resection of a spinous process nonunion. We collected demographic data on the patients, evaluated the radiographic studies, and reviewed operative reports and follow-up patient data.

Results

Dr. Hedequist operated on 3 patients with a spinous process nonunion over the study time period. The average age of the patients was 14 years; the location of the spinous process fracture was the T1 vertebra in all patients. Two patients sustained the injury while playing hockey and 1 during wrestling. The average duration of symptoms prior to operation was 10 months; all patients had seen physicians without a diagnosis prior to evaluation at out institution. All patients had a trial of physical therapy before surgery, and all had been unable to return to sport after injury secondary to pain.

Examination of all patients revealed pain directly over the fracture site and accentuated by forward flexion of the neck and shoulders. Evaluation of injury plain films revealed a fracture fragment in 2 patients (Figure 1). All 3 patients underwent MRI and CT scans confirming the diagnosis. MRI confirmed areas of increased signal at the tip of the T1 spinous process, with inflammation in the supraspinous ligament directly at that region (Figure 2). The CT scans confirmed the presence of a bony fragment correlating with the tip of the T1 spinous process (Figure 3).

   

Surgery was performed under general endotracheal anesthesia via a midline incision over the affected area down to the spinous process. The supraspinous ligament was opened revealing an easily identified and definable ununited ossicle, which was removed without taking down the interspinous ligament. All 3 nonunions were noted to be atrophic with no evidence of surrounding inflammatory tissue or bursa. The residual end of the spinous process was smoothed down with a rongeur. Standard closure was performed. There were no surgical complications.

All patients had complete relief of pain at follow-up; 1 patient returned to full sports activity at 6 weeks and the other 2 returned to full sports activity at 3 months. There was no loss of cervical motion or trapezial strength at follow-up. All patients voiced satisfaction with the decision for surgical intervention.

Discussion

Clay-shoveler’s fracture is an injury well known to orthopedists. This fracture is thought to be caused by a forceful contraction of the thoracic paraspinal and trapezial muscles, causing an avulsion fracture with pain and frequently a “pop” experienced by the patient.1 Usually considered self-limiting injuries, treatment involves a period of rest and activity modification with occasional physical therapy. Return to sports has been reported with occasional pain but with patient satisfaction.3,5,6

Our series of patients represent a group of adolescent athletes who sustained spinous process fractures of the T1 vertebra and, despite a significant period of rest and activity modification, were unable to return to sports given their pain. The examination of these patients revealed focal tenderness at the tip of the spinous process. The diagnosis is made clinically, with radiographic studies confirming the diagnosis. In our series of patients, MRI was the original modality used to confirm injury to the area, with hyperintensity seen in the area of the supraspinous ligament and tip of the spinous process. CT confirmed the nonunion and presence of an ossicle in all patients. Surgical exposure of that area easily exposed the ununited ossicle, which was removed in all patients.

 

 

To our knowledge, this is the first report in the literature describing surgical excision of an ununited spinous process fracture in adolescent athletes. The original descriptive case series by Hall1 states “in the minds of surgeons who have seen many of these cases that early operative removal of the fragments is the proper routine treatment.” Since that original series, we have not found articles in the literature that support surgical removal; however, persistent symptoms after fracture are described.5 It is not surprising that these patients developed pain at the site of the fracture given the forces acting in that area. The trapezial and paraspinal muscles acting on that area are forceful and repetitive during activities, especially sports. All our patients had pain with attempts at activity and all had had a significant period of rest. In a recent article, this injury was described in adolescents without the patients having clear relief of symptoms despite a period of inactivity.5 While physical therapy is therapeutic in some patients experiencing pain, it can be a source of aggravation due to neck and shoulder motion and muscle contraction. It is not surprising that therapy would not help in most cases, as neck and shoulder motion and muscle contraction are the sources of continuing discomfort.

Clinical practice suggests that most patients with spinous process fractures will become pain-free; however, that is not universal. This series demonstrates that a small subset of patients with this injury will continue to have significant symptoms despite a period of rest. In those patients who desire a pain-free return to sports, we recommend consideration of surgical excision after confirmation of nonunion with radiographic studies. The inherent risks of surgical treatment are minimal with this procedure, and the benefits include return to pain-free sports activity, with the resultant physical and psychosocial benefits for adolescent athletes.

Fractures of the spinous process of the lower cervical spine or upper thoracic spine are frequently referred to as clay-shoveler’s fractures. Originally reported by Hall1 in 1940, these fractures were described in workers in Australia who dug drains in clay soil and threw the clay overhead with long shovels. Occasionally, the mud would not release from the shovel, causing excess force to be transmitted to the supraspinous ligaments and resulting in a forceful avulsion fracture of one or multiple spinous processes. The few reports following the earliest description in the literature frequently describe the mechanism of injury as being athletic in nature.2-4 The forceful contraction of the paraspinal and trapezius muscles on the supraspinous ligaments and the resultant attachment to the spinous processes make this a not uncommon injury during athletics, especially with a flexed position of the neck and shoulders. The resultant fracture or apophyseal avulsion is painful and often necessitates a visit to the physician, with plain films, computed tomography (CT) scans, or magnetic resonance imaging (MRI) confirming the diagnosis.5

Treatment of these fractures has not been well described, but frequently a period of rest followed by physical therapy will allow a return to activity. We present a series of adolescent athletes who developed nonunion of the fracture of the T1 spinous process with continued symptoms, despite rest and conservative therapy, and who underwent surgical excision of the ununited fragment.

Materials and Methods

We obtained institutional review board permission for this study and searched the surgical database between 2006 and 2013 for patients who had undergone resection of a spinous process nonunion. We collected demographic data on the patients, evaluated the radiographic studies, and reviewed operative reports and follow-up patient data.

Results

Dr. Hedequist operated on 3 patients with a spinous process nonunion over the study time period. The average age of the patients was 14 years; the location of the spinous process fracture was the T1 vertebra in all patients. Two patients sustained the injury while playing hockey and 1 during wrestling. The average duration of symptoms prior to operation was 10 months; all patients had seen physicians without a diagnosis prior to evaluation at out institution. All patients had a trial of physical therapy before surgery, and all had been unable to return to sport after injury secondary to pain.

Examination of all patients revealed pain directly over the fracture site and accentuated by forward flexion of the neck and shoulders. Evaluation of injury plain films revealed a fracture fragment in 2 patients (Figure 1). All 3 patients underwent MRI and CT scans confirming the diagnosis. MRI confirmed areas of increased signal at the tip of the T1 spinous process, with inflammation in the supraspinous ligament directly at that region (Figure 2). The CT scans confirmed the presence of a bony fragment correlating with the tip of the T1 spinous process (Figure 3).

   

Surgery was performed under general endotracheal anesthesia via a midline incision over the affected area down to the spinous process. The supraspinous ligament was opened revealing an easily identified and definable ununited ossicle, which was removed without taking down the interspinous ligament. All 3 nonunions were noted to be atrophic with no evidence of surrounding inflammatory tissue or bursa. The residual end of the spinous process was smoothed down with a rongeur. Standard closure was performed. There were no surgical complications.

All patients had complete relief of pain at follow-up; 1 patient returned to full sports activity at 6 weeks and the other 2 returned to full sports activity at 3 months. There was no loss of cervical motion or trapezial strength at follow-up. All patients voiced satisfaction with the decision for surgical intervention.

Discussion

Clay-shoveler’s fracture is an injury well known to orthopedists. This fracture is thought to be caused by a forceful contraction of the thoracic paraspinal and trapezial muscles, causing an avulsion fracture with pain and frequently a “pop” experienced by the patient.1 Usually considered self-limiting injuries, treatment involves a period of rest and activity modification with occasional physical therapy. Return to sports has been reported with occasional pain but with patient satisfaction.3,5,6

Our series of patients represent a group of adolescent athletes who sustained spinous process fractures of the T1 vertebra and, despite a significant period of rest and activity modification, were unable to return to sports given their pain. The examination of these patients revealed focal tenderness at the tip of the spinous process. The diagnosis is made clinically, with radiographic studies confirming the diagnosis. In our series of patients, MRI was the original modality used to confirm injury to the area, with hyperintensity seen in the area of the supraspinous ligament and tip of the spinous process. CT confirmed the nonunion and presence of an ossicle in all patients. Surgical exposure of that area easily exposed the ununited ossicle, which was removed in all patients.

 

 

To our knowledge, this is the first report in the literature describing surgical excision of an ununited spinous process fracture in adolescent athletes. The original descriptive case series by Hall1 states “in the minds of surgeons who have seen many of these cases that early operative removal of the fragments is the proper routine treatment.” Since that original series, we have not found articles in the literature that support surgical removal; however, persistent symptoms after fracture are described.5 It is not surprising that these patients developed pain at the site of the fracture given the forces acting in that area. The trapezial and paraspinal muscles acting on that area are forceful and repetitive during activities, especially sports. All our patients had pain with attempts at activity and all had had a significant period of rest. In a recent article, this injury was described in adolescents without the patients having clear relief of symptoms despite a period of inactivity.5 While physical therapy is therapeutic in some patients experiencing pain, it can be a source of aggravation due to neck and shoulder motion and muscle contraction. It is not surprising that therapy would not help in most cases, as neck and shoulder motion and muscle contraction are the sources of continuing discomfort.

Clinical practice suggests that most patients with spinous process fractures will become pain-free; however, that is not universal. This series demonstrates that a small subset of patients with this injury will continue to have significant symptoms despite a period of rest. In those patients who desire a pain-free return to sports, we recommend consideration of surgical excision after confirmation of nonunion with radiographic studies. The inherent risks of surgical treatment are minimal with this procedure, and the benefits include return to pain-free sports activity, with the resultant physical and psychosocial benefits for adolescent athletes.

References

1.    Hall RDM. Clay-shoveler’s fracture. J Bone Joint Surg Am. 1940;22(1):63-75.

2.    Herrick RT. Clay-shoveler’s fracture in power-lifting. A case report. Am J Sports Med. 1981;9(1):29-30.

3.    Hetsroni I, Mann G, Dolev E, Morgenstern D, Nyska M. Clay shoveler’s fracture in a volleyball player. Phys Sportsmed. 2005;33(7):38-42.

4.    Kaloostian PE, Kim JE, Calabresi PA, Bydon A, Witham T. Clay-shoveler’s fracture during indoor rock climbing. Orthopedics. 2013;36(3):e381-e383.

5.    Yamaguchi KT Jr, Myung KS, Alonso MA, Skaggs DL. Clay-shoveler’s fracture equivalent in children. Spine. 2012;37(26):e1672-e1675.

6.    Kang DH, Lee SH. Multiple spinous process fractures of the thoracic vertebrae (clay-shoveler’s fracture) in a beginning golfer: a case report. Spine. 2009;34(15):e534-e537.

References

1.    Hall RDM. Clay-shoveler’s fracture. J Bone Joint Surg Am. 1940;22(1):63-75.

2.    Herrick RT. Clay-shoveler’s fracture in power-lifting. A case report. Am J Sports Med. 1981;9(1):29-30.

3.    Hetsroni I, Mann G, Dolev E, Morgenstern D, Nyska M. Clay shoveler’s fracture in a volleyball player. Phys Sportsmed. 2005;33(7):38-42.

4.    Kaloostian PE, Kim JE, Calabresi PA, Bydon A, Witham T. Clay-shoveler’s fracture during indoor rock climbing. Orthopedics. 2013;36(3):e381-e383.

5.    Yamaguchi KT Jr, Myung KS, Alonso MA, Skaggs DL. Clay-shoveler’s fracture equivalent in children. Spine. 2012;37(26):e1672-e1675.

6.    Kang DH, Lee SH. Multiple spinous process fractures of the thoracic vertebrae (clay-shoveler’s fracture) in a beginning golfer: a case report. Spine. 2009;34(15):e534-e537.

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Academic Characteristics of Orthopedic Team Physicians Affiliated With High School, Collegiate, and Professional Teams

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The responsibilities of team physicians have increased dramatically since the early 19th century, when these physicians first appeared on the sidelines during football games.1 Although the primary role of the team physician is to care for the athlete, other responsibilities include administrative and legal duties, equipment- and environment-related duties, teaching, and communication with parents, coaches, and other physicians.2-4 These responsibilities differ greatly by the level of the athlete and the team being covered. For example, compared with high school and collegiate sport physicians, physicians caring for professional athletes may have increased interaction with the media.5

Despite the increasing demands and responsibilities of team physicians, it is important that they continue to advance the field of sports medicine through teaching and research.3,6 Team physicians have direct access to athletes at multiple levels of competition, from novice to professional, and therefore have a unique understanding of the injuries that commonly affect these athletes. Efforts to both teach and study the prevention, diagnosis, and treatment of these injuries have dramatically advanced the field of sports medicine. In fact, several advancements in sports medicine have come from team physicians, including advancements in anterior cruciate ligament reconstruction,7,8 shoulder arthroscopy,9 and “Tommy John” surgery,10 to name a few.

Given the important role of team physicians (particularly orthopedic team physicians) in advancing sports medicine, it is important to understand the degree to which team physicians at all levels of sport contribute to teaching and research.

We conducted a study to determine the overall academic involvement of orthopedic team physicians at all levels of sport, including the degree to which these physicians are affiliated with academic medical centers (by level of sport and by professional sport) and the quantity and impact of these physicians’ scientific publications. We hypothesized that orthopedic physician academic involvement would be higher at the professional level of sport than at the collegiate or high school level and that the degree of physician academic involvement would differ between professional sporting leagues.

Materials and Methods

In August 2012, we performed a comprehensive telephone- and Internet-based search to identify a sample of team physicians caring for athletes at the high school, collegiate, and professional levels of sport. Data were collected on all team physicians, regardless of medical specialty. We defined a physician as any person listed as having either a doctor of medicine (MD) or a doctor of osteopathic medicine (DO) degree. A physician listed as a team physician at 2 different levels of competition (high school, college, professional) was included in both cohorts. A physician listed as a team physician in 2 different professional sports leagues was included independently for both leagues. All other medical personnel, including athletic trainers, therapists, and nursing staff, were excluded. Data on our sample population were collected as follows:

1. High school. Performing a comprehensive database search through the US Department of Education, we generated a list of all 20,989 US schools that include grades 9 to 12.11 We then used a random number generator (random.org) to randomly select a sample of 120 high schools. These schools were contacted by telephone and asked to identify the team physician(s) for their sports teams. Twenty of these schools reported not having an athletic team, so we randomly generated a list of 20 additional high schools. High schools that had an athletic team but denied having a team physician were included in the analysis.

2. College. We used the National Collegiate Athletic Association (NCAA) website (ncaa.org) to generate a list of all colleges affiliated with the NCAA. Of these colleges, 347 were Division I, 316 were Division II, and 443 were Division III. The random.org random number generator was used to generate a list of 40 schools for each division, for a total of 120 schools. An Internet-based search was then performed to identify any and all team physicians caring for athletes at that particular school. In select cases, telephone calls were made to determine all the team physicians involved in the care of athletes at that institution.

3. Professional. Team physician data were collected for 4 of the most popular professional sporting leagues12: Major League Baseball (MLB), National Basketball Association (NBA), National Football League (NFL), and National Hockey League (NHL). Each team’s official website was identified through its league website (mlb.com, nba.com, nfl.com, nhl.com), and the roster or directory listing of all team physicians was recorded. In 2 cases, the team’s medical personnel listing could not be retrieved through the Internet, and a telephone call had to be made to identify all team physicians. Team physicians were identified for 122 professional teams: 30 MLB, 30 NBA, 32 NFL, and 30 NHL.

 

 

For this study, all physicians were classified as either orthopedic or nonorthopedic. Orthopedic surgeons—the focus of this study—were defined as those who completed residency training in orthopedic surgery. Median number of orthopedic and nonorthopedic surgeons per team was calculated at the high school, collegiate, and professional levels.

After identifying all orthopedic team physicians, we performed additional Internet searches to determine any affiliation between each physician and an applicable academic medical center. Physicians were placed in 1 of 3 different categories based on “level” of academic affiliation. Orthopedists with no identifiable connection to an academic medical center were listed under none. The first 100 search results were studied before this determination was made. Orthopedists with any academic affiliation below the level of full professorship were placed in the category associate/assistant/adjunct professor, which included any physician who was an associate professor, adjunct professor, clinical instructor, or volunteer instructor at an academic medical center. Last, orthopedists listed as full professors were placed in the professor category.

Number of publications written by each orthopedic team physician was then calculated using SciVerse Scopus (scopus.com), a comprehensive abstract and citation database of research literature that offers complete coverage of the Medline and Embase databases.13 Scopus offers a Scopus Author Identifier, which assigns each author in Scopus a unique identification number.14 This number is based on an “algorithm that matches author names based on their affiliation, address, subject area, source title, dates of publication citations, and co-authors.”14 Authors whose names did not appear in Scopus were assumed to have no publications, and this was reported after cross-referencing with Medline to ensure no documents were missed. This study included all publications: original research articles, reviews, letters, and commentaries. Any level of authorship (first, second, etc) was included. All publications were scanned, and duplicate listings were not included. Median number of publications per orthopedic team physician was calculated at the high school, college, and professional levels.

We also determined the h-index for each orthopedic team physician. The h-index is used to measure the impact of the published work of a scholar: “A scientist has index h if h of his/her papers have at least h citations each, and the other papers have no more than h citations each.”15 For example, an h-index of 12 means that, out of an author’s total number of publications, 12 have been cited at least 12 times, and all of his or her other publications have been cited fewer than 12 times. All authors in Scopus are automatically assigned h-indexes, and we collected these numbers.16 Of note, citations for articles published before 1996 are not included in the h-index calculation. Median h-index score per orthopedic team physician was calculated at the high school, college, and professional levels.

Analysis of variance was used to compare continuous data (eg, number of publications per surgeon) across different groups (eg, physicians from respective sports). Chi-square tests were used to detect whole-number differences between groups (eg, difference in number of physicians per team across the various professional sports leagues). Statistical significance was set at P < .05.

Results

We identified 1054 team physicians among the 362 total high schools, colleges, and professional sports teams included in this study. Of the 1054 physicians, 678 (64%) were orthopedic surgeons (Table 1). Seventy-two (60%) of the 120 high schools did not have a team physician, whereas all the colleges and professional teams did. Number of orthopedic surgeons per team was higher at the collegiate level (2.29; range, 0-11) and professional level (2.21; range, 1-9) than at the high school level (1.11; range, 0-24) (Table 1). Median number of nonorthopedic surgeons was highest in professional sports (1.88; range, 0-9) followed by college sports (1.06; range, 0-9) and high school sports (0.16; range, 0-2) (Table 1).

Of the 678 orthopedic team physicians, 298 (44%) were officially affiliated with an academic medical center, either as clinical instructor, associate/adjunct professor, or full professor. Percentage of orthopedists affiliated with an academic medical center was highest in professional sports (173/270, 64%) followed by collegiate sports (98/275, 36%) and high school sports (27/133, 20%) (P < .001, Table 2). Percentage of orthopedists identified as full professors was highest at the professional level (42/270, 16%) followed by the collegiate level (14/275, 5.1%) and the high school level (3/133, 2.3%) (P < .001, Table 2).

We found 12,036 publications written by the 678 orthopedic team physicians included in this study. Median number of publications per orthopedist was significantly higher in professional sports (30.6; range, 0-460) than in collegiate sports (10.7; range, 0-581) and high school sports (6.0; range, 0-220) (P < .001). Number of authors with more than 25 publications was highest at the professional level (82) followed by the collegiate level (27) and the high school level (7) (Table 3). Median number of publications per orthopedist was also higher at the professional level (12) than at the collegiate level (2) and high school level (1). Median h-index was higher among orthopedists in professional sports (7.1; range, 0-50) than at colleges (2.7; range, 0-63) and high schools (1.8; range, 0-32) (P < .001). Median h-index was also significantly higher at the professional level (5) than at the collegiate level (1) and high school level (0).

 

 

At the professional level of sports, we identified 499 team physicians (270 orthopedic, 54%; 229 nonorthopedic, 46%). Median number of orthopedic team physicians varied by sport, with MLB (2.8; range, 1-8) and the NFL (2.4; range, 1-4) having relatively more of these physicians than the NHL (2.0; range, 1-6) and the NBA (1.7; range, 1-9) (Table 4). Percentage of orthopedic team physicians affiliated with academic medical centers was highest in MLB (58/83, 69.9%) followed by the NFL (47/76, 61.8%), the NHL (37/60, 61.7%), and the NBA (31/51, 60.8%) (Table 5). Median number of publications by orthopedists also varied by sport, with the highest number in MLB (37.9; range, 0-225) followed by the NBA (32.0; range, 0-227) and the NFL (30.4; range, 0-460), with the lowest number in the NHL (20.7; range, 0-144) (Table 6). Median number of publications was the same (17.5) in MLB and the NFL and lower in the NBA (11) and the NHL (7.5). Median h-index was highest in the NFL (8.2; range, 0-50) and MLB (7.9; range, 0-32) followed by the NBA (6.6; range, 0-35) and the NHL (4.9; range, 0-20) (Table 7) Median h-index was the same (6) in MLB and the NFL and lower (3) in the NBA and the NHL.

     

Discussion

To our knowledge, this is the first study of academic involvement and the research activities of orthopedic team physicians at the high school, college, and professional levels of sport. We found that, on average, there were almost twice as many orthopedists at the collegiate and professional levels than at the high school level—likely because 72 of the 120 high schools randomly selected did not have a team physician, despite having sports teams. We can attribute this to the organizational structure of teams in a high school setting, where it is fairly common that no medically educated health care provider is readily available for the student athletes.5 Although the median number of orthopedists was similar at the collegiate and professional levels, the number of nonorthopedic team physicians was higher at the professional level than at the collegiate level. Although most collegiate and professional teams have an internist and an orthopedist on staff, medical staff at the professional level may also include several subspecialists from a variety of medical fields (eg, dental medicine, ophthalmology, neurology).17

We found that a significantly larger proportion of orthopedists at the professional level (64%) were affiliated with academic medical centers as associate/adjunct professors and full professors compared with orthopedists at the collegiate level (36%) and high school level (20%). The academic relationship with collegiate teams was much lower than expected. Regarding professional sports, however, this finding confirmed our hypothesis, and the explanation is likely multifactorial and historical. Moreover, the median number of publications was higher for orthopedists at the professional level (30.8) than at the collegiate level (10.7) and high school level (6). In the late 1940s and early 1950s, many orthopedic team physicians entered into contracts with major universities.4 For many physicians, this contractual relationship increased their prestige, and some orthopedic groups were alleged to have endorsed scholarships at those schools.4 Given the high level of publicity and scrutiny surrounding medical decisions at the professional level of sports, it is possible that professional sports teams specifically seek orthopedists who are well respected within academia. Moreover, contracts between universities/academic medical centers and professional teams may mandate that a faculty member from that organization provide the orthopedic/medical care for the team. This may also increase the likelihood of professional teams being paired with academic orthopedic physicians. However, such contractual agreements are made between professional teams and large private medical groups as well.

In addition to measuring quantity of publications, we used the h-index to measure their quality. Following the same pattern as the publication rate, median h-index per orthopedic team physician was significantly higher at the professional level (7.1) than at the collegiate level (2.7) and high school level (1.8). As with publication volume, this is not entirely surprising, as h-index has been shown to correlate with academic rank in other surgical specialties,18 and there was a higher percentage of academic physicians at the professional level than at the collegiate and high school levels.

At the professional level of sports, 56% of all team physicians were orthopedic surgeons. Orthopedists caring for MLB teams had the highest median number of publications (37.9), followed by the NBA (32.0), the NFL (30.4), and the NHL (20.7). One likely explanation is the higher percentage of MLB physicians affiliated with academic medical centers. Regarding the h-index, MLB and NFL physicians had the highest values (7.9 and 8.2, respectively).

 

 

Our study had several limitations. First, we may not have captured data on all the team physicians at the high school, college, and professional levels. By following a detailed protocol in identifying surgeons, however, we tried to minimize the impact of any such omissions. In addition, teams may have had many unofficial consultants acting as team physicians, whether orthopedic or nonorthopedic, and, if these physicians were not listed in an official capacity, they may have been omitted from this study. We further realize that a true measure of academic productivity should also include book chapters and books published, research grants awarded, and patents registered. By including only peer-reviewed articles, we omitted these other criteria.

To our knowledge, the data presented here represent the first attempt to quantify the academic involvement and research productivity of orthopedic team physicians at the high school, college, and professional levels of sport. These data help us understand how research productivity varies by orthopedic team physicians at different levels of sport and may be useful to those considering a career as a team physician, as they can better evaluate their own productivity in the context of team physicians across different levels of competition.

References

1.    Thorndike A. Athletic Injuries: Prevention, Diagnosis, and Treatment. Philadelphia, PA: Lea & Febiger; 1956.

2.    The team physician. A statement of the Committee on the Medical Aspects of Sports of the American Medical Association, September 1967. J School Health. 1967;37(10):510-514.

3.     Team physician consensus statement. Am J Sports Med. 2000;28(3):440-441.

4.    Whiteside J, Andrews JR. Trends for the future as a team physician: Herodicus to hereafter. Clin Sports Med. 2007;26(2):285-304.

5.    Goforth M, Almquist J, Matney M, et al. Understanding organization structures of the college, university, high school, clinical, and professional settings. Clin Sports Med. 2007;26(2):201-226.

6.    Hughston JC. Want to be in sports medicine? Get involved. Am J Sports Med. 1979;7(2):79-80.

7.    Marshall JL, Warren RF, Wickiewicz TL, Reider B. The anterior cruciate ligament: a technique of repair and reconstruction. Clin Orthop Relat Res. 1979;(143):97-106.

8.    Clancy WG Jr, Nelson DA, Reider B, Narechania RG. Anterior cruciate ligament reconstruction using one-third of the patellar ligament, augmented by extra-articular tendon transfers. J Bone Joint Surg Am. 1982;64(3):352-359.

9.    Andrews JR, Carson WG Jr, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985;13(5):337-341.

10.  Indelicato PA, Jobe FW, Kerlan RK, Carter VS, Shields CL, Lombardo SJ. Correctable elbow lesions in professional baseball players: a review of 25 cases. Am J Sports Med. 1979;7(1):72-75.

11.  Elementary/Secondary Information System (EISi). National Center for Education Statistics, Institute of Education Sciences, US Department of Education website. http://nces.ed.gov/ccd/elsi/. Accessed September 21, 2015.

12.  Corso RA; Harris Interactive. Football is America’s favorite sport as lead over baseball continues to grow; college football and auto racing come next. Harris Interactive website. http://www.harrisinteractive.com/vault/Harris Poll 9 - Favorite sport_1.25.12.pdf. Harris Poll 9, January 25, 2012. Accessed September 21, 2015.

13.  [Scopus content]. Elsevier website. http://www.elsevier.com/solutions/scopus/content. Accessed September 21, 2015.

14.  Scopus Author Identifier. Scopus website. http://help.scopus.com/Content/h_autsrch_intro.htm. Accessed October 5, 2015.

15.  Hirsch JE. An index to quantify an individual’s scientific research output. Proc Natl Acad Sci U S A. 2005;102(46):16569-16572.

16.  Author Evaluator h Index Tab. Scopus website. http://help.scopus.com/Content/h_auteval_hindex.htm. Accessed October 5, 2015.

17.  Boyd JL. Understanding the politics of being a team physician. Clin Sports Med. 2007;26(2):161-172.

18.   Lee J, Kraus KL, Couldwell WT. Use of the h index in neurosurgery. Clinical article. J Neurosurg. 2009;111(2):387-

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Authors’ Disclosure Statement: Dr. Ahmad wishes to report that he is a consultant for Acumed and Arthrex, and receives research support from Arthrex, Major League Baseball, and Stryker. The other authors report no actual or potential conflict of interest in relation to this article.

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Authors’ Disclosure Statement: Dr. Ahmad wishes to report that he is a consultant for Acumed and Arthrex, and receives research support from Arthrex, Major League Baseball, and Stryker. The other authors report no actual or potential conflict of interest in relation to this article.

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The responsibilities of team physicians have increased dramatically since the early 19th century, when these physicians first appeared on the sidelines during football games.1 Although the primary role of the team physician is to care for the athlete, other responsibilities include administrative and legal duties, equipment- and environment-related duties, teaching, and communication with parents, coaches, and other physicians.2-4 These responsibilities differ greatly by the level of the athlete and the team being covered. For example, compared with high school and collegiate sport physicians, physicians caring for professional athletes may have increased interaction with the media.5

Despite the increasing demands and responsibilities of team physicians, it is important that they continue to advance the field of sports medicine through teaching and research.3,6 Team physicians have direct access to athletes at multiple levels of competition, from novice to professional, and therefore have a unique understanding of the injuries that commonly affect these athletes. Efforts to both teach and study the prevention, diagnosis, and treatment of these injuries have dramatically advanced the field of sports medicine. In fact, several advancements in sports medicine have come from team physicians, including advancements in anterior cruciate ligament reconstruction,7,8 shoulder arthroscopy,9 and “Tommy John” surgery,10 to name a few.

Given the important role of team physicians (particularly orthopedic team physicians) in advancing sports medicine, it is important to understand the degree to which team physicians at all levels of sport contribute to teaching and research.

We conducted a study to determine the overall academic involvement of orthopedic team physicians at all levels of sport, including the degree to which these physicians are affiliated with academic medical centers (by level of sport and by professional sport) and the quantity and impact of these physicians’ scientific publications. We hypothesized that orthopedic physician academic involvement would be higher at the professional level of sport than at the collegiate or high school level and that the degree of physician academic involvement would differ between professional sporting leagues.

Materials and Methods

In August 2012, we performed a comprehensive telephone- and Internet-based search to identify a sample of team physicians caring for athletes at the high school, collegiate, and professional levels of sport. Data were collected on all team physicians, regardless of medical specialty. We defined a physician as any person listed as having either a doctor of medicine (MD) or a doctor of osteopathic medicine (DO) degree. A physician listed as a team physician at 2 different levels of competition (high school, college, professional) was included in both cohorts. A physician listed as a team physician in 2 different professional sports leagues was included independently for both leagues. All other medical personnel, including athletic trainers, therapists, and nursing staff, were excluded. Data on our sample population were collected as follows:

1. High school. Performing a comprehensive database search through the US Department of Education, we generated a list of all 20,989 US schools that include grades 9 to 12.11 We then used a random number generator (random.org) to randomly select a sample of 120 high schools. These schools were contacted by telephone and asked to identify the team physician(s) for their sports teams. Twenty of these schools reported not having an athletic team, so we randomly generated a list of 20 additional high schools. High schools that had an athletic team but denied having a team physician were included in the analysis.

2. College. We used the National Collegiate Athletic Association (NCAA) website (ncaa.org) to generate a list of all colleges affiliated with the NCAA. Of these colleges, 347 were Division I, 316 were Division II, and 443 were Division III. The random.org random number generator was used to generate a list of 40 schools for each division, for a total of 120 schools. An Internet-based search was then performed to identify any and all team physicians caring for athletes at that particular school. In select cases, telephone calls were made to determine all the team physicians involved in the care of athletes at that institution.

3. Professional. Team physician data were collected for 4 of the most popular professional sporting leagues12: Major League Baseball (MLB), National Basketball Association (NBA), National Football League (NFL), and National Hockey League (NHL). Each team’s official website was identified through its league website (mlb.com, nba.com, nfl.com, nhl.com), and the roster or directory listing of all team physicians was recorded. In 2 cases, the team’s medical personnel listing could not be retrieved through the Internet, and a telephone call had to be made to identify all team physicians. Team physicians were identified for 122 professional teams: 30 MLB, 30 NBA, 32 NFL, and 30 NHL.

 

 

For this study, all physicians were classified as either orthopedic or nonorthopedic. Orthopedic surgeons—the focus of this study—were defined as those who completed residency training in orthopedic surgery. Median number of orthopedic and nonorthopedic surgeons per team was calculated at the high school, collegiate, and professional levels.

After identifying all orthopedic team physicians, we performed additional Internet searches to determine any affiliation between each physician and an applicable academic medical center. Physicians were placed in 1 of 3 different categories based on “level” of academic affiliation. Orthopedists with no identifiable connection to an academic medical center were listed under none. The first 100 search results were studied before this determination was made. Orthopedists with any academic affiliation below the level of full professorship were placed in the category associate/assistant/adjunct professor, which included any physician who was an associate professor, adjunct professor, clinical instructor, or volunteer instructor at an academic medical center. Last, orthopedists listed as full professors were placed in the professor category.

Number of publications written by each orthopedic team physician was then calculated using SciVerse Scopus (scopus.com), a comprehensive abstract and citation database of research literature that offers complete coverage of the Medline and Embase databases.13 Scopus offers a Scopus Author Identifier, which assigns each author in Scopus a unique identification number.14 This number is based on an “algorithm that matches author names based on their affiliation, address, subject area, source title, dates of publication citations, and co-authors.”14 Authors whose names did not appear in Scopus were assumed to have no publications, and this was reported after cross-referencing with Medline to ensure no documents were missed. This study included all publications: original research articles, reviews, letters, and commentaries. Any level of authorship (first, second, etc) was included. All publications were scanned, and duplicate listings were not included. Median number of publications per orthopedic team physician was calculated at the high school, college, and professional levels.

We also determined the h-index for each orthopedic team physician. The h-index is used to measure the impact of the published work of a scholar: “A scientist has index h if h of his/her papers have at least h citations each, and the other papers have no more than h citations each.”15 For example, an h-index of 12 means that, out of an author’s total number of publications, 12 have been cited at least 12 times, and all of his or her other publications have been cited fewer than 12 times. All authors in Scopus are automatically assigned h-indexes, and we collected these numbers.16 Of note, citations for articles published before 1996 are not included in the h-index calculation. Median h-index score per orthopedic team physician was calculated at the high school, college, and professional levels.

Analysis of variance was used to compare continuous data (eg, number of publications per surgeon) across different groups (eg, physicians from respective sports). Chi-square tests were used to detect whole-number differences between groups (eg, difference in number of physicians per team across the various professional sports leagues). Statistical significance was set at P < .05.

Results

We identified 1054 team physicians among the 362 total high schools, colleges, and professional sports teams included in this study. Of the 1054 physicians, 678 (64%) were orthopedic surgeons (Table 1). Seventy-two (60%) of the 120 high schools did not have a team physician, whereas all the colleges and professional teams did. Number of orthopedic surgeons per team was higher at the collegiate level (2.29; range, 0-11) and professional level (2.21; range, 1-9) than at the high school level (1.11; range, 0-24) (Table 1). Median number of nonorthopedic surgeons was highest in professional sports (1.88; range, 0-9) followed by college sports (1.06; range, 0-9) and high school sports (0.16; range, 0-2) (Table 1).

Of the 678 orthopedic team physicians, 298 (44%) were officially affiliated with an academic medical center, either as clinical instructor, associate/adjunct professor, or full professor. Percentage of orthopedists affiliated with an academic medical center was highest in professional sports (173/270, 64%) followed by collegiate sports (98/275, 36%) and high school sports (27/133, 20%) (P < .001, Table 2). Percentage of orthopedists identified as full professors was highest at the professional level (42/270, 16%) followed by the collegiate level (14/275, 5.1%) and the high school level (3/133, 2.3%) (P < .001, Table 2).

We found 12,036 publications written by the 678 orthopedic team physicians included in this study. Median number of publications per orthopedist was significantly higher in professional sports (30.6; range, 0-460) than in collegiate sports (10.7; range, 0-581) and high school sports (6.0; range, 0-220) (P < .001). Number of authors with more than 25 publications was highest at the professional level (82) followed by the collegiate level (27) and the high school level (7) (Table 3). Median number of publications per orthopedist was also higher at the professional level (12) than at the collegiate level (2) and high school level (1). Median h-index was higher among orthopedists in professional sports (7.1; range, 0-50) than at colleges (2.7; range, 0-63) and high schools (1.8; range, 0-32) (P < .001). Median h-index was also significantly higher at the professional level (5) than at the collegiate level (1) and high school level (0).

 

 

At the professional level of sports, we identified 499 team physicians (270 orthopedic, 54%; 229 nonorthopedic, 46%). Median number of orthopedic team physicians varied by sport, with MLB (2.8; range, 1-8) and the NFL (2.4; range, 1-4) having relatively more of these physicians than the NHL (2.0; range, 1-6) and the NBA (1.7; range, 1-9) (Table 4). Percentage of orthopedic team physicians affiliated with academic medical centers was highest in MLB (58/83, 69.9%) followed by the NFL (47/76, 61.8%), the NHL (37/60, 61.7%), and the NBA (31/51, 60.8%) (Table 5). Median number of publications by orthopedists also varied by sport, with the highest number in MLB (37.9; range, 0-225) followed by the NBA (32.0; range, 0-227) and the NFL (30.4; range, 0-460), with the lowest number in the NHL (20.7; range, 0-144) (Table 6). Median number of publications was the same (17.5) in MLB and the NFL and lower in the NBA (11) and the NHL (7.5). Median h-index was highest in the NFL (8.2; range, 0-50) and MLB (7.9; range, 0-32) followed by the NBA (6.6; range, 0-35) and the NHL (4.9; range, 0-20) (Table 7) Median h-index was the same (6) in MLB and the NFL and lower (3) in the NBA and the NHL.

     

Discussion

To our knowledge, this is the first study of academic involvement and the research activities of orthopedic team physicians at the high school, college, and professional levels of sport. We found that, on average, there were almost twice as many orthopedists at the collegiate and professional levels than at the high school level—likely because 72 of the 120 high schools randomly selected did not have a team physician, despite having sports teams. We can attribute this to the organizational structure of teams in a high school setting, where it is fairly common that no medically educated health care provider is readily available for the student athletes.5 Although the median number of orthopedists was similar at the collegiate and professional levels, the number of nonorthopedic team physicians was higher at the professional level than at the collegiate level. Although most collegiate and professional teams have an internist and an orthopedist on staff, medical staff at the professional level may also include several subspecialists from a variety of medical fields (eg, dental medicine, ophthalmology, neurology).17

We found that a significantly larger proportion of orthopedists at the professional level (64%) were affiliated with academic medical centers as associate/adjunct professors and full professors compared with orthopedists at the collegiate level (36%) and high school level (20%). The academic relationship with collegiate teams was much lower than expected. Regarding professional sports, however, this finding confirmed our hypothesis, and the explanation is likely multifactorial and historical. Moreover, the median number of publications was higher for orthopedists at the professional level (30.8) than at the collegiate level (10.7) and high school level (6). In the late 1940s and early 1950s, many orthopedic team physicians entered into contracts with major universities.4 For many physicians, this contractual relationship increased their prestige, and some orthopedic groups were alleged to have endorsed scholarships at those schools.4 Given the high level of publicity and scrutiny surrounding medical decisions at the professional level of sports, it is possible that professional sports teams specifically seek orthopedists who are well respected within academia. Moreover, contracts between universities/academic medical centers and professional teams may mandate that a faculty member from that organization provide the orthopedic/medical care for the team. This may also increase the likelihood of professional teams being paired with academic orthopedic physicians. However, such contractual agreements are made between professional teams and large private medical groups as well.

In addition to measuring quantity of publications, we used the h-index to measure their quality. Following the same pattern as the publication rate, median h-index per orthopedic team physician was significantly higher at the professional level (7.1) than at the collegiate level (2.7) and high school level (1.8). As with publication volume, this is not entirely surprising, as h-index has been shown to correlate with academic rank in other surgical specialties,18 and there was a higher percentage of academic physicians at the professional level than at the collegiate and high school levels.

At the professional level of sports, 56% of all team physicians were orthopedic surgeons. Orthopedists caring for MLB teams had the highest median number of publications (37.9), followed by the NBA (32.0), the NFL (30.4), and the NHL (20.7). One likely explanation is the higher percentage of MLB physicians affiliated with academic medical centers. Regarding the h-index, MLB and NFL physicians had the highest values (7.9 and 8.2, respectively).

 

 

Our study had several limitations. First, we may not have captured data on all the team physicians at the high school, college, and professional levels. By following a detailed protocol in identifying surgeons, however, we tried to minimize the impact of any such omissions. In addition, teams may have had many unofficial consultants acting as team physicians, whether orthopedic or nonorthopedic, and, if these physicians were not listed in an official capacity, they may have been omitted from this study. We further realize that a true measure of academic productivity should also include book chapters and books published, research grants awarded, and patents registered. By including only peer-reviewed articles, we omitted these other criteria.

To our knowledge, the data presented here represent the first attempt to quantify the academic involvement and research productivity of orthopedic team physicians at the high school, college, and professional levels of sport. These data help us understand how research productivity varies by orthopedic team physicians at different levels of sport and may be useful to those considering a career as a team physician, as they can better evaluate their own productivity in the context of team physicians across different levels of competition.

The responsibilities of team physicians have increased dramatically since the early 19th century, when these physicians first appeared on the sidelines during football games.1 Although the primary role of the team physician is to care for the athlete, other responsibilities include administrative and legal duties, equipment- and environment-related duties, teaching, and communication with parents, coaches, and other physicians.2-4 These responsibilities differ greatly by the level of the athlete and the team being covered. For example, compared with high school and collegiate sport physicians, physicians caring for professional athletes may have increased interaction with the media.5

Despite the increasing demands and responsibilities of team physicians, it is important that they continue to advance the field of sports medicine through teaching and research.3,6 Team physicians have direct access to athletes at multiple levels of competition, from novice to professional, and therefore have a unique understanding of the injuries that commonly affect these athletes. Efforts to both teach and study the prevention, diagnosis, and treatment of these injuries have dramatically advanced the field of sports medicine. In fact, several advancements in sports medicine have come from team physicians, including advancements in anterior cruciate ligament reconstruction,7,8 shoulder arthroscopy,9 and “Tommy John” surgery,10 to name a few.

Given the important role of team physicians (particularly orthopedic team physicians) in advancing sports medicine, it is important to understand the degree to which team physicians at all levels of sport contribute to teaching and research.

We conducted a study to determine the overall academic involvement of orthopedic team physicians at all levels of sport, including the degree to which these physicians are affiliated with academic medical centers (by level of sport and by professional sport) and the quantity and impact of these physicians’ scientific publications. We hypothesized that orthopedic physician academic involvement would be higher at the professional level of sport than at the collegiate or high school level and that the degree of physician academic involvement would differ between professional sporting leagues.

Materials and Methods

In August 2012, we performed a comprehensive telephone- and Internet-based search to identify a sample of team physicians caring for athletes at the high school, collegiate, and professional levels of sport. Data were collected on all team physicians, regardless of medical specialty. We defined a physician as any person listed as having either a doctor of medicine (MD) or a doctor of osteopathic medicine (DO) degree. A physician listed as a team physician at 2 different levels of competition (high school, college, professional) was included in both cohorts. A physician listed as a team physician in 2 different professional sports leagues was included independently for both leagues. All other medical personnel, including athletic trainers, therapists, and nursing staff, were excluded. Data on our sample population were collected as follows:

1. High school. Performing a comprehensive database search through the US Department of Education, we generated a list of all 20,989 US schools that include grades 9 to 12.11 We then used a random number generator (random.org) to randomly select a sample of 120 high schools. These schools were contacted by telephone and asked to identify the team physician(s) for their sports teams. Twenty of these schools reported not having an athletic team, so we randomly generated a list of 20 additional high schools. High schools that had an athletic team but denied having a team physician were included in the analysis.

2. College. We used the National Collegiate Athletic Association (NCAA) website (ncaa.org) to generate a list of all colleges affiliated with the NCAA. Of these colleges, 347 were Division I, 316 were Division II, and 443 were Division III. The random.org random number generator was used to generate a list of 40 schools for each division, for a total of 120 schools. An Internet-based search was then performed to identify any and all team physicians caring for athletes at that particular school. In select cases, telephone calls were made to determine all the team physicians involved in the care of athletes at that institution.

3. Professional. Team physician data were collected for 4 of the most popular professional sporting leagues12: Major League Baseball (MLB), National Basketball Association (NBA), National Football League (NFL), and National Hockey League (NHL). Each team’s official website was identified through its league website (mlb.com, nba.com, nfl.com, nhl.com), and the roster or directory listing of all team physicians was recorded. In 2 cases, the team’s medical personnel listing could not be retrieved through the Internet, and a telephone call had to be made to identify all team physicians. Team physicians were identified for 122 professional teams: 30 MLB, 30 NBA, 32 NFL, and 30 NHL.

 

 

For this study, all physicians were classified as either orthopedic or nonorthopedic. Orthopedic surgeons—the focus of this study—were defined as those who completed residency training in orthopedic surgery. Median number of orthopedic and nonorthopedic surgeons per team was calculated at the high school, collegiate, and professional levels.

After identifying all orthopedic team physicians, we performed additional Internet searches to determine any affiliation between each physician and an applicable academic medical center. Physicians were placed in 1 of 3 different categories based on “level” of academic affiliation. Orthopedists with no identifiable connection to an academic medical center were listed under none. The first 100 search results were studied before this determination was made. Orthopedists with any academic affiliation below the level of full professorship were placed in the category associate/assistant/adjunct professor, which included any physician who was an associate professor, adjunct professor, clinical instructor, or volunteer instructor at an academic medical center. Last, orthopedists listed as full professors were placed in the professor category.

Number of publications written by each orthopedic team physician was then calculated using SciVerse Scopus (scopus.com), a comprehensive abstract and citation database of research literature that offers complete coverage of the Medline and Embase databases.13 Scopus offers a Scopus Author Identifier, which assigns each author in Scopus a unique identification number.14 This number is based on an “algorithm that matches author names based on their affiliation, address, subject area, source title, dates of publication citations, and co-authors.”14 Authors whose names did not appear in Scopus were assumed to have no publications, and this was reported after cross-referencing with Medline to ensure no documents were missed. This study included all publications: original research articles, reviews, letters, and commentaries. Any level of authorship (first, second, etc) was included. All publications were scanned, and duplicate listings were not included. Median number of publications per orthopedic team physician was calculated at the high school, college, and professional levels.

We also determined the h-index for each orthopedic team physician. The h-index is used to measure the impact of the published work of a scholar: “A scientist has index h if h of his/her papers have at least h citations each, and the other papers have no more than h citations each.”15 For example, an h-index of 12 means that, out of an author’s total number of publications, 12 have been cited at least 12 times, and all of his or her other publications have been cited fewer than 12 times. All authors in Scopus are automatically assigned h-indexes, and we collected these numbers.16 Of note, citations for articles published before 1996 are not included in the h-index calculation. Median h-index score per orthopedic team physician was calculated at the high school, college, and professional levels.

Analysis of variance was used to compare continuous data (eg, number of publications per surgeon) across different groups (eg, physicians from respective sports). Chi-square tests were used to detect whole-number differences between groups (eg, difference in number of physicians per team across the various professional sports leagues). Statistical significance was set at P < .05.

Results

We identified 1054 team physicians among the 362 total high schools, colleges, and professional sports teams included in this study. Of the 1054 physicians, 678 (64%) were orthopedic surgeons (Table 1). Seventy-two (60%) of the 120 high schools did not have a team physician, whereas all the colleges and professional teams did. Number of orthopedic surgeons per team was higher at the collegiate level (2.29; range, 0-11) and professional level (2.21; range, 1-9) than at the high school level (1.11; range, 0-24) (Table 1). Median number of nonorthopedic surgeons was highest in professional sports (1.88; range, 0-9) followed by college sports (1.06; range, 0-9) and high school sports (0.16; range, 0-2) (Table 1).

Of the 678 orthopedic team physicians, 298 (44%) were officially affiliated with an academic medical center, either as clinical instructor, associate/adjunct professor, or full professor. Percentage of orthopedists affiliated with an academic medical center was highest in professional sports (173/270, 64%) followed by collegiate sports (98/275, 36%) and high school sports (27/133, 20%) (P < .001, Table 2). Percentage of orthopedists identified as full professors was highest at the professional level (42/270, 16%) followed by the collegiate level (14/275, 5.1%) and the high school level (3/133, 2.3%) (P < .001, Table 2).

We found 12,036 publications written by the 678 orthopedic team physicians included in this study. Median number of publications per orthopedist was significantly higher in professional sports (30.6; range, 0-460) than in collegiate sports (10.7; range, 0-581) and high school sports (6.0; range, 0-220) (P < .001). Number of authors with more than 25 publications was highest at the professional level (82) followed by the collegiate level (27) and the high school level (7) (Table 3). Median number of publications per orthopedist was also higher at the professional level (12) than at the collegiate level (2) and high school level (1). Median h-index was higher among orthopedists in professional sports (7.1; range, 0-50) than at colleges (2.7; range, 0-63) and high schools (1.8; range, 0-32) (P < .001). Median h-index was also significantly higher at the professional level (5) than at the collegiate level (1) and high school level (0).

 

 

At the professional level of sports, we identified 499 team physicians (270 orthopedic, 54%; 229 nonorthopedic, 46%). Median number of orthopedic team physicians varied by sport, with MLB (2.8; range, 1-8) and the NFL (2.4; range, 1-4) having relatively more of these physicians than the NHL (2.0; range, 1-6) and the NBA (1.7; range, 1-9) (Table 4). Percentage of orthopedic team physicians affiliated with academic medical centers was highest in MLB (58/83, 69.9%) followed by the NFL (47/76, 61.8%), the NHL (37/60, 61.7%), and the NBA (31/51, 60.8%) (Table 5). Median number of publications by orthopedists also varied by sport, with the highest number in MLB (37.9; range, 0-225) followed by the NBA (32.0; range, 0-227) and the NFL (30.4; range, 0-460), with the lowest number in the NHL (20.7; range, 0-144) (Table 6). Median number of publications was the same (17.5) in MLB and the NFL and lower in the NBA (11) and the NHL (7.5). Median h-index was highest in the NFL (8.2; range, 0-50) and MLB (7.9; range, 0-32) followed by the NBA (6.6; range, 0-35) and the NHL (4.9; range, 0-20) (Table 7) Median h-index was the same (6) in MLB and the NFL and lower (3) in the NBA and the NHL.

     

Discussion

To our knowledge, this is the first study of academic involvement and the research activities of orthopedic team physicians at the high school, college, and professional levels of sport. We found that, on average, there were almost twice as many orthopedists at the collegiate and professional levels than at the high school level—likely because 72 of the 120 high schools randomly selected did not have a team physician, despite having sports teams. We can attribute this to the organizational structure of teams in a high school setting, where it is fairly common that no medically educated health care provider is readily available for the student athletes.5 Although the median number of orthopedists was similar at the collegiate and professional levels, the number of nonorthopedic team physicians was higher at the professional level than at the collegiate level. Although most collegiate and professional teams have an internist and an orthopedist on staff, medical staff at the professional level may also include several subspecialists from a variety of medical fields (eg, dental medicine, ophthalmology, neurology).17

We found that a significantly larger proportion of orthopedists at the professional level (64%) were affiliated with academic medical centers as associate/adjunct professors and full professors compared with orthopedists at the collegiate level (36%) and high school level (20%). The academic relationship with collegiate teams was much lower than expected. Regarding professional sports, however, this finding confirmed our hypothesis, and the explanation is likely multifactorial and historical. Moreover, the median number of publications was higher for orthopedists at the professional level (30.8) than at the collegiate level (10.7) and high school level (6). In the late 1940s and early 1950s, many orthopedic team physicians entered into contracts with major universities.4 For many physicians, this contractual relationship increased their prestige, and some orthopedic groups were alleged to have endorsed scholarships at those schools.4 Given the high level of publicity and scrutiny surrounding medical decisions at the professional level of sports, it is possible that professional sports teams specifically seek orthopedists who are well respected within academia. Moreover, contracts between universities/academic medical centers and professional teams may mandate that a faculty member from that organization provide the orthopedic/medical care for the team. This may also increase the likelihood of professional teams being paired with academic orthopedic physicians. However, such contractual agreements are made between professional teams and large private medical groups as well.

In addition to measuring quantity of publications, we used the h-index to measure their quality. Following the same pattern as the publication rate, median h-index per orthopedic team physician was significantly higher at the professional level (7.1) than at the collegiate level (2.7) and high school level (1.8). As with publication volume, this is not entirely surprising, as h-index has been shown to correlate with academic rank in other surgical specialties,18 and there was a higher percentage of academic physicians at the professional level than at the collegiate and high school levels.

At the professional level of sports, 56% of all team physicians were orthopedic surgeons. Orthopedists caring for MLB teams had the highest median number of publications (37.9), followed by the NBA (32.0), the NFL (30.4), and the NHL (20.7). One likely explanation is the higher percentage of MLB physicians affiliated with academic medical centers. Regarding the h-index, MLB and NFL physicians had the highest values (7.9 and 8.2, respectively).

 

 

Our study had several limitations. First, we may not have captured data on all the team physicians at the high school, college, and professional levels. By following a detailed protocol in identifying surgeons, however, we tried to minimize the impact of any such omissions. In addition, teams may have had many unofficial consultants acting as team physicians, whether orthopedic or nonorthopedic, and, if these physicians were not listed in an official capacity, they may have been omitted from this study. We further realize that a true measure of academic productivity should also include book chapters and books published, research grants awarded, and patents registered. By including only peer-reviewed articles, we omitted these other criteria.

To our knowledge, the data presented here represent the first attempt to quantify the academic involvement and research productivity of orthopedic team physicians at the high school, college, and professional levels of sport. These data help us understand how research productivity varies by orthopedic team physicians at different levels of sport and may be useful to those considering a career as a team physician, as they can better evaluate their own productivity in the context of team physicians across different levels of competition.

References

1.    Thorndike A. Athletic Injuries: Prevention, Diagnosis, and Treatment. Philadelphia, PA: Lea & Febiger; 1956.

2.    The team physician. A statement of the Committee on the Medical Aspects of Sports of the American Medical Association, September 1967. J School Health. 1967;37(10):510-514.

3.     Team physician consensus statement. Am J Sports Med. 2000;28(3):440-441.

4.    Whiteside J, Andrews JR. Trends for the future as a team physician: Herodicus to hereafter. Clin Sports Med. 2007;26(2):285-304.

5.    Goforth M, Almquist J, Matney M, et al. Understanding organization structures of the college, university, high school, clinical, and professional settings. Clin Sports Med. 2007;26(2):201-226.

6.    Hughston JC. Want to be in sports medicine? Get involved. Am J Sports Med. 1979;7(2):79-80.

7.    Marshall JL, Warren RF, Wickiewicz TL, Reider B. The anterior cruciate ligament: a technique of repair and reconstruction. Clin Orthop Relat Res. 1979;(143):97-106.

8.    Clancy WG Jr, Nelson DA, Reider B, Narechania RG. Anterior cruciate ligament reconstruction using one-third of the patellar ligament, augmented by extra-articular tendon transfers. J Bone Joint Surg Am. 1982;64(3):352-359.

9.    Andrews JR, Carson WG Jr, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985;13(5):337-341.

10.  Indelicato PA, Jobe FW, Kerlan RK, Carter VS, Shields CL, Lombardo SJ. Correctable elbow lesions in professional baseball players: a review of 25 cases. Am J Sports Med. 1979;7(1):72-75.

11.  Elementary/Secondary Information System (EISi). National Center for Education Statistics, Institute of Education Sciences, US Department of Education website. http://nces.ed.gov/ccd/elsi/. Accessed September 21, 2015.

12.  Corso RA; Harris Interactive. Football is America’s favorite sport as lead over baseball continues to grow; college football and auto racing come next. Harris Interactive website. http://www.harrisinteractive.com/vault/Harris Poll 9 - Favorite sport_1.25.12.pdf. Harris Poll 9, January 25, 2012. Accessed September 21, 2015.

13.  [Scopus content]. Elsevier website. http://www.elsevier.com/solutions/scopus/content. Accessed September 21, 2015.

14.  Scopus Author Identifier. Scopus website. http://help.scopus.com/Content/h_autsrch_intro.htm. Accessed October 5, 2015.

15.  Hirsch JE. An index to quantify an individual’s scientific research output. Proc Natl Acad Sci U S A. 2005;102(46):16569-16572.

16.  Author Evaluator h Index Tab. Scopus website. http://help.scopus.com/Content/h_auteval_hindex.htm. Accessed October 5, 2015.

17.  Boyd JL. Understanding the politics of being a team physician. Clin Sports Med. 2007;26(2):161-172.

18.   Lee J, Kraus KL, Couldwell WT. Use of the h index in neurosurgery. Clinical article. J Neurosurg. 2009;111(2):387-

References

1.    Thorndike A. Athletic Injuries: Prevention, Diagnosis, and Treatment. Philadelphia, PA: Lea & Febiger; 1956.

2.    The team physician. A statement of the Committee on the Medical Aspects of Sports of the American Medical Association, September 1967. J School Health. 1967;37(10):510-514.

3.     Team physician consensus statement. Am J Sports Med. 2000;28(3):440-441.

4.    Whiteside J, Andrews JR. Trends for the future as a team physician: Herodicus to hereafter. Clin Sports Med. 2007;26(2):285-304.

5.    Goforth M, Almquist J, Matney M, et al. Understanding organization structures of the college, university, high school, clinical, and professional settings. Clin Sports Med. 2007;26(2):201-226.

6.    Hughston JC. Want to be in sports medicine? Get involved. Am J Sports Med. 1979;7(2):79-80.

7.    Marshall JL, Warren RF, Wickiewicz TL, Reider B. The anterior cruciate ligament: a technique of repair and reconstruction. Clin Orthop Relat Res. 1979;(143):97-106.

8.    Clancy WG Jr, Nelson DA, Reider B, Narechania RG. Anterior cruciate ligament reconstruction using one-third of the patellar ligament, augmented by extra-articular tendon transfers. J Bone Joint Surg Am. 1982;64(3):352-359.

9.    Andrews JR, Carson WG Jr, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985;13(5):337-341.

10.  Indelicato PA, Jobe FW, Kerlan RK, Carter VS, Shields CL, Lombardo SJ. Correctable elbow lesions in professional baseball players: a review of 25 cases. Am J Sports Med. 1979;7(1):72-75.

11.  Elementary/Secondary Information System (EISi). National Center for Education Statistics, Institute of Education Sciences, US Department of Education website. http://nces.ed.gov/ccd/elsi/. Accessed September 21, 2015.

12.  Corso RA; Harris Interactive. Football is America’s favorite sport as lead over baseball continues to grow; college football and auto racing come next. Harris Interactive website. http://www.harrisinteractive.com/vault/Harris Poll 9 - Favorite sport_1.25.12.pdf. Harris Poll 9, January 25, 2012. Accessed September 21, 2015.

13.  [Scopus content]. Elsevier website. http://www.elsevier.com/solutions/scopus/content. Accessed September 21, 2015.

14.  Scopus Author Identifier. Scopus website. http://help.scopus.com/Content/h_autsrch_intro.htm. Accessed October 5, 2015.

15.  Hirsch JE. An index to quantify an individual’s scientific research output. Proc Natl Acad Sci U S A. 2005;102(46):16569-16572.

16.  Author Evaluator h Index Tab. Scopus website. http://help.scopus.com/Content/h_auteval_hindex.htm. Accessed October 5, 2015.

17.  Boyd JL. Understanding the politics of being a team physician. Clin Sports Med. 2007;26(2):161-172.

18.   Lee J, Kraus KL, Couldwell WT. Use of the h index in neurosurgery. Clinical article. J Neurosurg. 2009;111(2):387-

Issue
The American Journal of Orthopedics - 44(11)
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The American Journal of Orthopedics - 44(11)
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510-514
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Academic Characteristics of Orthopedic Team Physicians Affiliated With High School, Collegiate, and Professional Teams
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Academic Characteristics of Orthopedic Team Physicians Affiliated With High School, Collegiate, and Professional Teams
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american journal of orthopedics, AJO, original study, study, sports medicine, academic, orthopedic, team, physicians, high school, college, collegiate, professional, athletes, athletics, sports, makhni, buza, byram, ahmad
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american journal of orthopedics, AJO, original study, study, sports medicine, academic, orthopedic, team, physicians, high school, college, collegiate, professional, athletes, athletics, sports, makhni, buza, byram, ahmad
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