Sports Medicine

The patient’s physical examination was unremarkable. His vital signs were normal, and there was no obvious external evidence of trauma. The posterior cervical spine was tender to palpation in the midline, but no step-off signs were appreciated. The neurological examination, including strength and sensation in all four extremities, was normal.

Since the patient’s only complaint was neck pain and his physical examination and history were otherwise normal, the emergency physician (EP) ordered radiographs of the cervical spine. The imaging studies were interpreted as showing advanced degenerative changes but no fractures, and the patient was prescribed an analgesic and discharged home.

When the patient woke up the next morning, he was unable to move his extremities, and returned to the same ED via EMS. He was placed in a cervical collar and found to have flaccid extremities on examination. A computed tomography (CT) scan of the cervical spine revealed a transverse fracture through the C6 vertebra. Radiology services also reviewed the cervical spine X-rays from the previous day, noting the presence of fracture.

The patient was taken to the operating room by neurosurgery services but remained paralyzed postoperatively. He never recovered from his injury and died 6 months later. His family sued the EP and the hospital for missed diagnosis of cervical spine fracture at the first ED presentation and the resulting paralysis. The case was settled for $1.3 million prior to trial.

Discussion

The evaluation of suspected cervical spine injury secondary to blunt trauma is a frequent and important skill practiced by EPs. Motor vehicle accidents are the most common cause of spinal cord injury in the United States (42%), followed by falls (27%), acts of violence (15%), and sports-related injuries (8%).¹ A review by Sekon and Fehlings² showed that 55% of all spinal injuries involve the cervical spine. Interestingly, the majority of cervical spine injuries occur at the upper or lower ends of the cervical spine; C2 vertebral fractures account for 33%, while C6 and C7 vertebral fractures account for approximately 50%.¹

There are two commonly used criteria to clinically clear the cervical spine (ie, no imaging studies necessary) in blunt-trauma patients. The first is the National Emergency X-Radiography Use Study (NEXUS), which has a sensitivity of 99.6% of identifying cervical spine fractures.¹ According to the NEXUS criteria, no imaging studies are required if: (1) there is no midline cervical spine tenderness; (2) there are no focal neurological deficits; (3) the patient exhibits a normal level of alertness; (4) the patient is not intoxicated; and (5) there is no distracting injury.¹

The other set of criteria used to clear the cervical spine is the Canadian Cervical Spine Rule. In these criteria, a patient is considered at very low risk for cervical spine fracture in the following cases: (1) the patient is fully alert with a Glasgow Coma scale of 15; (2) the patient has no high-risk factors (ie, age >65 years, dangerous mechanism of injury, fall greater than five stairs, axial load to the head, high-speed vehicular crash, bicycle or motorcycle crash, or the presence of paresthesias in the extremities); (3) the patient has low-risk factors (eg, simple vehicle crash, sitting position in the ED, ambulatory at any time, delayed onset of neck pain, and the absence of midline cervical tenderness); and (4) the patient can actively rotate his or her neck 45 degrees to the left and to the right. The Canadian group found the above criteria to have 100% sensitivity for predicting the absence of cervical spine injury.¹

The patient in this case failed both sets of criteria (ie, presence of cervical spine tenderness and age >65 years) and therefore required imaging. Historically, cervical spine X-ray (three views, anteroposterior, lateral, and odontoid; or five views, three views plus obliques) has been the imaging study of choice for such patients. Unfortunately, however, cervical spine radiographs have severe limitations in identifying spinal injury. In a large retrospective review, Woodring and Lee,³ found that the standard three-view cervical spine series failed to demonstrate 61% of all fractures and 36% of all subluxation and dislocations. Similarly, in a prospective study of 1,006 patients with 72 injuries, Diaz et al,⁴ found a 52.3% missed fracture rate when five-view radiographs were used to identify cervical spine injury. In addition, radiographic evaluation of elderly patients was found to be even more challenging in identifying cervical spine injury due to age-related degenerative changes.

Given the abovementioned limitations associated with radiographic imaging, CT scan of the cervical spine has become the imaging study of choice in moderate-to-severe risk patients with blunt cervical spine trauma. This modality has been shown to have a higher sensitivity and specificity for evaluating cervical spine injury compared to plain X-ray films, with CT detecting 97% to 100% of cervical spine fractures.⁵

In addition to demonstrating a higher sensitivity, CT also has the advantage of speed—especially when the patient is undergoing other CT studies (eg, head, abdomen, pelvis). While some clinicians criticize the higher cost of CT versus plain films, CT has been shown to decrease institutional costs (when settlement costs are taken into account) due to the reduction of the incidence of paralysis resulting from false-negative imaging studies.⁶

Forgotten Tourniquet

The patient’s vital signs were: blood pressure, 138/82 mm Hg; heart rate, 102 beats/minute; respiratory rate, 18 breaths/minute; temperature 98.6˚F. Oxygen saturation was 99% on room air.

The patient appeared uncomfortable overall. The physical examination was remarkable only for mild left-sided costovertebral angle tenderness. Her abdomen was soft, nontender, and without guarding or rebound.

The EP ordered the placement of an intravenous (IV) line, through which the patient was administered normal saline and morphine and promethazine, respectively, for pain and nausea. A complete blood count, basic metabolic panel, urinalysis, and urine pregnancy test were ordered. All of the laboratory bloodwork results were normal, and the urine pregnancy test was negative. The urinalysis was remarkable for 50 to 100 red blood cells.

A noncontrast CT scan of the abdomen and pelvis revealed a 3-mm ureteral stone on the left side. When the patient returned from radiology services, her pain was significantly decreased and she felt much improved. She was diagnosed with a kidney stone and discharged home with an analgesic and a strainer, along with instructions to follow-up with urology services. The patient was in the ED for a total of 5 hours.

The plaintiff sued the EP and hospital, claiming that the tourniquet used to start the IV line and draw blood was never removed, which in turn caused nerve damage resulting in reflex sympathetic dystrophy and complex regional pain syndrome. The defense denied all of these allegations, and the ED personnel testified that the tourniquet was removed as soon as the IV was established. The defense cited the plaintiff’s medical records, which contained documentation that the tourniquet had been removed. The defense further argued that if the tourniquet had been left on as the patient alleged, she would have experienced obvious physical signs, such as swelling, redness, infiltration of fluids, pain, and numbness. A defense verdict was returned.

Discussion

It is very tempting to simply dismiss this case as absurd, with nothing to be learned from it. It does defy common sense that no one would have noticed the tourniquet or, at the very least, that the patient would not have spoken up about it during her stay in the ED. While the jury clearly came to the correct conclusion,  it does highlight a real problem: forgotten tourniquets.

According to the Pennsylvania Patient Safety Advisory (PPSA), there were 125 reports of tourniquets being left on patients in Pennsylvania healthcare facilities in 1 year alone.¹ In 5% of these cases, the tourniquet was discovered within a half hour of application. In approximately 66% of cases, the tourniquet was left on for up to 2 hours, and the remaining were left in place for 2 to 18 hours.

Few locations within the hospital are without risk for this type of accident. The PPSA further noted that approximately 30% of retained tourniquets occurred on medical/surgical units, 14% in the ED, and 14% on inpatient and ambulatory surgical services departments. Approximately 19% were discovered when patients were transferred from one department to another.¹

In the analysis of these incidents, contributing factors to forgotten tourniquets included staff failing to follow proper procedures, inadequate staff proficiency, and staff distractions and/or interruptions.¹ In addition, some patients appeared to be at increased risk of having a retained tourniquet than others. Sixty percent of 125 patients with a forgotten tourniquet were aged 70 years or older, whereas some patients were younger than age 2 years.¹ Not surprisingly, patients who were unable to verbally communicate (eg, patients who were intubated, under anesthesia, had expressive aphasia, severe dementia), were at the highest risk.

In a review of recovery room incidents, Salman and Asfar² identified two cases of forgotten tourniquets out of approximately 7,000 patients. Potential strategies to avoid this mistake include: (1) only documenting procedures after they have been completed (eg, tourniquet removal); (2) double-checking that the tourniquet has been removed prior to leaving patient bedside; and (3) the use of extra-long tourniquets so the ends are more clearly visible.

The patient’s physical examination was unremarkable. His vital signs were normal, and there was no obvious external evidence of trauma. The posterior cervical spine was tender to palpation in the midline, but no step-off signs were appreciated. The neurological examination, including strength and sensation in all four extremities, was normal.

Since the patient’s only complaint was neck pain and his physical examination and history were otherwise normal, the emergency physician (EP) ordered radiographs of the cervical spine. The imaging studies were interpreted as showing advanced degenerative changes but no fractures, and the patient was prescribed an analgesic and discharged home.

When the patient woke up the next morning, he was unable to move his extremities, and returned to the same ED via EMS. He was placed in a cervical collar and found to have flaccid extremities on examination. A computed tomography (CT) scan of the cervical spine revealed a transverse fracture through the C6 vertebra. Radiology services also reviewed the cervical spine X-rays from the previous day, noting the presence of fracture.

The patient was taken to the operating room by neurosurgery services but remained paralyzed postoperatively. He never recovered from his injury and died 6 months later. His family sued the EP and the hospital for missed diagnosis of cervical spine fracture at the first ED presentation and the resulting paralysis. The case was settled for $1.3 million prior to trial.

Discussion

The evaluation of suspected cervical spine injury secondary to blunt trauma is a frequent and important skill practiced by EPs. Motor vehicle accidents are the most common cause of spinal cord injury in the United States (42%), followed by falls (27%), acts of violence (15%), and sports-related injuries (8%).¹ A review by Sekon and Fehlings² showed that 55% of all spinal injuries involve the cervical spine. Interestingly, the majority of cervical spine injuries occur at the upper or lower ends of the cervical spine; C2 vertebral fractures account for 33%, while C6 and C7 vertebral fractures account for approximately 50%.¹

There are two commonly used criteria to clinically clear the cervical spine (ie, no imaging studies necessary) in blunt-trauma patients. The first is the National Emergency X-Radiography Use Study (NEXUS), which has a sensitivity of 99.6% of identifying cervical spine fractures.¹ According to the NEXUS criteria, no imaging studies are required if: (1) there is no midline cervical spine tenderness; (2) there are no focal neurological deficits; (3) the patient exhibits a normal level of alertness; (4) the patient is not intoxicated; and (5) there is no distracting injury.¹

The other set of criteria used to clear the cervical spine is the Canadian Cervical Spine Rule. In these criteria, a patient is considered at very low risk for cervical spine fracture in the following cases: (1) the patient is fully alert with a Glasgow Coma scale of 15; (2) the patient has no high-risk factors (ie, age >65 years, dangerous mechanism of injury, fall greater than five stairs, axial load to the head, high-speed vehicular crash, bicycle or motorcycle crash, or the presence of paresthesias in the extremities); (3) the patient has low-risk factors (eg, simple vehicle crash, sitting position in the ED, ambulatory at any time, delayed onset of neck pain, and the absence of midline cervical tenderness); and (4) the patient can actively rotate his or her neck 45 degrees to the left and to the right. The Canadian group found the above criteria to have 100% sensitivity for predicting the absence of cervical spine injury.¹

The patient in this case failed both sets of criteria (ie, presence of cervical spine tenderness and age >65 years) and therefore required imaging. Historically, cervical spine X-ray (three views, anteroposterior, lateral, and odontoid; or five views, three views plus obliques) has been the imaging study of choice for such patients. Unfortunately, however, cervical spine radiographs have severe limitations in identifying spinal injury. In a large retrospective review, Woodring and Lee,³ found that the standard three-view cervical spine series failed to demonstrate 61% of all fractures and 36% of all subluxation and dislocations. Similarly, in a prospective study of 1,006 patients with 72 injuries, Diaz et al,⁴ found a 52.3% missed fracture rate when five-view radiographs were used to identify cervical spine injury. In addition, radiographic evaluation of elderly patients was found to be even more challenging in identifying cervical spine injury due to age-related degenerative changes.

Given the abovementioned limitations associated with radiographic imaging, CT scan of the cervical spine has become the imaging study of choice in moderate-to-severe risk patients with blunt cervical spine trauma. This modality has been shown to have a higher sensitivity and specificity for evaluating cervical spine injury compared to plain X-ray films, with CT detecting 97% to 100% of cervical spine fractures.⁵

In addition to demonstrating a higher sensitivity, CT also has the advantage of speed—especially when the patient is undergoing other CT studies (eg, head, abdomen, pelvis). While some clinicians criticize the higher cost of CT versus plain films, CT has been shown to decrease institutional costs (when settlement costs are taken into account) due to the reduction of the incidence of paralysis resulting from false-negative imaging studies.⁶

Forgotten Tourniquet

The patient’s vital signs were: blood pressure, 138/82 mm Hg; heart rate, 102 beats/minute; respiratory rate, 18 breaths/minute; temperature 98.6˚F. Oxygen saturation was 99% on room air.

The patient appeared uncomfortable overall. The physical examination was remarkable only for mild left-sided costovertebral angle tenderness. Her abdomen was soft, nontender, and without guarding or rebound.

The EP ordered the placement of an intravenous (IV) line, through which the patient was administered normal saline and morphine and promethazine, respectively, for pain and nausea. A complete blood count, basic metabolic panel, urinalysis, and urine pregnancy test were ordered. All of the laboratory bloodwork results were normal, and the urine pregnancy test was negative. The urinalysis was remarkable for 50 to 100 red blood cells.

A noncontrast CT scan of the abdomen and pelvis revealed a 3-mm ureteral stone on the left side. When the patient returned from radiology services, her pain was significantly decreased and she felt much improved. She was diagnosed with a kidney stone and discharged home with an analgesic and a strainer, along with instructions to follow-up with urology services. The patient was in the ED for a total of 5 hours.

The plaintiff sued the EP and hospital, claiming that the tourniquet used to start the IV line and draw blood was never removed, which in turn caused nerve damage resulting in reflex sympathetic dystrophy and complex regional pain syndrome. The defense denied all of these allegations, and the ED personnel testified that the tourniquet was removed as soon as the IV was established. The defense cited the plaintiff’s medical records, which contained documentation that the tourniquet had been removed. The defense further argued that if the tourniquet had been left on as the patient alleged, she would have experienced obvious physical signs, such as swelling, redness, infiltration of fluids, pain, and numbness. A defense verdict was returned.

Discussion

It is very tempting to simply dismiss this case as absurd, with nothing to be learned from it. It does defy common sense that no one would have noticed the tourniquet or, at the very least, that the patient would not have spoken up about it during her stay in the ED. While the jury clearly came to the correct conclusion,  it does highlight a real problem: forgotten tourniquets.

According to the Pennsylvania Patient Safety Advisory (PPSA), there were 125 reports of tourniquets being left on patients in Pennsylvania healthcare facilities in 1 year alone.¹ In 5% of these cases, the tourniquet was discovered within a half hour of application. In approximately 66% of cases, the tourniquet was left on for up to 2 hours, and the remaining were left in place for 2 to 18 hours.

Few locations within the hospital are without risk for this type of accident. The PPSA further noted that approximately 30% of retained tourniquets occurred on medical/surgical units, 14% in the ED, and 14% on inpatient and ambulatory surgical services departments. Approximately 19% were discovered when patients were transferred from one department to another.¹

In the analysis of these incidents, contributing factors to forgotten tourniquets included staff failing to follow proper procedures, inadequate staff proficiency, and staff distractions and/or interruptions.¹ In addition, some patients appeared to be at increased risk of having a retained tourniquet than others. Sixty percent of 125 patients with a forgotten tourniquet were aged 70 years or older, whereas some patients were younger than age 2 years.¹ Not surprisingly, patients who were unable to verbally communicate (eg, patients who were intubated, under anesthesia, had expressive aphasia, severe dementia), were at the highest risk.

In a review of recovery room incidents, Salman and Asfar² identified two cases of forgotten tourniquets out of approximately 7,000 patients. Potential strategies to avoid this mistake include: (1) only documenting procedures after they have been completed (eg, tourniquet removal); (2) double-checking that the tourniquet has been removed prior to leaving patient bedside; and (3) the use of extra-long tourniquets so the ends are more clearly visible.

The patient’s physical examination was unremarkable. His vital signs were normal, and there was no obvious external evidence of trauma. The posterior cervical spine was tender to palpation in the midline, but no step-off signs were appreciated. The neurological examination, including strength and sensation in all four extremities, was normal.

Since the patient’s only complaint was neck pain and his physical examination and history were otherwise normal, the emergency physician (EP) ordered radiographs of the cervical spine. The imaging studies were interpreted as showing advanced degenerative changes but no fractures, and the patient was prescribed an analgesic and discharged home.

When the patient woke up the next morning, he was unable to move his extremities, and returned to the same ED via EMS. He was placed in a cervical collar and found to have flaccid extremities on examination. A computed tomography (CT) scan of the cervical spine revealed a transverse fracture through the C6 vertebra. Radiology services also reviewed the cervical spine X-rays from the previous day, noting the presence of fracture.

The patient was taken to the operating room by neurosurgery services but remained paralyzed postoperatively. He never recovered from his injury and died 6 months later. His family sued the EP and the hospital for missed diagnosis of cervical spine fracture at the first ED presentation and the resulting paralysis. The case was settled for $1.3 million prior to trial.

Discussion

The evaluation of suspected cervical spine injury secondary to blunt trauma is a frequent and important skill practiced by EPs. Motor vehicle accidents are the most common cause of spinal cord injury in the United States (42%), followed by falls (27%), acts of violence (15%), and sports-related injuries (8%).¹ A review by Sekon and Fehlings² showed that 55% of all spinal injuries involve the cervical spine. Interestingly, the majority of cervical spine injuries occur at the upper or lower ends of the cervical spine; C2 vertebral fractures account for 33%, while C6 and C7 vertebral fractures account for approximately 50%.¹

There are two commonly used criteria to clinically clear the cervical spine (ie, no imaging studies necessary) in blunt-trauma patients. The first is the National Emergency X-Radiography Use Study (NEXUS), which has a sensitivity of 99.6% of identifying cervical spine fractures.¹ According to the NEXUS criteria, no imaging studies are required if: (1) there is no midline cervical spine tenderness; (2) there are no focal neurological deficits; (3) the patient exhibits a normal level of alertness; (4) the patient is not intoxicated; and (5) there is no distracting injury.¹

The other set of criteria used to clear the cervical spine is the Canadian Cervical Spine Rule. In these criteria, a patient is considered at very low risk for cervical spine fracture in the following cases: (1) the patient is fully alert with a Glasgow Coma scale of 15; (2) the patient has no high-risk factors (ie, age >65 years, dangerous mechanism of injury, fall greater than five stairs, axial load to the head, high-speed vehicular crash, bicycle or motorcycle crash, or the presence of paresthesias in the extremities); (3) the patient has low-risk factors (eg, simple vehicle crash, sitting position in the ED, ambulatory at any time, delayed onset of neck pain, and the absence of midline cervical tenderness); and (4) the patient can actively rotate his or her neck 45 degrees to the left and to the right. The Canadian group found the above criteria to have 100% sensitivity for predicting the absence of cervical spine injury.¹

The patient in this case failed both sets of criteria (ie, presence of cervical spine tenderness and age >65 years) and therefore required imaging. Historically, cervical spine X-ray (three views, anteroposterior, lateral, and odontoid; or five views, three views plus obliques) has been the imaging study of choice for such patients. Unfortunately, however, cervical spine radiographs have severe limitations in identifying spinal injury. In a large retrospective review, Woodring and Lee,³ found that the standard three-view cervical spine series failed to demonstrate 61% of all fractures and 36% of all subluxation and dislocations. Similarly, in a prospective study of 1,006 patients with 72 injuries, Diaz et al,⁴ found a 52.3% missed fracture rate when five-view radiographs were used to identify cervical spine injury. In addition, radiographic evaluation of elderly patients was found to be even more challenging in identifying cervical spine injury due to age-related degenerative changes.

Given the abovementioned limitations associated with radiographic imaging, CT scan of the cervical spine has become the imaging study of choice in moderate-to-severe risk patients with blunt cervical spine trauma. This modality has been shown to have a higher sensitivity and specificity for evaluating cervical spine injury compared to plain X-ray films, with CT detecting 97% to 100% of cervical spine fractures.⁵

In addition to demonstrating a higher sensitivity, CT also has the advantage of speed—especially when the patient is undergoing other CT studies (eg, head, abdomen, pelvis). While some clinicians criticize the higher cost of CT versus plain films, CT has been shown to decrease institutional costs (when settlement costs are taken into account) due to the reduction of the incidence of paralysis resulting from false-negative imaging studies.⁶

Forgotten Tourniquet

The patient’s vital signs were: blood pressure, 138/82 mm Hg; heart rate, 102 beats/minute; respiratory rate, 18 breaths/minute; temperature 98.6˚F. Oxygen saturation was 99% on room air.

The patient appeared uncomfortable overall. The physical examination was remarkable only for mild left-sided costovertebral angle tenderness. Her abdomen was soft, nontender, and without guarding or rebound.

The EP ordered the placement of an intravenous (IV) line, through which the patient was administered normal saline and morphine and promethazine, respectively, for pain and nausea. A complete blood count, basic metabolic panel, urinalysis, and urine pregnancy test were ordered. All of the laboratory bloodwork results were normal, and the urine pregnancy test was negative. The urinalysis was remarkable for 50 to 100 red blood cells.

A noncontrast CT scan of the abdomen and pelvis revealed a 3-mm ureteral stone on the left side. When the patient returned from radiology services, her pain was significantly decreased and she felt much improved. She was diagnosed with a kidney stone and discharged home with an analgesic and a strainer, along with instructions to follow-up with urology services. The patient was in the ED for a total of 5 hours.

The plaintiff sued the EP and hospital, claiming that the tourniquet used to start the IV line and draw blood was never removed, which in turn caused nerve damage resulting in reflex sympathetic dystrophy and complex regional pain syndrome. The defense denied all of these allegations, and the ED personnel testified that the tourniquet was removed as soon as the IV was established. The defense cited the plaintiff’s medical records, which contained documentation that the tourniquet had been removed. The defense further argued that if the tourniquet had been left on as the patient alleged, she would have experienced obvious physical signs, such as swelling, redness, infiltration of fluids, pain, and numbness. A defense verdict was returned.

Discussion

It is very tempting to simply dismiss this case as absurd, with nothing to be learned from it. It does defy common sense that no one would have noticed the tourniquet or, at the very least, that the patient would not have spoken up about it during her stay in the ED. While the jury clearly came to the correct conclusion,  it does highlight a real problem: forgotten tourniquets.

According to the Pennsylvania Patient Safety Advisory (PPSA), there were 125 reports of tourniquets being left on patients in Pennsylvania healthcare facilities in 1 year alone.¹ In 5% of these cases, the tourniquet was discovered within a half hour of application. In approximately 66% of cases, the tourniquet was left on for up to 2 hours, and the remaining were left in place for 2 to 18 hours.

Few locations within the hospital are without risk for this type of accident. The PPSA further noted that approximately 30% of retained tourniquets occurred on medical/surgical units, 14% in the ED, and 14% on inpatient and ambulatory surgical services departments. Approximately 19% were discovered when patients were transferred from one department to another.¹

In the analysis of these incidents, contributing factors to forgotten tourniquets included staff failing to follow proper procedures, inadequate staff proficiency, and staff distractions and/or interruptions.¹ In addition, some patients appeared to be at increased risk of having a retained tourniquet than others. Sixty percent of 125 patients with a forgotten tourniquet were aged 70 years or older, whereas some patients were younger than age 2 years.¹ Not surprisingly, patients who were unable to verbally communicate (eg, patients who were intubated, under anesthesia, had expressive aphasia, severe dementia), were at the highest risk.

In a review of recovery room incidents, Salman and Asfar² identified two cases of forgotten tourniquets out of approximately 7,000 patients. Potential strategies to avoid this mistake include: (1) only documenting procedures after they have been completed (eg, tourniquet removal); (2) double-checking that the tourniquet has been removed prior to leaving patient bedside; and (3) the use of extra-long tourniquets so the ends are more clearly visible.

Spondylolysis, a defect in the pars interarticularis, is the single most common identifiable source of persistent low back pain in adolescent athletes.^1,2 The diagnosis of spondylolysis is confirmed by radiographic imaging.³ However, there is controversy regarding which imaging modality is preferred—specifically, which to use for first-line advanced imaging after plain radiographs are obtained.³ Single-photon emission computed tomography (SPECT) consistently has been shown to be the most sensitive modality, and it is considered the gold standard.^4-7 Patients with a positive SPECT scan are then routinely imaged with computed tomography (CT) for bone detail and staging of the pars defect.⁸ This imaging or diagnostic sequence yields organ-specific radiation doses (15-30 mSv) as much as 50-fold higher than those of plain radiography.⁹ Recent epidemiologic studies have shown that this organ dose results in an increased risk of cancer, especially in children.¹⁰

Diagnosis is crucial in early-stage lumbar spondylolysis, as osseous healing can occur with conservative treatment.^11,12 High signal change (HSC) in the pedicle or pars interarticularis (Figure 1) on fluid-specific (T2) magnetic resonance imaging (MRI) sequences has been shown to be important in the diagnosis of early spondylolysis and, subsequently, a good predictor of bony healing.^13,14 We conducted a study to determine the clinical and radiographic characteristics associated with the diagnosis of early or active spondylolysis.

Materials and Methods

The study was reviewed and approved by the local institutional review board. Using the International Classification of Diseases, Ninth Revision (ICD-9) diagnosis code for spondylolysis (756.11), we retrospectively identified patients (age, 12-21 years) from 2002–2011 billing data from a single specialty spine practice. Baseline data—including height, weight, sex, age, symptom duration, sporting activities, defect location, pain score, and previous treatments—were collected from a standardized patient intake questionnaire and office medical records. We also determined radiographic data, including level, laterality (right vs left, unilateral vs bilateral), presence of listhesis, and slip grade and percentage. CT scans were reviewed to confirm the spondylolysis diagnosis and to measure parameters described by Fujii and colleagues.¹⁵ These parameters include spondylolysis chronicity (early, progressive, terminal) (Figure 2), distance from defect to posterior margin of vertebral body, and defect angle relative to posterior margin of vertebral body. We also measured sagittal radiographic parameters, including pelvic incidence and lumbar lordosis.

Pars lesions were divided into active and inactive defects¹⁶ based on signal characteristics on either MRI or SPECT (Figure 3). Defects with a positive SPECT or HSC on T2 MRI were classified as active; all other defects were classified as inactive. All MRIs were reviewed by a radiologist, and any mention of HSC in the pedicle or pars of the corresponding level was considered positive. For the sake of accuracy, all MRIs were also reviewed by a spine surgeon. All CT measurements were done by 1 of 2 authors. Demographic, clinical, and radiographic characteristics were compared between patients with active defects and patients with inactive defects. Independent t tests and Fisher exact tests were used to compare continuous and categorical variables, respectively. Threshold P was set at .01 to account for the small sample size and multiple concurrent comparisons.

Results

Fifty-seven patients (29 males, 28 females) with a total of 108 pars defects (6 unilateral, 102 bilateral) were identified. Mean age was 14.64 years. Of the 108 defects, 49 were classified as active and 59 as inactive. SPECT results were available for 52 defects, MRI results for 85, and CT results for 76 (Table 1). There was no difference between the active and inactive groups in age (14.7 vs 14.6 years; P = .083), body mass index (24.2 vs 21.7 kg/m²; P = .034), symptom duration (236.3 vs 397.4 days; P = .016), lumbar lordosis (27.4° vs 32.1°; P = .097), pelvic incidence (59.0° vs 61.2°; P = .488), slip percentage (9.5% vs 14.2%; P = .034), and laterality (right vs left, P = .847; unilateral vs bilateral, P = .281) (Table 2). There was a significant difference between the active and inactive groups in sex (35 vs 19 males; P < .0001) and presence of listhesis (16 vs 35; P = .006) (Table 2).

Of the 49 active defects, 3 were graded as early, 10 as progressive, and 11 as terminal (Table 3). There was a statistically significant (P < .0001) difference between active and inactive lesions for each stage. Mean distance from posterior margin of the vertebral body was 0.57 mm and 0.68 mm for inactive and active lesions, respectively (P = .007). There was no significant difference (P = .294) in the posterior angle of the vertebral body and the defect between inactive (20.54°) and active (24.73°) lesions (Table 3).

Subanalysis by sex showed no difference in age (males, 16.4 years vs females, 18.7 years; P = .073), slip percentage (10.4% vs 13.4%; P = .168), or presence or absence of slip (25 vs 26; P > .99) (Table 4).

Discussion

Increasing MRI resolution combined with increasing concern about unnecessary radiation exposure has added to the attractiveness of MRI in the diagnosis of spondylolysis. Spondylolysis progresses on a continuum, starting with a stress reaction (early or active defect) and ending with either healing or nonunion of the pars defect (terminal defect) (Figure 4). Although risk factors for progression are not clearly defined, Fujii and colleagues¹⁵ showed that the reaction around the defect is the most important factor for osseous union. It would then make sense that the earlier the spondylolytic defect is identified, the higher the likelihood for union, especially with nonoperative treatment such as rest, activity restriction, and bracing.^12,17

There is a lack of consensus regarding MRI use in the diagnosis of spondylolysis. Masci and colleagues¹⁸ prospectively evaluated 50 defects in 39 patients using a 1.5-Tesla MRI scanner, concluded MRI is inferior to SPECT/CT, and recommended that SPECT remain the first-line advanced imaging modality. Conversely, Campbell and colleagues⁴ prospectively evaluated 40 defects in 22 patients using a 1.0-Tesla magnet and concluded that MRI can be used as an effective and reliable first-line advanced imaging modality. These are the only 2 prospective studies conducted within the past decade. Both were underpowered and used outdated technology (newer MRI scanners use 3.0-Tesla magnets). In addition, specific imaging characteristics (eg, edema in pars or pedicle on fluid-specific sequences) that suggest a positive finding—versus overt fracture on T1 MRI—have been recently emphasized. Neither Masci and colleagues¹⁸ nor Campbell and colleagues⁴ detailed what constituted a positive MRI finding. Although an adequately powered prospective study will provide a better analysis of the utility of MRI versus SPECT, such a study is costly and time-consuming. It is important to identify patient and lesion characteristics to help optimize the usefulness of MRI. It is also important to identify the subset of patients most likely to experience osseous healing of active defects,¹⁶ as this is the same subset of patients most likely to respond to nonoperative treatment.

We conducted the present study to identify any clinical or radiographic characteristics associated with the diagnosis of early or active spondylolysis. Almost equal numbers of active and inactive defects (49, 59) were identified. There were no differences in patient characteristics, including age, body mass index, and symptom duration. However, there was a significant sex difference—a relatively high proportion of males with active spondylolysis. This finding, which had been reported before,^16,19,20 is probably the result of several factors, including males’ lower lumbar spine bone mineral density²¹; their relatively less spinal flexibility, which affects the distribution of torsional loads on the spine²²; and their relatively greater participation in sports, especially sports involving high-velocity, torsional loading of the lumbar spine.²³ Studies are needed to delineate the extent to which sex influences the development and persistence of active spondylolytic lesions. Alternatively, a subanalysis revealed an age difference, between our female and male cohorts (18.7 vs 16.4 years), that may have contributed to the high proportion of males with active spondylolysis.

Although the groups’ difference in symptom duration was not significant, it was trending toward significance. As discussed, it could be explained that, along the continuum of disease, earlier defects are more active and either achieve fibrous or osseous union or become chronic and “burn out” to inactive lesions, potentially leading to a listhesis.²⁴ The listhesis association was higher in the inactive group than in the active group (P = .006). The difference in numbers of active and inactive defects at each stage (early, progressive, late) confirms this finding, with no inactive lesions in the early and progressive stages and many fewer active lesions in the terminal stage. Overall, presence of a spondylolisthesis on plain radiographs may obviate the need for SPECT or MRI, as it indicates an inactive chronic lesion—unless new symptoms are suspicious for reactivation or development of previously described adjacent-level pars defects.

No other radiographic parameters were found to be significant—consistent with findings of other studies.^2,5,16 Pelvic incidence has been shown to predict progression of spondylisthesis, but under our study parameters it appears not to be associated with development of a slip.

This study had several weaknesses. First, it was retrospective, and imaging parameters were inconsistent, as we included patients who underwent imaging at other facilities. Second, the timing of imaging was inconsistent. Ideally, the same sequence protocol would be used, and all imaging studies (MRI, SPECT, CT) would be performed within a specific period after the initial concern for a spondylolysis was raised. Last, not all patients underwent all 3 advanced imaging modalities; having all 3 would have allowed for a retrospective comparison of MRI and SPECT sensitivity in detecting spondylolysis. Such a comparison would have been interesting, though it was not the goal of this study.

With its technological improvements and lack of radiation exposure, MRI is becoming more attractive as a first-line advanced imaging modality. Although the superiority of MRI over SPECT is yet to be confirmed, clinical use of MRI in the evaluation of spondylolysis seems to be increasing. It is therefore important to characterize the spondylolytic defects that are readily detected with MRI.

Active or early juvenile spondylolysis appears to be associated with males and absence of an associated listhesis. These clinical and radiographic characteristics may be important in the identification of patients with higher potential for osseous healing after nonoperative treatment.

Spondylolysis, a defect in the pars interarticularis, is the single most common identifiable source of persistent low back pain in adolescent athletes.^1,2 The diagnosis of spondylolysis is confirmed by radiographic imaging.³ However, there is controversy regarding which imaging modality is preferred—specifically, which to use for first-line advanced imaging after plain radiographs are obtained.³ Single-photon emission computed tomography (SPECT) consistently has been shown to be the most sensitive modality, and it is considered the gold standard.^4-7 Patients with a positive SPECT scan are then routinely imaged with computed tomography (CT) for bone detail and staging of the pars defect.⁸ This imaging or diagnostic sequence yields organ-specific radiation doses (15-30 mSv) as much as 50-fold higher than those of plain radiography.⁹ Recent epidemiologic studies have shown that this organ dose results in an increased risk of cancer, especially in children.¹⁰

Diagnosis is crucial in early-stage lumbar spondylolysis, as osseous healing can occur with conservative treatment.^11,12 High signal change (HSC) in the pedicle or pars interarticularis (Figure 1) on fluid-specific (T2) magnetic resonance imaging (MRI) sequences has been shown to be important in the diagnosis of early spondylolysis and, subsequently, a good predictor of bony healing.^13,14 We conducted a study to determine the clinical and radiographic characteristics associated with the diagnosis of early or active spondylolysis.

Materials and Methods

The study was reviewed and approved by the local institutional review board. Using the International Classification of Diseases, Ninth Revision (ICD-9) diagnosis code for spondylolysis (756.11), we retrospectively identified patients (age, 12-21 years) from 2002–2011 billing data from a single specialty spine practice. Baseline data—including height, weight, sex, age, symptom duration, sporting activities, defect location, pain score, and previous treatments—were collected from a standardized patient intake questionnaire and office medical records. We also determined radiographic data, including level, laterality (right vs left, unilateral vs bilateral), presence of listhesis, and slip grade and percentage. CT scans were reviewed to confirm the spondylolysis diagnosis and to measure parameters described by Fujii and colleagues.¹⁵ These parameters include spondylolysis chronicity (early, progressive, terminal) (Figure 2), distance from defect to posterior margin of vertebral body, and defect angle relative to posterior margin of vertebral body. We also measured sagittal radiographic parameters, including pelvic incidence and lumbar lordosis.

Pars lesions were divided into active and inactive defects¹⁶ based on signal characteristics on either MRI or SPECT (Figure 3). Defects with a positive SPECT or HSC on T2 MRI were classified as active; all other defects were classified as inactive. All MRIs were reviewed by a radiologist, and any mention of HSC in the pedicle or pars of the corresponding level was considered positive. For the sake of accuracy, all MRIs were also reviewed by a spine surgeon. All CT measurements were done by 1 of 2 authors. Demographic, clinical, and radiographic characteristics were compared between patients with active defects and patients with inactive defects. Independent t tests and Fisher exact tests were used to compare continuous and categorical variables, respectively. Threshold P was set at .01 to account for the small sample size and multiple concurrent comparisons.

Results

Fifty-seven patients (29 males, 28 females) with a total of 108 pars defects (6 unilateral, 102 bilateral) were identified. Mean age was 14.64 years. Of the 108 defects, 49 were classified as active and 59 as inactive. SPECT results were available for 52 defects, MRI results for 85, and CT results for 76 (Table 1). There was no difference between the active and inactive groups in age (14.7 vs 14.6 years; P = .083), body mass index (24.2 vs 21.7 kg/m²; P = .034), symptom duration (236.3 vs 397.4 days; P = .016), lumbar lordosis (27.4° vs 32.1°; P = .097), pelvic incidence (59.0° vs 61.2°; P = .488), slip percentage (9.5% vs 14.2%; P = .034), and laterality (right vs left, P = .847; unilateral vs bilateral, P = .281) (Table 2). There was a significant difference between the active and inactive groups in sex (35 vs 19 males; P < .0001) and presence of listhesis (16 vs 35; P = .006) (Table 2).

Of the 49 active defects, 3 were graded as early, 10 as progressive, and 11 as terminal (Table 3). There was a statistically significant (P < .0001) difference between active and inactive lesions for each stage. Mean distance from posterior margin of the vertebral body was 0.57 mm and 0.68 mm for inactive and active lesions, respectively (P = .007). There was no significant difference (P = .294) in the posterior angle of the vertebral body and the defect between inactive (20.54°) and active (24.73°) lesions (Table 3).

Subanalysis by sex showed no difference in age (males, 16.4 years vs females, 18.7 years; P = .073), slip percentage (10.4% vs 13.4%; P = .168), or presence or absence of slip (25 vs 26; P > .99) (Table 4).

Discussion

Increasing MRI resolution combined with increasing concern about unnecessary radiation exposure has added to the attractiveness of MRI in the diagnosis of spondylolysis. Spondylolysis progresses on a continuum, starting with a stress reaction (early or active defect) and ending with either healing or nonunion of the pars defect (terminal defect) (Figure 4). Although risk factors for progression are not clearly defined, Fujii and colleagues¹⁵ showed that the reaction around the defect is the most important factor for osseous union. It would then make sense that the earlier the spondylolytic defect is identified, the higher the likelihood for union, especially with nonoperative treatment such as rest, activity restriction, and bracing.^12,17

There is a lack of consensus regarding MRI use in the diagnosis of spondylolysis. Masci and colleagues¹⁸ prospectively evaluated 50 defects in 39 patients using a 1.5-Tesla MRI scanner, concluded MRI is inferior to SPECT/CT, and recommended that SPECT remain the first-line advanced imaging modality. Conversely, Campbell and colleagues⁴ prospectively evaluated 40 defects in 22 patients using a 1.0-Tesla magnet and concluded that MRI can be used as an effective and reliable first-line advanced imaging modality. These are the only 2 prospective studies conducted within the past decade. Both were underpowered and used outdated technology (newer MRI scanners use 3.0-Tesla magnets). In addition, specific imaging characteristics (eg, edema in pars or pedicle on fluid-specific sequences) that suggest a positive finding—versus overt fracture on T1 MRI—have been recently emphasized. Neither Masci and colleagues¹⁸ nor Campbell and colleagues⁴ detailed what constituted a positive MRI finding. Although an adequately powered prospective study will provide a better analysis of the utility of MRI versus SPECT, such a study is costly and time-consuming. It is important to identify patient and lesion characteristics to help optimize the usefulness of MRI. It is also important to identify the subset of patients most likely to experience osseous healing of active defects,¹⁶ as this is the same subset of patients most likely to respond to nonoperative treatment.

We conducted the present study to identify any clinical or radiographic characteristics associated with the diagnosis of early or active spondylolysis. Almost equal numbers of active and inactive defects (49, 59) were identified. There were no differences in patient characteristics, including age, body mass index, and symptom duration. However, there was a significant sex difference—a relatively high proportion of males with active spondylolysis. This finding, which had been reported before,^16,19,20 is probably the result of several factors, including males’ lower lumbar spine bone mineral density²¹; their relatively less spinal flexibility, which affects the distribution of torsional loads on the spine²²; and their relatively greater participation in sports, especially sports involving high-velocity, torsional loading of the lumbar spine.²³ Studies are needed to delineate the extent to which sex influences the development and persistence of active spondylolytic lesions. Alternatively, a subanalysis revealed an age difference, between our female and male cohorts (18.7 vs 16.4 years), that may have contributed to the high proportion of males with active spondylolysis.

Although the groups’ difference in symptom duration was not significant, it was trending toward significance. As discussed, it could be explained that, along the continuum of disease, earlier defects are more active and either achieve fibrous or osseous union or become chronic and “burn out” to inactive lesions, potentially leading to a listhesis.²⁴ The listhesis association was higher in the inactive group than in the active group (P = .006). The difference in numbers of active and inactive defects at each stage (early, progressive, late) confirms this finding, with no inactive lesions in the early and progressive stages and many fewer active lesions in the terminal stage. Overall, presence of a spondylolisthesis on plain radiographs may obviate the need for SPECT or MRI, as it indicates an inactive chronic lesion—unless new symptoms are suspicious for reactivation or development of previously described adjacent-level pars defects.

No other radiographic parameters were found to be significant—consistent with findings of other studies.^2,5,16 Pelvic incidence has been shown to predict progression of spondylisthesis, but under our study parameters it appears not to be associated with development of a slip.

This study had several weaknesses. First, it was retrospective, and imaging parameters were inconsistent, as we included patients who underwent imaging at other facilities. Second, the timing of imaging was inconsistent. Ideally, the same sequence protocol would be used, and all imaging studies (MRI, SPECT, CT) would be performed within a specific period after the initial concern for a spondylolysis was raised. Last, not all patients underwent all 3 advanced imaging modalities; having all 3 would have allowed for a retrospective comparison of MRI and SPECT sensitivity in detecting spondylolysis. Such a comparison would have been interesting, though it was not the goal of this study.

With its technological improvements and lack of radiation exposure, MRI is becoming more attractive as a first-line advanced imaging modality. Although the superiority of MRI over SPECT is yet to be confirmed, clinical use of MRI in the evaluation of spondylolysis seems to be increasing. It is therefore important to characterize the spondylolytic defects that are readily detected with MRI.

Active or early juvenile spondylolysis appears to be associated with males and absence of an associated listhesis. These clinical and radiographic characteristics may be important in the identification of patients with higher potential for osseous healing after nonoperative treatment.

Spondylolysis, a defect in the pars interarticularis, is the single most common identifiable source of persistent low back pain in adolescent athletes.^1,2 The diagnosis of spondylolysis is confirmed by radiographic imaging.³ However, there is controversy regarding which imaging modality is preferred—specifically, which to use for first-line advanced imaging after plain radiographs are obtained.³ Single-photon emission computed tomography (SPECT) consistently has been shown to be the most sensitive modality, and it is considered the gold standard.^4-7 Patients with a positive SPECT scan are then routinely imaged with computed tomography (CT) for bone detail and staging of the pars defect.⁸ This imaging or diagnostic sequence yields organ-specific radiation doses (15-30 mSv) as much as 50-fold higher than those of plain radiography.⁹ Recent epidemiologic studies have shown that this organ dose results in an increased risk of cancer, especially in children.¹⁰

Diagnosis is crucial in early-stage lumbar spondylolysis, as osseous healing can occur with conservative treatment.^11,12 High signal change (HSC) in the pedicle or pars interarticularis (Figure 1) on fluid-specific (T2) magnetic resonance imaging (MRI) sequences has been shown to be important in the diagnosis of early spondylolysis and, subsequently, a good predictor of bony healing.^13,14 We conducted a study to determine the clinical and radiographic characteristics associated with the diagnosis of early or active spondylolysis.

Materials and Methods

The study was reviewed and approved by the local institutional review board. Using the International Classification of Diseases, Ninth Revision (ICD-9) diagnosis code for spondylolysis (756.11), we retrospectively identified patients (age, 12-21 years) from 2002–2011 billing data from a single specialty spine practice. Baseline data—including height, weight, sex, age, symptom duration, sporting activities, defect location, pain score, and previous treatments—were collected from a standardized patient intake questionnaire and office medical records. We also determined radiographic data, including level, laterality (right vs left, unilateral vs bilateral), presence of listhesis, and slip grade and percentage. CT scans were reviewed to confirm the spondylolysis diagnosis and to measure parameters described by Fujii and colleagues.¹⁵ These parameters include spondylolysis chronicity (early, progressive, terminal) (Figure 2), distance from defect to posterior margin of vertebral body, and defect angle relative to posterior margin of vertebral body. We also measured sagittal radiographic parameters, including pelvic incidence and lumbar lordosis.

Pars lesions were divided into active and inactive defects¹⁶ based on signal characteristics on either MRI or SPECT (Figure 3). Defects with a positive SPECT or HSC on T2 MRI were classified as active; all other defects were classified as inactive. All MRIs were reviewed by a radiologist, and any mention of HSC in the pedicle or pars of the corresponding level was considered positive. For the sake of accuracy, all MRIs were also reviewed by a spine surgeon. All CT measurements were done by 1 of 2 authors. Demographic, clinical, and radiographic characteristics were compared between patients with active defects and patients with inactive defects. Independent t tests and Fisher exact tests were used to compare continuous and categorical variables, respectively. Threshold P was set at .01 to account for the small sample size and multiple concurrent comparisons.

Results

Fifty-seven patients (29 males, 28 females) with a total of 108 pars defects (6 unilateral, 102 bilateral) were identified. Mean age was 14.64 years. Of the 108 defects, 49 were classified as active and 59 as inactive. SPECT results were available for 52 defects, MRI results for 85, and CT results for 76 (Table 1). There was no difference between the active and inactive groups in age (14.7 vs 14.6 years; P = .083), body mass index (24.2 vs 21.7 kg/m²; P = .034), symptom duration (236.3 vs 397.4 days; P = .016), lumbar lordosis (27.4° vs 32.1°; P = .097), pelvic incidence (59.0° vs 61.2°; P = .488), slip percentage (9.5% vs 14.2%; P = .034), and laterality (right vs left, P = .847; unilateral vs bilateral, P = .281) (Table 2). There was a significant difference between the active and inactive groups in sex (35 vs 19 males; P < .0001) and presence of listhesis (16 vs 35; P = .006) (Table 2).

Of the 49 active defects, 3 were graded as early, 10 as progressive, and 11 as terminal (Table 3). There was a statistically significant (P < .0001) difference between active and inactive lesions for each stage. Mean distance from posterior margin of the vertebral body was 0.57 mm and 0.68 mm for inactive and active lesions, respectively (P = .007). There was no significant difference (P = .294) in the posterior angle of the vertebral body and the defect between inactive (20.54°) and active (24.73°) lesions (Table 3).

Subanalysis by sex showed no difference in age (males, 16.4 years vs females, 18.7 years; P = .073), slip percentage (10.4% vs 13.4%; P = .168), or presence or absence of slip (25 vs 26; P > .99) (Table 4).

Discussion

Increasing MRI resolution combined with increasing concern about unnecessary radiation exposure has added to the attractiveness of MRI in the diagnosis of spondylolysis. Spondylolysis progresses on a continuum, starting with a stress reaction (early or active defect) and ending with either healing or nonunion of the pars defect (terminal defect) (Figure 4). Although risk factors for progression are not clearly defined, Fujii and colleagues¹⁵ showed that the reaction around the defect is the most important factor for osseous union. It would then make sense that the earlier the spondylolytic defect is identified, the higher the likelihood for union, especially with nonoperative treatment such as rest, activity restriction, and bracing.^12,17

There is a lack of consensus regarding MRI use in the diagnosis of spondylolysis. Masci and colleagues¹⁸ prospectively evaluated 50 defects in 39 patients using a 1.5-Tesla MRI scanner, concluded MRI is inferior to SPECT/CT, and recommended that SPECT remain the first-line advanced imaging modality. Conversely, Campbell and colleagues⁴ prospectively evaluated 40 defects in 22 patients using a 1.0-Tesla magnet and concluded that MRI can be used as an effective and reliable first-line advanced imaging modality. These are the only 2 prospective studies conducted within the past decade. Both were underpowered and used outdated technology (newer MRI scanners use 3.0-Tesla magnets). In addition, specific imaging characteristics (eg, edema in pars or pedicle on fluid-specific sequences) that suggest a positive finding—versus overt fracture on T1 MRI—have been recently emphasized. Neither Masci and colleagues¹⁸ nor Campbell and colleagues⁴ detailed what constituted a positive MRI finding. Although an adequately powered prospective study will provide a better analysis of the utility of MRI versus SPECT, such a study is costly and time-consuming. It is important to identify patient and lesion characteristics to help optimize the usefulness of MRI. It is also important to identify the subset of patients most likely to experience osseous healing of active defects,¹⁶ as this is the same subset of patients most likely to respond to nonoperative treatment.

We conducted the present study to identify any clinical or radiographic characteristics associated with the diagnosis of early or active spondylolysis. Almost equal numbers of active and inactive defects (49, 59) were identified. There were no differences in patient characteristics, including age, body mass index, and symptom duration. However, there was a significant sex difference—a relatively high proportion of males with active spondylolysis. This finding, which had been reported before,^16,19,20 is probably the result of several factors, including males’ lower lumbar spine bone mineral density²¹; their relatively less spinal flexibility, which affects the distribution of torsional loads on the spine²²; and their relatively greater participation in sports, especially sports involving high-velocity, torsional loading of the lumbar spine.²³ Studies are needed to delineate the extent to which sex influences the development and persistence of active spondylolytic lesions. Alternatively, a subanalysis revealed an age difference, between our female and male cohorts (18.7 vs 16.4 years), that may have contributed to the high proportion of males with active spondylolysis.

Although the groups’ difference in symptom duration was not significant, it was trending toward significance. As discussed, it could be explained that, along the continuum of disease, earlier defects are more active and either achieve fibrous or osseous union or become chronic and “burn out” to inactive lesions, potentially leading to a listhesis.²⁴ The listhesis association was higher in the inactive group than in the active group (P = .006). The difference in numbers of active and inactive defects at each stage (early, progressive, late) confirms this finding, with no inactive lesions in the early and progressive stages and many fewer active lesions in the terminal stage. Overall, presence of a spondylolisthesis on plain radiographs may obviate the need for SPECT or MRI, as it indicates an inactive chronic lesion—unless new symptoms are suspicious for reactivation or development of previously described adjacent-level pars defects.

No other radiographic parameters were found to be significant—consistent with findings of other studies.^2,5,16 Pelvic incidence has been shown to predict progression of spondylisthesis, but under our study parameters it appears not to be associated with development of a slip.

This study had several weaknesses. First, it was retrospective, and imaging parameters were inconsistent, as we included patients who underwent imaging at other facilities. Second, the timing of imaging was inconsistent. Ideally, the same sequence protocol would be used, and all imaging studies (MRI, SPECT, CT) would be performed within a specific period after the initial concern for a spondylolysis was raised. Last, not all patients underwent all 3 advanced imaging modalities; having all 3 would have allowed for a retrospective comparison of MRI and SPECT sensitivity in detecting spondylolysis. Such a comparison would have been interesting, though it was not the goal of this study.

With its technological improvements and lack of radiation exposure, MRI is becoming more attractive as a first-line advanced imaging modality. Although the superiority of MRI over SPECT is yet to be confirmed, clinical use of MRI in the evaluation of spondylolysis seems to be increasing. It is therefore important to characterize the spondylolytic defects that are readily detected with MRI.

Active or early juvenile spondylolysis appears to be associated with males and absence of an associated listhesis. These clinical and radiographic characteristics may be important in the identification of patients with higher potential for osseous healing after nonoperative treatment.

The anterior cruciate ligament (ACL) restrains anterior translation of the tibia on the femur and controls rotation of the knee. The natural primary healing potential of the ACL has been extremely poor in clinical and experimental studies, and primary suture repair has not provided stability to the joint in most patients.^1-8 This has led surgeons to reconstruct the ACL, rather than to attempt nonoperative treatment. Anterior cruciate ligament reconstruction is recommended to help patients maintain activities that place shear and torque forces on the knee or to ameliorate persistent pain due to instability.⁹ Reconstruction of the ACL in adults is one of the most common procedures performed by orthopedic surgeons. However, reconstruction in the ACL-deficient adolescent remains a controversial subject, with debates surrounding operative timing and surgical technique.

This case report presents a skeletally immature patient who suffered a complete traumatic rupture of his ACL, which intrinsically healed. The patient had a protracted treatment course, complicated by an open tibial fracture with delayed union. He responded to a progressive rehabilitation program and has made a good functional recovery. Review of the literature has demonstrated limited evidence of intrinsic ACL healing, none of which has been shown to occur in a skeletally immature patient. The patient’s mother provided written informed consent for print and electronic publication of this case report.

Case Report

A 12-year-old boy was brought to our level I trauma center by ambulance after being hit by a car while riding a motorized scooter. He presented with a grade IIIB open tibial fracture and a distal fibula fracture of his left lower extremity and was taken to the operating room that night for irrigation and débridement, percutaneous fixation of the fibula, and intramedullary flexible nail fixation of the tibia. On postoperative day 1, he had increasing pain and, once his splint was removed, his compartments were found to be very tense. He was taken emergently to the operating room for 4 compartment fasciotomies of the left lower extremity with wound vacuum-assisted closure (VAC) placement. This was changed on hospital day 4 and was removed with definitive closure on day 7. Examination under anesthesia prior to the final wound VAC change was performed given the patient’s complaints during physical therapy. This showed anterior and posterior ligamentous instability of the knee, and he was placed in a knee immobilizer. He was discharged on hospital day 11.

At 2-week follow-up, the patient was doing well, except that he was nonadherent with the knee immobilizer and unable to fully extend his left knee. On examination, a posterior drawer sign was noted; therefore, the patient was referred for magnetic resonance imaging (MRI) to evaluate his ligaments. His MRI, 9 weeks after injury, showed: (1) complete tears of both the anterior and posterior cruciate ligaments (PCLs) (Figures 1A, 1B); (2) medial meniscus and lateral meniscus tears; (3) 2.0-cm plate-like avulsion fracture of the posterolateral femoral metaphysis involving the insertion of the lateral head of the gastrocnemius muscle, fibular collateral ligament, and popliteus muscle (Figure 2); and (4) left posterior lateral tibial plateau contusion.

The patient was started on a 6-week course of physical therapy with active and active-assisted extension exercises. At follow-up approximately 3½ months after injury, he was found to have a 35º flexion contracture with pain at the end extension. Unfortunately, his tibial fracture showed minimal signs of healing, and the decision was made to delay surgical intervention on the knee until the tibial fracture had healed. He was given a knee orthotic to wear at night to help regain his knee extension.

Six months after injury, the patient underwent open removal of the avulsed bony fragment, posterior knee capsule release, and autograft of the delayed union tibial fracture. He was placed in a straight leg cast postoperatively and was discharged home on postoperative day 2. He transitioned to a knee immobilizer after 2 weeks. Six weeks after the last surgery, he had range of motion of 0º to 130º. Ligamentous examination at this time showed anterior and posterior drawer signs, positive Lachman test, and dial test with 90º of external rotation. He was placed in physical therapy for a total of 10 weeks to work on his quadriceps muscle strength and 15º extension lag.

On 13-month postinjury radiographs, the patient was noted to have adequate healing of his tibial fracture, and ligamentous reconstruction was discussed. At this time, the patient did not have any instability or pain in the knee. Examination demonstrated a very mild effusion of the left knee. Range of motion determined by goniometer was from -3º to 140º, and Lachman test was positive but with solid 2+ endpoint. He also had a positive posterior drawer sign with no endpoint, positive sag sign of his tibia, and positive active quadriceps test of the left leg. His dial test showed some increased external rotation at 90º but was equivocal at 30º when compared with the contralateral knee, demonstrating involvement of the posterolateral corner.

Sixteen months after injury, repeat MRI to further evaluate the posterolateral corner showed: (1) complete medial and lateral meniscal healing without evidence of residual or recurrent tear, and (2) interval healing of the remote ACL and PCL tears with intact insertions (Figures 3A, 3B). This scan showed an end-to-end continuous ACL with homogeneous signal and disappearance of the secondary signs. Physical examination at this time showed a very firm endpoint on Lachman test but some laxity with his posterior drawer. Given these findings, the patient was given a brace and continued in physical therapy to strengthen his quadriceps muscle. By 20 months after injury, he had returned to competitive hockey and had no complaints of pain or instability. His physical examination showed full range of motion in a ligamentously stable knee with firm endpoint. The patient’s condition was unchanged at 29-month follow-up.

Discussion

There is a body of evidence that states a completely ruptured ACL does not heal.^3,6,10 In animal models, the ACL has been shown to have poor healing potential.^3,11 Some studies have suggested this is secondary to poor blood supply. Blood supply to the ACL is derived from a periligamentous, then endoligamentous, arterial network with a less vascularized area in the middle third of the ACL. Additionally, there is no blood supply from the tibia or femur, meaning the areas of attachment of the ligament are poorly vascularized.¹² With a minimal blood supply to the ACL, the supply of undifferentiated mesenchymal cells from the surrounding tissue during the initial healing process is limited. In vitro cell cultures of these cells have showed a reduced potential for proliferation and migration.⁹ Cells of the ACL have a lower response to growth factors than human medial collateral ligament cells, further suggesting a decreased reparative capacity.⁷ Joint fluid has been shown to inhibit the proliferation of these cells, further reducing their regenerative potential.¹³ Additionally, biomechanical factors that alter signaling pathways, sites of ligament reattachment, and injury to proprioceptive structures have been shown to negatively influence the healing response.^14-18

Review of the literature on healing of ACLs includes 2 case reports, totaling 3 patients, and 3 level IV therapeutic studies involving 74 patients total.^10,19-22 In most cases, the authors of these studies have indicated a nonoperative treatment protocol with bracing and a specific rehabilitation program. Malanga and colleagues¹⁰ demonstrated that an ACL torn from its attachment on the femur, with the majority of the ligament in good condition and no compromise in the length, healed back onto the femur. Kurosaka and coauthors²⁰ described case reports of isolated distal or proximal midsubstance tears that have healed spontaneously. However, none of the patients described in the literature were under the age of 20 years.

Treatment for pediatric patients with open physes causes some debate. Nonoperative management of ACL deficiency in adolescents is generally not recommended because the continued instability of the joint leads to intra-articular injury, functional impairment, and joint degeneration.^23-25 A recent systematic review found only 1 study that showed no increase in secondary intra-articular injury when surgery was delayed until skeletal maturity.²⁶ 

Our patient was a 12-year-old boy whose traumatic knee injury with multiple ruptured ligaments healed over the course of 20 months. It is likely that bracing associated with the patient’s second surgery and delayed union of his tibial fracture allowed healing tissue to be protected from excessive stress until it remodeled with sufficient strength. Most would assume that healing would occur early, during the first 6 to 9 months; however, our patient regained his stability between 8 and 13 months. It is possible that the hostile healing environment of the ACL, including the low blood supply, poor response to growth factors, and biomechanical environment, as described previously, played a factor in this delay.^7,9,12,13

It is important to recognize that our patient tore his ACL during a traumatic motorized scooter rollover collision, not the more common noncontact twisting injury. Additionally, given the patient’s knee surgery that was performed 6 months after the initial injury, it is possible that intra-articular scar formation contributed to his healing capacity. While this patient did not undergo arthroscopy to visualize the tear in the ACL, or its reconstitution, recent evidence suggests that the accuracy of MRI in diagnosing pediatric ACL injuries is excellent.^27,28 The diagnostic accuracy with new MRI machines has sensitivity and specificity approaching 100%.²⁹ Additionally, the patient’s subjective and objective improvements argue for a change in anatomy over a change in the quality of his examination.

Conclusion

The goal of ACL reconstruction in adolescents is to provide long-term stability to the knee while minimizing the risk of growth disturbance. This goal was achieved in our patient through the in situ healing of his ACL. Intrinsic reconstitution of a torn ACL is rare, and it is difficult to speculate which patients may have some healing potential. While this patient was an extreme example, his case demonstrated that protection of the knee from undue stress could favorably alter the environment of the knee to allow for healing of ACL tears. Such information could be valuable in managing select pediatric patients with open physes and ACL injuries nonoperatively, sparing them from the risks associated with surgical treatment. While we do not recommend nonoperative treatment for patients with acute tears of the ACL, we believe more investigation into the healing potential of the ACL, and potential pathways to augment this, is warranted.

The anterior cruciate ligament (ACL) restrains anterior translation of the tibia on the femur and controls rotation of the knee. The natural primary healing potential of the ACL has been extremely poor in clinical and experimental studies, and primary suture repair has not provided stability to the joint in most patients.^1-8 This has led surgeons to reconstruct the ACL, rather than to attempt nonoperative treatment. Anterior cruciate ligament reconstruction is recommended to help patients maintain activities that place shear and torque forces on the knee or to ameliorate persistent pain due to instability.⁹ Reconstruction of the ACL in adults is one of the most common procedures performed by orthopedic surgeons. However, reconstruction in the ACL-deficient adolescent remains a controversial subject, with debates surrounding operative timing and surgical technique.

This case report presents a skeletally immature patient who suffered a complete traumatic rupture of his ACL, which intrinsically healed. The patient had a protracted treatment course, complicated by an open tibial fracture with delayed union. He responded to a progressive rehabilitation program and has made a good functional recovery. Review of the literature has demonstrated limited evidence of intrinsic ACL healing, none of which has been shown to occur in a skeletally immature patient. The patient’s mother provided written informed consent for print and electronic publication of this case report.

Case Report

A 12-year-old boy was brought to our level I trauma center by ambulance after being hit by a car while riding a motorized scooter. He presented with a grade IIIB open tibial fracture and a distal fibula fracture of his left lower extremity and was taken to the operating room that night for irrigation and débridement, percutaneous fixation of the fibula, and intramedullary flexible nail fixation of the tibia. On postoperative day 1, he had increasing pain and, once his splint was removed, his compartments were found to be very tense. He was taken emergently to the operating room for 4 compartment fasciotomies of the left lower extremity with wound vacuum-assisted closure (VAC) placement. This was changed on hospital day 4 and was removed with definitive closure on day 7. Examination under anesthesia prior to the final wound VAC change was performed given the patient’s complaints during physical therapy. This showed anterior and posterior ligamentous instability of the knee, and he was placed in a knee immobilizer. He was discharged on hospital day 11.

At 2-week follow-up, the patient was doing well, except that he was nonadherent with the knee immobilizer and unable to fully extend his left knee. On examination, a posterior drawer sign was noted; therefore, the patient was referred for magnetic resonance imaging (MRI) to evaluate his ligaments. His MRI, 9 weeks after injury, showed: (1) complete tears of both the anterior and posterior cruciate ligaments (PCLs) (Figures 1A, 1B); (2) medial meniscus and lateral meniscus tears; (3) 2.0-cm plate-like avulsion fracture of the posterolateral femoral metaphysis involving the insertion of the lateral head of the gastrocnemius muscle, fibular collateral ligament, and popliteus muscle (Figure 2); and (4) left posterior lateral tibial plateau contusion.

The patient was started on a 6-week course of physical therapy with active and active-assisted extension exercises. At follow-up approximately 3½ months after injury, he was found to have a 35º flexion contracture with pain at the end extension. Unfortunately, his tibial fracture showed minimal signs of healing, and the decision was made to delay surgical intervention on the knee until the tibial fracture had healed. He was given a knee orthotic to wear at night to help regain his knee extension.

Six months after injury, the patient underwent open removal of the avulsed bony fragment, posterior knee capsule release, and autograft of the delayed union tibial fracture. He was placed in a straight leg cast postoperatively and was discharged home on postoperative day 2. He transitioned to a knee immobilizer after 2 weeks. Six weeks after the last surgery, he had range of motion of 0º to 130º. Ligamentous examination at this time showed anterior and posterior drawer signs, positive Lachman test, and dial test with 90º of external rotation. He was placed in physical therapy for a total of 10 weeks to work on his quadriceps muscle strength and 15º extension lag.

On 13-month postinjury radiographs, the patient was noted to have adequate healing of his tibial fracture, and ligamentous reconstruction was discussed. At this time, the patient did not have any instability or pain in the knee. Examination demonstrated a very mild effusion of the left knee. Range of motion determined by goniometer was from -3º to 140º, and Lachman test was positive but with solid 2+ endpoint. He also had a positive posterior drawer sign with no endpoint, positive sag sign of his tibia, and positive active quadriceps test of the left leg. His dial test showed some increased external rotation at 90º but was equivocal at 30º when compared with the contralateral knee, demonstrating involvement of the posterolateral corner.

Sixteen months after injury, repeat MRI to further evaluate the posterolateral corner showed: (1) complete medial and lateral meniscal healing without evidence of residual or recurrent tear, and (2) interval healing of the remote ACL and PCL tears with intact insertions (Figures 3A, 3B). This scan showed an end-to-end continuous ACL with homogeneous signal and disappearance of the secondary signs. Physical examination at this time showed a very firm endpoint on Lachman test but some laxity with his posterior drawer. Given these findings, the patient was given a brace and continued in physical therapy to strengthen his quadriceps muscle. By 20 months after injury, he had returned to competitive hockey and had no complaints of pain or instability. His physical examination showed full range of motion in a ligamentously stable knee with firm endpoint. The patient’s condition was unchanged at 29-month follow-up.

Discussion

There is a body of evidence that states a completely ruptured ACL does not heal.^3,6,10 In animal models, the ACL has been shown to have poor healing potential.^3,11 Some studies have suggested this is secondary to poor blood supply. Blood supply to the ACL is derived from a periligamentous, then endoligamentous, arterial network with a less vascularized area in the middle third of the ACL. Additionally, there is no blood supply from the tibia or femur, meaning the areas of attachment of the ligament are poorly vascularized.¹² With a minimal blood supply to the ACL, the supply of undifferentiated mesenchymal cells from the surrounding tissue during the initial healing process is limited. In vitro cell cultures of these cells have showed a reduced potential for proliferation and migration.⁹ Cells of the ACL have a lower response to growth factors than human medial collateral ligament cells, further suggesting a decreased reparative capacity.⁷ Joint fluid has been shown to inhibit the proliferation of these cells, further reducing their regenerative potential.¹³ Additionally, biomechanical factors that alter signaling pathways, sites of ligament reattachment, and injury to proprioceptive structures have been shown to negatively influence the healing response.^14-18

Review of the literature on healing of ACLs includes 2 case reports, totaling 3 patients, and 3 level IV therapeutic studies involving 74 patients total.^10,19-22 In most cases, the authors of these studies have indicated a nonoperative treatment protocol with bracing and a specific rehabilitation program. Malanga and colleagues¹⁰ demonstrated that an ACL torn from its attachment on the femur, with the majority of the ligament in good condition and no compromise in the length, healed back onto the femur. Kurosaka and coauthors²⁰ described case reports of isolated distal or proximal midsubstance tears that have healed spontaneously. However, none of the patients described in the literature were under the age of 20 years.

Treatment for pediatric patients with open physes causes some debate. Nonoperative management of ACL deficiency in adolescents is generally not recommended because the continued instability of the joint leads to intra-articular injury, functional impairment, and joint degeneration.^23-25 A recent systematic review found only 1 study that showed no increase in secondary intra-articular injury when surgery was delayed until skeletal maturity.²⁶ 

Our patient was a 12-year-old boy whose traumatic knee injury with multiple ruptured ligaments healed over the course of 20 months. It is likely that bracing associated with the patient’s second surgery and delayed union of his tibial fracture allowed healing tissue to be protected from excessive stress until it remodeled with sufficient strength. Most would assume that healing would occur early, during the first 6 to 9 months; however, our patient regained his stability between 8 and 13 months. It is possible that the hostile healing environment of the ACL, including the low blood supply, poor response to growth factors, and biomechanical environment, as described previously, played a factor in this delay.^7,9,12,13

It is important to recognize that our patient tore his ACL during a traumatic motorized scooter rollover collision, not the more common noncontact twisting injury. Additionally, given the patient’s knee surgery that was performed 6 months after the initial injury, it is possible that intra-articular scar formation contributed to his healing capacity. While this patient did not undergo arthroscopy to visualize the tear in the ACL, or its reconstitution, recent evidence suggests that the accuracy of MRI in diagnosing pediatric ACL injuries is excellent.^27,28 The diagnostic accuracy with new MRI machines has sensitivity and specificity approaching 100%.²⁹ Additionally, the patient’s subjective and objective improvements argue for a change in anatomy over a change in the quality of his examination.

Conclusion

The goal of ACL reconstruction in adolescents is to provide long-term stability to the knee while minimizing the risk of growth disturbance. This goal was achieved in our patient through the in situ healing of his ACL. Intrinsic reconstitution of a torn ACL is rare, and it is difficult to speculate which patients may have some healing potential. While this patient was an extreme example, his case demonstrated that protection of the knee from undue stress could favorably alter the environment of the knee to allow for healing of ACL tears. Such information could be valuable in managing select pediatric patients with open physes and ACL injuries nonoperatively, sparing them from the risks associated with surgical treatment. While we do not recommend nonoperative treatment for patients with acute tears of the ACL, we believe more investigation into the healing potential of the ACL, and potential pathways to augment this, is warranted.

The anterior cruciate ligament (ACL) restrains anterior translation of the tibia on the femur and controls rotation of the knee. The natural primary healing potential of the ACL has been extremely poor in clinical and experimental studies, and primary suture repair has not provided stability to the joint in most patients.^1-8 This has led surgeons to reconstruct the ACL, rather than to attempt nonoperative treatment. Anterior cruciate ligament reconstruction is recommended to help patients maintain activities that place shear and torque forces on the knee or to ameliorate persistent pain due to instability.⁹ Reconstruction of the ACL in adults is one of the most common procedures performed by orthopedic surgeons. However, reconstruction in the ACL-deficient adolescent remains a controversial subject, with debates surrounding operative timing and surgical technique.

This case report presents a skeletally immature patient who suffered a complete traumatic rupture of his ACL, which intrinsically healed. The patient had a protracted treatment course, complicated by an open tibial fracture with delayed union. He responded to a progressive rehabilitation program and has made a good functional recovery. Review of the literature has demonstrated limited evidence of intrinsic ACL healing, none of which has been shown to occur in a skeletally immature patient. The patient’s mother provided written informed consent for print and electronic publication of this case report.

Case Report

A 12-year-old boy was brought to our level I trauma center by ambulance after being hit by a car while riding a motorized scooter. He presented with a grade IIIB open tibial fracture and a distal fibula fracture of his left lower extremity and was taken to the operating room that night for irrigation and débridement, percutaneous fixation of the fibula, and intramedullary flexible nail fixation of the tibia. On postoperative day 1, he had increasing pain and, once his splint was removed, his compartments were found to be very tense. He was taken emergently to the operating room for 4 compartment fasciotomies of the left lower extremity with wound vacuum-assisted closure (VAC) placement. This was changed on hospital day 4 and was removed with definitive closure on day 7. Examination under anesthesia prior to the final wound VAC change was performed given the patient’s complaints during physical therapy. This showed anterior and posterior ligamentous instability of the knee, and he was placed in a knee immobilizer. He was discharged on hospital day 11.

At 2-week follow-up, the patient was doing well, except that he was nonadherent with the knee immobilizer and unable to fully extend his left knee. On examination, a posterior drawer sign was noted; therefore, the patient was referred for magnetic resonance imaging (MRI) to evaluate his ligaments. His MRI, 9 weeks after injury, showed: (1) complete tears of both the anterior and posterior cruciate ligaments (PCLs) (Figures 1A, 1B); (2) medial meniscus and lateral meniscus tears; (3) 2.0-cm plate-like avulsion fracture of the posterolateral femoral metaphysis involving the insertion of the lateral head of the gastrocnemius muscle, fibular collateral ligament, and popliteus muscle (Figure 2); and (4) left posterior lateral tibial plateau contusion.

The patient was started on a 6-week course of physical therapy with active and active-assisted extension exercises. At follow-up approximately 3½ months after injury, he was found to have a 35º flexion contracture with pain at the end extension. Unfortunately, his tibial fracture showed minimal signs of healing, and the decision was made to delay surgical intervention on the knee until the tibial fracture had healed. He was given a knee orthotic to wear at night to help regain his knee extension.

Six months after injury, the patient underwent open removal of the avulsed bony fragment, posterior knee capsule release, and autograft of the delayed union tibial fracture. He was placed in a straight leg cast postoperatively and was discharged home on postoperative day 2. He transitioned to a knee immobilizer after 2 weeks. Six weeks after the last surgery, he had range of motion of 0º to 130º. Ligamentous examination at this time showed anterior and posterior drawer signs, positive Lachman test, and dial test with 90º of external rotation. He was placed in physical therapy for a total of 10 weeks to work on his quadriceps muscle strength and 15º extension lag.

On 13-month postinjury radiographs, the patient was noted to have adequate healing of his tibial fracture, and ligamentous reconstruction was discussed. At this time, the patient did not have any instability or pain in the knee. Examination demonstrated a very mild effusion of the left knee. Range of motion determined by goniometer was from -3º to 140º, and Lachman test was positive but with solid 2+ endpoint. He also had a positive posterior drawer sign with no endpoint, positive sag sign of his tibia, and positive active quadriceps test of the left leg. His dial test showed some increased external rotation at 90º but was equivocal at 30º when compared with the contralateral knee, demonstrating involvement of the posterolateral corner.

Sixteen months after injury, repeat MRI to further evaluate the posterolateral corner showed: (1) complete medial and lateral meniscal healing without evidence of residual or recurrent tear, and (2) interval healing of the remote ACL and PCL tears with intact insertions (Figures 3A, 3B). This scan showed an end-to-end continuous ACL with homogeneous signal and disappearance of the secondary signs. Physical examination at this time showed a very firm endpoint on Lachman test but some laxity with his posterior drawer. Given these findings, the patient was given a brace and continued in physical therapy to strengthen his quadriceps muscle. By 20 months after injury, he had returned to competitive hockey and had no complaints of pain or instability. His physical examination showed full range of motion in a ligamentously stable knee with firm endpoint. The patient’s condition was unchanged at 29-month follow-up.

Discussion

There is a body of evidence that states a completely ruptured ACL does not heal.^3,6,10 In animal models, the ACL has been shown to have poor healing potential.^3,11 Some studies have suggested this is secondary to poor blood supply. Blood supply to the ACL is derived from a periligamentous, then endoligamentous, arterial network with a less vascularized area in the middle third of the ACL. Additionally, there is no blood supply from the tibia or femur, meaning the areas of attachment of the ligament are poorly vascularized.¹² With a minimal blood supply to the ACL, the supply of undifferentiated mesenchymal cells from the surrounding tissue during the initial healing process is limited. In vitro cell cultures of these cells have showed a reduced potential for proliferation and migration.⁹ Cells of the ACL have a lower response to growth factors than human medial collateral ligament cells, further suggesting a decreased reparative capacity.⁷ Joint fluid has been shown to inhibit the proliferation of these cells, further reducing their regenerative potential.¹³ Additionally, biomechanical factors that alter signaling pathways, sites of ligament reattachment, and injury to proprioceptive structures have been shown to negatively influence the healing response.^14-18

Review of the literature on healing of ACLs includes 2 case reports, totaling 3 patients, and 3 level IV therapeutic studies involving 74 patients total.^10,19-22 In most cases, the authors of these studies have indicated a nonoperative treatment protocol with bracing and a specific rehabilitation program. Malanga and colleagues¹⁰ demonstrated that an ACL torn from its attachment on the femur, with the majority of the ligament in good condition and no compromise in the length, healed back onto the femur. Kurosaka and coauthors²⁰ described case reports of isolated distal or proximal midsubstance tears that have healed spontaneously. However, none of the patients described in the literature were under the age of 20 years.

Treatment for pediatric patients with open physes causes some debate. Nonoperative management of ACL deficiency in adolescents is generally not recommended because the continued instability of the joint leads to intra-articular injury, functional impairment, and joint degeneration.^23-25 A recent systematic review found only 1 study that showed no increase in secondary intra-articular injury when surgery was delayed until skeletal maturity.²⁶ 

Our patient was a 12-year-old boy whose traumatic knee injury with multiple ruptured ligaments healed over the course of 20 months. It is likely that bracing associated with the patient’s second surgery and delayed union of his tibial fracture allowed healing tissue to be protected from excessive stress until it remodeled with sufficient strength. Most would assume that healing would occur early, during the first 6 to 9 months; however, our patient regained his stability between 8 and 13 months. It is possible that the hostile healing environment of the ACL, including the low blood supply, poor response to growth factors, and biomechanical environment, as described previously, played a factor in this delay.^7,9,12,13

It is important to recognize that our patient tore his ACL during a traumatic motorized scooter rollover collision, not the more common noncontact twisting injury. Additionally, given the patient’s knee surgery that was performed 6 months after the initial injury, it is possible that intra-articular scar formation contributed to his healing capacity. While this patient did not undergo arthroscopy to visualize the tear in the ACL, or its reconstitution, recent evidence suggests that the accuracy of MRI in diagnosing pediatric ACL injuries is excellent.^27,28 The diagnostic accuracy with new MRI machines has sensitivity and specificity approaching 100%.²⁹ Additionally, the patient’s subjective and objective improvements argue for a change in anatomy over a change in the quality of his examination.

Conclusion

The goal of ACL reconstruction in adolescents is to provide long-term stability to the knee while minimizing the risk of growth disturbance. This goal was achieved in our patient through the in situ healing of his ACL. Intrinsic reconstitution of a torn ACL is rare, and it is difficult to speculate which patients may have some healing potential. While this patient was an extreme example, his case demonstrated that protection of the knee from undue stress could favorably alter the environment of the knee to allow for healing of ACL tears. Such information could be valuable in managing select pediatric patients with open physes and ACL injuries nonoperatively, sparing them from the risks associated with surgical treatment. While we do not recommend nonoperative treatment for patients with acute tears of the ACL, we believe more investigation into the healing potential of the ACL, and potential pathways to augment this, is warranted.

The biceps brachii derives its name from the 2 heads of the muscle. The short head originates from the coracoid apex, with the coracobrachialis muscle. The long head of the biceps tendon (LHBT) starts within the capsule of the shoulder joint, running from the supraglenoid tubercle or labrum.¹ The tendon typically runs free along its intra-articular course, but it is also extrasynovial and ensheathed by a continuation of the synovial lining of the articular capsule that extends to the inferior-most extent of the bicipital groove.² Congenital anomalies of the LHBT are uncommon, although several atypical forms have been described. A literature search for anomalous LHBT identified several variations in anatomic descriptions, including Y-shaped variant, complete absence of tendon, extra-articular attachment, and a variety of intracapsular attachments. In all, 8 case reports of aberrant intracapsular attachment of LHBT^3-12 were identified. These cases presented with a variety of clinical manifestations and pathologic changes. Often, these anatomic variations are considered innocuous, yet some present with pathologic findings.

We present the clinical, magnetic resonance imaging (MRI), and arthroscopic findings of a relatively young athletic patient who was experiencing symptoms of bilateral superior labrum anterior to posterior (SLAP) tears that were unresponsive to conservative management. A unique anatomic variant of the LHBT that involved confluence of the LHBT with the undersurface of the anterosuperior capsule at the rotator interval, as well as a Buford complex anteriorly, was identified and treated. We believe that the tethering of the biceps tendon to the capsule combined with the Buford complex created increased stress on the superior labrum and biceps anchor variant, leading to the development of bilateral symptomatic type II SLAP tears. Knowledge of this variant, though perhaps rare, may be relevant for diagnostic recognition of young athletic patients who present with recalcitrant shoulder symptoms. The patient and the patient’s parents provided written informed consent for print and electronic publication of this case report.

Case Report

A 15-year-old healthy and active athletic boy presented with pain in the right shoulder without history of trauma. He was active in both swimming and baseball. He complained of pain that was present with activities, such as lifting weights, swimming, and throwing. His treatment prior to the office visit consisted of nonsteroidal anti-inflammatory medication, rest, and a therapy program initiated by his high school athletic trainer.

Physical examination demonstrated tenderness to palpation over the posterior capsule and biceps. Motion was full, cuff strength was normal, and SLAP signs (O’Brien, Speed, and Jobe relocation) were positive. A radiograph showed no sign of fracture or dislocation, and no evidence of bony abnormality.

The patient was sent for an MRI arthrogram, which showed a SLAP tear extending from 1 o’clock anteriorly to 10 o’clock posteriorly without intra-articular displacement. No rotator cuff tear was noted. The biceps tendon was noted to be unremarkable and located within the bicipital groove, although retrospective review of the MRI showed that the intra-articular biceps tendon was somewhat confluent with the adjacent tissues.

The patient underwent right shoulder arthroscopy. The shoulder was stable to ligamentous examination under anesthesia. Arthroscopic evaluation revealed that there was a type II SLAP tear extending from the 11-o’clock to the 2-o’clock positions. The superior glenohumeral ligament was identified as it arose from the upper pole of the glenoid labrum and then ran parallel and inferior to the tendon of the biceps towards the lesser tubercle. Surprisingly, there was a very unusual attachment of the intracapsular LHBT to the undersurface of the rotator interval, which restricted biceps excursion in relation to the rotator cuff. Additionally, there was a thick cord-like middle glenohumeral ligament anteriorly that lacked the normal glenoid attachments, thus representing a Buford complex. Interestingly, the labral tear could not only be displaced with a probe, but placing the shoulder through a range of motion also led to increased displacement of the labrum from the glenoid, likely because the biceps tendon was tethered to the undersurface of the capsule.

At the time of arthroscopy, the LHBT was released from its attachment to the capsule at the rotator interval with a radiofrequency wand and shaver. A labral repair was performed using three 2.9-mm bioabsorbable suture anchors, placing 2 posterior and 1 anterior to the biceps tendon. The integrity of the labral repair was observed while placing the shoulder through range of motion.  

Postoperatively, the patient was kept in a sling for 5 weeks. Home exercises were initiated at 2 weeks, and outpatient physical therapy was implemented at 4 weeks. The patient resumed swimming, throwing, and other activities—with minimal discomfort—at 6 months postoperatively.

Three years after his initial visit, the patient returned to the office with a similar complaint of pain and limitation of function in his left shoulder after returning to full athletic competition. Once again, there was no history of injury, and history, physical examination, and MRI arthrogram (Figures 1A, 1B) evaluation proved to be very similar to this young athlete’s right shoulder work-up.

The patient once again underwent shoulder arthroscopy and treatment. Although this was now the left shoulder, the findings were essentially identical to the right shoulder. Once again, the labrum was detached from the 11-o’clock to 2-o’clock positions, and a Buford complex was present anteriorly (Figure 2A). The labral tear was easily displaceable from the glenoid with a probe, and placing the shoulder through a range of motion led to increased displacement of the labrum from the glenoid. There was also confluence of the intra-articular LHBT with the undersurface of the capsule within the rotator interval (Figure 2B). A radiofrequency wand, shaver, and elevator were used to define the biceps tendon and separate it from the undersurface of the capsule. The SLAP repair was performed using three 2.9-mm absorbable suture anchors with 2 posterior and 1 anterior to the biceps tendon insertion. The labral repair was observed while placing the shoulder through range of motion and the shoulder was seen to be free of any undue tension on the labrum.

Postoperatively, the patient’s sling and rehabilitation protocol was identical to that of the right shoulder. The patient progressed well, was released to full activity at 6 months, and has not returned with any further complaints of left or right shoulder pain. Approximately 3 years after treatment the patient was contacted via phone and asked about symptoms, pain, and activity. He denies current symptoms of clicking or instability and has no pain that he can identify as being related to previous pathology or treatment. Since the surgery, he has ceased competitive sports and weight lifting, which he attributes to deconditioning associated with postsurgical immobilization and lack of motivation.

Discussion

Of the 8 case reports in the literature that identified variable intra-articular biceps insertional anatomy, only 2 reports represented confluence of the biceps within the rotator interval.⁷ Interestingly, of the cases identified, the single case that presented a patient with similar pathology of a type II SLAP lesion had an almost identical anatomical variant presentation consisting of both the anomalous insertion of the LHBT into the undersurface of the rotator interval and a Buford variant of the anterosuperior glenohumeral ligament complex. To our knowledge, our bilateral case of an altered intra-articular biceps insertion and a concomitant SLAP tear supports the theory that this pattern of anomalous insertion may very well have altered the biomechanics of the tendon, resulting in acquired pathology to the superior labrum.

The literature reviewed showed the prevalence of anatomic variations of the LHBT ranged from 1.9% to 7.4%.^13,14 These variations are generally considered benign; however, in some cases—as in the cases of the young athletes presented by Wahl and MacGillivray⁷ and in this report—anatomic variation may play an important role in pathogenesis of different injury patterns. The primary function of the LHBT is the stabilization of the glenohumeral joint during abduction and external rotation.¹⁵ When the insertion diverges from normal (eg, when the tendon is tethered to the undersurface of the rotator cuff), the biomechanical stresses on the tendon likely change. As a result of the anomalous position of the LHBT origin, there may be a change in the shoulder joint’s biomechanics, with increased strain on the glenohumeral ligament and its attachment onto the glenoid.¹⁶

This case report differs from publications on variable superior glenohumeral ligament attachments because a discrete superior glenohumeral ligament structure was isolated from the biceps tendon. Although a larger case series or patient cohort, as well as more involved biomechanical analysis, would certainly be necessary to prove our hypothesis, we believe that this case suggests certain anatomic LHBT and labral variations can contribute to the develop of SLAP tears in younger individuals.

The biceps brachii derives its name from the 2 heads of the muscle. The short head originates from the coracoid apex, with the coracobrachialis muscle. The long head of the biceps tendon (LHBT) starts within the capsule of the shoulder joint, running from the supraglenoid tubercle or labrum.¹ The tendon typically runs free along its intra-articular course, but it is also extrasynovial and ensheathed by a continuation of the synovial lining of the articular capsule that extends to the inferior-most extent of the bicipital groove.² Congenital anomalies of the LHBT are uncommon, although several atypical forms have been described. A literature search for anomalous LHBT identified several variations in anatomic descriptions, including Y-shaped variant, complete absence of tendon, extra-articular attachment, and a variety of intracapsular attachments. In all, 8 case reports of aberrant intracapsular attachment of LHBT^3-12 were identified. These cases presented with a variety of clinical manifestations and pathologic changes. Often, these anatomic variations are considered innocuous, yet some present with pathologic findings.

We present the clinical, magnetic resonance imaging (MRI), and arthroscopic findings of a relatively young athletic patient who was experiencing symptoms of bilateral superior labrum anterior to posterior (SLAP) tears that were unresponsive to conservative management. A unique anatomic variant of the LHBT that involved confluence of the LHBT with the undersurface of the anterosuperior capsule at the rotator interval, as well as a Buford complex anteriorly, was identified and treated. We believe that the tethering of the biceps tendon to the capsule combined with the Buford complex created increased stress on the superior labrum and biceps anchor variant, leading to the development of bilateral symptomatic type II SLAP tears. Knowledge of this variant, though perhaps rare, may be relevant for diagnostic recognition of young athletic patients who present with recalcitrant shoulder symptoms. The patient and the patient’s parents provided written informed consent for print and electronic publication of this case report.

Case Report

A 15-year-old healthy and active athletic boy presented with pain in the right shoulder without history of trauma. He was active in both swimming and baseball. He complained of pain that was present with activities, such as lifting weights, swimming, and throwing. His treatment prior to the office visit consisted of nonsteroidal anti-inflammatory medication, rest, and a therapy program initiated by his high school athletic trainer.

Physical examination demonstrated tenderness to palpation over the posterior capsule and biceps. Motion was full, cuff strength was normal, and SLAP signs (O’Brien, Speed, and Jobe relocation) were positive. A radiograph showed no sign of fracture or dislocation, and no evidence of bony abnormality.

The patient was sent for an MRI arthrogram, which showed a SLAP tear extending from 1 o’clock anteriorly to 10 o’clock posteriorly without intra-articular displacement. No rotator cuff tear was noted. The biceps tendon was noted to be unremarkable and located within the bicipital groove, although retrospective review of the MRI showed that the intra-articular biceps tendon was somewhat confluent with the adjacent tissues.

The patient underwent right shoulder arthroscopy. The shoulder was stable to ligamentous examination under anesthesia. Arthroscopic evaluation revealed that there was a type II SLAP tear extending from the 11-o’clock to the 2-o’clock positions. The superior glenohumeral ligament was identified as it arose from the upper pole of the glenoid labrum and then ran parallel and inferior to the tendon of the biceps towards the lesser tubercle. Surprisingly, there was a very unusual attachment of the intracapsular LHBT to the undersurface of the rotator interval, which restricted biceps excursion in relation to the rotator cuff. Additionally, there was a thick cord-like middle glenohumeral ligament anteriorly that lacked the normal glenoid attachments, thus representing a Buford complex. Interestingly, the labral tear could not only be displaced with a probe, but placing the shoulder through a range of motion also led to increased displacement of the labrum from the glenoid, likely because the biceps tendon was tethered to the undersurface of the capsule.

At the time of arthroscopy, the LHBT was released from its attachment to the capsule at the rotator interval with a radiofrequency wand and shaver. A labral repair was performed using three 2.9-mm bioabsorbable suture anchors, placing 2 posterior and 1 anterior to the biceps tendon. The integrity of the labral repair was observed while placing the shoulder through range of motion.  

Postoperatively, the patient was kept in a sling for 5 weeks. Home exercises were initiated at 2 weeks, and outpatient physical therapy was implemented at 4 weeks. The patient resumed swimming, throwing, and other activities—with minimal discomfort—at 6 months postoperatively.

Three years after his initial visit, the patient returned to the office with a similar complaint of pain and limitation of function in his left shoulder after returning to full athletic competition. Once again, there was no history of injury, and history, physical examination, and MRI arthrogram (Figures 1A, 1B) evaluation proved to be very similar to this young athlete’s right shoulder work-up.

The patient once again underwent shoulder arthroscopy and treatment. Although this was now the left shoulder, the findings were essentially identical to the right shoulder. Once again, the labrum was detached from the 11-o’clock to 2-o’clock positions, and a Buford complex was present anteriorly (Figure 2A). The labral tear was easily displaceable from the glenoid with a probe, and placing the shoulder through a range of motion led to increased displacement of the labrum from the glenoid. There was also confluence of the intra-articular LHBT with the undersurface of the capsule within the rotator interval (Figure 2B). A radiofrequency wand, shaver, and elevator were used to define the biceps tendon and separate it from the undersurface of the capsule. The SLAP repair was performed using three 2.9-mm absorbable suture anchors with 2 posterior and 1 anterior to the biceps tendon insertion. The labral repair was observed while placing the shoulder through range of motion and the shoulder was seen to be free of any undue tension on the labrum.

Postoperatively, the patient’s sling and rehabilitation protocol was identical to that of the right shoulder. The patient progressed well, was released to full activity at 6 months, and has not returned with any further complaints of left or right shoulder pain. Approximately 3 years after treatment the patient was contacted via phone and asked about symptoms, pain, and activity. He denies current symptoms of clicking or instability and has no pain that he can identify as being related to previous pathology or treatment. Since the surgery, he has ceased competitive sports and weight lifting, which he attributes to deconditioning associated with postsurgical immobilization and lack of motivation.

Discussion

Of the 8 case reports in the literature that identified variable intra-articular biceps insertional anatomy, only 2 reports represented confluence of the biceps within the rotator interval.⁷ Interestingly, of the cases identified, the single case that presented a patient with similar pathology of a type II SLAP lesion had an almost identical anatomical variant presentation consisting of both the anomalous insertion of the LHBT into the undersurface of the rotator interval and a Buford variant of the anterosuperior glenohumeral ligament complex. To our knowledge, our bilateral case of an altered intra-articular biceps insertion and a concomitant SLAP tear supports the theory that this pattern of anomalous insertion may very well have altered the biomechanics of the tendon, resulting in acquired pathology to the superior labrum.

The literature reviewed showed the prevalence of anatomic variations of the LHBT ranged from 1.9% to 7.4%.^13,14 These variations are generally considered benign; however, in some cases—as in the cases of the young athletes presented by Wahl and MacGillivray⁷ and in this report—anatomic variation may play an important role in pathogenesis of different injury patterns. The primary function of the LHBT is the stabilization of the glenohumeral joint during abduction and external rotation.¹⁵ When the insertion diverges from normal (eg, when the tendon is tethered to the undersurface of the rotator cuff), the biomechanical stresses on the tendon likely change. As a result of the anomalous position of the LHBT origin, there may be a change in the shoulder joint’s biomechanics, with increased strain on the glenohumeral ligament and its attachment onto the glenoid.¹⁶

This case report differs from publications on variable superior glenohumeral ligament attachments because a discrete superior glenohumeral ligament structure was isolated from the biceps tendon. Although a larger case series or patient cohort, as well as more involved biomechanical analysis, would certainly be necessary to prove our hypothesis, we believe that this case suggests certain anatomic LHBT and labral variations can contribute to the develop of SLAP tears in younger individuals.

The biceps brachii derives its name from the 2 heads of the muscle. The short head originates from the coracoid apex, with the coracobrachialis muscle. The long head of the biceps tendon (LHBT) starts within the capsule of the shoulder joint, running from the supraglenoid tubercle or labrum.¹ The tendon typically runs free along its intra-articular course, but it is also extrasynovial and ensheathed by a continuation of the synovial lining of the articular capsule that extends to the inferior-most extent of the bicipital groove.² Congenital anomalies of the LHBT are uncommon, although several atypical forms have been described. A literature search for anomalous LHBT identified several variations in anatomic descriptions, including Y-shaped variant, complete absence of tendon, extra-articular attachment, and a variety of intracapsular attachments. In all, 8 case reports of aberrant intracapsular attachment of LHBT^3-12 were identified. These cases presented with a variety of clinical manifestations and pathologic changes. Often, these anatomic variations are considered innocuous, yet some present with pathologic findings.

We present the clinical, magnetic resonance imaging (MRI), and arthroscopic findings of a relatively young athletic patient who was experiencing symptoms of bilateral superior labrum anterior to posterior (SLAP) tears that were unresponsive to conservative management. A unique anatomic variant of the LHBT that involved confluence of the LHBT with the undersurface of the anterosuperior capsule at the rotator interval, as well as a Buford complex anteriorly, was identified and treated. We believe that the tethering of the biceps tendon to the capsule combined with the Buford complex created increased stress on the superior labrum and biceps anchor variant, leading to the development of bilateral symptomatic type II SLAP tears. Knowledge of this variant, though perhaps rare, may be relevant for diagnostic recognition of young athletic patients who present with recalcitrant shoulder symptoms. The patient and the patient’s parents provided written informed consent for print and electronic publication of this case report.

Case Report

A 15-year-old healthy and active athletic boy presented with pain in the right shoulder without history of trauma. He was active in both swimming and baseball. He complained of pain that was present with activities, such as lifting weights, swimming, and throwing. His treatment prior to the office visit consisted of nonsteroidal anti-inflammatory medication, rest, and a therapy program initiated by his high school athletic trainer.

Physical examination demonstrated tenderness to palpation over the posterior capsule and biceps. Motion was full, cuff strength was normal, and SLAP signs (O’Brien, Speed, and Jobe relocation) were positive. A radiograph showed no sign of fracture or dislocation, and no evidence of bony abnormality.

The patient was sent for an MRI arthrogram, which showed a SLAP tear extending from 1 o’clock anteriorly to 10 o’clock posteriorly without intra-articular displacement. No rotator cuff tear was noted. The biceps tendon was noted to be unremarkable and located within the bicipital groove, although retrospective review of the MRI showed that the intra-articular biceps tendon was somewhat confluent with the adjacent tissues.

The patient underwent right shoulder arthroscopy. The shoulder was stable to ligamentous examination under anesthesia. Arthroscopic evaluation revealed that there was a type II SLAP tear extending from the 11-o’clock to the 2-o’clock positions. The superior glenohumeral ligament was identified as it arose from the upper pole of the glenoid labrum and then ran parallel and inferior to the tendon of the biceps towards the lesser tubercle. Surprisingly, there was a very unusual attachment of the intracapsular LHBT to the undersurface of the rotator interval, which restricted biceps excursion in relation to the rotator cuff. Additionally, there was a thick cord-like middle glenohumeral ligament anteriorly that lacked the normal glenoid attachments, thus representing a Buford complex. Interestingly, the labral tear could not only be displaced with a probe, but placing the shoulder through a range of motion also led to increased displacement of the labrum from the glenoid, likely because the biceps tendon was tethered to the undersurface of the capsule.

At the time of arthroscopy, the LHBT was released from its attachment to the capsule at the rotator interval with a radiofrequency wand and shaver. A labral repair was performed using three 2.9-mm bioabsorbable suture anchors, placing 2 posterior and 1 anterior to the biceps tendon. The integrity of the labral repair was observed while placing the shoulder through range of motion.  

Postoperatively, the patient was kept in a sling for 5 weeks. Home exercises were initiated at 2 weeks, and outpatient physical therapy was implemented at 4 weeks. The patient resumed swimming, throwing, and other activities—with minimal discomfort—at 6 months postoperatively.

Three years after his initial visit, the patient returned to the office with a similar complaint of pain and limitation of function in his left shoulder after returning to full athletic competition. Once again, there was no history of injury, and history, physical examination, and MRI arthrogram (Figures 1A, 1B) evaluation proved to be very similar to this young athlete’s right shoulder work-up.

The patient once again underwent shoulder arthroscopy and treatment. Although this was now the left shoulder, the findings were essentially identical to the right shoulder. Once again, the labrum was detached from the 11-o’clock to 2-o’clock positions, and a Buford complex was present anteriorly (Figure 2A). The labral tear was easily displaceable from the glenoid with a probe, and placing the shoulder through a range of motion led to increased displacement of the labrum from the glenoid. There was also confluence of the intra-articular LHBT with the undersurface of the capsule within the rotator interval (Figure 2B). A radiofrequency wand, shaver, and elevator were used to define the biceps tendon and separate it from the undersurface of the capsule. The SLAP repair was performed using three 2.9-mm absorbable suture anchors with 2 posterior and 1 anterior to the biceps tendon insertion. The labral repair was observed while placing the shoulder through range of motion and the shoulder was seen to be free of any undue tension on the labrum.

Postoperatively, the patient’s sling and rehabilitation protocol was identical to that of the right shoulder. The patient progressed well, was released to full activity at 6 months, and has not returned with any further complaints of left or right shoulder pain. Approximately 3 years after treatment the patient was contacted via phone and asked about symptoms, pain, and activity. He denies current symptoms of clicking or instability and has no pain that he can identify as being related to previous pathology or treatment. Since the surgery, he has ceased competitive sports and weight lifting, which he attributes to deconditioning associated with postsurgical immobilization and lack of motivation.

Discussion

Of the 8 case reports in the literature that identified variable intra-articular biceps insertional anatomy, only 2 reports represented confluence of the biceps within the rotator interval.⁷ Interestingly, of the cases identified, the single case that presented a patient with similar pathology of a type II SLAP lesion had an almost identical anatomical variant presentation consisting of both the anomalous insertion of the LHBT into the undersurface of the rotator interval and a Buford variant of the anterosuperior glenohumeral ligament complex. To our knowledge, our bilateral case of an altered intra-articular biceps insertion and a concomitant SLAP tear supports the theory that this pattern of anomalous insertion may very well have altered the biomechanics of the tendon, resulting in acquired pathology to the superior labrum.

The literature reviewed showed the prevalence of anatomic variations of the LHBT ranged from 1.9% to 7.4%.^13,14 These variations are generally considered benign; however, in some cases—as in the cases of the young athletes presented by Wahl and MacGillivray⁷ and in this report—anatomic variation may play an important role in pathogenesis of different injury patterns. The primary function of the LHBT is the stabilization of the glenohumeral joint during abduction and external rotation.¹⁵ When the insertion diverges from normal (eg, when the tendon is tethered to the undersurface of the rotator cuff), the biomechanical stresses on the tendon likely change. As a result of the anomalous position of the LHBT origin, there may be a change in the shoulder joint’s biomechanics, with increased strain on the glenohumeral ligament and its attachment onto the glenoid.¹⁶

This case report differs from publications on variable superior glenohumeral ligament attachments because a discrete superior glenohumeral ligament structure was isolated from the biceps tendon. Although a larger case series or patient cohort, as well as more involved biomechanical analysis, would certainly be necessary to prove our hypothesis, we believe that this case suggests certain anatomic LHBT and labral variations can contribute to the develop of SLAP tears in younger individuals.

The overhead athlete’s shoulder is exposed to extremes of stress and range of motion (ROM), predisposing this joint to unique injury patterns. Prompt diagnosis and management begin with a comprehensive history and a physical examination, supplemented by imaging studies as needed. Furthermore, the throwing shoulder undergoes adaptive changes, such as partial undersurface rotator cuff tears and capsular laxity. Imaging studies typically demonstrate abnormalities in asymptomatic throwers. Therefore, clinicians must be skilled in history taking and physical examination in throwing athletes to accurately determine the cause of symptoms and provide optimal treatment. This primer provides orthopedic surgeons with the key points in performing a thorough physical examination of the shoulder in overhead athletes.

When working with overhead athletes, surgeons must elicit the precise nature of symptoms. For example, it is important to distinguish pain from fatigue, as well as complaints related purely to decline in performance. Often, collaboration with the player’s parent or coach may help clarify the chief complaint. In addition, surgeons must have an intricate knowledge of the various stages of the overhead motion, as symptoms in specific stages (late cocking/early acceleration) may raise suspicion for distinctive pathology (labral/biceps complex). Last, it is imperative to understand that the shoulder represents only one part of the kinetic chain in overhead athletes. Successful throwing relies on integrity of the entire kinetic chain, starting with the lower extremity and trunk, extending through the spine, scapula, and shoulder, and terminating with the hand and fingers. Pathology anywhere in the chain must be evaluated and addressed.

When examining the shoulder in overhead athletes, surgeons must address several anatomical structures, both bony and soft tissue. Proper examination begins with comprehensive assessment of the ROM and strength of the various muscles around the shoulder, along with visual inspection to identify any asymmetry of these structures. In addition, the scapulothoracic structures must be examined in detail to rule out underlying dyskinesis. The capsular and ligamentous components of the shoulder joint must be further assessed to note any capsular contracture causing glenohumeral internal rotation deficit (GIRD) or any pathology with the rotator cuff or labral/biceps complex. Last, a comprehensive neurovascular examination should be performed to rule out any compression or neuropathy affecting the shoulder and overhead motion. Findings from the physical examination may then require further imaging to correlate the history and physical examination findings.

1. Inspection, palpation, strength testing

Every examination of the shoulder must begin with visual inspection, along with assessment of basic ROM and strength. The patient must be positioned and exposed adequately to promote visualization of the entire shoulder and scapular girdle, from both anterior and posterior. Visual inspection focuses on identifying any areas of asymmetry, such as position of the bony prominences or bulk of the muscular fossae. Asymmetry of the bony architecture may indicate prior trauma, and atrophy of the muscular fossae may indicate nerve compression. For example, atrophy of the infraspinatus fossa may be caused by compression of the suprascapular nerve at the spinoglenoid notch (likely by a cyst, often associated with labral pathology, but infraspinatus atrophy can result even without the presence of a compressive cyst¹). Alternatively, atrophy of both the supraspinatus and infraspinatus fossae may indicate underlying compression of the suprascapular nerve at the suprascapular notch (either by a cyst or by the transverse scapular ligament). Static and dynamic observation of the posterior aspect of the shoulder may help identify gross pathology with scapular positioning or retraction, indicating underlying dyskinesis (discussed later). Deformity of the acromioclavicular joint may indicate prior trauma or separation. Last, all prior surgical scars should be noted.

Selective palpation may help identify pathology in the shoulder of the throwing athlete. Tenderness at the acromioclavicular joint may be especially common in patients who have had prior sprains of this joint or who have degenerative changes. Tenderness along the biceps tendon may be present in those with biceps tendinitis or partial tear. In addition, tenderness at the coracoid may be present in those with scapular dyskinesis. Posteriorly, palpation at the inferomedial aspect of the scapula (Figure 1), as with palpation along the medial border of the scapula, may elicit tenderness in those with scapulothoracic bursitis.

Strength testing in the shoulder is performed to elicit any deficiencies of the rotator cuff/musculature or surrounding structures. Weakness in forward elevation may indicate pathology in the supraspinatus, whereas weakness in external rotation may reflect deficiency in the infraspinatus or teres minor. Teres minor deficiency may be more isolated with weakness in a position of shoulder abduction to 90°. Last, weakness in internal rotation may indicate subscapularis deficiency. Lag signs and other provocative maneuvers are similarly elicited but typically are positive only in the event of large tears of the rotator cuff. These signs and maneuvers include the internal rotation lag sign or belly press test for subscapularis integrity, the drop-arm sign for supraspinatus function, the external rotation lag sign for infraspinatus function, and the hornblower sign for teres minor integrity. Supporting muscles of the shoulder may also be tested. Latissimus strength may be tested with resisted downward rotation of the arm with the shoulder in abduction and the elbow flexed to 90°.

2. ROM and GIRD assessment

After inspection and palpation, the shoulder should be ranged in all relevant planes of motion. Our standard examination includes forward elevation in the frontal and scapular planes, along with external rotation at the side and at 90° of abduction, as well as internal rotation behind the back with documentation of the highest spinal level that the patient can reach. This examination may be performed with the patient upright, but supine positioning can help stabilize the scapula and provide more accurate views of motion. Deficits of internal rotation may be a common finding in overhead athletes, and the degree of this deficit should be quantitatively noted.

Bony and soft-tissue remodeling of the shoulder (and associated structures) in the overhead athlete can lead to contracture of the posterior capsule. This contracture can cause excessive external rotation and subsequent decrease in internal rotation, leading to pain and anterior instability in the throwing shoulder.² For precise measurements of the internal and external rotation arc, the scapula must be stabilized. This can be done with the patient supine on the examining table or seated upright with manual stabilization of the scapula by the examiner. Once the scapula is stabilized, the arc of internal and external rotation (with the arm in about 90° of abduction) can be measured with a goniometer, with maximum values obtained as the scapula begins to move along the posterior chest wall.² The difference in internal rotation between the dominant and nondominant arms defines the extent of the athlete’s GIRD. Internal rotation can also be qualitatively assessed by having the athlete internally rotate each arm and reach up the spine while the examiner notes the difference in level achieved. However, this does not provide a quantitative assessment of the patient’s GIRD.

In general, the sum of the internal and external rotation arcs on the 2 sides should be symmetric. Consequently, in GIRD, excessive external rotation is balanced by decreased internal rotation. Symptomatic GIRD may be present when there is more than 25° of discrepancy in internal rotation between the athlete’s dominant and nondominant arms.² The goal is to reduce this discrepancy to less than 20°.

3. Internal impingement: rotator cuff and labrum

In overhead athletes, an intricate relationship involving rotator cuff, labrum, and biceps tendon allows for efficient, pain-free force delivery at the shoulder. However, because of the significant external rotation and abduction required in the overhead motion, there may be internal impingement of the posterosuperior rotator cuff (infraspinatus and posterior aspect of supraspinatus) between the posterior labrum and the greater tuberosity. Detailed examination of these structures must be performed in any assessment of an overhead athlete. Symptomatic patients may complain of pain during the throwing cycle, particularly in late cocking and early acceleration.

The modified relocation examination is a common maneuver to detect internal impingement.³ In this examination, the patient’s arm is brought into a position of maximal external rotation and abduction mimicking that found in late cocking or early acceleration. In this position, a patient with internal impingement complains of pain in the posterior shoulder. A posteriorly directed force on the humerus relieves this pain.

There are also many examinations for detecting labral pathology, specifically a SLAP (superior labrum, anterior to posterior) lesion, which is commonly found in patients with internal impingement. One commonly tested maneuver is the O’Brien active compression test (Figures 2A, 2B), which has excellent sensitivity and specificity in detecting type II SLAP lesions.⁴ In this examination, the patient holds the arm in about 15° of adduction and 90° of forward elevation. A downward force is applied with the forearm pronated and subsequently supinated. If pain is noted on the force applied to the pronated arm, and if this pain decreases in the supinated examination, the test is positive for labral pathology.

Anterior instability is routinely found in these patients. Translation is measured with the anterior load and shift test. Anterior translation is tested with the patient supine, with the arm in abduction and external rotation, and with the examiner placing an anteriorly directed force on the humeral head. Translation is compared with the contralateral side and graded on a 3-point scale (1+ is translation to glenoid rim, 2+ is translation over glenoid rim but reduces, 3+ is translation over glenoid and locking). We also use the anterior release test, in which the patient is supine, the arm is brought into abduction and external rotation, and the examiner places a posteriorly directed force on the humeral head. When the examiner removes this force, the patient notices symptoms of instability caused by subluxation (Figures 3A, 3B).

Biceps tendon testing should also be performed to help elicit signs of labral pathology. The Speed test is performed by placing a downward force on the patient’s arm, which is held in 90° forward elevation, and with elbows in extension and forearm in supination. Pain in the long head of the biceps tendon is considered a positive sign and suggestive of SLAP lesion. Although not commonly found in these athletes, external impingement should also be elicited through both the Neer test and the Hawkins test. In the Neer test, the patient’s arm is brought to maximal forward elevation with the forearm supinated and elbow extended, while the scapula is stabilized by the examiner. Pain in the shoulder indicates a positive examination. In the Hawkins test, the patient’s arm is brought into a position of forward elevation, internal rotation, and elbow flexion. The arm is then further internally rotated, and shoulder pain defines a positive examination.

Any of these findings can be concomitant with scapular dyskinesis. Moreover, symptoms related to internal impingement may be exacerbated by concomitant scapular pathology, and therefore proper assessment of scapulothoracic motion must also be performed.

4. Scapulothoracic examination

Motion coupled between the scapula and the rest of the arm (scapular rhythm) allows for efficient use of the shoulder girdle. The scapula helps transfer the force generated by the core so that the hand can efficiently deliver it. Therefore, scapular pathology (or dyskinesis) results in inefficient functioning of the arm, which can be especially debilitating in an overhead athlete.

Scapular assessment begins with visual inspection of the patient, typically from the posterior view, which allows for assessment of the resting position of the scapula. Evidence of prominence of the medial or inferomedial border, coracoid malposition (or pain on palpation), or general scapular malposition should be noted. On active ROM, as the patient forward-elevates the arm, any asymmetric prominence of the inferomedial border of the scapula should be noted. Such asymmetry may indicate underlying scapular dyskinesis. In another important test, the lateral scapular slide test (described by Kibler⁵), the distance from the inferomedial angle of the scapula to the thoracic spine should be measured for both sides and in 3 difference positions, noting any asymmetry between the affected and nonaffected sides. These 3 positions (Figures 4A–4C) are with arms at side, with hands on hips (internal rotation of humerus in 45° abduction), and in 90° of shoulder abduction. Last, medial and lateral scapular winging—caused by long thoracic nerve and spinal accessory nerve pathology, respectively—can be detected by asking the patient to do a “push-up” against the wall while the examiner views from posterior.

After assessment of scapular position at rest and through motion, a series of provocative maneuvers⁶ may aid in the diagnosis of scapular dyskinesis. The first maneuver is the scapular assistance test, in which the examiner provides a gentle force at the inferomedial angle of the scapula, promoting upward rotation and posterior tilt as the patient elevates the arm (Figures 5A, 5B). If the patient experiences a decrease or absence of symptoms through this arc, the test is considered positive. The second maneuver is the scapular retraction test, in which strength testing of the supraspinatus is performed before and after retraction stabilization of the scapula. In the baseline state, the strength of the supraspinatus is tested in standard fashion, with resisted elevation of the internally rotated and abducted arm. The strength is then tested with the scapula stabilized in retraction (the examiner medially stabilizes the scapula). With scapular stabilization, an increase in strength or a decrease in symptoms is considered a positive test.

5. Neurovascular examination

It is essential to perform a comprehensive neurovascular examination in all overhead athletes. This includes basic cervical spine testing for any motor or sensory deficits, along with assessment of scapular winging to detect long thoracic or spinal accessory nerve palsy for medial and lateral winging, respectively. Although neurovascular injury may be a rare finding in the overhead athlete, a detailed examination must still be performed to rule it out.

Thoracic outlet syndrome

Thoracic syndrome is a compressive neuropathy of nerves and vasculature exiting the thorax and entering the upper extremity. Common symptoms include pain and tingling (sometimes vague) in the neck and upper extremity. These symptoms may be positional as well.

Diagnosis of thoracic outlet syndrome begins with visual inspection of the involved upper extremity, noting atrophy or asymmetry. Weakness may also be present. Additional provocative maneuvers can be used to detect decrease or loss of pulses, along with reproduction of symptoms, during a provocative maneuver with subsequent return of pulses and resolution of symptoms after the maneuver is completed.

One examination that can be used to detect thoracic outlet syndrome is the Adson test.⁷ During this maneuver, the radial pulse is palpated with the arm at rest on the patient’s side. The patient then turns to the symptomatic side, hyperextends the arm, and holds inspiration. A positive test coincides with both decreased pulse and reproduction of symptoms, indicating compression within the scalene triangle. In the Wright test,⁷ the pulse is again palpated at rest with the arm at the side. The patient then holds inspiration and places the arm in a position of abduction and external rotation. If the pulses decrease with this maneuver, the test is considered positive, indicating compression in the sub–pectoralis minor region deep to the coracoid. In a third test, the costoclavicular test, again pulses are measured before and during the provocative maneuver, which is with the shoulders thrust backward and depressed downward. A positive test indicates compression between the clavicle and the first rib. In our practice, we use a modified Wright test in which the arm is held in abduction and external rotation while radial pulses are palpated. The fist is then opened and clenched rapidly, and diminution of radial pulses is considered a positive examination (Figures 6A, 6B).

Effort thrombosis

Overhead athletes are at increased risk for developing effort thrombosis⁸ (Paget-Schroetter syndrome). This thrombosis, which results from repetitive motion involving the upper extremity, is not limited to overhead sports; it may be caused by underlying compression of or microtrauma to the venous infrastructure. On physical examination, there may be swelling of the affected limb, along with diffuse pain and fatigue, as well as dermatologic changes. Positive findings warrant further testing, such as coagulation profile testing and advanced imaging or venography.

Arterial aneurysm

Although rare, arterial aneurysms, especially of the axillary artery, must be ruled out in the overhead athlete with vague upper extremity pain (especially distally) and without clear diagnosis.⁹ Aneurysm of the axillary artery can result from repetitive microtrauma related to repetitive overhead motion of the upper extremity. This condition may cause showering of emboli distally to the vasculature of the hand and fingers (Figure 7). Patients may complain of pain in the fingers, difficulty with grip, cyanosis, or cold sensation. On examination, the sufficiency of the radial and ulnar arteries should be assessed, as with detailed sensorimotor examination of the fingers. The fingernails should be examined for splinter hemorrhages.

Conclusion

Overhead athletes place extreme stress on the shoulder during the throwing motion and are at high risk for injury because of repetitive stress on the shoulder girdle. When examining overhead athletes with shoulder pain, surgeons must consider the entire kinetic chain, as inefficiencies anywhere along the chain can lead to altered mechanics and pathology in the shoulder.

The overhead athlete’s shoulder is exposed to extremes of stress and range of motion (ROM), predisposing this joint to unique injury patterns. Prompt diagnosis and management begin with a comprehensive history and a physical examination, supplemented by imaging studies as needed. Furthermore, the throwing shoulder undergoes adaptive changes, such as partial undersurface rotator cuff tears and capsular laxity. Imaging studies typically demonstrate abnormalities in asymptomatic throwers. Therefore, clinicians must be skilled in history taking and physical examination in throwing athletes to accurately determine the cause of symptoms and provide optimal treatment. This primer provides orthopedic surgeons with the key points in performing a thorough physical examination of the shoulder in overhead athletes.

When working with overhead athletes, surgeons must elicit the precise nature of symptoms. For example, it is important to distinguish pain from fatigue, as well as complaints related purely to decline in performance. Often, collaboration with the player’s parent or coach may help clarify the chief complaint. In addition, surgeons must have an intricate knowledge of the various stages of the overhead motion, as symptoms in specific stages (late cocking/early acceleration) may raise suspicion for distinctive pathology (labral/biceps complex). Last, it is imperative to understand that the shoulder represents only one part of the kinetic chain in overhead athletes. Successful throwing relies on integrity of the entire kinetic chain, starting with the lower extremity and trunk, extending through the spine, scapula, and shoulder, and terminating with the hand and fingers. Pathology anywhere in the chain must be evaluated and addressed.

When examining the shoulder in overhead athletes, surgeons must address several anatomical structures, both bony and soft tissue. Proper examination begins with comprehensive assessment of the ROM and strength of the various muscles around the shoulder, along with visual inspection to identify any asymmetry of these structures. In addition, the scapulothoracic structures must be examined in detail to rule out underlying dyskinesis. The capsular and ligamentous components of the shoulder joint must be further assessed to note any capsular contracture causing glenohumeral internal rotation deficit (GIRD) or any pathology with the rotator cuff or labral/biceps complex. Last, a comprehensive neurovascular examination should be performed to rule out any compression or neuropathy affecting the shoulder and overhead motion. Findings from the physical examination may then require further imaging to correlate the history and physical examination findings.

1. Inspection, palpation, strength testing

Every examination of the shoulder must begin with visual inspection, along with assessment of basic ROM and strength. The patient must be positioned and exposed adequately to promote visualization of the entire shoulder and scapular girdle, from both anterior and posterior. Visual inspection focuses on identifying any areas of asymmetry, such as position of the bony prominences or bulk of the muscular fossae. Asymmetry of the bony architecture may indicate prior trauma, and atrophy of the muscular fossae may indicate nerve compression. For example, atrophy of the infraspinatus fossa may be caused by compression of the suprascapular nerve at the spinoglenoid notch (likely by a cyst, often associated with labral pathology, but infraspinatus atrophy can result even without the presence of a compressive cyst¹). Alternatively, atrophy of both the supraspinatus and infraspinatus fossae may indicate underlying compression of the suprascapular nerve at the suprascapular notch (either by a cyst or by the transverse scapular ligament). Static and dynamic observation of the posterior aspect of the shoulder may help identify gross pathology with scapular positioning or retraction, indicating underlying dyskinesis (discussed later). Deformity of the acromioclavicular joint may indicate prior trauma or separation. Last, all prior surgical scars should be noted.

Selective palpation may help identify pathology in the shoulder of the throwing athlete. Tenderness at the acromioclavicular joint may be especially common in patients who have had prior sprains of this joint or who have degenerative changes. Tenderness along the biceps tendon may be present in those with biceps tendinitis or partial tear. In addition, tenderness at the coracoid may be present in those with scapular dyskinesis. Posteriorly, palpation at the inferomedial aspect of the scapula (Figure 1), as with palpation along the medial border of the scapula, may elicit tenderness in those with scapulothoracic bursitis.

Strength testing in the shoulder is performed to elicit any deficiencies of the rotator cuff/musculature or surrounding structures. Weakness in forward elevation may indicate pathology in the supraspinatus, whereas weakness in external rotation may reflect deficiency in the infraspinatus or teres minor. Teres minor deficiency may be more isolated with weakness in a position of shoulder abduction to 90°. Last, weakness in internal rotation may indicate subscapularis deficiency. Lag signs and other provocative maneuvers are similarly elicited but typically are positive only in the event of large tears of the rotator cuff. These signs and maneuvers include the internal rotation lag sign or belly press test for subscapularis integrity, the drop-arm sign for supraspinatus function, the external rotation lag sign for infraspinatus function, and the hornblower sign for teres minor integrity. Supporting muscles of the shoulder may also be tested. Latissimus strength may be tested with resisted downward rotation of the arm with the shoulder in abduction and the elbow flexed to 90°.

2. ROM and GIRD assessment

After inspection and palpation, the shoulder should be ranged in all relevant planes of motion. Our standard examination includes forward elevation in the frontal and scapular planes, along with external rotation at the side and at 90° of abduction, as well as internal rotation behind the back with documentation of the highest spinal level that the patient can reach. This examination may be performed with the patient upright, but supine positioning can help stabilize the scapula and provide more accurate views of motion. Deficits of internal rotation may be a common finding in overhead athletes, and the degree of this deficit should be quantitatively noted.

Bony and soft-tissue remodeling of the shoulder (and associated structures) in the overhead athlete can lead to contracture of the posterior capsule. This contracture can cause excessive external rotation and subsequent decrease in internal rotation, leading to pain and anterior instability in the throwing shoulder.² For precise measurements of the internal and external rotation arc, the scapula must be stabilized. This can be done with the patient supine on the examining table or seated upright with manual stabilization of the scapula by the examiner. Once the scapula is stabilized, the arc of internal and external rotation (with the arm in about 90° of abduction) can be measured with a goniometer, with maximum values obtained as the scapula begins to move along the posterior chest wall.² The difference in internal rotation between the dominant and nondominant arms defines the extent of the athlete’s GIRD. Internal rotation can also be qualitatively assessed by having the athlete internally rotate each arm and reach up the spine while the examiner notes the difference in level achieved. However, this does not provide a quantitative assessment of the patient’s GIRD.

In general, the sum of the internal and external rotation arcs on the 2 sides should be symmetric. Consequently, in GIRD, excessive external rotation is balanced by decreased internal rotation. Symptomatic GIRD may be present when there is more than 25° of discrepancy in internal rotation between the athlete’s dominant and nondominant arms.² The goal is to reduce this discrepancy to less than 20°.

3. Internal impingement: rotator cuff and labrum

In overhead athletes, an intricate relationship involving rotator cuff, labrum, and biceps tendon allows for efficient, pain-free force delivery at the shoulder. However, because of the significant external rotation and abduction required in the overhead motion, there may be internal impingement of the posterosuperior rotator cuff (infraspinatus and posterior aspect of supraspinatus) between the posterior labrum and the greater tuberosity. Detailed examination of these structures must be performed in any assessment of an overhead athlete. Symptomatic patients may complain of pain during the throwing cycle, particularly in late cocking and early acceleration.

The modified relocation examination is a common maneuver to detect internal impingement.³ In this examination, the patient’s arm is brought into a position of maximal external rotation and abduction mimicking that found in late cocking or early acceleration. In this position, a patient with internal impingement complains of pain in the posterior shoulder. A posteriorly directed force on the humerus relieves this pain.

There are also many examinations for detecting labral pathology, specifically a SLAP (superior labrum, anterior to posterior) lesion, which is commonly found in patients with internal impingement. One commonly tested maneuver is the O’Brien active compression test (Figures 2A, 2B), which has excellent sensitivity and specificity in detecting type II SLAP lesions.⁴ In this examination, the patient holds the arm in about 15° of adduction and 90° of forward elevation. A downward force is applied with the forearm pronated and subsequently supinated. If pain is noted on the force applied to the pronated arm, and if this pain decreases in the supinated examination, the test is positive for labral pathology.

Anterior instability is routinely found in these patients. Translation is measured with the anterior load and shift test. Anterior translation is tested with the patient supine, with the arm in abduction and external rotation, and with the examiner placing an anteriorly directed force on the humeral head. Translation is compared with the contralateral side and graded on a 3-point scale (1+ is translation to glenoid rim, 2+ is translation over glenoid rim but reduces, 3+ is translation over glenoid and locking). We also use the anterior release test, in which the patient is supine, the arm is brought into abduction and external rotation, and the examiner places a posteriorly directed force on the humeral head. When the examiner removes this force, the patient notices symptoms of instability caused by subluxation (Figures 3A, 3B).

Biceps tendon testing should also be performed to help elicit signs of labral pathology. The Speed test is performed by placing a downward force on the patient’s arm, which is held in 90° forward elevation, and with elbows in extension and forearm in supination. Pain in the long head of the biceps tendon is considered a positive sign and suggestive of SLAP lesion. Although not commonly found in these athletes, external impingement should also be elicited through both the Neer test and the Hawkins test. In the Neer test, the patient’s arm is brought to maximal forward elevation with the forearm supinated and elbow extended, while the scapula is stabilized by the examiner. Pain in the shoulder indicates a positive examination. In the Hawkins test, the patient’s arm is brought into a position of forward elevation, internal rotation, and elbow flexion. The arm is then further internally rotated, and shoulder pain defines a positive examination.

Any of these findings can be concomitant with scapular dyskinesis. Moreover, symptoms related to internal impingement may be exacerbated by concomitant scapular pathology, and therefore proper assessment of scapulothoracic motion must also be performed.

4. Scapulothoracic examination

Motion coupled between the scapula and the rest of the arm (scapular rhythm) allows for efficient use of the shoulder girdle. The scapula helps transfer the force generated by the core so that the hand can efficiently deliver it. Therefore, scapular pathology (or dyskinesis) results in inefficient functioning of the arm, which can be especially debilitating in an overhead athlete.

Scapular assessment begins with visual inspection of the patient, typically from the posterior view, which allows for assessment of the resting position of the scapula. Evidence of prominence of the medial or inferomedial border, coracoid malposition (or pain on palpation), or general scapular malposition should be noted. On active ROM, as the patient forward-elevates the arm, any asymmetric prominence of the inferomedial border of the scapula should be noted. Such asymmetry may indicate underlying scapular dyskinesis. In another important test, the lateral scapular slide test (described by Kibler⁵), the distance from the inferomedial angle of the scapula to the thoracic spine should be measured for both sides and in 3 difference positions, noting any asymmetry between the affected and nonaffected sides. These 3 positions (Figures 4A–4C) are with arms at side, with hands on hips (internal rotation of humerus in 45° abduction), and in 90° of shoulder abduction. Last, medial and lateral scapular winging—caused by long thoracic nerve and spinal accessory nerve pathology, respectively—can be detected by asking the patient to do a “push-up” against the wall while the examiner views from posterior.

After assessment of scapular position at rest and through motion, a series of provocative maneuvers⁶ may aid in the diagnosis of scapular dyskinesis. The first maneuver is the scapular assistance test, in which the examiner provides a gentle force at the inferomedial angle of the scapula, promoting upward rotation and posterior tilt as the patient elevates the arm (Figures 5A, 5B). If the patient experiences a decrease or absence of symptoms through this arc, the test is considered positive. The second maneuver is the scapular retraction test, in which strength testing of the supraspinatus is performed before and after retraction stabilization of the scapula. In the baseline state, the strength of the supraspinatus is tested in standard fashion, with resisted elevation of the internally rotated and abducted arm. The strength is then tested with the scapula stabilized in retraction (the examiner medially stabilizes the scapula). With scapular stabilization, an increase in strength or a decrease in symptoms is considered a positive test.

5. Neurovascular examination

It is essential to perform a comprehensive neurovascular examination in all overhead athletes. This includes basic cervical spine testing for any motor or sensory deficits, along with assessment of scapular winging to detect long thoracic or spinal accessory nerve palsy for medial and lateral winging, respectively. Although neurovascular injury may be a rare finding in the overhead athlete, a detailed examination must still be performed to rule it out.

Thoracic outlet syndrome

Thoracic syndrome is a compressive neuropathy of nerves and vasculature exiting the thorax and entering the upper extremity. Common symptoms include pain and tingling (sometimes vague) in the neck and upper extremity. These symptoms may be positional as well.

Diagnosis of thoracic outlet syndrome begins with visual inspection of the involved upper extremity, noting atrophy or asymmetry. Weakness may also be present. Additional provocative maneuvers can be used to detect decrease or loss of pulses, along with reproduction of symptoms, during a provocative maneuver with subsequent return of pulses and resolution of symptoms after the maneuver is completed.

One examination that can be used to detect thoracic outlet syndrome is the Adson test.⁷ During this maneuver, the radial pulse is palpated with the arm at rest on the patient’s side. The patient then turns to the symptomatic side, hyperextends the arm, and holds inspiration. A positive test coincides with both decreased pulse and reproduction of symptoms, indicating compression within the scalene triangle. In the Wright test,⁷ the pulse is again palpated at rest with the arm at the side. The patient then holds inspiration and places the arm in a position of abduction and external rotation. If the pulses decrease with this maneuver, the test is considered positive, indicating compression in the sub–pectoralis minor region deep to the coracoid. In a third test, the costoclavicular test, again pulses are measured before and during the provocative maneuver, which is with the shoulders thrust backward and depressed downward. A positive test indicates compression between the clavicle and the first rib. In our practice, we use a modified Wright test in which the arm is held in abduction and external rotation while radial pulses are palpated. The fist is then opened and clenched rapidly, and diminution of radial pulses is considered a positive examination (Figures 6A, 6B).

Effort thrombosis

Overhead athletes are at increased risk for developing effort thrombosis⁸ (Paget-Schroetter syndrome). This thrombosis, which results from repetitive motion involving the upper extremity, is not limited to overhead sports; it may be caused by underlying compression of or microtrauma to the venous infrastructure. On physical examination, there may be swelling of the affected limb, along with diffuse pain and fatigue, as well as dermatologic changes. Positive findings warrant further testing, such as coagulation profile testing and advanced imaging or venography.

Arterial aneurysm

Although rare, arterial aneurysms, especially of the axillary artery, must be ruled out in the overhead athlete with vague upper extremity pain (especially distally) and without clear diagnosis.⁹ Aneurysm of the axillary artery can result from repetitive microtrauma related to repetitive overhead motion of the upper extremity. This condition may cause showering of emboli distally to the vasculature of the hand and fingers (Figure 7). Patients may complain of pain in the fingers, difficulty with grip, cyanosis, or cold sensation. On examination, the sufficiency of the radial and ulnar arteries should be assessed, as with detailed sensorimotor examination of the fingers. The fingernails should be examined for splinter hemorrhages.

Conclusion

Overhead athletes place extreme stress on the shoulder during the throwing motion and are at high risk for injury because of repetitive stress on the shoulder girdle. When examining overhead athletes with shoulder pain, surgeons must consider the entire kinetic chain, as inefficiencies anywhere along the chain can lead to altered mechanics and pathology in the shoulder.

The overhead athlete’s shoulder is exposed to extremes of stress and range of motion (ROM), predisposing this joint to unique injury patterns. Prompt diagnosis and management begin with a comprehensive history and a physical examination, supplemented by imaging studies as needed. Furthermore, the throwing shoulder undergoes adaptive changes, such as partial undersurface rotator cuff tears and capsular laxity. Imaging studies typically demonstrate abnormalities in asymptomatic throwers. Therefore, clinicians must be skilled in history taking and physical examination in throwing athletes to accurately determine the cause of symptoms and provide optimal treatment. This primer provides orthopedic surgeons with the key points in performing a thorough physical examination of the shoulder in overhead athletes.

When working with overhead athletes, surgeons must elicit the precise nature of symptoms. For example, it is important to distinguish pain from fatigue, as well as complaints related purely to decline in performance. Often, collaboration with the player’s parent or coach may help clarify the chief complaint. In addition, surgeons must have an intricate knowledge of the various stages of the overhead motion, as symptoms in specific stages (late cocking/early acceleration) may raise suspicion for distinctive pathology (labral/biceps complex). Last, it is imperative to understand that the shoulder represents only one part of the kinetic chain in overhead athletes. Successful throwing relies on integrity of the entire kinetic chain, starting with the lower extremity and trunk, extending through the spine, scapula, and shoulder, and terminating with the hand and fingers. Pathology anywhere in the chain must be evaluated and addressed.

When examining the shoulder in overhead athletes, surgeons must address several anatomical structures, both bony and soft tissue. Proper examination begins with comprehensive assessment of the ROM and strength of the various muscles around the shoulder, along with visual inspection to identify any asymmetry of these structures. In addition, the scapulothoracic structures must be examined in detail to rule out underlying dyskinesis. The capsular and ligamentous components of the shoulder joint must be further assessed to note any capsular contracture causing glenohumeral internal rotation deficit (GIRD) or any pathology with the rotator cuff or labral/biceps complex. Last, a comprehensive neurovascular examination should be performed to rule out any compression or neuropathy affecting the shoulder and overhead motion. Findings from the physical examination may then require further imaging to correlate the history and physical examination findings.

1. Inspection, palpation, strength testing

Every examination of the shoulder must begin with visual inspection, along with assessment of basic ROM and strength. The patient must be positioned and exposed adequately to promote visualization of the entire shoulder and scapular girdle, from both anterior and posterior. Visual inspection focuses on identifying any areas of asymmetry, such as position of the bony prominences or bulk of the muscular fossae. Asymmetry of the bony architecture may indicate prior trauma, and atrophy of the muscular fossae may indicate nerve compression. For example, atrophy of the infraspinatus fossa may be caused by compression of the suprascapular nerve at the spinoglenoid notch (likely by a cyst, often associated with labral pathology, but infraspinatus atrophy can result even without the presence of a compressive cyst¹). Alternatively, atrophy of both the supraspinatus and infraspinatus fossae may indicate underlying compression of the suprascapular nerve at the suprascapular notch (either by a cyst or by the transverse scapular ligament). Static and dynamic observation of the posterior aspect of the shoulder may help identify gross pathology with scapular positioning or retraction, indicating underlying dyskinesis (discussed later). Deformity of the acromioclavicular joint may indicate prior trauma or separation. Last, all prior surgical scars should be noted.

Selective palpation may help identify pathology in the shoulder of the throwing athlete. Tenderness at the acromioclavicular joint may be especially common in patients who have had prior sprains of this joint or who have degenerative changes. Tenderness along the biceps tendon may be present in those with biceps tendinitis or partial tear. In addition, tenderness at the coracoid may be present in those with scapular dyskinesis. Posteriorly, palpation at the inferomedial aspect of the scapula (Figure 1), as with palpation along the medial border of the scapula, may elicit tenderness in those with scapulothoracic bursitis.

Strength testing in the shoulder is performed to elicit any deficiencies of the rotator cuff/musculature or surrounding structures. Weakness in forward elevation may indicate pathology in the supraspinatus, whereas weakness in external rotation may reflect deficiency in the infraspinatus or teres minor. Teres minor deficiency may be more isolated with weakness in a position of shoulder abduction to 90°. Last, weakness in internal rotation may indicate subscapularis deficiency. Lag signs and other provocative maneuvers are similarly elicited but typically are positive only in the event of large tears of the rotator cuff. These signs and maneuvers include the internal rotation lag sign or belly press test for subscapularis integrity, the drop-arm sign for supraspinatus function, the external rotation lag sign for infraspinatus function, and the hornblower sign for teres minor integrity. Supporting muscles of the shoulder may also be tested. Latissimus strength may be tested with resisted downward rotation of the arm with the shoulder in abduction and the elbow flexed to 90°.

2. ROM and GIRD assessment

After inspection and palpation, the shoulder should be ranged in all relevant planes of motion. Our standard examination includes forward elevation in the frontal and scapular planes, along with external rotation at the side and at 90° of abduction, as well as internal rotation behind the back with documentation of the highest spinal level that the patient can reach. This examination may be performed with the patient upright, but supine positioning can help stabilize the scapula and provide more accurate views of motion. Deficits of internal rotation may be a common finding in overhead athletes, and the degree of this deficit should be quantitatively noted.

Bony and soft-tissue remodeling of the shoulder (and associated structures) in the overhead athlete can lead to contracture of the posterior capsule. This contracture can cause excessive external rotation and subsequent decrease in internal rotation, leading to pain and anterior instability in the throwing shoulder.² For precise measurements of the internal and external rotation arc, the scapula must be stabilized. This can be done with the patient supine on the examining table or seated upright with manual stabilization of the scapula by the examiner. Once the scapula is stabilized, the arc of internal and external rotation (with the arm in about 90° of abduction) can be measured with a goniometer, with maximum values obtained as the scapula begins to move along the posterior chest wall.² The difference in internal rotation between the dominant and nondominant arms defines the extent of the athlete’s GIRD. Internal rotation can also be qualitatively assessed by having the athlete internally rotate each arm and reach up the spine while the examiner notes the difference in level achieved. However, this does not provide a quantitative assessment of the patient’s GIRD.

In general, the sum of the internal and external rotation arcs on the 2 sides should be symmetric. Consequently, in GIRD, excessive external rotation is balanced by decreased internal rotation. Symptomatic GIRD may be present when there is more than 25° of discrepancy in internal rotation between the athlete’s dominant and nondominant arms.² The goal is to reduce this discrepancy to less than 20°.

3. Internal impingement: rotator cuff and labrum

In overhead athletes, an intricate relationship involving rotator cuff, labrum, and biceps tendon allows for efficient, pain-free force delivery at the shoulder. However, because of the significant external rotation and abduction required in the overhead motion, there may be internal impingement of the posterosuperior rotator cuff (infraspinatus and posterior aspect of supraspinatus) between the posterior labrum and the greater tuberosity. Detailed examination of these structures must be performed in any assessment of an overhead athlete. Symptomatic patients may complain of pain during the throwing cycle, particularly in late cocking and early acceleration.

The modified relocation examination is a common maneuver to detect internal impingement.³ In this examination, the patient’s arm is brought into a position of maximal external rotation and abduction mimicking that found in late cocking or early acceleration. In this position, a patient with internal impingement complains of pain in the posterior shoulder. A posteriorly directed force on the humerus relieves this pain.

There are also many examinations for detecting labral pathology, specifically a SLAP (superior labrum, anterior to posterior) lesion, which is commonly found in patients with internal impingement. One commonly tested maneuver is the O’Brien active compression test (Figures 2A, 2B), which has excellent sensitivity and specificity in detecting type II SLAP lesions.⁴ In this examination, the patient holds the arm in about 15° of adduction and 90° of forward elevation. A downward force is applied with the forearm pronated and subsequently supinated. If pain is noted on the force applied to the pronated arm, and if this pain decreases in the supinated examination, the test is positive for labral pathology.

Anterior instability is routinely found in these patients. Translation is measured with the anterior load and shift test. Anterior translation is tested with the patient supine, with the arm in abduction and external rotation, and with the examiner placing an anteriorly directed force on the humeral head. Translation is compared with the contralateral side and graded on a 3-point scale (1+ is translation to glenoid rim, 2+ is translation over glenoid rim but reduces, 3+ is translation over glenoid and locking). We also use the anterior release test, in which the patient is supine, the arm is brought into abduction and external rotation, and the examiner places a posteriorly directed force on the humeral head. When the examiner removes this force, the patient notices symptoms of instability caused by subluxation (Figures 3A, 3B).

Biceps tendon testing should also be performed to help elicit signs of labral pathology. The Speed test is performed by placing a downward force on the patient’s arm, which is held in 90° forward elevation, and with elbows in extension and forearm in supination. Pain in the long head of the biceps tendon is considered a positive sign and suggestive of SLAP lesion. Although not commonly found in these athletes, external impingement should also be elicited through both the Neer test and the Hawkins test. In the Neer test, the patient’s arm is brought to maximal forward elevation with the forearm supinated and elbow extended, while the scapula is stabilized by the examiner. Pain in the shoulder indicates a positive examination. In the Hawkins test, the patient’s arm is brought into a position of forward elevation, internal rotation, and elbow flexion. The arm is then further internally rotated, and shoulder pain defines a positive examination.

Any of these findings can be concomitant with scapular dyskinesis. Moreover, symptoms related to internal impingement may be exacerbated by concomitant scapular pathology, and therefore proper assessment of scapulothoracic motion must also be performed.

4. Scapulothoracic examination

Motion coupled between the scapula and the rest of the arm (scapular rhythm) allows for efficient use of the shoulder girdle. The scapula helps transfer the force generated by the core so that the hand can efficiently deliver it. Therefore, scapular pathology (or dyskinesis) results in inefficient functioning of the arm, which can be especially debilitating in an overhead athlete.

Scapular assessment begins with visual inspection of the patient, typically from the posterior view, which allows for assessment of the resting position of the scapula. Evidence of prominence of the medial or inferomedial border, coracoid malposition (or pain on palpation), or general scapular malposition should be noted. On active ROM, as the patient forward-elevates the arm, any asymmetric prominence of the inferomedial border of the scapula should be noted. Such asymmetry may indicate underlying scapular dyskinesis. In another important test, the lateral scapular slide test (described by Kibler⁵), the distance from the inferomedial angle of the scapula to the thoracic spine should be measured for both sides and in 3 difference positions, noting any asymmetry between the affected and nonaffected sides. These 3 positions (Figures 4A–4C) are with arms at side, with hands on hips (internal rotation of humerus in 45° abduction), and in 90° of shoulder abduction. Last, medial and lateral scapular winging—caused by long thoracic nerve and spinal accessory nerve pathology, respectively—can be detected by asking the patient to do a “push-up” against the wall while the examiner views from posterior.

After assessment of scapular position at rest and through motion, a series of provocative maneuvers⁶ may aid in the diagnosis of scapular dyskinesis. The first maneuver is the scapular assistance test, in which the examiner provides a gentle force at the inferomedial angle of the scapula, promoting upward rotation and posterior tilt as the patient elevates the arm (Figures 5A, 5B). If the patient experiences a decrease or absence of symptoms through this arc, the test is considered positive. The second maneuver is the scapular retraction test, in which strength testing of the supraspinatus is performed before and after retraction stabilization of the scapula. In the baseline state, the strength of the supraspinatus is tested in standard fashion, with resisted elevation of the internally rotated and abducted arm. The strength is then tested with the scapula stabilized in retraction (the examiner medially stabilizes the scapula). With scapular stabilization, an increase in strength or a decrease in symptoms is considered a positive test.

5. Neurovascular examination

It is essential to perform a comprehensive neurovascular examination in all overhead athletes. This includes basic cervical spine testing for any motor or sensory deficits, along with assessment of scapular winging to detect long thoracic or spinal accessory nerve palsy for medial and lateral winging, respectively. Although neurovascular injury may be a rare finding in the overhead athlete, a detailed examination must still be performed to rule it out.

Thoracic outlet syndrome

Thoracic syndrome is a compressive neuropathy of nerves and vasculature exiting the thorax and entering the upper extremity. Common symptoms include pain and tingling (sometimes vague) in the neck and upper extremity. These symptoms may be positional as well.

Diagnosis of thoracic outlet syndrome begins with visual inspection of the involved upper extremity, noting atrophy or asymmetry. Weakness may also be present. Additional provocative maneuvers can be used to detect decrease or loss of pulses, along with reproduction of symptoms, during a provocative maneuver with subsequent return of pulses and resolution of symptoms after the maneuver is completed.

One examination that can be used to detect thoracic outlet syndrome is the Adson test.⁷ During this maneuver, the radial pulse is palpated with the arm at rest on the patient’s side. The patient then turns to the symptomatic side, hyperextends the arm, and holds inspiration. A positive test coincides with both decreased pulse and reproduction of symptoms, indicating compression within the scalene triangle. In the Wright test,⁷ the pulse is again palpated at rest with the arm at the side. The patient then holds inspiration and places the arm in a position of abduction and external rotation. If the pulses decrease with this maneuver, the test is considered positive, indicating compression in the sub–pectoralis minor region deep to the coracoid. In a third test, the costoclavicular test, again pulses are measured before and during the provocative maneuver, which is with the shoulders thrust backward and depressed downward. A positive test indicates compression between the clavicle and the first rib. In our practice, we use a modified Wright test in which the arm is held in abduction and external rotation while radial pulses are palpated. The fist is then opened and clenched rapidly, and diminution of radial pulses is considered a positive examination (Figures 6A, 6B).

Effort thrombosis

Overhead athletes are at increased risk for developing effort thrombosis⁸ (Paget-Schroetter syndrome). This thrombosis, which results from repetitive motion involving the upper extremity, is not limited to overhead sports; it may be caused by underlying compression of or microtrauma to the venous infrastructure. On physical examination, there may be swelling of the affected limb, along with diffuse pain and fatigue, as well as dermatologic changes. Positive findings warrant further testing, such as coagulation profile testing and advanced imaging or venography.

Arterial aneurysm

Although rare, arterial aneurysms, especially of the axillary artery, must be ruled out in the overhead athlete with vague upper extremity pain (especially distally) and without clear diagnosis.⁹ Aneurysm of the axillary artery can result from repetitive microtrauma related to repetitive overhead motion of the upper extremity. This condition may cause showering of emboli distally to the vasculature of the hand and fingers (Figure 7). Patients may complain of pain in the fingers, difficulty with grip, cyanosis, or cold sensation. On examination, the sufficiency of the radial and ulnar arteries should be assessed, as with detailed sensorimotor examination of the fingers. The fingernails should be examined for splinter hemorrhages.

Conclusion

Overhead athletes place extreme stress on the shoulder during the throwing motion and are at high risk for injury because of repetitive stress on the shoulder girdle. When examining overhead athletes with shoulder pain, surgeons must consider the entire kinetic chain, as inefficiencies anywhere along the chain can lead to altered mechanics and pathology in the shoulder.

Glenohumeral internal rotation deficit (GIRD) can be observed in overhead athletes and is thought to play a role in generating pain and rotator cuff weakness in the dominant shoulder with sport. It is unclear what is an acceptable value of GIRD in a population of overhead athletes and whether it should be based solely on internal rotation deficit or should include total range of motion (ROM) deficit.^1,2 Acquired GIRD in the athlete’s throwing shoulder has been thoroughly documented in the literature as a loss of internal rotation relative to the nonthrowing shoulder, with etiologies including bony adaptations (increased humeral retroversion), muscular tightness, and posterior capsular tightness.^1,3-11 In particular, the repetitive torsional stresses acting on the throwing shoulder of baseball players is thought to produce, over the long term, structural adaptations such as increased humeral retroversion.^5,12-14 Further, for shoulders with posterior-inferior capsular tightness, cadaveric studies have shown increased contact pressure at the coracoacromial arch during simulated follow-through.¹⁵ Athletes of other overhead and throwing sports, such as football, softball, tennis, and volleyball, may show similar adaptations in overhead motion.^9,16,17

GIRD has been associated with a variety of pathologic conditions, including scapular dyskinesis, internal and secondary impingement, partial articular-sided rotator cuff tears, damage to the biceps–labral complex, and ulnar collateral ligament insufficiency.^10,12,18-22

Restriction from engaging in exacerbating activities (eg, throwing) and compliance with a specific stretching program reduces or eliminates GIRD in the majority of cases.^1,23-28 In the few cases in which conservative management fails, operative intervention may be indicated.^1,23,29,30 Few investigators have detailed an operative technique for selective arthroscopic capsular release of the posterior-inferior capsule or evaluated the ability of athletes to return to sport after such surgery.

In this article, we present our technique for arthroscopic posterior-inferior capsular release and report the results of applying this technique in a population of athletes with symptomatic GIRD that was unresponsive to nonoperative treatment and was preventing them from returning to sport.

We hypothesized that selective arthroscopic surgical release of the posterior-inferior capsule would improve symptomatic GIRD and result in a return to sport in the majority of cases unresponsive to nonoperative treatment.

Materials and Methods

Patients

After obtaining institutional review board approval, we retrospectively reviewed patient charts and collected data. Study inclusion criteria were arthroscopic selective posterior-inferior capsular release between 2004 and 2008; failure to resume sport after minimum 3 months of physical therapy, including use of sleeper stretch, active joint mobilization by licensed physical therapist, and sport-specific restriction from exacerbating activities (eg, throwing for baseball players); and active participation in overhead sport.^1,27 Exclusion criteria were generalized adhesive capsulitis, labral pathology producing glenohumeral joint instability (Bankart or reverse Bankart lesion), high-grade or full-thickness tearing of rotator cuff, and clinically significant partial-thickness tearing or instability of long head of biceps tendon.

Assessment

One of 3 authors (Dr. Buss, Dr. Codding, or Dr. Dahm) used a bubble goniometer to measure passive internal rotation. Patients were positioned supine with 90° of thoracohumeral abduction and 90° of elbow flexion. The examiner’s hand stabilized the scapula against the examination table, in accordance with published techniques.^1,26 Active internal rotation was measured at 0° of thoracohumeral abduction by noting the most superior spinal segment reached. Before and after surgery, passive internal rotation measurements were taken on both arms. GIRD was determined by the difference between dominant and nondominant arm measurements; segmental differences were obtained by subtracting segments achieved between the dominant and nondominant arms.

Before surgery and at minimum 2-year follow-up after surgery, patients completed a subjective questionnaire, which included the American Shoulder and Elbow Surgeons (ASES) Standardized Shoulder Assessment Form, for assessment of both arms. ASES scores are reliable, valid, and responsive in evaluating shoulder pain and function.^15,31 Patients also answered questions about their ability to return to play, their level of play after surgery, and whether they would undergo the procedure again.

Surgical Technique

After induction of general anesthesia and standard preparation and draping, the patient is placed in a standard beach-chair position and examined. Diagnostic arthroscopy is then performed. In all patients, intra-articular evaluation revealed a thickened, contracted posterior band of the inferior glenohumeral ligament. This finding is consistent with other studies of patients with significant GIRD.^1,14,22,30

On completion of the diagnostic portion of the arthroscopy, attention is turned to the selective posterior-inferior capsular release. Key to proper execution of the release is establishing a posterior-inferior accessory portal. This is accomplished while viewing from a standard posterior (“soft spot”) portal and determining the appropriate location and angle of entry by spinal needle localization. Typically, an entry point is selected about 4 cm distal and 1 cm lateral to the standard posterior portal. An 18-gauge spinal needle introduced at this location is angled about 15° superiorly and about 20° medially. Once the appropriate vector is determined, a skin incision is made, and a Wissinger rod is introduced, over which a small-diameter cannula is passed. A hooked-tip electrocautery device is used to divide the posterior capsule from the glenoid labrum between the 8- and 6-o’clock positions in the right shoulder (Figure). Care is taken to perform the release immediately adjacent to the glenoid labrum and using short bursts of cautery in order to minimize risk of injury to the teres minor branch of the axillary nerve. Adequate release is confirmed by reassessing passive internal rotation under anesthesia. Additional procedures are performed, if necessary, after completion of the capsular release.

Postoperative rehabilitation consists initially of pendulum exercises and scapular retraction starting on postoperative day 1. Once the swelling from the surgical procedure subsides, typically within 1 week, passive and active-assisted ROM and gentle posterior capsular mobilization are initiated under the direction of a licensed physical therapist. Active ROM is allowed once the patient regains normal scapulothoracic rhythm. Strengthening consists initially of isometrics followed by light resistance strengthening for the rotator cuff and scapular stabilizers once active ROM and scapulothoracic rhythm return to normal. Passive internal rotation stretching, including use of the sleeper stretch, is implemented as soon as tolerated and continues throughout the rehabilitation process.³²

Statistical Analysis

Statistical analysis was performed with Stata Release 11 (StataCorp, College Station, Texas). Paired t tests were used to assess preoperative and postoperative mean differences in ASES scores, in passive glenohumeral internal rotation, and in active glenohumeral internal rotation; independent-samples t tests were used to assess side-to-side differences. Significance was set at P < .05.

Results

Fifteen overhead athletes met the study inclusion criteria. Two were lost to follow-up. Of the remaining 13 patients, 6 underwent isolated arthroscopic posterior-inferior capsular release, and 7 had concomitant procedures (6 subacromial decompressions, 1 superior labrum anterior-posterior [SLAP] repair). There were 11 male athletes and 2 female athletes. Twelve of the 13 patients were right-hand–dominant. Mean age at time of surgery was 21 years (range, 16-33 years). There were 10 baseball players (6 pitchers, 4 position players); the other 3 patients played softball (1), volleyball (1), or tennis (1). Six patients played at high school level, 5 at college level, 1 at professional level, and 1 at amateur level. All 13 patients underwent a minimum of 3 months of comprehensive rehabilitation, which included use of the sleeper stretch, active joint mobilization by a licensed physical therapist, and sport-specific restriction from exacerbating activities. Mean duration of symptoms before surgery was 18 months (range, 4-48 months). Mean postoperative follow-up was 31 months (range, 24-59 months). Mean ASES score was 71.5 (range, 33-95) before surgery and 86.9 (range, 60-100) after surgery (P < .001). Mean GIRD improved from 43.1° (range, 30°-60°) before surgery to 9.7° (range, –7° to 40°) after surgery (P < .001). Mean active internal rotation difference improved from 3.8 vertebral segments before surgery to 2.6 vertebral segments after surgery; this difference was not statistically significant (P = .459). Ten (77%) of the 13 patients returned to their preoperative level of play or a higher level; the other 3 (23%) did not return to their preoperative level of play but continued to compete in a different position (Table). Eleven patients (85%) stated they would repeat the procedure. One of the 2 patients who would not repeat the procedure was in the isolated posterior-inferior capsular release group; the other was in the concomitant-procedure group (subacromial decompression). Total glenohumeral ROM of dominant arm was 122° before surgery and 136° after surgery (P = .04). There was no significant difference in total ROM between dominant and nondominant arms after surgery (136° and 141°; P = .12), but the preoperative difference was significant (122° vs 141°; P = .022).

Discussion

GIRD has been associated with various pathologic conditions of the upper extremity. In 1991, Verna²⁸ found that a majority of 39 professional baseball pitchers with significant GIRD had shoulder problems that affected playing time. More recently, GIRD has been associated with a progression of injuries, including scapular dyskinesia, internal and secondary impingement, articular-sided partial rotator cuff tears, rotator cuff weakness, damage to the biceps–labral complex, and ulnar collateral ligament insufficiency.^12,18-22 In a cadaveric study of humeral head translation, Harryman and colleagues³³ noted an anterosuperior migration of the humeral head during flexion and concluded it resulted from a loose anterior and tight posterior glenohumeral capsule, leading to loss of glenohumeral internal rotation. More recently, posterosuperior migration of the humeral head has been postulated, with GIRD secondary to an essential posterior capsular contracture.¹ Tyler and colleagues³⁴ clinically linked posterior capsular tightness with GIRD, and both cadaveric and magnetic resonance imaging studies have supported the finding that posterior capsular contracture leads to posterosuperior humeral head migration in association with GIRD.^14,20 Such a disruption in normal glenohumeral joint mechanics could produce phenomena of internal or secondary acromiohumeral impingement and pain.

More recently, in a large cohort of professional baseball pitchers, a significant correlation was found between the incidence of rotator cuff strength deficits and GIRD.³⁵ More than 40% of the pitchers with GIRD of at least 35° had a measureable rotator cuff strength deficit in the throwing shoulder.

Burkhart and colleagues²³ concluded that the shoulder most at risk for developing “dead arm” has GIRD and an advanced form of scapular dyskinesia known as SICK scapula (the phenomenon involves Scapula malposition, Inferior medial border prominence, Coracoid pain and malposition, and dysKinesis of scapular movement).

Most athletes with symptoms attributed to GIRD respond to conservative management. A posterior-inferior capsular stretching program focused on regaining internal rotation in the throwing arm has been shown to return about 90% of athletes to play.¹ Numerous studies have indicated that enrollment in a compliant stretching program reduces GIRD.^1,23-27 However, nonoperative treatment fails in a reported 10% of patients with GIRD; these patients may respond to operative treatment.¹

More specifically, for patients who do not respond to conservative treatment, a posterior-inferior capsular release may be indicated.^1,29 Ticker and colleagues²² identified 9 patients who had lost internal rotation and had a posterior capsular contracture at arthroscopy. That study, however, was not performed on overhead or throwing athletes. Yoneda and colleagues³⁰ followed 16 overhead throwing athletes after arthroscopic posterior-inferior capsular release and found favorable preliminary clinical results. Eleven of the 16 patients returned to their preinjury level of performance; the other 5 returned to a lower level. In addition, all 4 patients who underwent isolated arthroscopic capsular release had throwing power restored to between 90% and 100%.

In the present study, 10 of 13 patients who underwent arthroscopic posterior-inferior capsular release returned to their preoperative level of play or a higher level. Mean passive GIRD improved significantly from before surgery to after surgery. ASES scores likewise were significantly improved from before surgery to after surgery. The active internal rotation difference as measured by vertebral segment level was not significantly changed after surgery. This lack of improvement may stem from the more complex musculoligamentous interactions governing active internal rotation versus isolated, passive internal rotation. Another possible explanation for lack of improvement is that the interobserver and intraobserver reliability of this method is lower.³⁶

At 2-year follow-up, the patient who had undergone concomitant SLAP repair demonstrated a 23% improvement in ASES score and more internal rotation on the dominant arm relative to the nondominant arm. This patient returned to a level of play at least as good as his preoperative level. Although we could not determine its statistical significance, this patient’s improvement suggests that the SLAP repair did not reduce the efficacy of the posterior-inferior capsular release.

Limitations of this study include its relatively small cohort (precluded statistical comparisons between groups), the proportion of patients (7/13) who had concomitant surgeries, and the limited options for patient outcome scores. Although the ASES score is a validated outcome score, the Kerlan-Jobe Orthopaedic Clinic Shoulder and Elbow (KJOC) score or the Disabilities of the Arm, Shoulder, and Hand (DASH) score may be more appropriate in an athletic population. In addition, although all study patients had GIRD that was unresponsive to a concerted trial of nonoperative management, we did not have a control group (nonoperatively treated patients) for comparison. Finally, we did not obtain computed tomography scans or account for the potential contribution of humeral retroversion to GIRD in this group of patients.

Conclusion

Selective arthroscopic posterior-inferior capsular release can be recommended as a reasonable operative solution for overhead athletes with symptomatic GIRD that has not responded to conservative management. In the present study, ASES scores improved significantly, and 77% of our athlete-patients returned to sport at their preoperative level of play or a higher level.

Glenohumeral internal rotation deficit (GIRD) can be observed in overhead athletes and is thought to play a role in generating pain and rotator cuff weakness in the dominant shoulder with sport. It is unclear what is an acceptable value of GIRD in a population of overhead athletes and whether it should be based solely on internal rotation deficit or should include total range of motion (ROM) deficit.^1,2 Acquired GIRD in the athlete’s throwing shoulder has been thoroughly documented in the literature as a loss of internal rotation relative to the nonthrowing shoulder, with etiologies including bony adaptations (increased humeral retroversion), muscular tightness, and posterior capsular tightness.^1,3-11 In particular, the repetitive torsional stresses acting on the throwing shoulder of baseball players is thought to produce, over the long term, structural adaptations such as increased humeral retroversion.^5,12-14 Further, for shoulders with posterior-inferior capsular tightness, cadaveric studies have shown increased contact pressure at the coracoacromial arch during simulated follow-through.¹⁵ Athletes of other overhead and throwing sports, such as football, softball, tennis, and volleyball, may show similar adaptations in overhead motion.^9,16,17

GIRD has been associated with a variety of pathologic conditions, including scapular dyskinesis, internal and secondary impingement, partial articular-sided rotator cuff tears, damage to the biceps–labral complex, and ulnar collateral ligament insufficiency.^10,12,18-22

Restriction from engaging in exacerbating activities (eg, throwing) and compliance with a specific stretching program reduces or eliminates GIRD in the majority of cases.^1,23-28 In the few cases in which conservative management fails, operative intervention may be indicated.^1,23,29,30 Few investigators have detailed an operative technique for selective arthroscopic capsular release of the posterior-inferior capsule or evaluated the ability of athletes to return to sport after such surgery.

In this article, we present our technique for arthroscopic posterior-inferior capsular release and report the results of applying this technique in a population of athletes with symptomatic GIRD that was unresponsive to nonoperative treatment and was preventing them from returning to sport.

We hypothesized that selective arthroscopic surgical release of the posterior-inferior capsule would improve symptomatic GIRD and result in a return to sport in the majority of cases unresponsive to nonoperative treatment.

Materials and Methods

Patients

After obtaining institutional review board approval, we retrospectively reviewed patient charts and collected data. Study inclusion criteria were arthroscopic selective posterior-inferior capsular release between 2004 and 2008; failure to resume sport after minimum 3 months of physical therapy, including use of sleeper stretch, active joint mobilization by licensed physical therapist, and sport-specific restriction from exacerbating activities (eg, throwing for baseball players); and active participation in overhead sport.^1,27 Exclusion criteria were generalized adhesive capsulitis, labral pathology producing glenohumeral joint instability (Bankart or reverse Bankart lesion), high-grade or full-thickness tearing of rotator cuff, and clinically significant partial-thickness tearing or instability of long head of biceps tendon.

Assessment

One of 3 authors (Dr. Buss, Dr. Codding, or Dr. Dahm) used a bubble goniometer to measure passive internal rotation. Patients were positioned supine with 90° of thoracohumeral abduction and 90° of elbow flexion. The examiner’s hand stabilized the scapula against the examination table, in accordance with published techniques.^1,26 Active internal rotation was measured at 0° of thoracohumeral abduction by noting the most superior spinal segment reached. Before and after surgery, passive internal rotation measurements were taken on both arms. GIRD was determined by the difference between dominant and nondominant arm measurements; segmental differences were obtained by subtracting segments achieved between the dominant and nondominant arms.

Before surgery and at minimum 2-year follow-up after surgery, patients completed a subjective questionnaire, which included the American Shoulder and Elbow Surgeons (ASES) Standardized Shoulder Assessment Form, for assessment of both arms. ASES scores are reliable, valid, and responsive in evaluating shoulder pain and function.^15,31 Patients also answered questions about their ability to return to play, their level of play after surgery, and whether they would undergo the procedure again.

Surgical Technique

After induction of general anesthesia and standard preparation and draping, the patient is placed in a standard beach-chair position and examined. Diagnostic arthroscopy is then performed. In all patients, intra-articular evaluation revealed a thickened, contracted posterior band of the inferior glenohumeral ligament. This finding is consistent with other studies of patients with significant GIRD.^1,14,22,30

On completion of the diagnostic portion of the arthroscopy, attention is turned to the selective posterior-inferior capsular release. Key to proper execution of the release is establishing a posterior-inferior accessory portal. This is accomplished while viewing from a standard posterior (“soft spot”) portal and determining the appropriate location and angle of entry by spinal needle localization. Typically, an entry point is selected about 4 cm distal and 1 cm lateral to the standard posterior portal. An 18-gauge spinal needle introduced at this location is angled about 15° superiorly and about 20° medially. Once the appropriate vector is determined, a skin incision is made, and a Wissinger rod is introduced, over which a small-diameter cannula is passed. A hooked-tip electrocautery device is used to divide the posterior capsule from the glenoid labrum between the 8- and 6-o’clock positions in the right shoulder (Figure). Care is taken to perform the release immediately adjacent to the glenoid labrum and using short bursts of cautery in order to minimize risk of injury to the teres minor branch of the axillary nerve. Adequate release is confirmed by reassessing passive internal rotation under anesthesia. Additional procedures are performed, if necessary, after completion of the capsular release.

Postoperative rehabilitation consists initially of pendulum exercises and scapular retraction starting on postoperative day 1. Once the swelling from the surgical procedure subsides, typically within 1 week, passive and active-assisted ROM and gentle posterior capsular mobilization are initiated under the direction of a licensed physical therapist. Active ROM is allowed once the patient regains normal scapulothoracic rhythm. Strengthening consists initially of isometrics followed by light resistance strengthening for the rotator cuff and scapular stabilizers once active ROM and scapulothoracic rhythm return to normal. Passive internal rotation stretching, including use of the sleeper stretch, is implemented as soon as tolerated and continues throughout the rehabilitation process.³²

Statistical Analysis

Statistical analysis was performed with Stata Release 11 (StataCorp, College Station, Texas). Paired t tests were used to assess preoperative and postoperative mean differences in ASES scores, in passive glenohumeral internal rotation, and in active glenohumeral internal rotation; independent-samples t tests were used to assess side-to-side differences. Significance was set at P < .05.

Results

Fifteen overhead athletes met the study inclusion criteria. Two were lost to follow-up. Of the remaining 13 patients, 6 underwent isolated arthroscopic posterior-inferior capsular release, and 7 had concomitant procedures (6 subacromial decompressions, 1 superior labrum anterior-posterior [SLAP] repair). There were 11 male athletes and 2 female athletes. Twelve of the 13 patients were right-hand–dominant. Mean age at time of surgery was 21 years (range, 16-33 years). There were 10 baseball players (6 pitchers, 4 position players); the other 3 patients played softball (1), volleyball (1), or tennis (1). Six patients played at high school level, 5 at college level, 1 at professional level, and 1 at amateur level. All 13 patients underwent a minimum of 3 months of comprehensive rehabilitation, which included use of the sleeper stretch, active joint mobilization by a licensed physical therapist, and sport-specific restriction from exacerbating activities. Mean duration of symptoms before surgery was 18 months (range, 4-48 months). Mean postoperative follow-up was 31 months (range, 24-59 months). Mean ASES score was 71.5 (range, 33-95) before surgery and 86.9 (range, 60-100) after surgery (P < .001). Mean GIRD improved from 43.1° (range, 30°-60°) before surgery to 9.7° (range, –7° to 40°) after surgery (P < .001). Mean active internal rotation difference improved from 3.8 vertebral segments before surgery to 2.6 vertebral segments after surgery; this difference was not statistically significant (P = .459). Ten (77%) of the 13 patients returned to their preoperative level of play or a higher level; the other 3 (23%) did not return to their preoperative level of play but continued to compete in a different position (Table). Eleven patients (85%) stated they would repeat the procedure. One of the 2 patients who would not repeat the procedure was in the isolated posterior-inferior capsular release group; the other was in the concomitant-procedure group (subacromial decompression). Total glenohumeral ROM of dominant arm was 122° before surgery and 136° after surgery (P = .04). There was no significant difference in total ROM between dominant and nondominant arms after surgery (136° and 141°; P = .12), but the preoperative difference was significant (122° vs 141°; P = .022).

Discussion

GIRD has been associated with various pathologic conditions of the upper extremity. In 1991, Verna²⁸ found that a majority of 39 professional baseball pitchers with significant GIRD had shoulder problems that affected playing time. More recently, GIRD has been associated with a progression of injuries, including scapular dyskinesia, internal and secondary impingement, articular-sided partial rotator cuff tears, rotator cuff weakness, damage to the biceps–labral complex, and ulnar collateral ligament insufficiency.^12,18-22 In a cadaveric study of humeral head translation, Harryman and colleagues³³ noted an anterosuperior migration of the humeral head during flexion and concluded it resulted from a loose anterior and tight posterior glenohumeral capsule, leading to loss of glenohumeral internal rotation. More recently, posterosuperior migration of the humeral head has been postulated, with GIRD secondary to an essential posterior capsular contracture.¹ Tyler and colleagues³⁴ clinically linked posterior capsular tightness with GIRD, and both cadaveric and magnetic resonance imaging studies have supported the finding that posterior capsular contracture leads to posterosuperior humeral head migration in association with GIRD.^14,20 Such a disruption in normal glenohumeral joint mechanics could produce phenomena of internal or secondary acromiohumeral impingement and pain.

More recently, in a large cohort of professional baseball pitchers, a significant correlation was found between the incidence of rotator cuff strength deficits and GIRD.³⁵ More than 40% of the pitchers with GIRD of at least 35° had a measureable rotator cuff strength deficit in the throwing shoulder.

Burkhart and colleagues²³ concluded that the shoulder most at risk for developing “dead arm” has GIRD and an advanced form of scapular dyskinesia known as SICK scapula (the phenomenon involves Scapula malposition, Inferior medial border prominence, Coracoid pain and malposition, and dysKinesis of scapular movement).

Most athletes with symptoms attributed to GIRD respond to conservative management. A posterior-inferior capsular stretching program focused on regaining internal rotation in the throwing arm has been shown to return about 90% of athletes to play.¹ Numerous studies have indicated that enrollment in a compliant stretching program reduces GIRD.^1,23-27 However, nonoperative treatment fails in a reported 10% of patients with GIRD; these patients may respond to operative treatment.¹

More specifically, for patients who do not respond to conservative treatment, a posterior-inferior capsular release may be indicated.^1,29 Ticker and colleagues²² identified 9 patients who had lost internal rotation and had a posterior capsular contracture at arthroscopy. That study, however, was not performed on overhead or throwing athletes. Yoneda and colleagues³⁰ followed 16 overhead throwing athletes after arthroscopic posterior-inferior capsular release and found favorable preliminary clinical results. Eleven of the 16 patients returned to their preinjury level of performance; the other 5 returned to a lower level. In addition, all 4 patients who underwent isolated arthroscopic capsular release had throwing power restored to between 90% and 100%.

In the present study, 10 of 13 patients who underwent arthroscopic posterior-inferior capsular release returned to their preoperative level of play or a higher level. Mean passive GIRD improved significantly from before surgery to after surgery. ASES scores likewise were significantly improved from before surgery to after surgery. The active internal rotation difference as measured by vertebral segment level was not significantly changed after surgery. This lack of improvement may stem from the more complex musculoligamentous interactions governing active internal rotation versus isolated, passive internal rotation. Another possible explanation for lack of improvement is that the interobserver and intraobserver reliability of this method is lower.³⁶

At 2-year follow-up, the patient who had undergone concomitant SLAP repair demonstrated a 23% improvement in ASES score and more internal rotation on the dominant arm relative to the nondominant arm. This patient returned to a level of play at least as good as his preoperative level. Although we could not determine its statistical significance, this patient’s improvement suggests that the SLAP repair did not reduce the efficacy of the posterior-inferior capsular release.

Limitations of this study include its relatively small cohort (precluded statistical comparisons between groups), the proportion of patients (7/13) who had concomitant surgeries, and the limited options for patient outcome scores. Although the ASES score is a validated outcome score, the Kerlan-Jobe Orthopaedic Clinic Shoulder and Elbow (KJOC) score or the Disabilities of the Arm, Shoulder, and Hand (DASH) score may be more appropriate in an athletic population. In addition, although all study patients had GIRD that was unresponsive to a concerted trial of nonoperative management, we did not have a control group (nonoperatively treated patients) for comparison. Finally, we did not obtain computed tomography scans or account for the potential contribution of humeral retroversion to GIRD in this group of patients.

Conclusion

Selective arthroscopic posterior-inferior capsular release can be recommended as a reasonable operative solution for overhead athletes with symptomatic GIRD that has not responded to conservative management. In the present study, ASES scores improved significantly, and 77% of our athlete-patients returned to sport at their preoperative level of play or a higher level.

Glenohumeral internal rotation deficit (GIRD) can be observed in overhead athletes and is thought to play a role in generating pain and rotator cuff weakness in the dominant shoulder with sport. It is unclear what is an acceptable value of GIRD in a population of overhead athletes and whether it should be based solely on internal rotation deficit or should include total range of motion (ROM) deficit.^1,2 Acquired GIRD in the athlete’s throwing shoulder has been thoroughly documented in the literature as a loss of internal rotation relative to the nonthrowing shoulder, with etiologies including bony adaptations (increased humeral retroversion), muscular tightness, and posterior capsular tightness.^1,3-11 In particular, the repetitive torsional stresses acting on the throwing shoulder of baseball players is thought to produce, over the long term, structural adaptations such as increased humeral retroversion.^5,12-14 Further, for shoulders with posterior-inferior capsular tightness, cadaveric studies have shown increased contact pressure at the coracoacromial arch during simulated follow-through.¹⁵ Athletes of other overhead and throwing sports, such as football, softball, tennis, and volleyball, may show similar adaptations in overhead motion.^9,16,17

GIRD has been associated with a variety of pathologic conditions, including scapular dyskinesis, internal and secondary impingement, partial articular-sided rotator cuff tears, damage to the biceps–labral complex, and ulnar collateral ligament insufficiency.^10,12,18-22

Restriction from engaging in exacerbating activities (eg, throwing) and compliance with a specific stretching program reduces or eliminates GIRD in the majority of cases.^1,23-28 In the few cases in which conservative management fails, operative intervention may be indicated.^1,23,29,30 Few investigators have detailed an operative technique for selective arthroscopic capsular release of the posterior-inferior capsule or evaluated the ability of athletes to return to sport after such surgery.

In this article, we present our technique for arthroscopic posterior-inferior capsular release and report the results of applying this technique in a population of athletes with symptomatic GIRD that was unresponsive to nonoperative treatment and was preventing them from returning to sport.

We hypothesized that selective arthroscopic surgical release of the posterior-inferior capsule would improve symptomatic GIRD and result in a return to sport in the majority of cases unresponsive to nonoperative treatment.

Materials and Methods

Patients

After obtaining institutional review board approval, we retrospectively reviewed patient charts and collected data. Study inclusion criteria were arthroscopic selective posterior-inferior capsular release between 2004 and 2008; failure to resume sport after minimum 3 months of physical therapy, including use of sleeper stretch, active joint mobilization by licensed physical therapist, and sport-specific restriction from exacerbating activities (eg, throwing for baseball players); and active participation in overhead sport.^1,27 Exclusion criteria were generalized adhesive capsulitis, labral pathology producing glenohumeral joint instability (Bankart or reverse Bankart lesion), high-grade or full-thickness tearing of rotator cuff, and clinically significant partial-thickness tearing or instability of long head of biceps tendon.

Assessment

One of 3 authors (Dr. Buss, Dr. Codding, or Dr. Dahm) used a bubble goniometer to measure passive internal rotation. Patients were positioned supine with 90° of thoracohumeral abduction and 90° of elbow flexion. The examiner’s hand stabilized the scapula against the examination table, in accordance with published techniques.^1,26 Active internal rotation was measured at 0° of thoracohumeral abduction by noting the most superior spinal segment reached. Before and after surgery, passive internal rotation measurements were taken on both arms. GIRD was determined by the difference between dominant and nondominant arm measurements; segmental differences were obtained by subtracting segments achieved between the dominant and nondominant arms.

Before surgery and at minimum 2-year follow-up after surgery, patients completed a subjective questionnaire, which included the American Shoulder and Elbow Surgeons (ASES) Standardized Shoulder Assessment Form, for assessment of both arms. ASES scores are reliable, valid, and responsive in evaluating shoulder pain and function.^15,31 Patients also answered questions about their ability to return to play, their level of play after surgery, and whether they would undergo the procedure again.

Surgical Technique

After induction of general anesthesia and standard preparation and draping, the patient is placed in a standard beach-chair position and examined. Diagnostic arthroscopy is then performed. In all patients, intra-articular evaluation revealed a thickened, contracted posterior band of the inferior glenohumeral ligament. This finding is consistent with other studies of patients with significant GIRD.^1,14,22,30

On completion of the diagnostic portion of the arthroscopy, attention is turned to the selective posterior-inferior capsular release. Key to proper execution of the release is establishing a posterior-inferior accessory portal. This is accomplished while viewing from a standard posterior (“soft spot”) portal and determining the appropriate location and angle of entry by spinal needle localization. Typically, an entry point is selected about 4 cm distal and 1 cm lateral to the standard posterior portal. An 18-gauge spinal needle introduced at this location is angled about 15° superiorly and about 20° medially. Once the appropriate vector is determined, a skin incision is made, and a Wissinger rod is introduced, over which a small-diameter cannula is passed. A hooked-tip electrocautery device is used to divide the posterior capsule from the glenoid labrum between the 8- and 6-o’clock positions in the right shoulder (Figure). Care is taken to perform the release immediately adjacent to the glenoid labrum and using short bursts of cautery in order to minimize risk of injury to the teres minor branch of the axillary nerve. Adequate release is confirmed by reassessing passive internal rotation under anesthesia. Additional procedures are performed, if necessary, after completion of the capsular release.

Postoperative rehabilitation consists initially of pendulum exercises and scapular retraction starting on postoperative day 1. Once the swelling from the surgical procedure subsides, typically within 1 week, passive and active-assisted ROM and gentle posterior capsular mobilization are initiated under the direction of a licensed physical therapist. Active ROM is allowed once the patient regains normal scapulothoracic rhythm. Strengthening consists initially of isometrics followed by light resistance strengthening for the rotator cuff and scapular stabilizers once active ROM and scapulothoracic rhythm return to normal. Passive internal rotation stretching, including use of the sleeper stretch, is implemented as soon as tolerated and continues throughout the rehabilitation process.³²

Statistical Analysis

Statistical analysis was performed with Stata Release 11 (StataCorp, College Station, Texas). Paired t tests were used to assess preoperative and postoperative mean differences in ASES scores, in passive glenohumeral internal rotation, and in active glenohumeral internal rotation; independent-samples t tests were used to assess side-to-side differences. Significance was set at P < .05.

Results

Fifteen overhead athletes met the study inclusion criteria. Two were lost to follow-up. Of the remaining 13 patients, 6 underwent isolated arthroscopic posterior-inferior capsular release, and 7 had concomitant procedures (6 subacromial decompressions, 1 superior labrum anterior-posterior [SLAP] repair). There were 11 male athletes and 2 female athletes. Twelve of the 13 patients were right-hand–dominant. Mean age at time of surgery was 21 years (range, 16-33 years). There were 10 baseball players (6 pitchers, 4 position players); the other 3 patients played softball (1), volleyball (1), or tennis (1). Six patients played at high school level, 5 at college level, 1 at professional level, and 1 at amateur level. All 13 patients underwent a minimum of 3 months of comprehensive rehabilitation, which included use of the sleeper stretch, active joint mobilization by a licensed physical therapist, and sport-specific restriction from exacerbating activities. Mean duration of symptoms before surgery was 18 months (range, 4-48 months). Mean postoperative follow-up was 31 months (range, 24-59 months). Mean ASES score was 71.5 (range, 33-95) before surgery and 86.9 (range, 60-100) after surgery (P < .001). Mean GIRD improved from 43.1° (range, 30°-60°) before surgery to 9.7° (range, –7° to 40°) after surgery (P < .001). Mean active internal rotation difference improved from 3.8 vertebral segments before surgery to 2.6 vertebral segments after surgery; this difference was not statistically significant (P = .459). Ten (77%) of the 13 patients returned to their preoperative level of play or a higher level; the other 3 (23%) did not return to their preoperative level of play but continued to compete in a different position (Table). Eleven patients (85%) stated they would repeat the procedure. One of the 2 patients who would not repeat the procedure was in the isolated posterior-inferior capsular release group; the other was in the concomitant-procedure group (subacromial decompression). Total glenohumeral ROM of dominant arm was 122° before surgery and 136° after surgery (P = .04). There was no significant difference in total ROM between dominant and nondominant arms after surgery (136° and 141°; P = .12), but the preoperative difference was significant (122° vs 141°; P = .022).

Discussion

GIRD has been associated with various pathologic conditions of the upper extremity. In 1991, Verna²⁸ found that a majority of 39 professional baseball pitchers with significant GIRD had shoulder problems that affected playing time. More recently, GIRD has been associated with a progression of injuries, including scapular dyskinesia, internal and secondary impingement, articular-sided partial rotator cuff tears, rotator cuff weakness, damage to the biceps–labral complex, and ulnar collateral ligament insufficiency.^12,18-22 In a cadaveric study of humeral head translation, Harryman and colleagues³³ noted an anterosuperior migration of the humeral head during flexion and concluded it resulted from a loose anterior and tight posterior glenohumeral capsule, leading to loss of glenohumeral internal rotation. More recently, posterosuperior migration of the humeral head has been postulated, with GIRD secondary to an essential posterior capsular contracture.¹ Tyler and colleagues³⁴ clinically linked posterior capsular tightness with GIRD, and both cadaveric and magnetic resonance imaging studies have supported the finding that posterior capsular contracture leads to posterosuperior humeral head migration in association with GIRD.^14,20 Such a disruption in normal glenohumeral joint mechanics could produce phenomena of internal or secondary acromiohumeral impingement and pain.

More recently, in a large cohort of professional baseball pitchers, a significant correlation was found between the incidence of rotator cuff strength deficits and GIRD.³⁵ More than 40% of the pitchers with GIRD of at least 35° had a measureable rotator cuff strength deficit in the throwing shoulder.

Burkhart and colleagues²³ concluded that the shoulder most at risk for developing “dead arm” has GIRD and an advanced form of scapular dyskinesia known as SICK scapula (the phenomenon involves Scapula malposition, Inferior medial border prominence, Coracoid pain and malposition, and dysKinesis of scapular movement).

Most athletes with symptoms attributed to GIRD respond to conservative management. A posterior-inferior capsular stretching program focused on regaining internal rotation in the throwing arm has been shown to return about 90% of athletes to play.¹ Numerous studies have indicated that enrollment in a compliant stretching program reduces GIRD.^1,23-27 However, nonoperative treatment fails in a reported 10% of patients with GIRD; these patients may respond to operative treatment.¹

More specifically, for patients who do not respond to conservative treatment, a posterior-inferior capsular release may be indicated.^1,29 Ticker and colleagues²² identified 9 patients who had lost internal rotation and had a posterior capsular contracture at arthroscopy. That study, however, was not performed on overhead or throwing athletes. Yoneda and colleagues³⁰ followed 16 overhead throwing athletes after arthroscopic posterior-inferior capsular release and found favorable preliminary clinical results. Eleven of the 16 patients returned to their preinjury level of performance; the other 5 returned to a lower level. In addition, all 4 patients who underwent isolated arthroscopic capsular release had throwing power restored to between 90% and 100%.

In the present study, 10 of 13 patients who underwent arthroscopic posterior-inferior capsular release returned to their preoperative level of play or a higher level. Mean passive GIRD improved significantly from before surgery to after surgery. ASES scores likewise were significantly improved from before surgery to after surgery. The active internal rotation difference as measured by vertebral segment level was not significantly changed after surgery. This lack of improvement may stem from the more complex musculoligamentous interactions governing active internal rotation versus isolated, passive internal rotation. Another possible explanation for lack of improvement is that the interobserver and intraobserver reliability of this method is lower.³⁶

At 2-year follow-up, the patient who had undergone concomitant SLAP repair demonstrated a 23% improvement in ASES score and more internal rotation on the dominant arm relative to the nondominant arm. This patient returned to a level of play at least as good as his preoperative level. Although we could not determine its statistical significance, this patient’s improvement suggests that the SLAP repair did not reduce the efficacy of the posterior-inferior capsular release.

Limitations of this study include its relatively small cohort (precluded statistical comparisons between groups), the proportion of patients (7/13) who had concomitant surgeries, and the limited options for patient outcome scores. Although the ASES score is a validated outcome score, the Kerlan-Jobe Orthopaedic Clinic Shoulder and Elbow (KJOC) score or the Disabilities of the Arm, Shoulder, and Hand (DASH) score may be more appropriate in an athletic population. In addition, although all study patients had GIRD that was unresponsive to a concerted trial of nonoperative management, we did not have a control group (nonoperatively treated patients) for comparison. Finally, we did not obtain computed tomography scans or account for the potential contribution of humeral retroversion to GIRD in this group of patients.

Conclusion

Selective arthroscopic posterior-inferior capsular release can be recommended as a reasonable operative solution for overhead athletes with symptomatic GIRD that has not responded to conservative management. In the present study, ASES scores improved significantly, and 77% of our athlete-patients returned to sport at their preoperative level of play or a higher level.