Arthroplasty/Joint Replacement

Developing arthritis increases a person’s risk of falling into poverty, especially for women, according to a study published online ahead of print September 8 in Arthritis & Rheumatology.

For this study of more than 4,000 Australian adults, females who developed arthritis were 51% more likely to fall into income poverty than nonarthritic women. In men, having arthritis was associated with a 22% increased risk of poverty.

Women with arthritis also were 87% more likely to fall into “multidimensional poverty,” which includes income, health, and education attainment, while the arthritis-related risk in men was 29%. The investigators noted that given the high prevalence of arthritis, the condition is an overlooked driver of poverty.

“With population ageing occurring in most of the developed nations around the world, health conditions such as arthritis will become increasingly common. That developing arthritis has such a pronounced impact on the risk of falling into poverty should flag to policy makers in welfare departments the influence of the condition on national living standards,” said lead author Emily Callander, PhD, from the Faculty of Pharmacy at the University of Sydney in Australia.

Researchers utilized survey data from the Household Income and Labour Dynamics in Australia (HILDA) Survey. Survival analysis using Cox regression models were applied to the nationally representative, longitudinal data between the years 2007 and 2012 for Australian adults ages 21 and older.

The hazard ratio for falling into income poverty for females who develop arthritis was 1.51, and for males the hazard ratio for falling into income poverty was 1.22, compared with people who never developed arthritis. The hazard ratio for falling into multidimensional poverty for females who develop arthritis was 1.87 and for males the hazard ratio was 1.29.

According to Dr. Callander, “The high risk of poverty should be kept in mind by clinicians seeking the most appropriate treatment for their patients with arthritis, as affordability of out-of-pocket costs may be an important factor.”

Developing arthritis increases a person’s risk of falling into poverty, especially for women, according to a study published online ahead of print September 8 in Arthritis & Rheumatology.

For this study of more than 4,000 Australian adults, females who developed arthritis were 51% more likely to fall into income poverty than nonarthritic women. In men, having arthritis was associated with a 22% increased risk of poverty.

Women with arthritis also were 87% more likely to fall into “multidimensional poverty,” which includes income, health, and education attainment, while the arthritis-related risk in men was 29%. The investigators noted that given the high prevalence of arthritis, the condition is an overlooked driver of poverty.

“With population ageing occurring in most of the developed nations around the world, health conditions such as arthritis will become increasingly common. That developing arthritis has such a pronounced impact on the risk of falling into poverty should flag to policy makers in welfare departments the influence of the condition on national living standards,” said lead author Emily Callander, PhD, from the Faculty of Pharmacy at the University of Sydney in Australia.

Researchers utilized survey data from the Household Income and Labour Dynamics in Australia (HILDA) Survey. Survival analysis using Cox regression models were applied to the nationally representative, longitudinal data between the years 2007 and 2012 for Australian adults ages 21 and older.

The hazard ratio for falling into income poverty for females who develop arthritis was 1.51, and for males the hazard ratio for falling into income poverty was 1.22, compared with people who never developed arthritis. The hazard ratio for falling into multidimensional poverty for females who develop arthritis was 1.87 and for males the hazard ratio was 1.29.

According to Dr. Callander, “The high risk of poverty should be kept in mind by clinicians seeking the most appropriate treatment for their patients with arthritis, as affordability of out-of-pocket costs may be an important factor.”

Developing arthritis increases a person’s risk of falling into poverty, especially for women, according to a study published online ahead of print September 8 in Arthritis & Rheumatology.

For this study of more than 4,000 Australian adults, females who developed arthritis were 51% more likely to fall into income poverty than nonarthritic women. In men, having arthritis was associated with a 22% increased risk of poverty.

Women with arthritis also were 87% more likely to fall into “multidimensional poverty,” which includes income, health, and education attainment, while the arthritis-related risk in men was 29%. The investigators noted that given the high prevalence of arthritis, the condition is an overlooked driver of poverty.

“With population ageing occurring in most of the developed nations around the world, health conditions such as arthritis will become increasingly common. That developing arthritis has such a pronounced impact on the risk of falling into poverty should flag to policy makers in welfare departments the influence of the condition on national living standards,” said lead author Emily Callander, PhD, from the Faculty of Pharmacy at the University of Sydney in Australia.

Researchers utilized survey data from the Household Income and Labour Dynamics in Australia (HILDA) Survey. Survival analysis using Cox regression models were applied to the nationally representative, longitudinal data between the years 2007 and 2012 for Australian adults ages 21 and older.

The hazard ratio for falling into income poverty for females who develop arthritis was 1.51, and for males the hazard ratio for falling into income poverty was 1.22, compared with people who never developed arthritis. The hazard ratio for falling into multidimensional poverty for females who develop arthritis was 1.87 and for males the hazard ratio was 1.29.

According to Dr. Callander, “The high risk of poverty should be kept in mind by clinicians seeking the most appropriate treatment for their patients with arthritis, as affordability of out-of-pocket costs may be an important factor.”

Supracondylar humerus fractures, which are the most common elbow fractures in the pediatric population, account for approximately 3% of all pediatric fractures.¹ Complications of the injury or surgery include pin migration (2%), pin-site infection (1%), malunion, loss of reduction, compartment syndrome, nerve injury, and cubitus varus.¹ A less frequently reported complication is avascular necrosis (AVN) of the trochlea.

First reported in 1948, posttraumatic deformity of the trochlea has appeared sparingly throughout the literature.² This complication has been reported in varying fracture patterns and degrees of injury. The exact incidence is unknown because AVN of the humerus can occur without known trauma. The etiology of the deformity is thought to be interruption of the blood supply of the trochlea. Patterns include type A (AVN of the lateral ossification center) and type B (AVN of the entire medial crista along with a metaphyseal portion). Type A necrosis leads to early degenerative joint disease and loss of range of motion (ROM); angular deformities are uncommon. Type B AVN results in a progressive varus deformity of the trochlea.³ The deformities typically worsen as the child ages. Late-onset ulnar neuropathy can be seen, as medial condyle hypoplasia allows the ulnar nerve to move anterior with the medial head of the triceps. Treatment options address the sequelae and include observation, muscle strengthening, supracondylar osteotomy, and ulnar nerve transposition. Arthroscopic joint débridement has been shown, in short-term follow-up, to relieve pain and restore motion.⁴

We present 5 cases of AVN of the trochlea after supracondylar humerus fractures to highlight this unusual complication. Unlike more common complications of supracondylar humerus fractures, AVN of the trochlea can be a late clinical finding. We speculate that, in cases resulting from nondisplaced fractures, tamponade from fracture hematoma may play a role. It is important to keep this complication in the differential diagnosis of patients with a history of a supracondylar humerus fracture and unexplained elbow motion loss or pain. 

Case Reports 

Retrospective data were collected for all patients after approval by the institutional review board at our institution. Patients were identified by a computerized search using the Current Procedural Terminology code for closed reduction percutaneous pinning of supracondylar humerus fracture. The search was limited to patients treated at our institution from 2000 to 2012; 1159 patients were initially identified. Three patients were found to have postoperative AVN of the trochlea; 2 other patients were treated at an outside hospital and were identified by surgeon recall. These 5 cases are presented here.

Case 1

A girl aged 5 years, 3 months sustained a Gartland type III supracondylar humerus fracture. She was originally seen at an outside facility and transferred to our tertiary care facility for definitive management. She underwent closed reduction and fixation with 3 lateral-based pins 1 day after her injury. Her pins and cast were removed 22 days postoperatively. She returned to full elbow function after her fracture care; 6 months later, she returned to the clinic with painless, decreased flexion of her elbow to 95º. Radiographs showed a lucency of the trochlea extending into the metaphysis (Figure 1). Thirteen months postoperatively, her examination was unchanged with motion at 0º to 95º; her radiographs showed a persistent lateral and medial lucency of the trochlea consistent with type B AVN involving the medial crista.

Case 2

An 8-year-old girl sustained a Gartland type III supracondylar humerus fracture that was treated at an outside facility with closed reduction and fixation with lateral pins. She had an uneventful postoperative course with painless return of motion. She presented 6 months after her surgery with progressive decreased ROM. She underwent conservative treatment with therapy and stretching without much improvement. She presented to our institution 4 years postoperatively with painless decreased motion from 40º to 110º. Radiographs showed dissolution of the lateral ossification center of the trochlea with a fishtail deformity consistent with type A AVN. Magnetic resonance imaging (MRI) confirmed AVN of the trochlea (Figure 2). 

Case 3

A girl aged 5 years, 6 months sustained a Gartland type I supracondylar humerus fracture that was treated uneventfully by casting. She did not have a reduction or manipulation and healed without complications. She returned to the clinic 3 years after the injury complaining of intermittent elbow pain, neglect, and loss of motion. Her ROM was 0º to 110º. Radiographs showed dissolution of the lateral trochlea with sclerosis of the metaphysis consistent with a type A deformity (Figure 3). Contralateral radiographs were not obtained. MRI confirmed AVN of the trochlea. 

Case 4

A 10-year-old girl sustained a Gartland type III supracondylar humerus fracture treated with closed reduction and pinning at an outside facility. She experienced full return to function postoperatively until developing stiffness and popping 1 year after surgery. She was evaluated at our institution 5 years postoperatively with elbow popping in full extension. Radiographs showed a type A deformity; MRI confirmed the diagnosis of AVN of the humerus (Figure 4). She underwent elbow arthroscopy with débridement of a posterior cartilage flap and synovial band. After elbow arthroscopy and débridement, she had resolution of symptoms with full elbow ROM.

Case 5

A 5-year-old boy sustained a Gartland III supracondylar humerus fracture that was treated with closed reduction and pinning at our institution. He had full return of painless motion postoperatively. Seven years after surgery, he presented with popping sensation in his elbow. Examination showed a 5º lack of full extension without effusion or crepitus. Radiographs showed a type A deformity with dissolution of the lateral ossification center (Figure 5).

Discussion

Avascular necrosis of the trochlea after supracondylar humerus fractures was first reported by McDonnell and Wilson in 1948.² Four of 53 patients (7.5%) developed AVN of the trochlea. Clinical presentation happened at 2 to 7 years after injury. No causative effect was given; however, 2 cases of AVN were associated with narrowing of joint space and thinning of articular cartilage. One incident was associated with multiple reduction attempts.² The etiology and exact incidence remain unclear, but both vascular insult and idiopathic growth disturbance have been proposed.⁴

Morrissy and Wilkins⁵ in 1984 reported 3 cases of dissolution of the trochlea after supracondylar humerus fractures: 1 fracture was casted, 1 was splinted, and 1 underwent closed reduction and pinning. Radiographic abnormality was noted at 5 years, 1 year, and 9 months, respectively. These authors explained the dissolution as a vascular phenomenon. Interruption of the medial or lateral vessels supplying the cartilage of the trochlea would lead to the central necrosis pattern seen in their 3 cases. In addition, the rapid onset in Morrissy and Wilkin’s second and third cases (both 7 years old) supports a vascular etiology.⁵ 

A more recent study of 6 cases found dissolution of the trochlea occurred as a result of severe displaced supracondylar fractures.⁶ Four of the 6 cases involved nerve injuries. Evidence of fishtail deformity was delayed from fracture time until 7 to 8 years of age, consistent with the ossification of the trochlea. Additionally, MRI findings, as well as loose body formation, added to the plausibility of AVN.⁶

Haraldsson⁷ demonstrated the 2 main sources of blood supply to the medial crista of the trochlea. The lateral vessels are intra-articular and supply the apex and lateral aspect of the trochlea. The medial vessels supply the medial aspect of the medial crista of the trochlea and are extra-articular. The lateral and medial vessels do not have an anastomosis between them (Figure 6).⁷ Disruption of the lateral vessels results in a type A deformity; disruption of the lateral and medial vessels results in a type B deformity. Displaced supracondylar humerus fractures disrupt the periosteum and can result in disruption of the medial and/or lateral vessels, resulting in AVN and deformity.

Another case of AVN of the trochlea after a Gartland type I fracture was reported by Schulte and Ramseier.⁸ Similar to our case 3, the patient developed type A AVN of the distal humerus,⁹ illustrating an interruption of the lateral, intra-articular vessels. The etiology of vascular disruption in these nondisplaced supracondylar humerus fractures is less clear, but we propose that tamponade may play a role. Nondisplaced fractures result in a fracture hematoma contained in an intact capsule, having the potential to increase pressures and lead to occlusion of the lateral, intra-articular vessels. This would result in a type A deformity. Nondisplaced supracondylar humerus fractures are common, and this complication is very rare. Typically, they would be expected to generate modest fracture hematoma. However, patient factors, such as bleeding disorders or anatomic variants, including a constricted capsule, could predispose patients to development of increased intracapsular pressure. In contrast, Gartland type II and III fractures, although higher-energy, presumably tear the surrounding capsule leading to release of the fracture hematoma. We do not have direct evidence to support this theory, but measurement of intracapsular pressures could help support or refute the occurrence of tamponade. Similar studies have been reported in hip fracture and slipped capital femoral epiphysis, in which hematoma has been shown to increase intracapsular pressure.^8,10 This pressure increase can theoretically cause a tamponade of the femoral head blood supply leading to AVN. Additional alternate explanations for AVN of the trochlea after type I fractures may include a rare occurrence of direct trauma to the vessels at the moment of fracture, increased intracapsular pressure from cast positioning, or that they are unrelated events that occurred in the same elbow (because atraumatic AVN has also been reported).

Conclusion

Avascular necrosis of the trochlea is a rare but important complication of supracondylar humerus fractures. Generally, this complication has a late clinical presentation, and its cause is interruption of the trochlea blood supply. In displaced fractures, the medial and/or lateral vessels are injured, leading to Gartland type A or type B deformity. In nondisplaced fractures, the lateral vessels are affected. We propose that the lateral vessels may be interrupted by tamponade caused by encased fracture hematoma; this presents as a type A deformity. Both type A and type B deformities can be clinically significant. Avascular necrosis of the trochlea should be considered in patients with late presentation of pain or loss of motion after treatment of supracondylar humerus fractures.

Supracondylar humerus fractures, which are the most common elbow fractures in the pediatric population, account for approximately 3% of all pediatric fractures.¹ Complications of the injury or surgery include pin migration (2%), pin-site infection (1%), malunion, loss of reduction, compartment syndrome, nerve injury, and cubitus varus.¹ A less frequently reported complication is avascular necrosis (AVN) of the trochlea.

First reported in 1948, posttraumatic deformity of the trochlea has appeared sparingly throughout the literature.² This complication has been reported in varying fracture patterns and degrees of injury. The exact incidence is unknown because AVN of the humerus can occur without known trauma. The etiology of the deformity is thought to be interruption of the blood supply of the trochlea. Patterns include type A (AVN of the lateral ossification center) and type B (AVN of the entire medial crista along with a metaphyseal portion). Type A necrosis leads to early degenerative joint disease and loss of range of motion (ROM); angular deformities are uncommon. Type B AVN results in a progressive varus deformity of the trochlea.³ The deformities typically worsen as the child ages. Late-onset ulnar neuropathy can be seen, as medial condyle hypoplasia allows the ulnar nerve to move anterior with the medial head of the triceps. Treatment options address the sequelae and include observation, muscle strengthening, supracondylar osteotomy, and ulnar nerve transposition. Arthroscopic joint débridement has been shown, in short-term follow-up, to relieve pain and restore motion.⁴

We present 5 cases of AVN of the trochlea after supracondylar humerus fractures to highlight this unusual complication. Unlike more common complications of supracondylar humerus fractures, AVN of the trochlea can be a late clinical finding. We speculate that, in cases resulting from nondisplaced fractures, tamponade from fracture hematoma may play a role. It is important to keep this complication in the differential diagnosis of patients with a history of a supracondylar humerus fracture and unexplained elbow motion loss or pain. 

Case Reports 

Retrospective data were collected for all patients after approval by the institutional review board at our institution. Patients were identified by a computerized search using the Current Procedural Terminology code for closed reduction percutaneous pinning of supracondylar humerus fracture. The search was limited to patients treated at our institution from 2000 to 2012; 1159 patients were initially identified. Three patients were found to have postoperative AVN of the trochlea; 2 other patients were treated at an outside hospital and were identified by surgeon recall. These 5 cases are presented here.

Case 1

A girl aged 5 years, 3 months sustained a Gartland type III supracondylar humerus fracture. She was originally seen at an outside facility and transferred to our tertiary care facility for definitive management. She underwent closed reduction and fixation with 3 lateral-based pins 1 day after her injury. Her pins and cast were removed 22 days postoperatively. She returned to full elbow function after her fracture care; 6 months later, she returned to the clinic with painless, decreased flexion of her elbow to 95º. Radiographs showed a lucency of the trochlea extending into the metaphysis (Figure 1). Thirteen months postoperatively, her examination was unchanged with motion at 0º to 95º; her radiographs showed a persistent lateral and medial lucency of the trochlea consistent with type B AVN involving the medial crista.

Case 2

An 8-year-old girl sustained a Gartland type III supracondylar humerus fracture that was treated at an outside facility with closed reduction and fixation with lateral pins. She had an uneventful postoperative course with painless return of motion. She presented 6 months after her surgery with progressive decreased ROM. She underwent conservative treatment with therapy and stretching without much improvement. She presented to our institution 4 years postoperatively with painless decreased motion from 40º to 110º. Radiographs showed dissolution of the lateral ossification center of the trochlea with a fishtail deformity consistent with type A AVN. Magnetic resonance imaging (MRI) confirmed AVN of the trochlea (Figure 2). 

Case 3

A girl aged 5 years, 6 months sustained a Gartland type I supracondylar humerus fracture that was treated uneventfully by casting. She did not have a reduction or manipulation and healed without complications. She returned to the clinic 3 years after the injury complaining of intermittent elbow pain, neglect, and loss of motion. Her ROM was 0º to 110º. Radiographs showed dissolution of the lateral trochlea with sclerosis of the metaphysis consistent with a type A deformity (Figure 3). Contralateral radiographs were not obtained. MRI confirmed AVN of the trochlea. 

Case 4

A 10-year-old girl sustained a Gartland type III supracondylar humerus fracture treated with closed reduction and pinning at an outside facility. She experienced full return to function postoperatively until developing stiffness and popping 1 year after surgery. She was evaluated at our institution 5 years postoperatively with elbow popping in full extension. Radiographs showed a type A deformity; MRI confirmed the diagnosis of AVN of the humerus (Figure 4). She underwent elbow arthroscopy with débridement of a posterior cartilage flap and synovial band. After elbow arthroscopy and débridement, she had resolution of symptoms with full elbow ROM.

Case 5

A 5-year-old boy sustained a Gartland III supracondylar humerus fracture that was treated with closed reduction and pinning at our institution. He had full return of painless motion postoperatively. Seven years after surgery, he presented with popping sensation in his elbow. Examination showed a 5º lack of full extension without effusion or crepitus. Radiographs showed a type A deformity with dissolution of the lateral ossification center (Figure 5).

Discussion

Avascular necrosis of the trochlea after supracondylar humerus fractures was first reported by McDonnell and Wilson in 1948.² Four of 53 patients (7.5%) developed AVN of the trochlea. Clinical presentation happened at 2 to 7 years after injury. No causative effect was given; however, 2 cases of AVN were associated with narrowing of joint space and thinning of articular cartilage. One incident was associated with multiple reduction attempts.² The etiology and exact incidence remain unclear, but both vascular insult and idiopathic growth disturbance have been proposed.⁴

Morrissy and Wilkins⁵ in 1984 reported 3 cases of dissolution of the trochlea after supracondylar humerus fractures: 1 fracture was casted, 1 was splinted, and 1 underwent closed reduction and pinning. Radiographic abnormality was noted at 5 years, 1 year, and 9 months, respectively. These authors explained the dissolution as a vascular phenomenon. Interruption of the medial or lateral vessels supplying the cartilage of the trochlea would lead to the central necrosis pattern seen in their 3 cases. In addition, the rapid onset in Morrissy and Wilkin’s second and third cases (both 7 years old) supports a vascular etiology.⁵ 

A more recent study of 6 cases found dissolution of the trochlea occurred as a result of severe displaced supracondylar fractures.⁶ Four of the 6 cases involved nerve injuries. Evidence of fishtail deformity was delayed from fracture time until 7 to 8 years of age, consistent with the ossification of the trochlea. Additionally, MRI findings, as well as loose body formation, added to the plausibility of AVN.⁶

Haraldsson⁷ demonstrated the 2 main sources of blood supply to the medial crista of the trochlea. The lateral vessels are intra-articular and supply the apex and lateral aspect of the trochlea. The medial vessels supply the medial aspect of the medial crista of the trochlea and are extra-articular. The lateral and medial vessels do not have an anastomosis between them (Figure 6).⁷ Disruption of the lateral vessels results in a type A deformity; disruption of the lateral and medial vessels results in a type B deformity. Displaced supracondylar humerus fractures disrupt the periosteum and can result in disruption of the medial and/or lateral vessels, resulting in AVN and deformity.

Another case of AVN of the trochlea after a Gartland type I fracture was reported by Schulte and Ramseier.⁸ Similar to our case 3, the patient developed type A AVN of the distal humerus,⁹ illustrating an interruption of the lateral, intra-articular vessels. The etiology of vascular disruption in these nondisplaced supracondylar humerus fractures is less clear, but we propose that tamponade may play a role. Nondisplaced fractures result in a fracture hematoma contained in an intact capsule, having the potential to increase pressures and lead to occlusion of the lateral, intra-articular vessels. This would result in a type A deformity. Nondisplaced supracondylar humerus fractures are common, and this complication is very rare. Typically, they would be expected to generate modest fracture hematoma. However, patient factors, such as bleeding disorders or anatomic variants, including a constricted capsule, could predispose patients to development of increased intracapsular pressure. In contrast, Gartland type II and III fractures, although higher-energy, presumably tear the surrounding capsule leading to release of the fracture hematoma. We do not have direct evidence to support this theory, but measurement of intracapsular pressures could help support or refute the occurrence of tamponade. Similar studies have been reported in hip fracture and slipped capital femoral epiphysis, in which hematoma has been shown to increase intracapsular pressure.^8,10 This pressure increase can theoretically cause a tamponade of the femoral head blood supply leading to AVN. Additional alternate explanations for AVN of the trochlea after type I fractures may include a rare occurrence of direct trauma to the vessels at the moment of fracture, increased intracapsular pressure from cast positioning, or that they are unrelated events that occurred in the same elbow (because atraumatic AVN has also been reported).

Conclusion

Avascular necrosis of the trochlea is a rare but important complication of supracondylar humerus fractures. Generally, this complication has a late clinical presentation, and its cause is interruption of the trochlea blood supply. In displaced fractures, the medial and/or lateral vessels are injured, leading to Gartland type A or type B deformity. In nondisplaced fractures, the lateral vessels are affected. We propose that the lateral vessels may be interrupted by tamponade caused by encased fracture hematoma; this presents as a type A deformity. Both type A and type B deformities can be clinically significant. Avascular necrosis of the trochlea should be considered in patients with late presentation of pain or loss of motion after treatment of supracondylar humerus fractures.

Supracondylar humerus fractures, which are the most common elbow fractures in the pediatric population, account for approximately 3% of all pediatric fractures.¹ Complications of the injury or surgery include pin migration (2%), pin-site infection (1%), malunion, loss of reduction, compartment syndrome, nerve injury, and cubitus varus.¹ A less frequently reported complication is avascular necrosis (AVN) of the trochlea.

First reported in 1948, posttraumatic deformity of the trochlea has appeared sparingly throughout the literature.² This complication has been reported in varying fracture patterns and degrees of injury. The exact incidence is unknown because AVN of the humerus can occur without known trauma. The etiology of the deformity is thought to be interruption of the blood supply of the trochlea. Patterns include type A (AVN of the lateral ossification center) and type B (AVN of the entire medial crista along with a metaphyseal portion). Type A necrosis leads to early degenerative joint disease and loss of range of motion (ROM); angular deformities are uncommon. Type B AVN results in a progressive varus deformity of the trochlea.³ The deformities typically worsen as the child ages. Late-onset ulnar neuropathy can be seen, as medial condyle hypoplasia allows the ulnar nerve to move anterior with the medial head of the triceps. Treatment options address the sequelae and include observation, muscle strengthening, supracondylar osteotomy, and ulnar nerve transposition. Arthroscopic joint débridement has been shown, in short-term follow-up, to relieve pain and restore motion.⁴

We present 5 cases of AVN of the trochlea after supracondylar humerus fractures to highlight this unusual complication. Unlike more common complications of supracondylar humerus fractures, AVN of the trochlea can be a late clinical finding. We speculate that, in cases resulting from nondisplaced fractures, tamponade from fracture hematoma may play a role. It is important to keep this complication in the differential diagnosis of patients with a history of a supracondylar humerus fracture and unexplained elbow motion loss or pain. 

Case Reports 

Retrospective data were collected for all patients after approval by the institutional review board at our institution. Patients were identified by a computerized search using the Current Procedural Terminology code for closed reduction percutaneous pinning of supracondylar humerus fracture. The search was limited to patients treated at our institution from 2000 to 2012; 1159 patients were initially identified. Three patients were found to have postoperative AVN of the trochlea; 2 other patients were treated at an outside hospital and were identified by surgeon recall. These 5 cases are presented here.

Case 1

A girl aged 5 years, 3 months sustained a Gartland type III supracondylar humerus fracture. She was originally seen at an outside facility and transferred to our tertiary care facility for definitive management. She underwent closed reduction and fixation with 3 lateral-based pins 1 day after her injury. Her pins and cast were removed 22 days postoperatively. She returned to full elbow function after her fracture care; 6 months later, she returned to the clinic with painless, decreased flexion of her elbow to 95º. Radiographs showed a lucency of the trochlea extending into the metaphysis (Figure 1). Thirteen months postoperatively, her examination was unchanged with motion at 0º to 95º; her radiographs showed a persistent lateral and medial lucency of the trochlea consistent with type B AVN involving the medial crista.

Case 2

An 8-year-old girl sustained a Gartland type III supracondylar humerus fracture that was treated at an outside facility with closed reduction and fixation with lateral pins. She had an uneventful postoperative course with painless return of motion. She presented 6 months after her surgery with progressive decreased ROM. She underwent conservative treatment with therapy and stretching without much improvement. She presented to our institution 4 years postoperatively with painless decreased motion from 40º to 110º. Radiographs showed dissolution of the lateral ossification center of the trochlea with a fishtail deformity consistent with type A AVN. Magnetic resonance imaging (MRI) confirmed AVN of the trochlea (Figure 2). 

Case 3

A girl aged 5 years, 6 months sustained a Gartland type I supracondylar humerus fracture that was treated uneventfully by casting. She did not have a reduction or manipulation and healed without complications. She returned to the clinic 3 years after the injury complaining of intermittent elbow pain, neglect, and loss of motion. Her ROM was 0º to 110º. Radiographs showed dissolution of the lateral trochlea with sclerosis of the metaphysis consistent with a type A deformity (Figure 3). Contralateral radiographs were not obtained. MRI confirmed AVN of the trochlea. 

Case 4

A 10-year-old girl sustained a Gartland type III supracondylar humerus fracture treated with closed reduction and pinning at an outside facility. She experienced full return to function postoperatively until developing stiffness and popping 1 year after surgery. She was evaluated at our institution 5 years postoperatively with elbow popping in full extension. Radiographs showed a type A deformity; MRI confirmed the diagnosis of AVN of the humerus (Figure 4). She underwent elbow arthroscopy with débridement of a posterior cartilage flap and synovial band. After elbow arthroscopy and débridement, she had resolution of symptoms with full elbow ROM.

Case 5

A 5-year-old boy sustained a Gartland III supracondylar humerus fracture that was treated with closed reduction and pinning at our institution. He had full return of painless motion postoperatively. Seven years after surgery, he presented with popping sensation in his elbow. Examination showed a 5º lack of full extension without effusion or crepitus. Radiographs showed a type A deformity with dissolution of the lateral ossification center (Figure 5).

Discussion

Avascular necrosis of the trochlea after supracondylar humerus fractures was first reported by McDonnell and Wilson in 1948.² Four of 53 patients (7.5%) developed AVN of the trochlea. Clinical presentation happened at 2 to 7 years after injury. No causative effect was given; however, 2 cases of AVN were associated with narrowing of joint space and thinning of articular cartilage. One incident was associated with multiple reduction attempts.² The etiology and exact incidence remain unclear, but both vascular insult and idiopathic growth disturbance have been proposed.⁴

Morrissy and Wilkins⁵ in 1984 reported 3 cases of dissolution of the trochlea after supracondylar humerus fractures: 1 fracture was casted, 1 was splinted, and 1 underwent closed reduction and pinning. Radiographic abnormality was noted at 5 years, 1 year, and 9 months, respectively. These authors explained the dissolution as a vascular phenomenon. Interruption of the medial or lateral vessels supplying the cartilage of the trochlea would lead to the central necrosis pattern seen in their 3 cases. In addition, the rapid onset in Morrissy and Wilkin’s second and third cases (both 7 years old) supports a vascular etiology.⁵ 

A more recent study of 6 cases found dissolution of the trochlea occurred as a result of severe displaced supracondylar fractures.⁶ Four of the 6 cases involved nerve injuries. Evidence of fishtail deformity was delayed from fracture time until 7 to 8 years of age, consistent with the ossification of the trochlea. Additionally, MRI findings, as well as loose body formation, added to the plausibility of AVN.⁶

Haraldsson⁷ demonstrated the 2 main sources of blood supply to the medial crista of the trochlea. The lateral vessels are intra-articular and supply the apex and lateral aspect of the trochlea. The medial vessels supply the medial aspect of the medial crista of the trochlea and are extra-articular. The lateral and medial vessels do not have an anastomosis between them (Figure 6).⁷ Disruption of the lateral vessels results in a type A deformity; disruption of the lateral and medial vessels results in a type B deformity. Displaced supracondylar humerus fractures disrupt the periosteum and can result in disruption of the medial and/or lateral vessels, resulting in AVN and deformity.

Another case of AVN of the trochlea after a Gartland type I fracture was reported by Schulte and Ramseier.⁸ Similar to our case 3, the patient developed type A AVN of the distal humerus,⁹ illustrating an interruption of the lateral, intra-articular vessels. The etiology of vascular disruption in these nondisplaced supracondylar humerus fractures is less clear, but we propose that tamponade may play a role. Nondisplaced fractures result in a fracture hematoma contained in an intact capsule, having the potential to increase pressures and lead to occlusion of the lateral, intra-articular vessels. This would result in a type A deformity. Nondisplaced supracondylar humerus fractures are common, and this complication is very rare. Typically, they would be expected to generate modest fracture hematoma. However, patient factors, such as bleeding disorders or anatomic variants, including a constricted capsule, could predispose patients to development of increased intracapsular pressure. In contrast, Gartland type II and III fractures, although higher-energy, presumably tear the surrounding capsule leading to release of the fracture hematoma. We do not have direct evidence to support this theory, but measurement of intracapsular pressures could help support or refute the occurrence of tamponade. Similar studies have been reported in hip fracture and slipped capital femoral epiphysis, in which hematoma has been shown to increase intracapsular pressure.^8,10 This pressure increase can theoretically cause a tamponade of the femoral head blood supply leading to AVN. Additional alternate explanations for AVN of the trochlea after type I fractures may include a rare occurrence of direct trauma to the vessels at the moment of fracture, increased intracapsular pressure from cast positioning, or that they are unrelated events that occurred in the same elbow (because atraumatic AVN has also been reported).

Conclusion

Avascular necrosis of the trochlea is a rare but important complication of supracondylar humerus fractures. Generally, this complication has a late clinical presentation, and its cause is interruption of the trochlea blood supply. In displaced fractures, the medial and/or lateral vessels are injured, leading to Gartland type A or type B deformity. In nondisplaced fractures, the lateral vessels are affected. We propose that the lateral vessels may be interrupted by tamponade caused by encased fracture hematoma; this presents as a type A deformity. Both type A and type B deformities can be clinically significant. Avascular necrosis of the trochlea should be considered in patients with late presentation of pain or loss of motion after treatment of supracondylar humerus fractures.

Chronic exertional compartment syndrome (CECS) is a common cause of leg pain during exertion in athletic and active-duty populations.¹ It is caused by an increase in intramuscular pressure to a point that the tissues within the involved compartment become ischemic because of a decrease in arteriolar blood flow.² This relative ischemia causes pain and may also be associated with neurologic symptoms. By definition, the pain associated with CECS resolves with rest. Patients typically describe a feeling of fullness or tightness, which eventually evolves into pain as they continue exercising. Pain onset is usually predictable and reproducible after a finite amount of time and/or intensity of exercise.

The differential diagnosis of leg pain during exercise includes CECS, medial tibial stress syndrome, popliteal entrapment syndrome, myopathy, peripheral nerve entrapment syndromes, stress fracture, and effort-induced rhabdomyolysis.³ CECS can be differentiated from other causes of leg pain with measurement of compartment pressures (the standard recommendation).⁴ Compartment pressure measurement, however, is invasive, time-consuming, and painful and may be associated with bleeding risk, infection, and nerve injury. Noninvasive means of testing for CECS (eg, magnetic resonance imaging [MRI], near-infrared spectroscopy [NIRS], thallium stress testing) remain experimental and expensive and are not easily accessible at all institutions.^5-8 While invasive compartment pressure (ICP) testing remains an important tool in the diagnosis of CECS, its criteria and execution vary considerably. Aweid and colleagues⁴ performed a meta-analysis of use of ICP testing in the diagnosis of CECS and concluded that, though elevated ICP measurements are accepted as the gold standard for diagnosing CECS, the criteria outlined for a positive test lack high-level supporting evidence. In addition, how the test is performed has been inconsistent across studies—further clouding the literature.⁴

The review by Aweid and colleagues⁴ highlights the deficiencies in diagnosing CECS by ICP testing. In clinical practice, ICP testing is challenging for both the patient and physician. As other validated, less-invasive tests are lacking, emphasis should remain on the history and the physical examination. Although all athletic populations are at risk for CECS, the active-duty military population is at particularly high risk because of the physical requirements and demands of military service.^1,9

We surveyed military orthopedic surgeons to investigate the clinical practice of performing ICP testing in patients with suspected CECS. We hypothesized that the rate of ICP testing among military orthopedic surgeons would not be 100% for patients with the typical signs and symptoms of CECS.

Materials and Methods

This study was approved by the institutional review board at Wright-Patterson Medical Center at Wright-Patterson Air Force Base in Ohio. A link to an online survey was distributed by email to members of the Society of Military Orthopaedic Surgeons. The anonymous survey polled the surgeons regarding basic demographic data and clinical practice as it pertains to the evaluation and treatment of CECS. No patient-protected health information was obtained. Survey results were compiled in a Microsoft Excel file for analysis.

Results

The survey was distributed to 606 email accounts; the response rate was 19% (114/606). Ninety-one surgeons (80%) indicated they have patients with CECS in their practice (Figure 1). Surgeons were asked how many CECS patients they see per year (responses are summarized in Figure 2) and how many years they have been in practice (Table).

Ninety-three percent of the respondents agreed or strongly agreed that ICP testing is unpleasant for the patient (Figure 3), and 90% would prefer a less-invasive test for confirmatory testing for CECS (Figure 4). Only 13% of respondents indicated they actually use noninvasive modalities (eg, MRI, NIRS) to confirm the diagnosis of CECS (Figure 5).

Respondents were asked about the practice of using ICP testing in the diagnosis of CECS (responses are summarized in Figures 6, 7). Although 85% of respondents agreed or strongly agreed with always confirming the diagnosis of CECS with ICP testing, 39% stated they would recommend surgical treatment without ICP testing if they were confident about the diagnosis based on clinical examination findings.

To better understand the apparent discrepancy between the percentage of surgeons who agreed or strongly agreed with always recommending ICP testing (85%) and the percentage who would recommend treatment without testing (39%), responses were stratified by clinical experience. Surgeons in practice more than 11 years (n = 35) were compared with those in practice 5 years or less (n = 31) (Table). Although the vast majority (85%) of respondents from both groups agreed or strongly agreed with always recommending ICP testing, 49% of those in practice more than 11 years and 29% in practice 5 years or less indicated they would recommend surgical treatment for CECS based solely on clinical examination findings (Figures 8, 9).

Responses were also stratified by number of CECS patients seen by each surgeon per year. Twenty-eight respondents saw 1 or 2 patients per year, and 12 saw more than 8 patients per year—31% and 13% of the total number of respondents, respectively. Of the respondents who saw 1 or 2 patients, 86% (24/28) agreed or strongly agreed with always recommending ICP testing—comparable to the 75% (9/12) who saw more than 8 patients (Figure 10). However, of the respondents who saw 1 or 2 patients, 36% (10/28) indicated they would recommend surgical treatment, without ICP testing, if they were confident about the clinical diagnosis of CECS—in contrast to the 75% (9/12) who saw more than 8 patients (Figure 11).

Discussion

CECS is a common cause of leg pain and a significant cause of disability among the active-duty military population. This was illustrated in 2 recent studies by Waterman and colleagues.^1,9 The first¹ investigated failure rates and disability after surgery for CECS among those on active duty. The authors showed that CECS is a substantial contributor to lower extremity disability in the military population and that there is a substantial risk for persistent symptoms despite surgical treatment. Nearly 1 in 5 patients experienced surgical failure after elective fasciotomy, and about 28% of patients were unable to return to the full activity required in the military. The second, more recent study⁹ was an epidemiologic study of risk factors associated with CECS in a physically active military population. The authors identified 4100 cases diagnosed between 2006 and 2011—representing an overall annual incidence of 0.49 per 1000 at-risk person-years, or about 683 cases per year; the authors also showed the incidence increased during the time period studied.

The diagnosis of CECS remains imperfect. A clinical history of exercise-induced lower leg pain that is relieved with rest suggests the diagnosis, but a confirmatory test is needed to distinguish CECS from other causes of exercise-induced leg pain. Although direct measurement of compartment pressures is the test used most often, it is invasive and time-consuming, can be uncomfortable for the patient, and may be associated with bleeding risk, infection, and nerve injury. Pedowitz and colleagues¹⁰ described the ICP testing criteria now generally used in the diagnosis of CECS. Unfortunately, there is little objective evidence supporting these criteria.⁴ Although less invasive tests (eg, MRI, NIRS) have been described,^5-8 they may not be readily available across institutions, and further study is needed to validate their use in diagnosing CECS.

While an objective, validated test or measurement for confirming the diagnosis of CECS remains elusive, the outcomes after surgical treatment of CECS also remain imperfect. Surgery consists of both open and endoscopically assisted fasciotomy of the involved compartments.^2,11-17 Reports of improvement after treatment range from 81% to 100%³; however, symptom relief does not come for all patients, particularly those in the military. Waterman and colleagues¹ found a failure rate of about 20% among an active-duty military population. Packer and colleagues¹⁸ examined civilians with CECS, treated both operatively and nonoperatively. Patients in this series were diagnosed with CECS based on clinical symptoms as well as compartment pressure measurements according to the Pedowitz criteria. Although overall outcomes were better for operatively treated patients than for nonoperatively treated patients, only 47% of patients were completely pain-free, and 21% were unable to return to full activity.

More recent studies have explored use of other nonoperative treatment modalities. Diebal and colleagues^19,20 used a running retraining program to treat patients with CECS. They based this treatment on the hypothesis that a heel-strike running pattern is associated with increased anterior compartment pressures.²¹ CECS patients who underwent a 6-week systematic treatment program focused on forefoot running, stride shortening, and hamstring activation during push-off experienced a decrease in clinical symptoms and posttreatment intracompartmental pressures.²⁰ The improvements in clinical scores were maintained at 1-year follow-up. Another nonoperative intervention, recently described by Isner-Horobeti and colleagues,²² involves injecting botulinum toxin A (BoNT-A) into the anterior and lateral compartments of the leg. Sixteen patients with CECS received BoNT-A injections. On average, intracompartmental pressures were lower after injection than they were before injection. In addition, exertional pain was eliminated in 15 patients at an average follow-up of 4.4 months.

This survey-based study examined the practice patterns of military orthopedic surgeons who performed ICP testing for cases of suspected CECS. Our hypothesis was that, though ICP testing is the most commonly accepted method for confirming the diagnosis of CECS, the ICP testing rate would not be 100% among those surveyed.

The results of our study uncover an apparent inconsistency in survey responses among physicians who evaluate and treat patients with CECS. About 85% of respondents stated they would always recommend confirming the diagnosis of CECS with ICP testing. However, about 40% stated they would recommend surgical treatment without confirmatory testing if they were confident about the diagnosis based on clinical findings. In other words, only 60% of the respondents disagreed or strongly disagreed with pursuing surgical treatment without testing. One would expect a closer correlation between respondents who would always recommend ICP testing and those who disagreed with recommending surgical treatment without ICP testing. This raises the question of what actually occurs when CECS is suspected in clinical practice.

To better understand the apparent discrepancy between respondents who agreed or strongly agreed with always recommending ICP testing and respondents who would recommend treatment without testing, we grouped responses by clinical experience. Although 85% of respondents (no matter the number of years in practice) agreed or strongly agreed with the statement, “I always recommend confirming the diagnosis of CECS with ICP measurements,” 49% of those in practice more than 11 years (vs. 29% of those in practice 5 years or less) agreed or strongly agreed with recommending surgery without testing if they were 100% confident about the diagnosis of CECS based solely on clinical findings. This may suggest that, though most agreed that the gold standard for confirming the diagnosis of CECS remains ICP testing, those with more clinical experience were more comfortable forgoing this diagnostic measure and recommending treatment without testing.

Another measure of clinical experience used in this survey was based on number of CECS patients seen per year. Responses of surgeons who saw 1 or 2 patients with CECS per year were compared with responses of surgeons who saw more than 8 patients with CECS per year. Of the respondents who saw 1 or 2 patients, 86% agreed or strongly agreed with always recommending ICP testing to confirm CECS—comparable to the 75% who saw more than 8 patients. However, of the respondents who saw 1 or 2 patients, 36% indicated they would recommend surgical treatment, without ICP testing, if they were confident about the clinical diagnosis of CECS—in contrast to the 75% who saw more than 8 patients.

Responses regarding the absolute of always recommending ICP testing and the absolute of being 100% confident about the clinical diagnosis of CECS highlight differences between the surgeons with more experience (>11 years in practice, >8 CECS patients per year) and those with less experience (≤5 years in practice, 1 or 2 CECS patients per year). Surgeons in practice longer, and surgeons who saw more patients with suspected CECS per year, were more likely to recommend surgical treatment based solely on clinical findings.

Conclusion

CECS can cause debilitating activity-related leg pain in both civilian and military populations. Treatment with fasciotomy is often curative, but a significant number of patients may continue to have pain and disability. As the incidence of treatment failures may be higher in the military than in civilians, proper evaluation of patients with suspected CECS is particularly important for military orthopedic surgeons. The diagnosis of CECS can be challenging to both the clinician and patient, and diagnostic modalities remain imperfect. The results of this study highlight this, revealing less than 100% agreement regarding use of ICP testing (the gold standard) for diagnosis of CECS.

This study also highlights the need for an improved method of diagnosing CECS since 93% of respondents agreed or strongly agreed that ICP testing is unpleasant for the patient, and 90% would prefer a less-invasive test. In addition, the ICP testing criteria for establishing the diagnosis of CECS remain inconsistent. If a reliable, consistent, and less-invasive test were available, perhaps there would be less variability in practitioners’ evaluations of patients with CECS.

This study shows an inconsistency among military orthopedic surgeons evaluating and treating patients with CECS. As testing modalities for CECS remain imperfect, clinical acumen and experience assume an important role in the assessment of patients with suspected CECS.

Chronic exertional compartment syndrome (CECS) is a common cause of leg pain during exertion in athletic and active-duty populations.¹ It is caused by an increase in intramuscular pressure to a point that the tissues within the involved compartment become ischemic because of a decrease in arteriolar blood flow.² This relative ischemia causes pain and may also be associated with neurologic symptoms. By definition, the pain associated with CECS resolves with rest. Patients typically describe a feeling of fullness or tightness, which eventually evolves into pain as they continue exercising. Pain onset is usually predictable and reproducible after a finite amount of time and/or intensity of exercise.

The differential diagnosis of leg pain during exercise includes CECS, medial tibial stress syndrome, popliteal entrapment syndrome, myopathy, peripheral nerve entrapment syndromes, stress fracture, and effort-induced rhabdomyolysis.³ CECS can be differentiated from other causes of leg pain with measurement of compartment pressures (the standard recommendation).⁴ Compartment pressure measurement, however, is invasive, time-consuming, and painful and may be associated with bleeding risk, infection, and nerve injury. Noninvasive means of testing for CECS (eg, magnetic resonance imaging [MRI], near-infrared spectroscopy [NIRS], thallium stress testing) remain experimental and expensive and are not easily accessible at all institutions.^5-8 While invasive compartment pressure (ICP) testing remains an important tool in the diagnosis of CECS, its criteria and execution vary considerably. Aweid and colleagues⁴ performed a meta-analysis of use of ICP testing in the diagnosis of CECS and concluded that, though elevated ICP measurements are accepted as the gold standard for diagnosing CECS, the criteria outlined for a positive test lack high-level supporting evidence. In addition, how the test is performed has been inconsistent across studies—further clouding the literature.⁴

The review by Aweid and colleagues⁴ highlights the deficiencies in diagnosing CECS by ICP testing. In clinical practice, ICP testing is challenging for both the patient and physician. As other validated, less-invasive tests are lacking, emphasis should remain on the history and the physical examination. Although all athletic populations are at risk for CECS, the active-duty military population is at particularly high risk because of the physical requirements and demands of military service.^1,9

We surveyed military orthopedic surgeons to investigate the clinical practice of performing ICP testing in patients with suspected CECS. We hypothesized that the rate of ICP testing among military orthopedic surgeons would not be 100% for patients with the typical signs and symptoms of CECS.

Materials and Methods

This study was approved by the institutional review board at Wright-Patterson Medical Center at Wright-Patterson Air Force Base in Ohio. A link to an online survey was distributed by email to members of the Society of Military Orthopaedic Surgeons. The anonymous survey polled the surgeons regarding basic demographic data and clinical practice as it pertains to the evaluation and treatment of CECS. No patient-protected health information was obtained. Survey results were compiled in a Microsoft Excel file for analysis.

Results

The survey was distributed to 606 email accounts; the response rate was 19% (114/606). Ninety-one surgeons (80%) indicated they have patients with CECS in their practice (Figure 1). Surgeons were asked how many CECS patients they see per year (responses are summarized in Figure 2) and how many years they have been in practice (Table).

Ninety-three percent of the respondents agreed or strongly agreed that ICP testing is unpleasant for the patient (Figure 3), and 90% would prefer a less-invasive test for confirmatory testing for CECS (Figure 4). Only 13% of respondents indicated they actually use noninvasive modalities (eg, MRI, NIRS) to confirm the diagnosis of CECS (Figure 5).

Respondents were asked about the practice of using ICP testing in the diagnosis of CECS (responses are summarized in Figures 6, 7). Although 85% of respondents agreed or strongly agreed with always confirming the diagnosis of CECS with ICP testing, 39% stated they would recommend surgical treatment without ICP testing if they were confident about the diagnosis based on clinical examination findings.

To better understand the apparent discrepancy between the percentage of surgeons who agreed or strongly agreed with always recommending ICP testing (85%) and the percentage who would recommend treatment without testing (39%), responses were stratified by clinical experience. Surgeons in practice more than 11 years (n = 35) were compared with those in practice 5 years or less (n = 31) (Table). Although the vast majority (85%) of respondents from both groups agreed or strongly agreed with always recommending ICP testing, 49% of those in practice more than 11 years and 29% in practice 5 years or less indicated they would recommend surgical treatment for CECS based solely on clinical examination findings (Figures 8, 9).

Responses were also stratified by number of CECS patients seen by each surgeon per year. Twenty-eight respondents saw 1 or 2 patients per year, and 12 saw more than 8 patients per year—31% and 13% of the total number of respondents, respectively. Of the respondents who saw 1 or 2 patients, 86% (24/28) agreed or strongly agreed with always recommending ICP testing—comparable to the 75% (9/12) who saw more than 8 patients (Figure 10). However, of the respondents who saw 1 or 2 patients, 36% (10/28) indicated they would recommend surgical treatment, without ICP testing, if they were confident about the clinical diagnosis of CECS—in contrast to the 75% (9/12) who saw more than 8 patients (Figure 11).

Discussion

CECS is a common cause of leg pain and a significant cause of disability among the active-duty military population. This was illustrated in 2 recent studies by Waterman and colleagues.^1,9 The first¹ investigated failure rates and disability after surgery for CECS among those on active duty. The authors showed that CECS is a substantial contributor to lower extremity disability in the military population and that there is a substantial risk for persistent symptoms despite surgical treatment. Nearly 1 in 5 patients experienced surgical failure after elective fasciotomy, and about 28% of patients were unable to return to the full activity required in the military. The second, more recent study⁹ was an epidemiologic study of risk factors associated with CECS in a physically active military population. The authors identified 4100 cases diagnosed between 2006 and 2011—representing an overall annual incidence of 0.49 per 1000 at-risk person-years, or about 683 cases per year; the authors also showed the incidence increased during the time period studied.

The diagnosis of CECS remains imperfect. A clinical history of exercise-induced lower leg pain that is relieved with rest suggests the diagnosis, but a confirmatory test is needed to distinguish CECS from other causes of exercise-induced leg pain. Although direct measurement of compartment pressures is the test used most often, it is invasive and time-consuming, can be uncomfortable for the patient, and may be associated with bleeding risk, infection, and nerve injury. Pedowitz and colleagues¹⁰ described the ICP testing criteria now generally used in the diagnosis of CECS. Unfortunately, there is little objective evidence supporting these criteria.⁴ Although less invasive tests (eg, MRI, NIRS) have been described,^5-8 they may not be readily available across institutions, and further study is needed to validate their use in diagnosing CECS.

While an objective, validated test or measurement for confirming the diagnosis of CECS remains elusive, the outcomes after surgical treatment of CECS also remain imperfect. Surgery consists of both open and endoscopically assisted fasciotomy of the involved compartments.^2,11-17 Reports of improvement after treatment range from 81% to 100%³; however, symptom relief does not come for all patients, particularly those in the military. Waterman and colleagues¹ found a failure rate of about 20% among an active-duty military population. Packer and colleagues¹⁸ examined civilians with CECS, treated both operatively and nonoperatively. Patients in this series were diagnosed with CECS based on clinical symptoms as well as compartment pressure measurements according to the Pedowitz criteria. Although overall outcomes were better for operatively treated patients than for nonoperatively treated patients, only 47% of patients were completely pain-free, and 21% were unable to return to full activity.

More recent studies have explored use of other nonoperative treatment modalities. Diebal and colleagues^19,20 used a running retraining program to treat patients with CECS. They based this treatment on the hypothesis that a heel-strike running pattern is associated with increased anterior compartment pressures.²¹ CECS patients who underwent a 6-week systematic treatment program focused on forefoot running, stride shortening, and hamstring activation during push-off experienced a decrease in clinical symptoms and posttreatment intracompartmental pressures.²⁰ The improvements in clinical scores were maintained at 1-year follow-up. Another nonoperative intervention, recently described by Isner-Horobeti and colleagues,²² involves injecting botulinum toxin A (BoNT-A) into the anterior and lateral compartments of the leg. Sixteen patients with CECS received BoNT-A injections. On average, intracompartmental pressures were lower after injection than they were before injection. In addition, exertional pain was eliminated in 15 patients at an average follow-up of 4.4 months.

This survey-based study examined the practice patterns of military orthopedic surgeons who performed ICP testing for cases of suspected CECS. Our hypothesis was that, though ICP testing is the most commonly accepted method for confirming the diagnosis of CECS, the ICP testing rate would not be 100% among those surveyed.

The results of our study uncover an apparent inconsistency in survey responses among physicians who evaluate and treat patients with CECS. About 85% of respondents stated they would always recommend confirming the diagnosis of CECS with ICP testing. However, about 40% stated they would recommend surgical treatment without confirmatory testing if they were confident about the diagnosis based on clinical findings. In other words, only 60% of the respondents disagreed or strongly disagreed with pursuing surgical treatment without testing. One would expect a closer correlation between respondents who would always recommend ICP testing and those who disagreed with recommending surgical treatment without ICP testing. This raises the question of what actually occurs when CECS is suspected in clinical practice.

To better understand the apparent discrepancy between respondents who agreed or strongly agreed with always recommending ICP testing and respondents who would recommend treatment without testing, we grouped responses by clinical experience. Although 85% of respondents (no matter the number of years in practice) agreed or strongly agreed with the statement, “I always recommend confirming the diagnosis of CECS with ICP measurements,” 49% of those in practice more than 11 years (vs. 29% of those in practice 5 years or less) agreed or strongly agreed with recommending surgery without testing if they were 100% confident about the diagnosis of CECS based solely on clinical findings. This may suggest that, though most agreed that the gold standard for confirming the diagnosis of CECS remains ICP testing, those with more clinical experience were more comfortable forgoing this diagnostic measure and recommending treatment without testing.

Another measure of clinical experience used in this survey was based on number of CECS patients seen per year. Responses of surgeons who saw 1 or 2 patients with CECS per year were compared with responses of surgeons who saw more than 8 patients with CECS per year. Of the respondents who saw 1 or 2 patients, 86% agreed or strongly agreed with always recommending ICP testing to confirm CECS—comparable to the 75% who saw more than 8 patients. However, of the respondents who saw 1 or 2 patients, 36% indicated they would recommend surgical treatment, without ICP testing, if they were confident about the clinical diagnosis of CECS—in contrast to the 75% who saw more than 8 patients.

Responses regarding the absolute of always recommending ICP testing and the absolute of being 100% confident about the clinical diagnosis of CECS highlight differences between the surgeons with more experience (>11 years in practice, >8 CECS patients per year) and those with less experience (≤5 years in practice, 1 or 2 CECS patients per year). Surgeons in practice longer, and surgeons who saw more patients with suspected CECS per year, were more likely to recommend surgical treatment based solely on clinical findings.

Conclusion

CECS can cause debilitating activity-related leg pain in both civilian and military populations. Treatment with fasciotomy is often curative, but a significant number of patients may continue to have pain and disability. As the incidence of treatment failures may be higher in the military than in civilians, proper evaluation of patients with suspected CECS is particularly important for military orthopedic surgeons. The diagnosis of CECS can be challenging to both the clinician and patient, and diagnostic modalities remain imperfect. The results of this study highlight this, revealing less than 100% agreement regarding use of ICP testing (the gold standard) for diagnosis of CECS.

This study also highlights the need for an improved method of diagnosing CECS since 93% of respondents agreed or strongly agreed that ICP testing is unpleasant for the patient, and 90% would prefer a less-invasive test. In addition, the ICP testing criteria for establishing the diagnosis of CECS remain inconsistent. If a reliable, consistent, and less-invasive test were available, perhaps there would be less variability in practitioners’ evaluations of patients with CECS.

This study shows an inconsistency among military orthopedic surgeons evaluating and treating patients with CECS. As testing modalities for CECS remain imperfect, clinical acumen and experience assume an important role in the assessment of patients with suspected CECS.

Chronic exertional compartment syndrome (CECS) is a common cause of leg pain during exertion in athletic and active-duty populations.¹ It is caused by an increase in intramuscular pressure to a point that the tissues within the involved compartment become ischemic because of a decrease in arteriolar blood flow.² This relative ischemia causes pain and may also be associated with neurologic symptoms. By definition, the pain associated with CECS resolves with rest. Patients typically describe a feeling of fullness or tightness, which eventually evolves into pain as they continue exercising. Pain onset is usually predictable and reproducible after a finite amount of time and/or intensity of exercise.

The differential diagnosis of leg pain during exercise includes CECS, medial tibial stress syndrome, popliteal entrapment syndrome, myopathy, peripheral nerve entrapment syndromes, stress fracture, and effort-induced rhabdomyolysis.³ CECS can be differentiated from other causes of leg pain with measurement of compartment pressures (the standard recommendation).⁴ Compartment pressure measurement, however, is invasive, time-consuming, and painful and may be associated with bleeding risk, infection, and nerve injury. Noninvasive means of testing for CECS (eg, magnetic resonance imaging [MRI], near-infrared spectroscopy [NIRS], thallium stress testing) remain experimental and expensive and are not easily accessible at all institutions.^5-8 While invasive compartment pressure (ICP) testing remains an important tool in the diagnosis of CECS, its criteria and execution vary considerably. Aweid and colleagues⁴ performed a meta-analysis of use of ICP testing in the diagnosis of CECS and concluded that, though elevated ICP measurements are accepted as the gold standard for diagnosing CECS, the criteria outlined for a positive test lack high-level supporting evidence. In addition, how the test is performed has been inconsistent across studies—further clouding the literature.⁴

The review by Aweid and colleagues⁴ highlights the deficiencies in diagnosing CECS by ICP testing. In clinical practice, ICP testing is challenging for both the patient and physician. As other validated, less-invasive tests are lacking, emphasis should remain on the history and the physical examination. Although all athletic populations are at risk for CECS, the active-duty military population is at particularly high risk because of the physical requirements and demands of military service.^1,9

We surveyed military orthopedic surgeons to investigate the clinical practice of performing ICP testing in patients with suspected CECS. We hypothesized that the rate of ICP testing among military orthopedic surgeons would not be 100% for patients with the typical signs and symptoms of CECS.

Materials and Methods

This study was approved by the institutional review board at Wright-Patterson Medical Center at Wright-Patterson Air Force Base in Ohio. A link to an online survey was distributed by email to members of the Society of Military Orthopaedic Surgeons. The anonymous survey polled the surgeons regarding basic demographic data and clinical practice as it pertains to the evaluation and treatment of CECS. No patient-protected health information was obtained. Survey results were compiled in a Microsoft Excel file for analysis.

Results

The survey was distributed to 606 email accounts; the response rate was 19% (114/606). Ninety-one surgeons (80%) indicated they have patients with CECS in their practice (Figure 1). Surgeons were asked how many CECS patients they see per year (responses are summarized in Figure 2) and how many years they have been in practice (Table).

Ninety-three percent of the respondents agreed or strongly agreed that ICP testing is unpleasant for the patient (Figure 3), and 90% would prefer a less-invasive test for confirmatory testing for CECS (Figure 4). Only 13% of respondents indicated they actually use noninvasive modalities (eg, MRI, NIRS) to confirm the diagnosis of CECS (Figure 5).

Respondents were asked about the practice of using ICP testing in the diagnosis of CECS (responses are summarized in Figures 6, 7). Although 85% of respondents agreed or strongly agreed with always confirming the diagnosis of CECS with ICP testing, 39% stated they would recommend surgical treatment without ICP testing if they were confident about the diagnosis based on clinical examination findings.

To better understand the apparent discrepancy between the percentage of surgeons who agreed or strongly agreed with always recommending ICP testing (85%) and the percentage who would recommend treatment without testing (39%), responses were stratified by clinical experience. Surgeons in practice more than 11 years (n = 35) were compared with those in practice 5 years or less (n = 31) (Table). Although the vast majority (85%) of respondents from both groups agreed or strongly agreed with always recommending ICP testing, 49% of those in practice more than 11 years and 29% in practice 5 years or less indicated they would recommend surgical treatment for CECS based solely on clinical examination findings (Figures 8, 9).

Responses were also stratified by number of CECS patients seen by each surgeon per year. Twenty-eight respondents saw 1 or 2 patients per year, and 12 saw more than 8 patients per year—31% and 13% of the total number of respondents, respectively. Of the respondents who saw 1 or 2 patients, 86% (24/28) agreed or strongly agreed with always recommending ICP testing—comparable to the 75% (9/12) who saw more than 8 patients (Figure 10). However, of the respondents who saw 1 or 2 patients, 36% (10/28) indicated they would recommend surgical treatment, without ICP testing, if they were confident about the clinical diagnosis of CECS—in contrast to the 75% (9/12) who saw more than 8 patients (Figure 11).

Discussion

CECS is a common cause of leg pain and a significant cause of disability among the active-duty military population. This was illustrated in 2 recent studies by Waterman and colleagues.^1,9 The first¹ investigated failure rates and disability after surgery for CECS among those on active duty. The authors showed that CECS is a substantial contributor to lower extremity disability in the military population and that there is a substantial risk for persistent symptoms despite surgical treatment. Nearly 1 in 5 patients experienced surgical failure after elective fasciotomy, and about 28% of patients were unable to return to the full activity required in the military. The second, more recent study⁹ was an epidemiologic study of risk factors associated with CECS in a physically active military population. The authors identified 4100 cases diagnosed between 2006 and 2011—representing an overall annual incidence of 0.49 per 1000 at-risk person-years, or about 683 cases per year; the authors also showed the incidence increased during the time period studied.

The diagnosis of CECS remains imperfect. A clinical history of exercise-induced lower leg pain that is relieved with rest suggests the diagnosis, but a confirmatory test is needed to distinguish CECS from other causes of exercise-induced leg pain. Although direct measurement of compartment pressures is the test used most often, it is invasive and time-consuming, can be uncomfortable for the patient, and may be associated with bleeding risk, infection, and nerve injury. Pedowitz and colleagues¹⁰ described the ICP testing criteria now generally used in the diagnosis of CECS. Unfortunately, there is little objective evidence supporting these criteria.⁴ Although less invasive tests (eg, MRI, NIRS) have been described,^5-8 they may not be readily available across institutions, and further study is needed to validate their use in diagnosing CECS.

While an objective, validated test or measurement for confirming the diagnosis of CECS remains elusive, the outcomes after surgical treatment of CECS also remain imperfect. Surgery consists of both open and endoscopically assisted fasciotomy of the involved compartments.^2,11-17 Reports of improvement after treatment range from 81% to 100%³; however, symptom relief does not come for all patients, particularly those in the military. Waterman and colleagues¹ found a failure rate of about 20% among an active-duty military population. Packer and colleagues¹⁸ examined civilians with CECS, treated both operatively and nonoperatively. Patients in this series were diagnosed with CECS based on clinical symptoms as well as compartment pressure measurements according to the Pedowitz criteria. Although overall outcomes were better for operatively treated patients than for nonoperatively treated patients, only 47% of patients were completely pain-free, and 21% were unable to return to full activity.

More recent studies have explored use of other nonoperative treatment modalities. Diebal and colleagues^19,20 used a running retraining program to treat patients with CECS. They based this treatment on the hypothesis that a heel-strike running pattern is associated with increased anterior compartment pressures.²¹ CECS patients who underwent a 6-week systematic treatment program focused on forefoot running, stride shortening, and hamstring activation during push-off experienced a decrease in clinical symptoms and posttreatment intracompartmental pressures.²⁰ The improvements in clinical scores were maintained at 1-year follow-up. Another nonoperative intervention, recently described by Isner-Horobeti and colleagues,²² involves injecting botulinum toxin A (BoNT-A) into the anterior and lateral compartments of the leg. Sixteen patients with CECS received BoNT-A injections. On average, intracompartmental pressures were lower after injection than they were before injection. In addition, exertional pain was eliminated in 15 patients at an average follow-up of 4.4 months.

This survey-based study examined the practice patterns of military orthopedic surgeons who performed ICP testing for cases of suspected CECS. Our hypothesis was that, though ICP testing is the most commonly accepted method for confirming the diagnosis of CECS, the ICP testing rate would not be 100% among those surveyed.

The results of our study uncover an apparent inconsistency in survey responses among physicians who evaluate and treat patients with CECS. About 85% of respondents stated they would always recommend confirming the diagnosis of CECS with ICP testing. However, about 40% stated they would recommend surgical treatment without confirmatory testing if they were confident about the diagnosis based on clinical findings. In other words, only 60% of the respondents disagreed or strongly disagreed with pursuing surgical treatment without testing. One would expect a closer correlation between respondents who would always recommend ICP testing and those who disagreed with recommending surgical treatment without ICP testing. This raises the question of what actually occurs when CECS is suspected in clinical practice.

To better understand the apparent discrepancy between respondents who agreed or strongly agreed with always recommending ICP testing and respondents who would recommend treatment without testing, we grouped responses by clinical experience. Although 85% of respondents (no matter the number of years in practice) agreed or strongly agreed with the statement, “I always recommend confirming the diagnosis of CECS with ICP measurements,” 49% of those in practice more than 11 years (vs. 29% of those in practice 5 years or less) agreed or strongly agreed with recommending surgery without testing if they were 100% confident about the diagnosis of CECS based solely on clinical findings. This may suggest that, though most agreed that the gold standard for confirming the diagnosis of CECS remains ICP testing, those with more clinical experience were more comfortable forgoing this diagnostic measure and recommending treatment without testing.

Another measure of clinical experience used in this survey was based on number of CECS patients seen per year. Responses of surgeons who saw 1 or 2 patients with CECS per year were compared with responses of surgeons who saw more than 8 patients with CECS per year. Of the respondents who saw 1 or 2 patients, 86% agreed or strongly agreed with always recommending ICP testing to confirm CECS—comparable to the 75% who saw more than 8 patients. However, of the respondents who saw 1 or 2 patients, 36% indicated they would recommend surgical treatment, without ICP testing, if they were confident about the clinical diagnosis of CECS—in contrast to the 75% who saw more than 8 patients.

Responses regarding the absolute of always recommending ICP testing and the absolute of being 100% confident about the clinical diagnosis of CECS highlight differences between the surgeons with more experience (>11 years in practice, >8 CECS patients per year) and those with less experience (≤5 years in practice, 1 or 2 CECS patients per year). Surgeons in practice longer, and surgeons who saw more patients with suspected CECS per year, were more likely to recommend surgical treatment based solely on clinical findings.

Conclusion

CECS can cause debilitating activity-related leg pain in both civilian and military populations. Treatment with fasciotomy is often curative, but a significant number of patients may continue to have pain and disability. As the incidence of treatment failures may be higher in the military than in civilians, proper evaluation of patients with suspected CECS is particularly important for military orthopedic surgeons. The diagnosis of CECS can be challenging to both the clinician and patient, and diagnostic modalities remain imperfect. The results of this study highlight this, revealing less than 100% agreement regarding use of ICP testing (the gold standard) for diagnosis of CECS.

This study also highlights the need for an improved method of diagnosing CECS since 93% of respondents agreed or strongly agreed that ICP testing is unpleasant for the patient, and 90% would prefer a less-invasive test. In addition, the ICP testing criteria for establishing the diagnosis of CECS remain inconsistent. If a reliable, consistent, and less-invasive test were available, perhaps there would be less variability in practitioners’ evaluations of patients with CECS.

This study shows an inconsistency among military orthopedic surgeons evaluating and treating patients with CECS. As testing modalities for CECS remain imperfect, clinical acumen and experience assume an important role in the assessment of patients with suspected CECS.

Distal biceps tendon ruptures have been reported with increasing frequency, occurring 1.2 times per 100,000 patients per year, representing 3% of tendinous avulsions involving this muscle.^1,2 This injury occurs most commonly in men between the ages of 40 and 60 years, and more often in the dominant extremity after an unexpected or violent eccentric contraction.^2,3 Generally, the patient is performing a task that is more strenuous than usual and only performed occasionally; usually, it is a flexion task. The biceps muscle is the most superficial muscle in the anterior compartment of the arm with the distal tendon passing deep in the antecubital fossa to insert at the radial tuberosity (Figure 1). Pronation of the forearm rotates the radial tuberosity medially and posteriorly, drawing the biceps tendon distally with it (Figures 1-3). The biceps muscle is primarily responsible for supination of the forearm, although it is also important in elbow flexion.^4,5 The bicipital aponeurosis (lacertus fibrosus) arises from the medial aspect of the muscle belly at the junction of the musculotendinous unit and the distal biceps tendon. This passes distally and medially across the antecubital fossa, blending with the fascia overlying the proximal flexor mass of the forearm, and inserts on the subcutaneous border of the ulna.³ A complete rupture of the distal biceps insertion can produce a 40% loss of supination strength, a 47% loss of supination endurance, and a 21% to 30% loss of flexion strength at the elbow when compared with the contralateral intact extremity.^1,2,4 

Background

Prompt diagnosis of a distal biceps tendon complete rupture increases the ability to perform a primary repair, and to restore motion and strength.³ Patients with acute ruptures of the distal biceps typically present with a history of experiencing a painful “pop” after a violent eccentric load force at the time of injury. Clinical examination of a patient with a distal biceps tendon rupture shows a loss of the normal upper arm contour, pain with flexion and supination of the forearm, ecchymosis, and an inability to palpate the distal biceps tendon in the antecubital fossa.⁵ It is important to note that a false-negative test can be elicited when examining the integrity of the muscle contour if the lacertus fibrosus remains intact when there is a complete rupture of the distal biceps tendon.⁶ This false negative also can occur with examination of the upper arm contour as the elbow flexes. Radiographic studies to evaluate the distal biceps tendon can aid in the diagnosis of ruptures but are not a substitute for a thorough history taking and physical examination.³ Plain radiographs may show hypertrophic bone formation at the radial tuberosity, although they are generally unrevealing.^3,6 After a complete clinical examination of the distal biceps tendon, magnetic resonance imaging (MRI) can be an important tool for evaluation of the distal biceps tendon.³ This article introduces a special test used as a diagnostic tool during the physical examination to isolate the distal biceps tendon from the lacertus fibrosus and to evaluate the integrity of the distal biceps brachii tendon. 

Test Description

To perform the supination-pronation test, the patient is positioned with both shoulders abducted to 90º and the elbows flexed to approximately 60º to 70º (Figures 4, 5). The examiner stands in front of the patient and observes the contour of the biceps muscle; the unaffected arm is used as a comparison. The examiner may either visually observe the contour of the muscle or may place a hand on the muscle belly throughout the test to feel for movement. The patient is asked to actively supinate and pronate the forearms by turning the hands. Through trial and error, we have found that the change in contour is most pronounced when placing the elbow in 60º to 70º of flexion. Additionally, through clinical experience, we have found testing the patient with both shoulders abducted to 90º provides the examiner with a reproducible examination that is easy to demonstrate to the patient; however, this shoulder position is not mandatory and can be modified if the patient struggles to get into testing position. Forearm position will maximize the size of the biceps, so the result is visually easier to appreciate. If the distal biceps tendon is intact, there is a substantial change in the shape of the biceps as the arm is supinated (the biceps moves proximally), then pronated (the biceps moves distally). Lack of migration of the biceps muscle during supination and pronation is considered a positive test, indicating rupture of the distal biceps tendon from its insertion on the radial tuberosity (Figure 6). We have found the anatomic correlations to a distal biceps injury may be clearly observed through the maneuver of the supination-pronation test and, therefore, provide a reliable clinical method to diagnose a complete distal biceps tendon rupture.

We have been using the supination-pronation test in our clinical practice for 2.5 years. In our experience, opportunities to use the supination-pronation test are very limited and specific. This type of tendon avulsion is rare, and the number of patients who warrant clinical examination using the supination-pronation test is small. We have had 5 positive supination-pronation tests in patients with suspected distal biceps tendon ruptures. To confirm if the supination-pronation test correctly demonstrated a full biceps tendon rupture in these 5 patients, we followed their clinical examination with MRI of the involved arm. Only 4 of the 5 patients were able to obtain MRI. Of these 4, all studies showed complete tearing of the distal biceps tendon from its attachment on the radial tuberosity. All 5 patients were taken into the operating room to confirm the clinical diagnosis and then repair it surgically. Through surgical exploration, we observed a full and complete tear of the distal biceps tendon in all patients, and the tears were repaired successfully. Postoperatively, all patients showed a full recovery with no complications, and all were able to regain full range of motion and strength in the involved arm. All 5 patients were discharged with no complaints. 

Although we have not encountered false positive and false negatives using the supination-pronation test in clinical practice, we speculate that there would be a low rate of incidence for these outcomes. There is a possibility of a false-positive test in obese patients in whom the contours of the biceps are difficult to appreciate (although we have not observed this clinically). In these patients, the examiner may not see the migration of the biceps that is occurring. In practice, we have found that, if the contours of the bicep are difficult to appreciate, the test can be performed with the examiner placing his/her hand on the muscle belly during the test to actively feel for movement. This could decrease the risk of a false-positive supination-pronation test. A false negative may occur if the distal biceps tendon is almost completely torn. In this case, enough of the tendon fibers may remain intact to pull the biceps muscle belly distally as the hand is pronated. In our experience, this was not observed but should be noted as a potential risk for a false-negative test. 

If the lacertus fibrosus is intact, and the distal biceps tendon is ruptured, the biceps will still change shape as the elbow is flexed and extended but will not change shape with supination and pronation. The biceps brachii muscle attaches distally to the radial tuberosity of the radius; contraction of the muscle pulls the tuberosity anteriorly, rotating the forearm into supination. When the forearm rotates into pronation, the tendon is pulled distally and the muscle lengthens, which causes the contour to be more elongated. Since the lacertus fibrosus attaches to the proximal ulna, it is not involved in forearm supination and pronation. It does, however, assist with elbow flexion. 

It is very important to isolate the biceps brachii tendon from the lacertus fibrosus and the brachialis because the examiner may miss a distal tendon rupture by not isolating supination and pronation. The supination-pronation test is a novel clinical test that allows the examiner to isolate the biceps brachii tendon in supination and pronation to evaluate for distal biceps tendon rupture. It has been well established that early anatomic repair of distal biceps tendon rupture is advocated for optimal results in returning flexion and supination strength.^3,4,6 Although some patients may choose nonoperative management of complete ruptures, prompt diagnosis of the injury is vital so that the option of surgical management at the time of presentation is not compromised by delay in diagnosis. Clinically, we have found that a delayed diagnosis results in more difficulty performing the surgery, and it may not be possible to obtain enough excursion for the biceps to be reattached with the passage of time. The literature suggests that patients with chronic ruptures (more than 4 weeks) often present with proximal retraction of the biceps muscles and scarring to the brachialis, which can make anatomic repair a difficult challenge.^3,7

It is important to note the differences in treatment of proximal versus distal bicep tendon ruptures. Proximally, there are 2 tendon attachments. The tendon of the short head attaches to the coracoid process of the scapula. The tendon of the long head runs into the shoulder joint, attaching intra-articularly to the superior aspect of the glenoid. This tendon is often involved in degeneration concurrently with the adjacent rotator cuff and is vulnerable to rupture. Rupture of this tendon is usually treated nonoperatively. Because proximal rupture nearly always affects only the tendon to the long head, the muscle preserves 1 proximal attachment and continues to function, both as a supinator and as a flexor. Also, this type of rupture tends to occur in more elderly and less active patients who are less adversely affected by the modest loss of function associated with proximal ruptures.

Conclusion

The supination-pronation test properly isolates the distal biceps tendon and does not cause significant discomfort, which can be a problem with other physical examination tests for acute distal biceps ruptures. The squeeze test involves placing the patient in 60º to 80º of elbow flexion with the forearm pronated. The examiner places 1 hand at the distal myotendinous junction, and the other around the belly of the muscle and squeezes, looking for forearm supination.⁵ We have not found the squeeze test to be optimal because the amount of forearm supination obtained by performing this test can be subtle. Additionally, the patient commonly has significant ecchymosis and pain associated with this rupture, and it may be too painful to squeeze the muscle belly hard enough to have a reliable test. Another test is the hook test, which is performed by the examiner “hooking” an index finger under the intact biceps tendon from the lateral side.⁸ Clinically, we have found this test difficult to administer because it requires palpation of the tendon, which is often painful for the patient with an acute injury.

The supination-pronation test can easily be performed in the acute setting, and confirms attachment of the biceps tendon distally to the bicipital tuberosity of the radius. It will not show an incomplete tear, but in that case, the muscle retains its normal length, alleviating the urgency of surgical management. We have found the supination-pronation test to be a reliable and pain-free test that should be incorporated in the physical examination to evaluate patients for distal biceps injury.

Distal biceps tendon ruptures have been reported with increasing frequency, occurring 1.2 times per 100,000 patients per year, representing 3% of tendinous avulsions involving this muscle.^1,2 This injury occurs most commonly in men between the ages of 40 and 60 years, and more often in the dominant extremity after an unexpected or violent eccentric contraction.^2,3 Generally, the patient is performing a task that is more strenuous than usual and only performed occasionally; usually, it is a flexion task. The biceps muscle is the most superficial muscle in the anterior compartment of the arm with the distal tendon passing deep in the antecubital fossa to insert at the radial tuberosity (Figure 1). Pronation of the forearm rotates the radial tuberosity medially and posteriorly, drawing the biceps tendon distally with it (Figures 1-3). The biceps muscle is primarily responsible for supination of the forearm, although it is also important in elbow flexion.^4,5 The bicipital aponeurosis (lacertus fibrosus) arises from the medial aspect of the muscle belly at the junction of the musculotendinous unit and the distal biceps tendon. This passes distally and medially across the antecubital fossa, blending with the fascia overlying the proximal flexor mass of the forearm, and inserts on the subcutaneous border of the ulna.³ A complete rupture of the distal biceps insertion can produce a 40% loss of supination strength, a 47% loss of supination endurance, and a 21% to 30% loss of flexion strength at the elbow when compared with the contralateral intact extremity.^1,2,4 

Background

Prompt diagnosis of a distal biceps tendon complete rupture increases the ability to perform a primary repair, and to restore motion and strength.³ Patients with acute ruptures of the distal biceps typically present with a history of experiencing a painful “pop” after a violent eccentric load force at the time of injury. Clinical examination of a patient with a distal biceps tendon rupture shows a loss of the normal upper arm contour, pain with flexion and supination of the forearm, ecchymosis, and an inability to palpate the distal biceps tendon in the antecubital fossa.⁵ It is important to note that a false-negative test can be elicited when examining the integrity of the muscle contour if the lacertus fibrosus remains intact when there is a complete rupture of the distal biceps tendon.⁶ This false negative also can occur with examination of the upper arm contour as the elbow flexes. Radiographic studies to evaluate the distal biceps tendon can aid in the diagnosis of ruptures but are not a substitute for a thorough history taking and physical examination.³ Plain radiographs may show hypertrophic bone formation at the radial tuberosity, although they are generally unrevealing.^3,6 After a complete clinical examination of the distal biceps tendon, magnetic resonance imaging (MRI) can be an important tool for evaluation of the distal biceps tendon.³ This article introduces a special test used as a diagnostic tool during the physical examination to isolate the distal biceps tendon from the lacertus fibrosus and to evaluate the integrity of the distal biceps brachii tendon. 

Test Description

To perform the supination-pronation test, the patient is positioned with both shoulders abducted to 90º and the elbows flexed to approximately 60º to 70º (Figures 4, 5). The examiner stands in front of the patient and observes the contour of the biceps muscle; the unaffected arm is used as a comparison. The examiner may either visually observe the contour of the muscle or may place a hand on the muscle belly throughout the test to feel for movement. The patient is asked to actively supinate and pronate the forearms by turning the hands. Through trial and error, we have found that the change in contour is most pronounced when placing the elbow in 60º to 70º of flexion. Additionally, through clinical experience, we have found testing the patient with both shoulders abducted to 90º provides the examiner with a reproducible examination that is easy to demonstrate to the patient; however, this shoulder position is not mandatory and can be modified if the patient struggles to get into testing position. Forearm position will maximize the size of the biceps, so the result is visually easier to appreciate. If the distal biceps tendon is intact, there is a substantial change in the shape of the biceps as the arm is supinated (the biceps moves proximally), then pronated (the biceps moves distally). Lack of migration of the biceps muscle during supination and pronation is considered a positive test, indicating rupture of the distal biceps tendon from its insertion on the radial tuberosity (Figure 6). We have found the anatomic correlations to a distal biceps injury may be clearly observed through the maneuver of the supination-pronation test and, therefore, provide a reliable clinical method to diagnose a complete distal biceps tendon rupture.

We have been using the supination-pronation test in our clinical practice for 2.5 years. In our experience, opportunities to use the supination-pronation test are very limited and specific. This type of tendon avulsion is rare, and the number of patients who warrant clinical examination using the supination-pronation test is small. We have had 5 positive supination-pronation tests in patients with suspected distal biceps tendon ruptures. To confirm if the supination-pronation test correctly demonstrated a full biceps tendon rupture in these 5 patients, we followed their clinical examination with MRI of the involved arm. Only 4 of the 5 patients were able to obtain MRI. Of these 4, all studies showed complete tearing of the distal biceps tendon from its attachment on the radial tuberosity. All 5 patients were taken into the operating room to confirm the clinical diagnosis and then repair it surgically. Through surgical exploration, we observed a full and complete tear of the distal biceps tendon in all patients, and the tears were repaired successfully. Postoperatively, all patients showed a full recovery with no complications, and all were able to regain full range of motion and strength in the involved arm. All 5 patients were discharged with no complaints. 

Although we have not encountered false positive and false negatives using the supination-pronation test in clinical practice, we speculate that there would be a low rate of incidence for these outcomes. There is a possibility of a false-positive test in obese patients in whom the contours of the biceps are difficult to appreciate (although we have not observed this clinically). In these patients, the examiner may not see the migration of the biceps that is occurring. In practice, we have found that, if the contours of the bicep are difficult to appreciate, the test can be performed with the examiner placing his/her hand on the muscle belly during the test to actively feel for movement. This could decrease the risk of a false-positive supination-pronation test. A false negative may occur if the distal biceps tendon is almost completely torn. In this case, enough of the tendon fibers may remain intact to pull the biceps muscle belly distally as the hand is pronated. In our experience, this was not observed but should be noted as a potential risk for a false-negative test. 

If the lacertus fibrosus is intact, and the distal biceps tendon is ruptured, the biceps will still change shape as the elbow is flexed and extended but will not change shape with supination and pronation. The biceps brachii muscle attaches distally to the radial tuberosity of the radius; contraction of the muscle pulls the tuberosity anteriorly, rotating the forearm into supination. When the forearm rotates into pronation, the tendon is pulled distally and the muscle lengthens, which causes the contour to be more elongated. Since the lacertus fibrosus attaches to the proximal ulna, it is not involved in forearm supination and pronation. It does, however, assist with elbow flexion. 

It is very important to isolate the biceps brachii tendon from the lacertus fibrosus and the brachialis because the examiner may miss a distal tendon rupture by not isolating supination and pronation. The supination-pronation test is a novel clinical test that allows the examiner to isolate the biceps brachii tendon in supination and pronation to evaluate for distal biceps tendon rupture. It has been well established that early anatomic repair of distal biceps tendon rupture is advocated for optimal results in returning flexion and supination strength.^3,4,6 Although some patients may choose nonoperative management of complete ruptures, prompt diagnosis of the injury is vital so that the option of surgical management at the time of presentation is not compromised by delay in diagnosis. Clinically, we have found that a delayed diagnosis results in more difficulty performing the surgery, and it may not be possible to obtain enough excursion for the biceps to be reattached with the passage of time. The literature suggests that patients with chronic ruptures (more than 4 weeks) often present with proximal retraction of the biceps muscles and scarring to the brachialis, which can make anatomic repair a difficult challenge.^3,7

It is important to note the differences in treatment of proximal versus distal bicep tendon ruptures. Proximally, there are 2 tendon attachments. The tendon of the short head attaches to the coracoid process of the scapula. The tendon of the long head runs into the shoulder joint, attaching intra-articularly to the superior aspect of the glenoid. This tendon is often involved in degeneration concurrently with the adjacent rotator cuff and is vulnerable to rupture. Rupture of this tendon is usually treated nonoperatively. Because proximal rupture nearly always affects only the tendon to the long head, the muscle preserves 1 proximal attachment and continues to function, both as a supinator and as a flexor. Also, this type of rupture tends to occur in more elderly and less active patients who are less adversely affected by the modest loss of function associated with proximal ruptures.

Conclusion

The supination-pronation test properly isolates the distal biceps tendon and does not cause significant discomfort, which can be a problem with other physical examination tests for acute distal biceps ruptures. The squeeze test involves placing the patient in 60º to 80º of elbow flexion with the forearm pronated. The examiner places 1 hand at the distal myotendinous junction, and the other around the belly of the muscle and squeezes, looking for forearm supination.⁵ We have not found the squeeze test to be optimal because the amount of forearm supination obtained by performing this test can be subtle. Additionally, the patient commonly has significant ecchymosis and pain associated with this rupture, and it may be too painful to squeeze the muscle belly hard enough to have a reliable test. Another test is the hook test, which is performed by the examiner “hooking” an index finger under the intact biceps tendon from the lateral side.⁸ Clinically, we have found this test difficult to administer because it requires palpation of the tendon, which is often painful for the patient with an acute injury.

The supination-pronation test can easily be performed in the acute setting, and confirms attachment of the biceps tendon distally to the bicipital tuberosity of the radius. It will not show an incomplete tear, but in that case, the muscle retains its normal length, alleviating the urgency of surgical management. We have found the supination-pronation test to be a reliable and pain-free test that should be incorporated in the physical examination to evaluate patients for distal biceps injury.

Distal biceps tendon ruptures have been reported with increasing frequency, occurring 1.2 times per 100,000 patients per year, representing 3% of tendinous avulsions involving this muscle.^1,2 This injury occurs most commonly in men between the ages of 40 and 60 years, and more often in the dominant extremity after an unexpected or violent eccentric contraction.^2,3 Generally, the patient is performing a task that is more strenuous than usual and only performed occasionally; usually, it is a flexion task. The biceps muscle is the most superficial muscle in the anterior compartment of the arm with the distal tendon passing deep in the antecubital fossa to insert at the radial tuberosity (Figure 1). Pronation of the forearm rotates the radial tuberosity medially and posteriorly, drawing the biceps tendon distally with it (Figures 1-3). The biceps muscle is primarily responsible for supination of the forearm, although it is also important in elbow flexion.^4,5 The bicipital aponeurosis (lacertus fibrosus) arises from the medial aspect of the muscle belly at the junction of the musculotendinous unit and the distal biceps tendon. This passes distally and medially across the antecubital fossa, blending with the fascia overlying the proximal flexor mass of the forearm, and inserts on the subcutaneous border of the ulna.³ A complete rupture of the distal biceps insertion can produce a 40% loss of supination strength, a 47% loss of supination endurance, and a 21% to 30% loss of flexion strength at the elbow when compared with the contralateral intact extremity.^1,2,4 

Background

Prompt diagnosis of a distal biceps tendon complete rupture increases the ability to perform a primary repair, and to restore motion and strength.³ Patients with acute ruptures of the distal biceps typically present with a history of experiencing a painful “pop” after a violent eccentric load force at the time of injury. Clinical examination of a patient with a distal biceps tendon rupture shows a loss of the normal upper arm contour, pain with flexion and supination of the forearm, ecchymosis, and an inability to palpate the distal biceps tendon in the antecubital fossa.⁵ It is important to note that a false-negative test can be elicited when examining the integrity of the muscle contour if the lacertus fibrosus remains intact when there is a complete rupture of the distal biceps tendon.⁶ This false negative also can occur with examination of the upper arm contour as the elbow flexes. Radiographic studies to evaluate the distal biceps tendon can aid in the diagnosis of ruptures but are not a substitute for a thorough history taking and physical examination.³ Plain radiographs may show hypertrophic bone formation at the radial tuberosity, although they are generally unrevealing.^3,6 After a complete clinical examination of the distal biceps tendon, magnetic resonance imaging (MRI) can be an important tool for evaluation of the distal biceps tendon.³ This article introduces a special test used as a diagnostic tool during the physical examination to isolate the distal biceps tendon from the lacertus fibrosus and to evaluate the integrity of the distal biceps brachii tendon. 

Test Description

To perform the supination-pronation test, the patient is positioned with both shoulders abducted to 90º and the elbows flexed to approximately 60º to 70º (Figures 4, 5). The examiner stands in front of the patient and observes the contour of the biceps muscle; the unaffected arm is used as a comparison. The examiner may either visually observe the contour of the muscle or may place a hand on the muscle belly throughout the test to feel for movement. The patient is asked to actively supinate and pronate the forearms by turning the hands. Through trial and error, we have found that the change in contour is most pronounced when placing the elbow in 60º to 70º of flexion. Additionally, through clinical experience, we have found testing the patient with both shoulders abducted to 90º provides the examiner with a reproducible examination that is easy to demonstrate to the patient; however, this shoulder position is not mandatory and can be modified if the patient struggles to get into testing position. Forearm position will maximize the size of the biceps, so the result is visually easier to appreciate. If the distal biceps tendon is intact, there is a substantial change in the shape of the biceps as the arm is supinated (the biceps moves proximally), then pronated (the biceps moves distally). Lack of migration of the biceps muscle during supination and pronation is considered a positive test, indicating rupture of the distal biceps tendon from its insertion on the radial tuberosity (Figure 6). We have found the anatomic correlations to a distal biceps injury may be clearly observed through the maneuver of the supination-pronation test and, therefore, provide a reliable clinical method to diagnose a complete distal biceps tendon rupture.

We have been using the supination-pronation test in our clinical practice for 2.5 years. In our experience, opportunities to use the supination-pronation test are very limited and specific. This type of tendon avulsion is rare, and the number of patients who warrant clinical examination using the supination-pronation test is small. We have had 5 positive supination-pronation tests in patients with suspected distal biceps tendon ruptures. To confirm if the supination-pronation test correctly demonstrated a full biceps tendon rupture in these 5 patients, we followed their clinical examination with MRI of the involved arm. Only 4 of the 5 patients were able to obtain MRI. Of these 4, all studies showed complete tearing of the distal biceps tendon from its attachment on the radial tuberosity. All 5 patients were taken into the operating room to confirm the clinical diagnosis and then repair it surgically. Through surgical exploration, we observed a full and complete tear of the distal biceps tendon in all patients, and the tears were repaired successfully. Postoperatively, all patients showed a full recovery with no complications, and all were able to regain full range of motion and strength in the involved arm. All 5 patients were discharged with no complaints. 

Although we have not encountered false positive and false negatives using the supination-pronation test in clinical practice, we speculate that there would be a low rate of incidence for these outcomes. There is a possibility of a false-positive test in obese patients in whom the contours of the biceps are difficult to appreciate (although we have not observed this clinically). In these patients, the examiner may not see the migration of the biceps that is occurring. In practice, we have found that, if the contours of the bicep are difficult to appreciate, the test can be performed with the examiner placing his/her hand on the muscle belly during the test to actively feel for movement. This could decrease the risk of a false-positive supination-pronation test. A false negative may occur if the distal biceps tendon is almost completely torn. In this case, enough of the tendon fibers may remain intact to pull the biceps muscle belly distally as the hand is pronated. In our experience, this was not observed but should be noted as a potential risk for a false-negative test. 

If the lacertus fibrosus is intact, and the distal biceps tendon is ruptured, the biceps will still change shape as the elbow is flexed and extended but will not change shape with supination and pronation. The biceps brachii muscle attaches distally to the radial tuberosity of the radius; contraction of the muscle pulls the tuberosity anteriorly, rotating the forearm into supination. When the forearm rotates into pronation, the tendon is pulled distally and the muscle lengthens, which causes the contour to be more elongated. Since the lacertus fibrosus attaches to the proximal ulna, it is not involved in forearm supination and pronation. It does, however, assist with elbow flexion. 

It is very important to isolate the biceps brachii tendon from the lacertus fibrosus and the brachialis because the examiner may miss a distal tendon rupture by not isolating supination and pronation. The supination-pronation test is a novel clinical test that allows the examiner to isolate the biceps brachii tendon in supination and pronation to evaluate for distal biceps tendon rupture. It has been well established that early anatomic repair of distal biceps tendon rupture is advocated for optimal results in returning flexion and supination strength.^3,4,6 Although some patients may choose nonoperative management of complete ruptures, prompt diagnosis of the injury is vital so that the option of surgical management at the time of presentation is not compromised by delay in diagnosis. Clinically, we have found that a delayed diagnosis results in more difficulty performing the surgery, and it may not be possible to obtain enough excursion for the biceps to be reattached with the passage of time. The literature suggests that patients with chronic ruptures (more than 4 weeks) often present with proximal retraction of the biceps muscles and scarring to the brachialis, which can make anatomic repair a difficult challenge.^3,7

It is important to note the differences in treatment of proximal versus distal bicep tendon ruptures. Proximally, there are 2 tendon attachments. The tendon of the short head attaches to the coracoid process of the scapula. The tendon of the long head runs into the shoulder joint, attaching intra-articularly to the superior aspect of the glenoid. This tendon is often involved in degeneration concurrently with the adjacent rotator cuff and is vulnerable to rupture. Rupture of this tendon is usually treated nonoperatively. Because proximal rupture nearly always affects only the tendon to the long head, the muscle preserves 1 proximal attachment and continues to function, both as a supinator and as a flexor. Also, this type of rupture tends to occur in more elderly and less active patients who are less adversely affected by the modest loss of function associated with proximal ruptures.

Conclusion

The supination-pronation test properly isolates the distal biceps tendon and does not cause significant discomfort, which can be a problem with other physical examination tests for acute distal biceps ruptures. The squeeze test involves placing the patient in 60º to 80º of elbow flexion with the forearm pronated. The examiner places 1 hand at the distal myotendinous junction, and the other around the belly of the muscle and squeezes, looking for forearm supination.⁵ We have not found the squeeze test to be optimal because the amount of forearm supination obtained by performing this test can be subtle. Additionally, the patient commonly has significant ecchymosis and pain associated with this rupture, and it may be too painful to squeeze the muscle belly hard enough to have a reliable test. Another test is the hook test, which is performed by the examiner “hooking” an index finger under the intact biceps tendon from the lateral side.⁸ Clinically, we have found this test difficult to administer because it requires palpation of the tendon, which is often painful for the patient with an acute injury.

The supination-pronation test can easily be performed in the acute setting, and confirms attachment of the biceps tendon distally to the bicipital tuberosity of the radius. It will not show an incomplete tear, but in that case, the muscle retains its normal length, alleviating the urgency of surgical management. We have found the supination-pronation test to be a reliable and pain-free test that should be incorporated in the physical examination to evaluate patients for distal biceps injury.

In this month’s issue of The American Journal of Orthopedics, Tannenbaum and colleagues present a “5 Points” article on “Measurement of Resource Utilization for Total and Reverse Shoulder Arthroplasty.” This is an excellent article that summarizes the authors’ methodology of determining not only the overall cost of hospital care for shoulder replacement but a detailed analysis of many components contributing to that cost.

The steps are fairly straightforward: identify the various components of the cost, gather the data contributing to those costs, and then analyze what are the major expenditures that contribute to the overall cost. Sounds simple, but, in practice, it is anything but!

As health care expenditures in the United States continue to increase and approach 20% of the gross domestic product, every sector of the health care industry is searching for ways to curtail and eventually decrease the cost of health care. However, one cannot control costs without accurate data that defines those costs. In this article, Tannenbaum and colleagues have provided a methodology to help both hospital administrators and surgeons determine the overall cost of shoulder arthroplasty, but their principles of analysis can be applied to all aspects of hospital care.

Such efforts are gaining the attention of many leaders of the health care industry. For example, in the September 8, 2015, edition of The New York Times, I was very interested to read the article “What are a Hospital’s Costs? Utah System Is Trying to Learn.”¹ The article reviewed the efforts of Dr. Vivian Lee, chief executive at University of Utah Health Care, to determine the actual cost of all care provided by the university hospital, the same goal as the present 5 Points article on shoulder arthroplasty but on a vastly greater scale. Analyzing those costs guided Dr. Lee and her colleagues to alter clinical programs, which led to a decrease of 30% in hospital expenditures and fewer complications.¹

We are all indebted to Mr. Tannenbaum and his coauthors for providing the journal’s readers with a clear map that we can use to both understand and navigate the current maze of hospital costs. Using such a guide, we will be able to gather information that not only saves money, but will improve care by directing resources to services that actually benefit our patients.

In this month’s issue of The American Journal of Orthopedics, Tannenbaum and colleagues present a “5 Points” article on “Measurement of Resource Utilization for Total and Reverse Shoulder Arthroplasty.” This is an excellent article that summarizes the authors’ methodology of determining not only the overall cost of hospital care for shoulder replacement but a detailed analysis of many components contributing to that cost.

The steps are fairly straightforward: identify the various components of the cost, gather the data contributing to those costs, and then analyze what are the major expenditures that contribute to the overall cost. Sounds simple, but, in practice, it is anything but!

As health care expenditures in the United States continue to increase and approach 20% of the gross domestic product, every sector of the health care industry is searching for ways to curtail and eventually decrease the cost of health care. However, one cannot control costs without accurate data that defines those costs. In this article, Tannenbaum and colleagues have provided a methodology to help both hospital administrators and surgeons determine the overall cost of shoulder arthroplasty, but their principles of analysis can be applied to all aspects of hospital care.

Such efforts are gaining the attention of many leaders of the health care industry. For example, in the September 8, 2015, edition of The New York Times, I was very interested to read the article “What are a Hospital’s Costs? Utah System Is Trying to Learn.”¹ The article reviewed the efforts of Dr. Vivian Lee, chief executive at University of Utah Health Care, to determine the actual cost of all care provided by the university hospital, the same goal as the present 5 Points article on shoulder arthroplasty but on a vastly greater scale. Analyzing those costs guided Dr. Lee and her colleagues to alter clinical programs, which led to a decrease of 30% in hospital expenditures and fewer complications.¹

We are all indebted to Mr. Tannenbaum and his coauthors for providing the journal’s readers with a clear map that we can use to both understand and navigate the current maze of hospital costs. Using such a guide, we will be able to gather information that not only saves money, but will improve care by directing resources to services that actually benefit our patients.

In this month’s issue of The American Journal of Orthopedics, Tannenbaum and colleagues present a “5 Points” article on “Measurement of Resource Utilization for Total and Reverse Shoulder Arthroplasty.” This is an excellent article that summarizes the authors’ methodology of determining not only the overall cost of hospital care for shoulder replacement but a detailed analysis of many components contributing to that cost.

The steps are fairly straightforward: identify the various components of the cost, gather the data contributing to those costs, and then analyze what are the major expenditures that contribute to the overall cost. Sounds simple, but, in practice, it is anything but!

As health care expenditures in the United States continue to increase and approach 20% of the gross domestic product, every sector of the health care industry is searching for ways to curtail and eventually decrease the cost of health care. However, one cannot control costs without accurate data that defines those costs. In this article, Tannenbaum and colleagues have provided a methodology to help both hospital administrators and surgeons determine the overall cost of shoulder arthroplasty, but their principles of analysis can be applied to all aspects of hospital care.

Such efforts are gaining the attention of many leaders of the health care industry. For example, in the September 8, 2015, edition of The New York Times, I was very interested to read the article “What are a Hospital’s Costs? Utah System Is Trying to Learn.”¹ The article reviewed the efforts of Dr. Vivian Lee, chief executive at University of Utah Health Care, to determine the actual cost of all care provided by the university hospital, the same goal as the present 5 Points article on shoulder arthroplasty but on a vastly greater scale. Analyzing those costs guided Dr. Lee and her colleagues to alter clinical programs, which led to a decrease of 30% in hospital expenditures and fewer complications.¹

We are all indebted to Mr. Tannenbaum and his coauthors for providing the journal’s readers with a clear map that we can use to both understand and navigate the current maze of hospital costs. Using such a guide, we will be able to gather information that not only saves money, but will improve care by directing resources to services that actually benefit our patients.