Clinical Review

The beach-chair position (BCP) is commonly used for both arthroscopic and open shoulder surgery. This technique positions the shoulder in an anatomical upright position, facilitating shoulder access and visualization.¹ Compared with the lateral decubitus position, the BCP also improves airway access, reduces bleeding, and lessens the risk for brachial plexus injury.²

Despite the advantages of using the BCP, there have been multiple reports of catastrophic neurologic complications, including severe brain damage and death, in relatively healthy patients without any known risk factors.^3-6 The definitive etiology of these complications remains unclear, but it has been hypothesized that BCP use may be an independent risk factor for cerebrovascular ischemia,^1,5-16 as the upright position can cause hypotension leading to increased risk for cerebral hypoperfusion.^7-11,17 Reducing cerebral perfusion pressure below critical thresholds may result in permanent neurologic injury.^4-6,14 Therefore, monitoring of cerebral perfusion and optimization of intraoperative cerebral oxygenation have been recommended to help avoid potential neurologic complications. However, a direct relationship between intraoperative cerebral desaturation events (CDEs) and postoperative neurocognitive deficits has not been definitively established.^1,9-12

To put into perspective the importance of detecting and preventing CDEs and neurologic complications, we can consider the incidence of fatal pulmonary embolism associated with total joint arthroplasty. Although the incidence is very low, about 0.1% to 2.0%, some form of venous thromboembolism prophylaxis is the standard of care for helping prevent this serious complication. Similarly, catastrophic neurologic complications of upright shoulder arthroscopy are very rare, but it is still important to consider measures that help minimize them.

We reviewed the literature for the incidence of postoperative neurocognitive deficits, number of reported neurocognitive complications, and incidence of intraoperative CDEs in patients who underwent arthroscopic shoulder surgery in the BCP.

Methods

Dr. Salazar and Dr. Hazel independently searched the Medline, Cochrane, and Embase databases for case series, prospective studies, and cohort studies that reported neurocognitive complications associated with the BCP and the incidence of intraoperative CDEs. The authors used beach chair, desaturation, near infrared spectroscopy, and shoulder as medical subject headings (MeSH). In addition, bibliographies of retrieved articles were checked for studies that the search terms may have missed. Eighty-one publications were identified and reviewed for possible inclusion.

Next, the same 2 authors reviewed the titles and abstracts for relevance and determined which articles had potential to contribute to the study. Only English-language publications were considered for inclusion. To review the incidence of postoperative neurocognitive deficits, we included only those studies with more than 25 patients, documentation of postoperative complications, and arthroscopic shoulder surgery performed with the patient in the seated, semi-upright, or BCP. Only studies with at least 25 patients were used in order to increase the power and improve the level of evidence. To review reported cases of neurocognitive complications, we included all relevant case reports and case series. To review the incidence of intraoperative CDEs and investigate their relationship with postoperative neurocognitive deficits, we included studies that reported on use of intraoperative cerebral perfusion monitoring. Modalities used in these studies included near infrared spectroscopy, electroencephalography, and invasive blood pressure monitoring calculated at the brain level. Studies were excluded if they did not involve arthroscopic shoulder surgery or were not conducted with human subjects.

Information recorded for each study included general information such as author and publication year, type of study, number of patients enrolled, type of intraoperative monitoring, anesthesia protocol, number of patients with CDEs, and number of patients with neurocognitive complications after surgery.

Results

Our search identified 81 publications for potential inclusion. Our first aim was to identify the overall incidence of reported neurocognitive deficits after arthroscopic shoulder surgery with the patient in the BCP. We identified 10 studies (Table 1) that met the inclusion criteria. Among the 24,701 patients in these 10 studies, there was only 1 reported case of neurocognitive deficit after surgery, in a mixed prospective-retrospective study of 15,014 cases by Rohrbaugh and colleagues.18 The deficit they reported was an ischemic cerebral vascular accident. The 0.0067% incidence in their study demonstrates how rare the complication is. Two large retrospective studies (Ns = 4169 and 5177 patients) found no postoperative neurocognitive complications.^19,20 Only 3 studies performed formal postoperative cognitive testing. Salazar and colleagues²¹ used the Repeatable Battery for the Assessment of Neuropsychological Status before and after surgery, and Gillespie and colleagues⁸ and Lee and colleagues¹⁰ used the Mini–Mental State Examination before and after surgery. Total incidence of reported neurocognitive deficits from our review was 0.004% (1/24,701).

Our second aim was to review all reported cases of neurocognitive complications after arthroscopic shoulder surgery with the patient in the BCP. We identified 4 publications that fit our inclusion criteria (Table 2). Pohl and Cullen6 described 4 cases of ischemic brain injury after arthroscopic shoulder surgery with the patient in the BCP. Age range was 47 to 57 years. Specific intraoperative cerebral monitoring was not used. However, these patients had several episodes of intraoperative hypotension (systolic blood pressures, 80-90 mm Hg), measured with a traditional blood pressure cuff on the arm. In general, these patients had minimal cerebrovascular risk factors and no known preexisting cerebrovascular disease. Drummond and colleagues²² described an ischemic stroke in a 50-year-old man after arthroscopic subacromial decompression and open rotator cuff repair that resulted in unresolved right hemiplegia. Subsequent diagnostic investigation revealed an asymmetry of the circle of Willis resulting in limited flow to the left anterior and middle cerebral artery distributions. Bhatti and Enneking³ reported the case of a 64-year-old man who lost vision in the right eye immediately after arthroscopic rotator cuff repair. His vision improved spontaneously the next morning and continued to improve over the next 6 months—he regained 20/20 vision with some residual optic neuropathy.

Our third aim was to determine the incidence of intraoperative CDEs during arthroscopic shoulder surgery with the patient in the BCP. Incidence of CDEs varied widely among the 7 studies reviewed (Table 3). Minimum incidence of intraoperative CDE was 0% in a cohort of 30 patients,¹ and maximum incidence was 80% in a study of 61 patients,¹² all of whom underwent elective arthroscopic shoulder surgery in the BCP. Although there was wide variability in CDE incidence, the studies were consistent with respect to their definition of a CDE. Most authors used a decrease in regional cerebral tissue oxygen saturation of 20% or more from baseline, or an absolute value up to 55%, to define a CDE. None of the 7 studies reviewed reported a clinically significant adverse neurocognitive event.

Discussion

Of concern, there have been several surveys, case reports, and small case series of previously healthy patients who had no known risk factors, underwent arthroscopic shoulder surgery in the BCP, and developed unanticipated postoperative neurologic complications.^4-6,14 Beach-chair positioning during surgical procedures has been implicated as a contributing factor leading to cerebral hypoperfusion with potential for cerebral ischemia.^1,12,23 These changes in cerebral perfusion pressure are thought to be the major determinant of poor neurologic outcomes. Such reports have exposed the potential need for heightened vigilance, alternative anesthesia techniques, and improved monitoring, though the exact etiology of the central nervous system injuries in this patient population is incompletely understood and is likely multifactorial. Therefore, in this study we wanted to determine the incidence of postoperative neurocognitive deficits and review all reported cases of neurocognitive complications in patients who have undergone arthroscopic shoulder surgery in the BCP. In addition, we wanted to define the incidence of intraoperative CDEs and investigate their relationship with postoperative neurocognitive complications.

According to our review, the incidence of postoperative neurocognitive complications after surgery in the BCP is 0.004% (1/24,701). However, this finding is based only on what has been reported; the true incidence is not known. It is also important to note that the incidence of neurocognitive deficits after many other types of surgery is not known and that surgery itself may be a risk factor for postoperative neurocognitive deficits.²⁴ In their retrospective review of 15,014 patients who underwent arthroscopic shoulder surgery in the BCP at a single institution over an 11-year period, Rohrbaugh and colleagues18 found an overall postoperative complication rate of 0.37% and a 0.0067% incidence of neurocognitive deficits. One patient in the series was given a diagnosis of ischemic stroke on the basis of neurologic deficits that occurred 24 hours after surgery. Yadeau and colleagues²⁰ found no postoperative neurocognitive complications in a mixed prospective-retrospective study of 4169 patients—3000 identified retrospectively, 1169 prospectively—who underwent arthroscopic shoulder surgery in the BCP at an ambulatory surgery center. Pin-on and colleagues¹⁹ reported on a series of 5177 orthopedic and neurosurgical patients who underwent surgery in the BCP. In those who had arthroscopic shoulder surgery, intraoperative systolic blood pressures obtained from an arterial line referenced to heart level decreased a mean (SD) of 14.4% (12.7%), whereas in those whose pressures were obtained from a noninvasive blood pressure cuff referenced to heart level decreased 19.3% (12.6%). However, the authors reported no incidence of postoperative stroke or neurologic deficits.

Although uncommon, perioperative cerebral ischemic accidents are potentially devastating for patients, their families, and the health care professionals involved. These events have tremendous economic, social, professional, and medicolegal implications, with perioperative stroke being particularly morbid. Perioperative stroke has a mortality rate of 60%, versus 15% to 46% for stroke in general.^25,26 In 2005, Pohl and Cullen⁶ published a landmark article on a series of 4 relatively healthy middle-aged patients who were at low risk for stroke but had catastrophic neurocognitive complications (including 1 death) after arthroscopic shoulder surgery in the BCP. Bhatti and Enneking³ described a case of acute postoperative vision loss and ophthalmoplegia attributed to intraoperative hypotension leading to ischemia in a patient who underwent an elective shoulder arthroscopic procedure in the BCP. These reports prompted multiple investigations into the physiologic hemodynamic changes associated with surgery in the BCP and the treatment strategies used to improve patient safety.

In the normal physiologic state, the sympathetic nervous system is activated when a person assumes the seated position. The result is increased systemic vascular resistance and heart rate alterations to maintain cardiac output and mean arterial pressure. In anesthetized patients, this response is blunted by the vasodilatory effects of intravenous and volatile anesthetics. Multiple studies have demonstrated substantial hemodynamic changes in both awake and anesthetized patients during the maneuver from the supine position to the seated position^1,27,28; these changes include diminished cardiac index, stroke volume, and arterial pressure.¹⁷ The data underscore the need for attentiveness and accurate monitoring of cerebral perfusion when the transition is made from the supine position to the BCP, particularly in the early phase of surgery and in high-risk patients.

Knowledge of these hemodynamic changes has led several authors to recommend additional intraoperative monitoring of cerebral perfusion. Monitoring techniques have included use of invasive blood pressure monitoring adjusted to brain level, cerebral oximetry using near infrared spectroscopy, and electroencephalography. However, the clinical relevance of intraoperative CDEs in isolation is not well understood.^1,6,7,23 In addition, cost and availability of additional advanced monitoring likely factor into why it is not more commonly used. For this patient population, the severity, frequency, and duration of desaturation that causes cerebral ischemia and the relationship with postoperative neurocognitive deficits remain undefined.

The incidence of CDEs in patients being monitored with near infrared spectroscopy while undergoing elective arthroscopic shoulder surgery in the BCP varies widely, from 0% to 80% (mean, 41%).^{1,4,7,10,12,21} Magnitude and duration of cerebral ischemia required to produce neurocognitive dysfunction in this patient population remain unidentified as well. In conscious patients, a 20% reduction in frontal lobe oxygenation is associated with clinical manifestations of cerebral hypoperfusion, such as syncope.^15,29 As none of the patients in the studies we reviewed experienced any sort of deficit, we cannot definitively state there is a correlation between CDE occurrence and neurocognitive deficit.

One limitation of our investigation is that it was a systemic review, and thus there was substantial heterogeneity in the methods and designs of the studies included in the analysis. Among the different series, there was variability in multiple aspects of the study design, including type of anesthetic, patient inclusion criteria, type of surgery, type of intraoperative cerebral perfusion monitoring, and type of neurocognitive testing. As a result, comparing the groups was difficult, and the generalizability of our findings may be limited. In addition, it is difficult to accurately establish incidence and comprehensively review these events because of the paucity of literature.

Conclusion

Neurocognitive complications after shoulder arthroscopy with the patient in the BCP are extremely rare but potentially devastating events that can affect healthy patients with no preexisting cerebrovascular risk factors. Our review indicated the incidence of permanent neurologic deficit after arthroscopy in the BCP may be as low as 0.004%. The exact etiology of such complications is not clear. Basic science research and large prospective studies are needed to identify the clinically relevant thresholds of magnitude, duration, and frequency of intraoperative CDEs in order to establish their relationship with postoperative neurocognitive complications. Such large studies may also elucidate modifiable patient-specific risk factors and establish the most sensitive, safe, and cost-effective intraoperative monitoring tools. Current literature suggests that accurate intraoperative monitoring of cerebral perfusion, alternatives to general anesthesia, and prudent use of intraoperative blood pressure control may improve patient safety.

The beach-chair position (BCP) is commonly used for both arthroscopic and open shoulder surgery. This technique positions the shoulder in an anatomical upright position, facilitating shoulder access and visualization.¹ Compared with the lateral decubitus position, the BCP also improves airway access, reduces bleeding, and lessens the risk for brachial plexus injury.²

Despite the advantages of using the BCP, there have been multiple reports of catastrophic neurologic complications, including severe brain damage and death, in relatively healthy patients without any known risk factors.^3-6 The definitive etiology of these complications remains unclear, but it has been hypothesized that BCP use may be an independent risk factor for cerebrovascular ischemia,^1,5-16 as the upright position can cause hypotension leading to increased risk for cerebral hypoperfusion.^7-11,17 Reducing cerebral perfusion pressure below critical thresholds may result in permanent neurologic injury.^4-6,14 Therefore, monitoring of cerebral perfusion and optimization of intraoperative cerebral oxygenation have been recommended to help avoid potential neurologic complications. However, a direct relationship between intraoperative cerebral desaturation events (CDEs) and postoperative neurocognitive deficits has not been definitively established.^1,9-12

To put into perspective the importance of detecting and preventing CDEs and neurologic complications, we can consider the incidence of fatal pulmonary embolism associated with total joint arthroplasty. Although the incidence is very low, about 0.1% to 2.0%, some form of venous thromboembolism prophylaxis is the standard of care for helping prevent this serious complication. Similarly, catastrophic neurologic complications of upright shoulder arthroscopy are very rare, but it is still important to consider measures that help minimize them.

We reviewed the literature for the incidence of postoperative neurocognitive deficits, number of reported neurocognitive complications, and incidence of intraoperative CDEs in patients who underwent arthroscopic shoulder surgery in the BCP.

Methods

Dr. Salazar and Dr. Hazel independently searched the Medline, Cochrane, and Embase databases for case series, prospective studies, and cohort studies that reported neurocognitive complications associated with the BCP and the incidence of intraoperative CDEs. The authors used beach chair, desaturation, near infrared spectroscopy, and shoulder as medical subject headings (MeSH). In addition, bibliographies of retrieved articles were checked for studies that the search terms may have missed. Eighty-one publications were identified and reviewed for possible inclusion.

Next, the same 2 authors reviewed the titles and abstracts for relevance and determined which articles had potential to contribute to the study. Only English-language publications were considered for inclusion. To review the incidence of postoperative neurocognitive deficits, we included only those studies with more than 25 patients, documentation of postoperative complications, and arthroscopic shoulder surgery performed with the patient in the seated, semi-upright, or BCP. Only studies with at least 25 patients were used in order to increase the power and improve the level of evidence. To review reported cases of neurocognitive complications, we included all relevant case reports and case series. To review the incidence of intraoperative CDEs and investigate their relationship with postoperative neurocognitive deficits, we included studies that reported on use of intraoperative cerebral perfusion monitoring. Modalities used in these studies included near infrared spectroscopy, electroencephalography, and invasive blood pressure monitoring calculated at the brain level. Studies were excluded if they did not involve arthroscopic shoulder surgery or were not conducted with human subjects.

Information recorded for each study included general information such as author and publication year, type of study, number of patients enrolled, type of intraoperative monitoring, anesthesia protocol, number of patients with CDEs, and number of patients with neurocognitive complications after surgery.

Results

Our search identified 81 publications for potential inclusion. Our first aim was to identify the overall incidence of reported neurocognitive deficits after arthroscopic shoulder surgery with the patient in the BCP. We identified 10 studies (Table 1) that met the inclusion criteria. Among the 24,701 patients in these 10 studies, there was only 1 reported case of neurocognitive deficit after surgery, in a mixed prospective-retrospective study of 15,014 cases by Rohrbaugh and colleagues.18 The deficit they reported was an ischemic cerebral vascular accident. The 0.0067% incidence in their study demonstrates how rare the complication is. Two large retrospective studies (Ns = 4169 and 5177 patients) found no postoperative neurocognitive complications.^19,20 Only 3 studies performed formal postoperative cognitive testing. Salazar and colleagues²¹ used the Repeatable Battery for the Assessment of Neuropsychological Status before and after surgery, and Gillespie and colleagues⁸ and Lee and colleagues¹⁰ used the Mini–Mental State Examination before and after surgery. Total incidence of reported neurocognitive deficits from our review was 0.004% (1/24,701).

Our second aim was to review all reported cases of neurocognitive complications after arthroscopic shoulder surgery with the patient in the BCP. We identified 4 publications that fit our inclusion criteria (Table 2). Pohl and Cullen6 described 4 cases of ischemic brain injury after arthroscopic shoulder surgery with the patient in the BCP. Age range was 47 to 57 years. Specific intraoperative cerebral monitoring was not used. However, these patients had several episodes of intraoperative hypotension (systolic blood pressures, 80-90 mm Hg), measured with a traditional blood pressure cuff on the arm. In general, these patients had minimal cerebrovascular risk factors and no known preexisting cerebrovascular disease. Drummond and colleagues²² described an ischemic stroke in a 50-year-old man after arthroscopic subacromial decompression and open rotator cuff repair that resulted in unresolved right hemiplegia. Subsequent diagnostic investigation revealed an asymmetry of the circle of Willis resulting in limited flow to the left anterior and middle cerebral artery distributions. Bhatti and Enneking³ reported the case of a 64-year-old man who lost vision in the right eye immediately after arthroscopic rotator cuff repair. His vision improved spontaneously the next morning and continued to improve over the next 6 months—he regained 20/20 vision with some residual optic neuropathy.

Our third aim was to determine the incidence of intraoperative CDEs during arthroscopic shoulder surgery with the patient in the BCP. Incidence of CDEs varied widely among the 7 studies reviewed (Table 3). Minimum incidence of intraoperative CDE was 0% in a cohort of 30 patients,¹ and maximum incidence was 80% in a study of 61 patients,¹² all of whom underwent elective arthroscopic shoulder surgery in the BCP. Although there was wide variability in CDE incidence, the studies were consistent with respect to their definition of a CDE. Most authors used a decrease in regional cerebral tissue oxygen saturation of 20% or more from baseline, or an absolute value up to 55%, to define a CDE. None of the 7 studies reviewed reported a clinically significant adverse neurocognitive event.

Discussion

Of concern, there have been several surveys, case reports, and small case series of previously healthy patients who had no known risk factors, underwent arthroscopic shoulder surgery in the BCP, and developed unanticipated postoperative neurologic complications.^4-6,14 Beach-chair positioning during surgical procedures has been implicated as a contributing factor leading to cerebral hypoperfusion with potential for cerebral ischemia.^1,12,23 These changes in cerebral perfusion pressure are thought to be the major determinant of poor neurologic outcomes. Such reports have exposed the potential need for heightened vigilance, alternative anesthesia techniques, and improved monitoring, though the exact etiology of the central nervous system injuries in this patient population is incompletely understood and is likely multifactorial. Therefore, in this study we wanted to determine the incidence of postoperative neurocognitive deficits and review all reported cases of neurocognitive complications in patients who have undergone arthroscopic shoulder surgery in the BCP. In addition, we wanted to define the incidence of intraoperative CDEs and investigate their relationship with postoperative neurocognitive complications.

According to our review, the incidence of postoperative neurocognitive complications after surgery in the BCP is 0.004% (1/24,701). However, this finding is based only on what has been reported; the true incidence is not known. It is also important to note that the incidence of neurocognitive deficits after many other types of surgery is not known and that surgery itself may be a risk factor for postoperative neurocognitive deficits.²⁴ In their retrospective review of 15,014 patients who underwent arthroscopic shoulder surgery in the BCP at a single institution over an 11-year period, Rohrbaugh and colleagues18 found an overall postoperative complication rate of 0.37% and a 0.0067% incidence of neurocognitive deficits. One patient in the series was given a diagnosis of ischemic stroke on the basis of neurologic deficits that occurred 24 hours after surgery. Yadeau and colleagues²⁰ found no postoperative neurocognitive complications in a mixed prospective-retrospective study of 4169 patients—3000 identified retrospectively, 1169 prospectively—who underwent arthroscopic shoulder surgery in the BCP at an ambulatory surgery center. Pin-on and colleagues¹⁹ reported on a series of 5177 orthopedic and neurosurgical patients who underwent surgery in the BCP. In those who had arthroscopic shoulder surgery, intraoperative systolic blood pressures obtained from an arterial line referenced to heart level decreased a mean (SD) of 14.4% (12.7%), whereas in those whose pressures were obtained from a noninvasive blood pressure cuff referenced to heart level decreased 19.3% (12.6%). However, the authors reported no incidence of postoperative stroke or neurologic deficits.

Although uncommon, perioperative cerebral ischemic accidents are potentially devastating for patients, their families, and the health care professionals involved. These events have tremendous economic, social, professional, and medicolegal implications, with perioperative stroke being particularly morbid. Perioperative stroke has a mortality rate of 60%, versus 15% to 46% for stroke in general.^25,26 In 2005, Pohl and Cullen⁶ published a landmark article on a series of 4 relatively healthy middle-aged patients who were at low risk for stroke but had catastrophic neurocognitive complications (including 1 death) after arthroscopic shoulder surgery in the BCP. Bhatti and Enneking³ described a case of acute postoperative vision loss and ophthalmoplegia attributed to intraoperative hypotension leading to ischemia in a patient who underwent an elective shoulder arthroscopic procedure in the BCP. These reports prompted multiple investigations into the physiologic hemodynamic changes associated with surgery in the BCP and the treatment strategies used to improve patient safety.

In the normal physiologic state, the sympathetic nervous system is activated when a person assumes the seated position. The result is increased systemic vascular resistance and heart rate alterations to maintain cardiac output and mean arterial pressure. In anesthetized patients, this response is blunted by the vasodilatory effects of intravenous and volatile anesthetics. Multiple studies have demonstrated substantial hemodynamic changes in both awake and anesthetized patients during the maneuver from the supine position to the seated position^1,27,28; these changes include diminished cardiac index, stroke volume, and arterial pressure.¹⁷ The data underscore the need for attentiveness and accurate monitoring of cerebral perfusion when the transition is made from the supine position to the BCP, particularly in the early phase of surgery and in high-risk patients.

Knowledge of these hemodynamic changes has led several authors to recommend additional intraoperative monitoring of cerebral perfusion. Monitoring techniques have included use of invasive blood pressure monitoring adjusted to brain level, cerebral oximetry using near infrared spectroscopy, and electroencephalography. However, the clinical relevance of intraoperative CDEs in isolation is not well understood.^1,6,7,23 In addition, cost and availability of additional advanced monitoring likely factor into why it is not more commonly used. For this patient population, the severity, frequency, and duration of desaturation that causes cerebral ischemia and the relationship with postoperative neurocognitive deficits remain undefined.

The incidence of CDEs in patients being monitored with near infrared spectroscopy while undergoing elective arthroscopic shoulder surgery in the BCP varies widely, from 0% to 80% (mean, 41%).^{1,4,7,10,12,21} Magnitude and duration of cerebral ischemia required to produce neurocognitive dysfunction in this patient population remain unidentified as well. In conscious patients, a 20% reduction in frontal lobe oxygenation is associated with clinical manifestations of cerebral hypoperfusion, such as syncope.^15,29 As none of the patients in the studies we reviewed experienced any sort of deficit, we cannot definitively state there is a correlation between CDE occurrence and neurocognitive deficit.

One limitation of our investigation is that it was a systemic review, and thus there was substantial heterogeneity in the methods and designs of the studies included in the analysis. Among the different series, there was variability in multiple aspects of the study design, including type of anesthetic, patient inclusion criteria, type of surgery, type of intraoperative cerebral perfusion monitoring, and type of neurocognitive testing. As a result, comparing the groups was difficult, and the generalizability of our findings may be limited. In addition, it is difficult to accurately establish incidence and comprehensively review these events because of the paucity of literature.

Conclusion

Neurocognitive complications after shoulder arthroscopy with the patient in the BCP are extremely rare but potentially devastating events that can affect healthy patients with no preexisting cerebrovascular risk factors. Our review indicated the incidence of permanent neurologic deficit after arthroscopy in the BCP may be as low as 0.004%. The exact etiology of such complications is not clear. Basic science research and large prospective studies are needed to identify the clinically relevant thresholds of magnitude, duration, and frequency of intraoperative CDEs in order to establish their relationship with postoperative neurocognitive complications. Such large studies may also elucidate modifiable patient-specific risk factors and establish the most sensitive, safe, and cost-effective intraoperative monitoring tools. Current literature suggests that accurate intraoperative monitoring of cerebral perfusion, alternatives to general anesthesia, and prudent use of intraoperative blood pressure control may improve patient safety.

The beach-chair position (BCP) is commonly used for both arthroscopic and open shoulder surgery. This technique positions the shoulder in an anatomical upright position, facilitating shoulder access and visualization.¹ Compared with the lateral decubitus position, the BCP also improves airway access, reduces bleeding, and lessens the risk for brachial plexus injury.²

Despite the advantages of using the BCP, there have been multiple reports of catastrophic neurologic complications, including severe brain damage and death, in relatively healthy patients without any known risk factors.^3-6 The definitive etiology of these complications remains unclear, but it has been hypothesized that BCP use may be an independent risk factor for cerebrovascular ischemia,^1,5-16 as the upright position can cause hypotension leading to increased risk for cerebral hypoperfusion.^7-11,17 Reducing cerebral perfusion pressure below critical thresholds may result in permanent neurologic injury.^4-6,14 Therefore, monitoring of cerebral perfusion and optimization of intraoperative cerebral oxygenation have been recommended to help avoid potential neurologic complications. However, a direct relationship between intraoperative cerebral desaturation events (CDEs) and postoperative neurocognitive deficits has not been definitively established.^1,9-12

To put into perspective the importance of detecting and preventing CDEs and neurologic complications, we can consider the incidence of fatal pulmonary embolism associated with total joint arthroplasty. Although the incidence is very low, about 0.1% to 2.0%, some form of venous thromboembolism prophylaxis is the standard of care for helping prevent this serious complication. Similarly, catastrophic neurologic complications of upright shoulder arthroscopy are very rare, but it is still important to consider measures that help minimize them.

We reviewed the literature for the incidence of postoperative neurocognitive deficits, number of reported neurocognitive complications, and incidence of intraoperative CDEs in patients who underwent arthroscopic shoulder surgery in the BCP.

Methods

Dr. Salazar and Dr. Hazel independently searched the Medline, Cochrane, and Embase databases for case series, prospective studies, and cohort studies that reported neurocognitive complications associated with the BCP and the incidence of intraoperative CDEs. The authors used beach chair, desaturation, near infrared spectroscopy, and shoulder as medical subject headings (MeSH). In addition, bibliographies of retrieved articles were checked for studies that the search terms may have missed. Eighty-one publications were identified and reviewed for possible inclusion.

Next, the same 2 authors reviewed the titles and abstracts for relevance and determined which articles had potential to contribute to the study. Only English-language publications were considered for inclusion. To review the incidence of postoperative neurocognitive deficits, we included only those studies with more than 25 patients, documentation of postoperative complications, and arthroscopic shoulder surgery performed with the patient in the seated, semi-upright, or BCP. Only studies with at least 25 patients were used in order to increase the power and improve the level of evidence. To review reported cases of neurocognitive complications, we included all relevant case reports and case series. To review the incidence of intraoperative CDEs and investigate their relationship with postoperative neurocognitive deficits, we included studies that reported on use of intraoperative cerebral perfusion monitoring. Modalities used in these studies included near infrared spectroscopy, electroencephalography, and invasive blood pressure monitoring calculated at the brain level. Studies were excluded if they did not involve arthroscopic shoulder surgery or were not conducted with human subjects.

Information recorded for each study included general information such as author and publication year, type of study, number of patients enrolled, type of intraoperative monitoring, anesthesia protocol, number of patients with CDEs, and number of patients with neurocognitive complications after surgery.

Results

Our search identified 81 publications for potential inclusion. Our first aim was to identify the overall incidence of reported neurocognitive deficits after arthroscopic shoulder surgery with the patient in the BCP. We identified 10 studies (Table 1) that met the inclusion criteria. Among the 24,701 patients in these 10 studies, there was only 1 reported case of neurocognitive deficit after surgery, in a mixed prospective-retrospective study of 15,014 cases by Rohrbaugh and colleagues.18 The deficit they reported was an ischemic cerebral vascular accident. The 0.0067% incidence in their study demonstrates how rare the complication is. Two large retrospective studies (Ns = 4169 and 5177 patients) found no postoperative neurocognitive complications.^19,20 Only 3 studies performed formal postoperative cognitive testing. Salazar and colleagues²¹ used the Repeatable Battery for the Assessment of Neuropsychological Status before and after surgery, and Gillespie and colleagues⁸ and Lee and colleagues¹⁰ used the Mini–Mental State Examination before and after surgery. Total incidence of reported neurocognitive deficits from our review was 0.004% (1/24,701).

Our second aim was to review all reported cases of neurocognitive complications after arthroscopic shoulder surgery with the patient in the BCP. We identified 4 publications that fit our inclusion criteria (Table 2). Pohl and Cullen6 described 4 cases of ischemic brain injury after arthroscopic shoulder surgery with the patient in the BCP. Age range was 47 to 57 years. Specific intraoperative cerebral monitoring was not used. However, these patients had several episodes of intraoperative hypotension (systolic blood pressures, 80-90 mm Hg), measured with a traditional blood pressure cuff on the arm. In general, these patients had minimal cerebrovascular risk factors and no known preexisting cerebrovascular disease. Drummond and colleagues²² described an ischemic stroke in a 50-year-old man after arthroscopic subacromial decompression and open rotator cuff repair that resulted in unresolved right hemiplegia. Subsequent diagnostic investigation revealed an asymmetry of the circle of Willis resulting in limited flow to the left anterior and middle cerebral artery distributions. Bhatti and Enneking³ reported the case of a 64-year-old man who lost vision in the right eye immediately after arthroscopic rotator cuff repair. His vision improved spontaneously the next morning and continued to improve over the next 6 months—he regained 20/20 vision with some residual optic neuropathy.

Our third aim was to determine the incidence of intraoperative CDEs during arthroscopic shoulder surgery with the patient in the BCP. Incidence of CDEs varied widely among the 7 studies reviewed (Table 3). Minimum incidence of intraoperative CDE was 0% in a cohort of 30 patients,¹ and maximum incidence was 80% in a study of 61 patients,¹² all of whom underwent elective arthroscopic shoulder surgery in the BCP. Although there was wide variability in CDE incidence, the studies were consistent with respect to their definition of a CDE. Most authors used a decrease in regional cerebral tissue oxygen saturation of 20% or more from baseline, or an absolute value up to 55%, to define a CDE. None of the 7 studies reviewed reported a clinically significant adverse neurocognitive event.

Discussion

Of concern, there have been several surveys, case reports, and small case series of previously healthy patients who had no known risk factors, underwent arthroscopic shoulder surgery in the BCP, and developed unanticipated postoperative neurologic complications.^4-6,14 Beach-chair positioning during surgical procedures has been implicated as a contributing factor leading to cerebral hypoperfusion with potential for cerebral ischemia.^1,12,23 These changes in cerebral perfusion pressure are thought to be the major determinant of poor neurologic outcomes. Such reports have exposed the potential need for heightened vigilance, alternative anesthesia techniques, and improved monitoring, though the exact etiology of the central nervous system injuries in this patient population is incompletely understood and is likely multifactorial. Therefore, in this study we wanted to determine the incidence of postoperative neurocognitive deficits and review all reported cases of neurocognitive complications in patients who have undergone arthroscopic shoulder surgery in the BCP. In addition, we wanted to define the incidence of intraoperative CDEs and investigate their relationship with postoperative neurocognitive complications.

According to our review, the incidence of postoperative neurocognitive complications after surgery in the BCP is 0.004% (1/24,701). However, this finding is based only on what has been reported; the true incidence is not known. It is also important to note that the incidence of neurocognitive deficits after many other types of surgery is not known and that surgery itself may be a risk factor for postoperative neurocognitive deficits.²⁴ In their retrospective review of 15,014 patients who underwent arthroscopic shoulder surgery in the BCP at a single institution over an 11-year period, Rohrbaugh and colleagues18 found an overall postoperative complication rate of 0.37% and a 0.0067% incidence of neurocognitive deficits. One patient in the series was given a diagnosis of ischemic stroke on the basis of neurologic deficits that occurred 24 hours after surgery. Yadeau and colleagues²⁰ found no postoperative neurocognitive complications in a mixed prospective-retrospective study of 4169 patients—3000 identified retrospectively, 1169 prospectively—who underwent arthroscopic shoulder surgery in the BCP at an ambulatory surgery center. Pin-on and colleagues¹⁹ reported on a series of 5177 orthopedic and neurosurgical patients who underwent surgery in the BCP. In those who had arthroscopic shoulder surgery, intraoperative systolic blood pressures obtained from an arterial line referenced to heart level decreased a mean (SD) of 14.4% (12.7%), whereas in those whose pressures were obtained from a noninvasive blood pressure cuff referenced to heart level decreased 19.3% (12.6%). However, the authors reported no incidence of postoperative stroke or neurologic deficits.

Although uncommon, perioperative cerebral ischemic accidents are potentially devastating for patients, their families, and the health care professionals involved. These events have tremendous economic, social, professional, and medicolegal implications, with perioperative stroke being particularly morbid. Perioperative stroke has a mortality rate of 60%, versus 15% to 46% for stroke in general.^25,26 In 2005, Pohl and Cullen⁶ published a landmark article on a series of 4 relatively healthy middle-aged patients who were at low risk for stroke but had catastrophic neurocognitive complications (including 1 death) after arthroscopic shoulder surgery in the BCP. Bhatti and Enneking³ described a case of acute postoperative vision loss and ophthalmoplegia attributed to intraoperative hypotension leading to ischemia in a patient who underwent an elective shoulder arthroscopic procedure in the BCP. These reports prompted multiple investigations into the physiologic hemodynamic changes associated with surgery in the BCP and the treatment strategies used to improve patient safety.

In the normal physiologic state, the sympathetic nervous system is activated when a person assumes the seated position. The result is increased systemic vascular resistance and heart rate alterations to maintain cardiac output and mean arterial pressure. In anesthetized patients, this response is blunted by the vasodilatory effects of intravenous and volatile anesthetics. Multiple studies have demonstrated substantial hemodynamic changes in both awake and anesthetized patients during the maneuver from the supine position to the seated position^1,27,28; these changes include diminished cardiac index, stroke volume, and arterial pressure.¹⁷ The data underscore the need for attentiveness and accurate monitoring of cerebral perfusion when the transition is made from the supine position to the BCP, particularly in the early phase of surgery and in high-risk patients.

Knowledge of these hemodynamic changes has led several authors to recommend additional intraoperative monitoring of cerebral perfusion. Monitoring techniques have included use of invasive blood pressure monitoring adjusted to brain level, cerebral oximetry using near infrared spectroscopy, and electroencephalography. However, the clinical relevance of intraoperative CDEs in isolation is not well understood.^1,6,7,23 In addition, cost and availability of additional advanced monitoring likely factor into why it is not more commonly used. For this patient population, the severity, frequency, and duration of desaturation that causes cerebral ischemia and the relationship with postoperative neurocognitive deficits remain undefined.

The incidence of CDEs in patients being monitored with near infrared spectroscopy while undergoing elective arthroscopic shoulder surgery in the BCP varies widely, from 0% to 80% (mean, 41%).^{1,4,7,10,12,21} Magnitude and duration of cerebral ischemia required to produce neurocognitive dysfunction in this patient population remain unidentified as well. In conscious patients, a 20% reduction in frontal lobe oxygenation is associated with clinical manifestations of cerebral hypoperfusion, such as syncope.^15,29 As none of the patients in the studies we reviewed experienced any sort of deficit, we cannot definitively state there is a correlation between CDE occurrence and neurocognitive deficit.

One limitation of our investigation is that it was a systemic review, and thus there was substantial heterogeneity in the methods and designs of the studies included in the analysis. Among the different series, there was variability in multiple aspects of the study design, including type of anesthetic, patient inclusion criteria, type of surgery, type of intraoperative cerebral perfusion monitoring, and type of neurocognitive testing. As a result, comparing the groups was difficult, and the generalizability of our findings may be limited. In addition, it is difficult to accurately establish incidence and comprehensively review these events because of the paucity of literature.

Conclusion

Neurocognitive complications after shoulder arthroscopy with the patient in the BCP are extremely rare but potentially devastating events that can affect healthy patients with no preexisting cerebrovascular risk factors. Our review indicated the incidence of permanent neurologic deficit after arthroscopy in the BCP may be as low as 0.004%. The exact etiology of such complications is not clear. Basic science research and large prospective studies are needed to identify the clinically relevant thresholds of magnitude, duration, and frequency of intraoperative CDEs in order to establish their relationship with postoperative neurocognitive complications. Such large studies may also elucidate modifiable patient-specific risk factors and establish the most sensitive, safe, and cost-effective intraoperative monitoring tools. Current literature suggests that accurate intraoperative monitoring of cerebral perfusion, alternatives to general anesthesia, and prudent use of intraoperative blood pressure control may improve patient safety.

Upper extremity injuries are very common in pitchers in amateur and professional baseball. The vast majority involving labral or rotator cuff pathology.^1-3 While uncommon, injuries to the latissimus dorsi (LD) (Figure) and teres major (TM) have been reported in Major League Baseball (MLB) pitchers.⁴ Jobe and colleagues⁵ demonstrated the role of the LD during the various phases of pitching. The LD is most active during the acceleration phase and remains active during the deceleration phase and follow-through.⁶ Anatomically, the TM lies posterior to the LD separated by bursal tissue. The tendon fibers converge and unite along their lower borders, leading to a synergistic mechanism of action.

Due to the rarity of LD and TM injuries, literature on the pathology and appropriate treatments for these injuries is limited. The goal of this review is to present the current literature on professional baseball players who have undergone either nonsurgical treatment or surgery for LD and TM strains and/or avulsion injuries. This review will ultimately assist clinicians when deciding on the optimal treatment method for professional baseball players.

Methods

We performed an extensive Medline database search with the following search algorithm: ([latissimus OR latissimus dorsi OR teres major] AND baseball). The search returned 20 citations. Inclusion criteria consisted of clinical studies that focused on professional baseball pitchers with TM and/or LD injuries that underwent either conservative nonsurgical treatment or surgical repair. There was no exclusion based on the type of injury present, such as avulsion vs strain. Any study with amateur athletes or athletes from other sports such as handball or rugby were excluded. Due to the limited amount of data available, the majority of included studies were case reports and case series.

Based on these parameters, 5 articles met criteria for inclusion. Of the 5 included studies, 3 were case reports and 2 were case series. From the eligible articles, the following information was obtained: publication year, sample size, mean age, mean follow-up duration, type of treatment (conservative vs surgical), ability to return to original level of play, time required to return to original form, and complications (Tables 1, 2).

Results

Nonoperative Management

Four of the 5 included studies implemented only conservative therapy for their patients.^4,7-9 The average duration these patients were followed for during treatment and rehabilitation was 26.3 months. Malcolm and colleagues⁷ followed patients for 8 months, the shortest length among the 4 conservative studies in this review. Leland and colleagues8 followed patients for 17 months, and Nagda and colleagues⁹ had the longest length of observation of 36 months (range 12 to 82 months).Schickendantz and colleagues⁴ followed patients for >12 months, but the exact duration was not specified. In order to calculate the average duration of observation, each patient was assigned a duration of 12 months.

Of the 30 patients included in this review, 29 were treated conservatively. All of the included studies consisted of male patients. The mean age was 26.8 years (range 22 to 28.1 years). Of the 29 injuries treated conservatively, there were 2 LD tendon avulsions, 4 TM tendon avulsions, 1 LD and TM tendon avulsion, 7 LD intramuscular strains, 9 TM intramuscular strains, and 6 LD and TM intramuscular strains.

Treatment Protocol

The various treatment and rehabilitation programs used for the conservative patient population all followed a similar pathway. After initial injury, a rest period focused on stretching was implemented. Patients were started on steroid or anti-inflammatory medications, cryotherapy, or other therapeutic modalities. Once pain-free and full range of motion was achieved, patients began the strength and throwing components of the rehabilitation program. Reoccurrence of symptoms would halt the throwing component of the rehabilitation program until symptoms improved. Patients were progressed through a return-to-throw program and once they could throw off the mound and achieve their preinjury velocity, strength, and range of motion, they were cleared to return to competitive pitching.

In the senior author’s (MSS) practice, all throwers are managed with the same nonoperative protocol.⁴ Initial treatment consists of short periods of rest and symptom control via the application of cryotherapy, among other modalities. Restoration of preinjury range of motion is achieved with active-assisted stretching exercises. As range of motion begins approaching pre-injury levels, strength training is initiated with isometric strengthening of the LD and TM progressing to resistance exercises. Exercising the abdominal core, strengthening the lower body, and cardiovascular conditioning are focal points of the rehabilitation period. Once patients regain preinjury shoulder strength and range of motion without pain, they begin a throwing program that consists of 4 weeks of long toss followed by 2 weeks of throwing from the pitching mound. After completion of the throwing program, the patient is allowed to return to competitive pitching. For patients who did not suffer season-ending injury, the average time required to return to play was 99.8 days (range 72.3 to 182.6 days).

Complications and Reinjury

The patients in Leland and colleagues⁸ and Malcolm and colleagues⁷ did not suffer any complications or reinjuries. In Schickendantz and colleagues⁴, all but 3 of the 10 patients were able to return to full speed pitching by 3 months. The other 3 required 4, 6, and 10 months. The patient that required 10 months tore both his LD and TM and the patient that required 6 months tore his TM and was never able to regain his pre-injury throwing velocity. None of the TM tears had a recurrence, while 1 LD tear had a recurrence of injury 6 months after returning to competitive pitching. This patient was successfully treated with 6 weeks of conservative rest and rehabilitation.

In Nagda and colleagues⁹, 2 athletes suffered injury recurrence. One athlete with a LD strain suffered 2 subsequent LD strains, 4 months and 1 year after initial injury. The other athlete with a LD avulsion suffered a subsequent TM avulsion 13 months after initial injury. One pitcher who had an LD and TM strain suffered a superior labrum anterior and posterior (SLAP) tear and was never able to return to his prior level of play.

Surgical Treatment

Only 1 of the 5 included studies utilized surgical repair for their patient.¹⁰ The single patient suffered an avulsion injury of the distal LD tendon and its insertion on the humerus. The LD tendon was retracted approximately 5 cm from the distal humeral insertion. The TM was not involved. Eight days post-injury, the patient underwent surgical repair.¹¹ Postoperatively, the patient started passive range of motion after 2 weeks and active range of motion after 6 weeks. He started throwing at 12 weeks and returned to play at 30 weeks after he had returned to his preinjury form in regards to muscle strength, pitch control, and velocity. The patient was able to resume pitching at a high level in MLB.

Discussion

Overhand throwing athletes, especially professional baseball players, have to constantly deal with a variety of shoulder injuries.^12,13 Currently, there is minimal literature on isolated TM and LD injuries. As a result, there is still debate about the optimal treatment method for these injuries, especially in athletes who compete at the highest level. In order to treat isolated injuries of these muscles, it is important to understand their anatomic relationship, as these 2 muscles are intimately associated. The LD originates from the thoracolumbar spine and inserts on the proximal humerus between the pectoralis<hl name="2"/> major and TM tendons. The TM originates from the scapula and, similar to the LD, inserts on the proximal humerus. In an anatomic study, the TM tendon inserted into the LD tendon before its humeral insertion in the majority of cadavers.^14,15

The LD is responsible for extension, adduction, and internal rotation of the humerus. The TM, while not as extensively studied, is believed to also contribute to extension, adduction, and internal rotation of the humerus.¹⁶ As Jobe and colleagues⁵ demonstrated, the LD is vital during the acceleration phase of pitching. While they were unable to make any conclusions about the role of the TM during the pitching cycle, it is reasonable to hypothesize that these 2 muscles work together. While it is thought that these 2 muscles work as a unit, it is significant to note that a professional pitcher can sustain an isolated injury to the TM without injury to the LD, and vice versa. This questions whether these 2 muscles work more independently than once thought. One hypothesis is that the physical size of the LD provides protection from injuries that the smaller TM cannot overcome. This is a potential area of further research.

The most common findings in patients with TM injuries include swelling, bruising, tenderness of the proximal arm, and limitations of shoulder range of motion in abduction, flexion, and external rotation. There is also weakness when resistance is applied against internal rotation and extension. Similar to the TM, common findings in patients with LD injuries include pain in the posterior shoulder, bruising, and weakness when resistance is applied against internal rotation of the shoulder. Pitchers are often able to pinpoint the occurrence of their acute pain during a specific time in the game. They commonly experience a pulling sensation and sometimes even feel a “pop” in their shoulder followed by an acute onset of pain and stiffness in the posterior aspect of the axilla. These injuries seem to be associated with the pitcher throwing a “breaking ball,” a pitch that requires greater shoulder rotation since it changes trajectory while traveling towards home plate. Despite the clear role of the LD and hypothesized role of the TM in the pitching sequence, there has been limited research on the optimal treatment of isolated injuries of these muscles in MLB pitchers. The majority of studies in this review opted for conservative treatment for both LD and TM injuries. The only study that presented a surgical option was for a LD avulsion injury.

Athletes undergoing either conservative or surgical treatment required a significant period of recovery and rehabilitation before they were able to compete at the professional level. In Leland and colleagues⁸, it took about 10 to 12 weeks of rehabilitation for both pitchers to return to pitching against competition. In Schickendantz and colleagues⁴, barring any complications or injury recurrence, it took patients 12 weeks to return to their preinjury level. In Malcolm and colleagues⁷, magnetic resonance imaging after 8 weeks showed marked recovery, and shortly after the pitcher was able to return to the pitching rotation. In Nagda and colleagues⁹, the time lost to injury ranged from 7 weeks to an entire season. Of the 9 pitchers who were lost for the season, 6 had avulsion injuries. The other 3 consisted of an LD strain, TM strain, and LD plus TM strain.⁹ In this study, it seems that avulsion injuries had a more significant impact on patient recovery. On average, it took 35.6 days after injury for players to begin throwing. In contrast, it took an average of 65.5 days after an avulsion injury for players to begin throwing. Ellman and colleagues¹⁰ included the only surgically repaired injury, and it was for an avulsion of the LD tendon. In the surgical case, it took slightly longer for the pitcher to return to preinjury form. It took him 12 to 16 weeks to begin light throwing and his full return to pitching took about 20 to 30 weeks. Since muscle strains and tendon avulsions are significantly different injuries in regards to the type of soft tissue damage and healing potential, they may require different treatment strategies. An avulsion injury may require more aggressive intervention, whereas a strain may only require conservative rehabilitation. Ultimately, there does not seem to be a significant benefit of one treatment option compared to the other. The majority of conservatively managed pitchers were able to return to previous form in a reasonable time frame. While each rehabilitation protocol was slightly different, multiple studies advocated for rehab programs that centered around the following goals: slowly progressing pitchers to light throwing once their pain resolved, followed by long throwing, then throwing off of the mound, and finally returning to competitive pitching. It is important to discuss with patients that rehabilitation generally takes 12 to 16 weeks before they are able to fully return to pitching against competition and that rest should immediately follow any recurrence of pain or stiffness. Once those symptoms resolve, patients may continue the rehabilitation protocol.

As with any form of treatment, there are risks involved. This holds true for both conservative and nonconservative therapy for LD and TM injuries. One risk of nonoperative treatment of an LD avulsion is the development of strength deficits in the muscle.¹⁷ While this deficit may go unnoticed in a recreational athlete, it may be more pronounced in a professional athlete, especially since the LD of a professional baseball pitcher is more active on electromyography during the acceleration phase of the pitching cycle compared to a recreational athlete.¹⁸ Another risk of conservative treatment of an LD avulsion is jeopardizing the potential for future surgery. As a result, some advocate for early surgical intervention of an acute LD avulsion.^19,20 Others, however, recommend conservative management with subsequent surgical intervention if conservative measures fail. One caveat is that surgical intervention to restore the original anatomy may become difficult after a certain period of time due to the buildup of scar tissue. Surgical intervention also has associated risks, such as nerve injury, infection, vascular damage, persistent pain, and the buildup of large amounts of scar tissue. It is important to discuss these risks with patients when deciding on a treatment option.

LD and TM avulsion and tears typically present after an acute event in throwing athletes. There are a number of case reports published that demonstrate successful outcomes with both nonoperative management²¹ and operative repair of LD injuries in non-throwing athletes such as competitive water skiers,^22,23 steer wrestlers,²⁴ professional wrestlers,²⁵ and recreational rock climbers.²⁶ The 5 studies included in this review were the first ones to present LD and TM injuries in MLB pitchers. They discussed the outcomes of mainly conservative and surgical management of LD and TM avulsion and tears. Unfortunately, there remains a limited number of cases on the treatment of these injuries in highly competitive throwing athletes. Further research is required to elucidate the advantages and disadvantages of operative vs nonoperative treatment. The goal of this review is to provide clinicians with a concise summary of the current literature so that they may offer some evidence to their patients when discussing appropriate treatment plans.

Upper extremity injuries are very common in pitchers in amateur and professional baseball. The vast majority involving labral or rotator cuff pathology.^1-3 While uncommon, injuries to the latissimus dorsi (LD) (Figure) and teres major (TM) have been reported in Major League Baseball (MLB) pitchers.⁴ Jobe and colleagues⁵ demonstrated the role of the LD during the various phases of pitching. The LD is most active during the acceleration phase and remains active during the deceleration phase and follow-through.⁶ Anatomically, the TM lies posterior to the LD separated by bursal tissue. The tendon fibers converge and unite along their lower borders, leading to a synergistic mechanism of action.

Due to the rarity of LD and TM injuries, literature on the pathology and appropriate treatments for these injuries is limited. The goal of this review is to present the current literature on professional baseball players who have undergone either nonsurgical treatment or surgery for LD and TM strains and/or avulsion injuries. This review will ultimately assist clinicians when deciding on the optimal treatment method for professional baseball players.

Methods

We performed an extensive Medline database search with the following search algorithm: ([latissimus OR latissimus dorsi OR teres major] AND baseball). The search returned 20 citations. Inclusion criteria consisted of clinical studies that focused on professional baseball pitchers with TM and/or LD injuries that underwent either conservative nonsurgical treatment or surgical repair. There was no exclusion based on the type of injury present, such as avulsion vs strain. Any study with amateur athletes or athletes from other sports such as handball or rugby were excluded. Due to the limited amount of data available, the majority of included studies were case reports and case series.

Based on these parameters, 5 articles met criteria for inclusion. Of the 5 included studies, 3 were case reports and 2 were case series. From the eligible articles, the following information was obtained: publication year, sample size, mean age, mean follow-up duration, type of treatment (conservative vs surgical), ability to return to original level of play, time required to return to original form, and complications (Tables 1, 2).

Results

Nonoperative Management

Four of the 5 included studies implemented only conservative therapy for their patients.^4,7-9 The average duration these patients were followed for during treatment and rehabilitation was 26.3 months. Malcolm and colleagues⁷ followed patients for 8 months, the shortest length among the 4 conservative studies in this review. Leland and colleagues8 followed patients for 17 months, and Nagda and colleagues⁹ had the longest length of observation of 36 months (range 12 to 82 months).Schickendantz and colleagues⁴ followed patients for >12 months, but the exact duration was not specified. In order to calculate the average duration of observation, each patient was assigned a duration of 12 months.

Of the 30 patients included in this review, 29 were treated conservatively. All of the included studies consisted of male patients. The mean age was 26.8 years (range 22 to 28.1 years). Of the 29 injuries treated conservatively, there were 2 LD tendon avulsions, 4 TM tendon avulsions, 1 LD and TM tendon avulsion, 7 LD intramuscular strains, 9 TM intramuscular strains, and 6 LD and TM intramuscular strains.

Treatment Protocol

The various treatment and rehabilitation programs used for the conservative patient population all followed a similar pathway. After initial injury, a rest period focused on stretching was implemented. Patients were started on steroid or anti-inflammatory medications, cryotherapy, or other therapeutic modalities. Once pain-free and full range of motion was achieved, patients began the strength and throwing components of the rehabilitation program. Reoccurrence of symptoms would halt the throwing component of the rehabilitation program until symptoms improved. Patients were progressed through a return-to-throw program and once they could throw off the mound and achieve their preinjury velocity, strength, and range of motion, they were cleared to return to competitive pitching.

In the senior author’s (MSS) practice, all throwers are managed with the same nonoperative protocol.⁴ Initial treatment consists of short periods of rest and symptom control via the application of cryotherapy, among other modalities. Restoration of preinjury range of motion is achieved with active-assisted stretching exercises. As range of motion begins approaching pre-injury levels, strength training is initiated with isometric strengthening of the LD and TM progressing to resistance exercises. Exercising the abdominal core, strengthening the lower body, and cardiovascular conditioning are focal points of the rehabilitation period. Once patients regain preinjury shoulder strength and range of motion without pain, they begin a throwing program that consists of 4 weeks of long toss followed by 2 weeks of throwing from the pitching mound. After completion of the throwing program, the patient is allowed to return to competitive pitching. For patients who did not suffer season-ending injury, the average time required to return to play was 99.8 days (range 72.3 to 182.6 days).

Complications and Reinjury

The patients in Leland and colleagues⁸ and Malcolm and colleagues⁷ did not suffer any complications or reinjuries. In Schickendantz and colleagues⁴, all but 3 of the 10 patients were able to return to full speed pitching by 3 months. The other 3 required 4, 6, and 10 months. The patient that required 10 months tore both his LD and TM and the patient that required 6 months tore his TM and was never able to regain his pre-injury throwing velocity. None of the TM tears had a recurrence, while 1 LD tear had a recurrence of injury 6 months after returning to competitive pitching. This patient was successfully treated with 6 weeks of conservative rest and rehabilitation.

In Nagda and colleagues⁹, 2 athletes suffered injury recurrence. One athlete with a LD strain suffered 2 subsequent LD strains, 4 months and 1 year after initial injury. The other athlete with a LD avulsion suffered a subsequent TM avulsion 13 months after initial injury. One pitcher who had an LD and TM strain suffered a superior labrum anterior and posterior (SLAP) tear and was never able to return to his prior level of play.

Surgical Treatment

Only 1 of the 5 included studies utilized surgical repair for their patient.¹⁰ The single patient suffered an avulsion injury of the distal LD tendon and its insertion on the humerus. The LD tendon was retracted approximately 5 cm from the distal humeral insertion. The TM was not involved. Eight days post-injury, the patient underwent surgical repair.¹¹ Postoperatively, the patient started passive range of motion after 2 weeks and active range of motion after 6 weeks. He started throwing at 12 weeks and returned to play at 30 weeks after he had returned to his preinjury form in regards to muscle strength, pitch control, and velocity. The patient was able to resume pitching at a high level in MLB.

Discussion

Overhand throwing athletes, especially professional baseball players, have to constantly deal with a variety of shoulder injuries.^12,13 Currently, there is minimal literature on isolated TM and LD injuries. As a result, there is still debate about the optimal treatment method for these injuries, especially in athletes who compete at the highest level. In order to treat isolated injuries of these muscles, it is important to understand their anatomic relationship, as these 2 muscles are intimately associated. The LD originates from the thoracolumbar spine and inserts on the proximal humerus between the pectoralis<hl name="2"/> major and TM tendons. The TM originates from the scapula and, similar to the LD, inserts on the proximal humerus. In an anatomic study, the TM tendon inserted into the LD tendon before its humeral insertion in the majority of cadavers.^14,15

The LD is responsible for extension, adduction, and internal rotation of the humerus. The TM, while not as extensively studied, is believed to also contribute to extension, adduction, and internal rotation of the humerus.¹⁶ As Jobe and colleagues⁵ demonstrated, the LD is vital during the acceleration phase of pitching. While they were unable to make any conclusions about the role of the TM during the pitching cycle, it is reasonable to hypothesize that these 2 muscles work together. While it is thought that these 2 muscles work as a unit, it is significant to note that a professional pitcher can sustain an isolated injury to the TM without injury to the LD, and vice versa. This questions whether these 2 muscles work more independently than once thought. One hypothesis is that the physical size of the LD provides protection from injuries that the smaller TM cannot overcome. This is a potential area of further research.

The most common findings in patients with TM injuries include swelling, bruising, tenderness of the proximal arm, and limitations of shoulder range of motion in abduction, flexion, and external rotation. There is also weakness when resistance is applied against internal rotation and extension. Similar to the TM, common findings in patients with LD injuries include pain in the posterior shoulder, bruising, and weakness when resistance is applied against internal rotation of the shoulder. Pitchers are often able to pinpoint the occurrence of their acute pain during a specific time in the game. They commonly experience a pulling sensation and sometimes even feel a “pop” in their shoulder followed by an acute onset of pain and stiffness in the posterior aspect of the axilla. These injuries seem to be associated with the pitcher throwing a “breaking ball,” a pitch that requires greater shoulder rotation since it changes trajectory while traveling towards home plate. Despite the clear role of the LD and hypothesized role of the TM in the pitching sequence, there has been limited research on the optimal treatment of isolated injuries of these muscles in MLB pitchers. The majority of studies in this review opted for conservative treatment for both LD and TM injuries. The only study that presented a surgical option was for a LD avulsion injury.

Athletes undergoing either conservative or surgical treatment required a significant period of recovery and rehabilitation before they were able to compete at the professional level. In Leland and colleagues⁸, it took about 10 to 12 weeks of rehabilitation for both pitchers to return to pitching against competition. In Schickendantz and colleagues⁴, barring any complications or injury recurrence, it took patients 12 weeks to return to their preinjury level. In Malcolm and colleagues⁷, magnetic resonance imaging after 8 weeks showed marked recovery, and shortly after the pitcher was able to return to the pitching rotation. In Nagda and colleagues⁹, the time lost to injury ranged from 7 weeks to an entire season. Of the 9 pitchers who were lost for the season, 6 had avulsion injuries. The other 3 consisted of an LD strain, TM strain, and LD plus TM strain.⁹ In this study, it seems that avulsion injuries had a more significant impact on patient recovery. On average, it took 35.6 days after injury for players to begin throwing. In contrast, it took an average of 65.5 days after an avulsion injury for players to begin throwing. Ellman and colleagues¹⁰ included the only surgically repaired injury, and it was for an avulsion of the LD tendon. In the surgical case, it took slightly longer for the pitcher to return to preinjury form. It took him 12 to 16 weeks to begin light throwing and his full return to pitching took about 20 to 30 weeks. Since muscle strains and tendon avulsions are significantly different injuries in regards to the type of soft tissue damage and healing potential, they may require different treatment strategies. An avulsion injury may require more aggressive intervention, whereas a strain may only require conservative rehabilitation. Ultimately, there does not seem to be a significant benefit of one treatment option compared to the other. The majority of conservatively managed pitchers were able to return to previous form in a reasonable time frame. While each rehabilitation protocol was slightly different, multiple studies advocated for rehab programs that centered around the following goals: slowly progressing pitchers to light throwing once their pain resolved, followed by long throwing, then throwing off of the mound, and finally returning to competitive pitching. It is important to discuss with patients that rehabilitation generally takes 12 to 16 weeks before they are able to fully return to pitching against competition and that rest should immediately follow any recurrence of pain or stiffness. Once those symptoms resolve, patients may continue the rehabilitation protocol.

As with any form of treatment, there are risks involved. This holds true for both conservative and nonconservative therapy for LD and TM injuries. One risk of nonoperative treatment of an LD avulsion is the development of strength deficits in the muscle.¹⁷ While this deficit may go unnoticed in a recreational athlete, it may be more pronounced in a professional athlete, especially since the LD of a professional baseball pitcher is more active on electromyography during the acceleration phase of the pitching cycle compared to a recreational athlete.¹⁸ Another risk of conservative treatment of an LD avulsion is jeopardizing the potential for future surgery. As a result, some advocate for early surgical intervention of an acute LD avulsion.^19,20 Others, however, recommend conservative management with subsequent surgical intervention if conservative measures fail. One caveat is that surgical intervention to restore the original anatomy may become difficult after a certain period of time due to the buildup of scar tissue. Surgical intervention also has associated risks, such as nerve injury, infection, vascular damage, persistent pain, and the buildup of large amounts of scar tissue. It is important to discuss these risks with patients when deciding on a treatment option.

LD and TM avulsion and tears typically present after an acute event in throwing athletes. There are a number of case reports published that demonstrate successful outcomes with both nonoperative management²¹ and operative repair of LD injuries in non-throwing athletes such as competitive water skiers,^22,23 steer wrestlers,²⁴ professional wrestlers,²⁵ and recreational rock climbers.²⁶ The 5 studies included in this review were the first ones to present LD and TM injuries in MLB pitchers. They discussed the outcomes of mainly conservative and surgical management of LD and TM avulsion and tears. Unfortunately, there remains a limited number of cases on the treatment of these injuries in highly competitive throwing athletes. Further research is required to elucidate the advantages and disadvantages of operative vs nonoperative treatment. The goal of this review is to provide clinicians with a concise summary of the current literature so that they may offer some evidence to their patients when discussing appropriate treatment plans.

Upper extremity injuries are very common in pitchers in amateur and professional baseball. The vast majority involving labral or rotator cuff pathology.^1-3 While uncommon, injuries to the latissimus dorsi (LD) (Figure) and teres major (TM) have been reported in Major League Baseball (MLB) pitchers.⁴ Jobe and colleagues⁵ demonstrated the role of the LD during the various phases of pitching. The LD is most active during the acceleration phase and remains active during the deceleration phase and follow-through.⁶ Anatomically, the TM lies posterior to the LD separated by bursal tissue. The tendon fibers converge and unite along their lower borders, leading to a synergistic mechanism of action.

Due to the rarity of LD and TM injuries, literature on the pathology and appropriate treatments for these injuries is limited. The goal of this review is to present the current literature on professional baseball players who have undergone either nonsurgical treatment or surgery for LD and TM strains and/or avulsion injuries. This review will ultimately assist clinicians when deciding on the optimal treatment method for professional baseball players.

Methods

We performed an extensive Medline database search with the following search algorithm: ([latissimus OR latissimus dorsi OR teres major] AND baseball). The search returned 20 citations. Inclusion criteria consisted of clinical studies that focused on professional baseball pitchers with TM and/or LD injuries that underwent either conservative nonsurgical treatment or surgical repair. There was no exclusion based on the type of injury present, such as avulsion vs strain. Any study with amateur athletes or athletes from other sports such as handball or rugby were excluded. Due to the limited amount of data available, the majority of included studies were case reports and case series.

Based on these parameters, 5 articles met criteria for inclusion. Of the 5 included studies, 3 were case reports and 2 were case series. From the eligible articles, the following information was obtained: publication year, sample size, mean age, mean follow-up duration, type of treatment (conservative vs surgical), ability to return to original level of play, time required to return to original form, and complications (Tables 1, 2).

Results

Nonoperative Management

Four of the 5 included studies implemented only conservative therapy for their patients.^4,7-9 The average duration these patients were followed for during treatment and rehabilitation was 26.3 months. Malcolm and colleagues⁷ followed patients for 8 months, the shortest length among the 4 conservative studies in this review. Leland and colleagues8 followed patients for 17 months, and Nagda and colleagues⁹ had the longest length of observation of 36 months (range 12 to 82 months).Schickendantz and colleagues⁴ followed patients for >12 months, but the exact duration was not specified. In order to calculate the average duration of observation, each patient was assigned a duration of 12 months.

Of the 30 patients included in this review, 29 were treated conservatively. All of the included studies consisted of male patients. The mean age was 26.8 years (range 22 to 28.1 years). Of the 29 injuries treated conservatively, there were 2 LD tendon avulsions, 4 TM tendon avulsions, 1 LD and TM tendon avulsion, 7 LD intramuscular strains, 9 TM intramuscular strains, and 6 LD and TM intramuscular strains.

Treatment Protocol

The various treatment and rehabilitation programs used for the conservative patient population all followed a similar pathway. After initial injury, a rest period focused on stretching was implemented. Patients were started on steroid or anti-inflammatory medications, cryotherapy, or other therapeutic modalities. Once pain-free and full range of motion was achieved, patients began the strength and throwing components of the rehabilitation program. Reoccurrence of symptoms would halt the throwing component of the rehabilitation program until symptoms improved. Patients were progressed through a return-to-throw program and once they could throw off the mound and achieve their preinjury velocity, strength, and range of motion, they were cleared to return to competitive pitching.

In the senior author’s (MSS) practice, all throwers are managed with the same nonoperative protocol.⁴ Initial treatment consists of short periods of rest and symptom control via the application of cryotherapy, among other modalities. Restoration of preinjury range of motion is achieved with active-assisted stretching exercises. As range of motion begins approaching pre-injury levels, strength training is initiated with isometric strengthening of the LD and TM progressing to resistance exercises. Exercising the abdominal core, strengthening the lower body, and cardiovascular conditioning are focal points of the rehabilitation period. Once patients regain preinjury shoulder strength and range of motion without pain, they begin a throwing program that consists of 4 weeks of long toss followed by 2 weeks of throwing from the pitching mound. After completion of the throwing program, the patient is allowed to return to competitive pitching. For patients who did not suffer season-ending injury, the average time required to return to play was 99.8 days (range 72.3 to 182.6 days).

Complications and Reinjury

The patients in Leland and colleagues⁸ and Malcolm and colleagues⁷ did not suffer any complications or reinjuries. In Schickendantz and colleagues⁴, all but 3 of the 10 patients were able to return to full speed pitching by 3 months. The other 3 required 4, 6, and 10 months. The patient that required 10 months tore both his LD and TM and the patient that required 6 months tore his TM and was never able to regain his pre-injury throwing velocity. None of the TM tears had a recurrence, while 1 LD tear had a recurrence of injury 6 months after returning to competitive pitching. This patient was successfully treated with 6 weeks of conservative rest and rehabilitation.

In Nagda and colleagues⁹, 2 athletes suffered injury recurrence. One athlete with a LD strain suffered 2 subsequent LD strains, 4 months and 1 year after initial injury. The other athlete with a LD avulsion suffered a subsequent TM avulsion 13 months after initial injury. One pitcher who had an LD and TM strain suffered a superior labrum anterior and posterior (SLAP) tear and was never able to return to his prior level of play.

Surgical Treatment

Only 1 of the 5 included studies utilized surgical repair for their patient.¹⁰ The single patient suffered an avulsion injury of the distal LD tendon and its insertion on the humerus. The LD tendon was retracted approximately 5 cm from the distal humeral insertion. The TM was not involved. Eight days post-injury, the patient underwent surgical repair.¹¹ Postoperatively, the patient started passive range of motion after 2 weeks and active range of motion after 6 weeks. He started throwing at 12 weeks and returned to play at 30 weeks after he had returned to his preinjury form in regards to muscle strength, pitch control, and velocity. The patient was able to resume pitching at a high level in MLB.

Discussion

Overhand throwing athletes, especially professional baseball players, have to constantly deal with a variety of shoulder injuries.^12,13 Currently, there is minimal literature on isolated TM and LD injuries. As a result, there is still debate about the optimal treatment method for these injuries, especially in athletes who compete at the highest level. In order to treat isolated injuries of these muscles, it is important to understand their anatomic relationship, as these 2 muscles are intimately associated. The LD originates from the thoracolumbar spine and inserts on the proximal humerus between the pectoralis<hl name="2"/> major and TM tendons. The TM originates from the scapula and, similar to the LD, inserts on the proximal humerus. In an anatomic study, the TM tendon inserted into the LD tendon before its humeral insertion in the majority of cadavers.^14,15

The LD is responsible for extension, adduction, and internal rotation of the humerus. The TM, while not as extensively studied, is believed to also contribute to extension, adduction, and internal rotation of the humerus.¹⁶ As Jobe and colleagues⁵ demonstrated, the LD is vital during the acceleration phase of pitching. While they were unable to make any conclusions about the role of the TM during the pitching cycle, it is reasonable to hypothesize that these 2 muscles work together. While it is thought that these 2 muscles work as a unit, it is significant to note that a professional pitcher can sustain an isolated injury to the TM without injury to the LD, and vice versa. This questions whether these 2 muscles work more independently than once thought. One hypothesis is that the physical size of the LD provides protection from injuries that the smaller TM cannot overcome. This is a potential area of further research.

The most common findings in patients with TM injuries include swelling, bruising, tenderness of the proximal arm, and limitations of shoulder range of motion in abduction, flexion, and external rotation. There is also weakness when resistance is applied against internal rotation and extension. Similar to the TM, common findings in patients with LD injuries include pain in the posterior shoulder, bruising, and weakness when resistance is applied against internal rotation of the shoulder. Pitchers are often able to pinpoint the occurrence of their acute pain during a specific time in the game. They commonly experience a pulling sensation and sometimes even feel a “pop” in their shoulder followed by an acute onset of pain and stiffness in the posterior aspect of the axilla. These injuries seem to be associated with the pitcher throwing a “breaking ball,” a pitch that requires greater shoulder rotation since it changes trajectory while traveling towards home plate. Despite the clear role of the LD and hypothesized role of the TM in the pitching sequence, there has been limited research on the optimal treatment of isolated injuries of these muscles in MLB pitchers. The majority of studies in this review opted for conservative treatment for both LD and TM injuries. The only study that presented a surgical option was for a LD avulsion injury.

Athletes undergoing either conservative or surgical treatment required a significant period of recovery and rehabilitation before they were able to compete at the professional level. In Leland and colleagues⁸, it took about 10 to 12 weeks of rehabilitation for both pitchers to return to pitching against competition. In Schickendantz and colleagues⁴, barring any complications or injury recurrence, it took patients 12 weeks to return to their preinjury level. In Malcolm and colleagues⁷, magnetic resonance imaging after 8 weeks showed marked recovery, and shortly after the pitcher was able to return to the pitching rotation. In Nagda and colleagues⁹, the time lost to injury ranged from 7 weeks to an entire season. Of the 9 pitchers who were lost for the season, 6 had avulsion injuries. The other 3 consisted of an LD strain, TM strain, and LD plus TM strain.⁹ In this study, it seems that avulsion injuries had a more significant impact on patient recovery. On average, it took 35.6 days after injury for players to begin throwing. In contrast, it took an average of 65.5 days after an avulsion injury for players to begin throwing. Ellman and colleagues¹⁰ included the only surgically repaired injury, and it was for an avulsion of the LD tendon. In the surgical case, it took slightly longer for the pitcher to return to preinjury form. It took him 12 to 16 weeks to begin light throwing and his full return to pitching took about 20 to 30 weeks. Since muscle strains and tendon avulsions are significantly different injuries in regards to the type of soft tissue damage and healing potential, they may require different treatment strategies. An avulsion injury may require more aggressive intervention, whereas a strain may only require conservative rehabilitation. Ultimately, there does not seem to be a significant benefit of one treatment option compared to the other. The majority of conservatively managed pitchers were able to return to previous form in a reasonable time frame. While each rehabilitation protocol was slightly different, multiple studies advocated for rehab programs that centered around the following goals: slowly progressing pitchers to light throwing once their pain resolved, followed by long throwing, then throwing off of the mound, and finally returning to competitive pitching. It is important to discuss with patients that rehabilitation generally takes 12 to 16 weeks before they are able to fully return to pitching against competition and that rest should immediately follow any recurrence of pain or stiffness. Once those symptoms resolve, patients may continue the rehabilitation protocol.

As with any form of treatment, there are risks involved. This holds true for both conservative and nonconservative therapy for LD and TM injuries. One risk of nonoperative treatment of an LD avulsion is the development of strength deficits in the muscle.¹⁷ While this deficit may go unnoticed in a recreational athlete, it may be more pronounced in a professional athlete, especially since the LD of a professional baseball pitcher is more active on electromyography during the acceleration phase of the pitching cycle compared to a recreational athlete.¹⁸ Another risk of conservative treatment of an LD avulsion is jeopardizing the potential for future surgery. As a result, some advocate for early surgical intervention of an acute LD avulsion.^19,20 Others, however, recommend conservative management with subsequent surgical intervention if conservative measures fail. One caveat is that surgical intervention to restore the original anatomy may become difficult after a certain period of time due to the buildup of scar tissue. Surgical intervention also has associated risks, such as nerve injury, infection, vascular damage, persistent pain, and the buildup of large amounts of scar tissue. It is important to discuss these risks with patients when deciding on a treatment option.

LD and TM avulsion and tears typically present after an acute event in throwing athletes. There are a number of case reports published that demonstrate successful outcomes with both nonoperative management²¹ and operative repair of LD injuries in non-throwing athletes such as competitive water skiers,^22,23 steer wrestlers,²⁴ professional wrestlers,²⁵ and recreational rock climbers.²⁶ The 5 studies included in this review were the first ones to present LD and TM injuries in MLB pitchers. They discussed the outcomes of mainly conservative and surgical management of LD and TM avulsion and tears. Unfortunately, there remains a limited number of cases on the treatment of these injuries in highly competitive throwing athletes. Further research is required to elucidate the advantages and disadvantages of operative vs nonoperative treatment. The goal of this review is to provide clinicians with a concise summary of the current literature so that they may offer some evidence to their patients when discussing appropriate treatment plans.

Throwing and batting each require repetitive motions that can result in injuries unique to baseball. Fortuantely, advances in operative and nonoperative treatments have allowed players to return to competition after sustaining what previously would have been considered a career-ending injury. Once a player has been deemed ready to return to throwing or hitting, a comprehensive, multiphased approach to rehabilitation is necessary to reintroduce the athlete back to baseball activities and avoid re-injury. This article reviews the biomechanics of both throwing and hitting, and outlines the phases of rehabilitation necessary to allow the athlete to return to competition.

Throwing

Biomechanical Overview

The overhead throwing motion is complex and involves full body coordination from the initial force generation through the follow-through phase of throwing. The “kinetic chain”—the concept that movements in the body are connected through segments culminating with the highest energy in the final segment—is paramount to achieving the force and energy needed for throwing.^1-8 The kinetic chain begins in the lower body and trunk and transmits the energy distally to the shoulder, elbow, and hand, ending with kinetic energy transfer to the ball.^3-5,7 The progression of motion through the kinetic chain during throwing includes stride, pelvis rotation, upper torso rotation, elbow extension, shoulder internal rotation, and wrist flexion. Disruptions in this chain due to muscle imbalance or weakness can lead to injury downstream, particularly in the upper extremity.^3,7,9

The importance of the kinetic chain can be highlighted in the 6 phases of throwing motion. These include wind-up, early arm cocking, late arm cocking, arm acceleration, arm deceleration, and follow-through (Figure 1).^1,2,9,10

The wind-up phase starts with initiation of motion and ends with maximal knee lift of the lead leg; its objective is to place the body in an optimal stance to throw.^3-5,7 There are minimal forces, torques, and muscle activity in the upper extremity during this phase, but up to 50% of throw speed is created through stride and trunk rotation.⁶ During the early cocking phase, the thrower keeps his stance foot planted and drives his lead leg towards the target, while bringing both arms into abduction. This is coupled with internal rotation of the stance hip, external rotation of the lead hip, and external rotation of the throwing shoulder. This creates linear velocity by maximizing the length of the elastic components of the body. Elbow, wrist, and finger extensors are also contracting during this phase to control elbow flexion and wrist hyperextension.³

The late cocking phase begins when the lead foot contacts the ground and ends with maximum shoulder external rotation.^3-5 Lead foot contact is followed by quadriceps contraction to decelerate and stabilize the lead leg. This is followed by rotation of the pelvis and upper torso. The result is energy transfer to the throwing arm with a shear force across the anterior shoulder of 400 N.⁴ The shoulder stays in 90° of abduction, 15° of horizontal adduction, and externally rotates to between 150° and 180°. This produces a maximum horizontal adduction moment of 100 N^.m and internal rotation torque of 70 N^.m.⁴ Simultaneously, the elbow generates maximum flexion and a 65 N^.m varus torque.⁷ Forces about the elbow are generated to resist the large angular velocity experienced (up to 3000°/second). This places an extreme amount of valgus stress along the medial elbow, particularly on the ulnar collateral ligament. The shoulder girdle and rotator cuff muscles simultaneously act to stabilize the scapula and glenohumeral joint.

The arm acceleration phase is from maximal shoulder external rotation until ball release.^3-5 In this phase, the thrower flexes his trunk from an extended position, returning to neutral by the time of ball release while the lead leg straightens. The shoulder stays abducted at 90° throughout while the rotator cuff internal rotators and scapular stabilizers contract to explosively internally rotate the shoulder, creating a maximal internal rotation velocity greater than 7000°/second by ball release.^1,4,7 The elbow also begins to extend, reaching maximum velocity during mid-acceleration phase from a combination of triceps contraction and torque generated from rotation at the shoulder and upper trunk.³ Finally, the wrist flexors contract to move the wrist to a neutral position from hyperextension as the ball is released.

During arm deceleration, the shoulder achieves maximum internal rotation until reaching a neutral position and horizontally adducts across the body. This is controlled by contraction of the shoulder girdle musculature; the teres minor has the highest activity.^3,4 The greatest forces produced during the throwing motion act at the shoulder and elbow during deceleration and can contribute to injury.² These include compressive forces of greater than 1000 N, posterior shear forces of 400 N, and inferior shear forces of 300 N.^4,7

The final phase, the follow-through phase, starts at shoulder maximum internal rotation and ends when the arm assumes a balanced position across the trunk. Lower extremity extension and trunk flexion help distribute forces throughout the body, taking stress away from the throwing arm. The posterior shoulder musculature and scapular protractors contribute to continued deceleration and muscle firing returns to resting levels. This complex motion of throwing fueled by the kinetic chain lasts less than 2 seconds and can result in ball release speeds as high as 100 miles per hour.^3,4

Return to Throwing: Principles

Nonoperative and postoperative rehabilitation programs allow restoration of motion, strength, static and dynamic stability, and neuromuscular control. The initiation of an interval throwing program (ITP) is based on the assumption that tissue healing is complete and a complete physical examination has been conducted to the treating physician’s approval.¹¹ An ITP progressively applies forces along the kinetic chain in a controlled manner through graduated throwing distances, while minimizing the risk of re-injury.

Reinold and colleagues¹² described guidelines that were used in the development of the ITP.¹² These factors include: (1) The act of throwing a baseball involves the transfer of energy from the feet up to the hand and therefore careful attention must be paid along the entire kinetic chain; (2) gradual progression of interval throwing decreases the chance for re-injury; (3) proper warm-up; and (4) proper throwing mechanics minimizes the chance of re-injury.

Variability. Unlike traditional rehabilitation programs that advance an athlete based on a specific timetable, the ITP requires that each level or phase to be completed pain-free or without complications prior to starting the next level. Therefore, an ITP can be used for overhead athletes of varying skill levels because progression will be different from one athlete to another. It is also important to have the athlete adhere strictly to the program, as over-eagerness to complete the ITP as quickly as possible can increase the chance of re-injury and thus slow the rehabilitation process.¹²

Warm-up. An adequate warm-up is recommended prior to initiating ITP. An athlete should jog or cycle to develop a light sweat and then progress to stretching and flexibility exercises. As emphasized before, throwing involves nearly all the muscles in the body. Therefore, all muscle groups should be stretched beginning with the legs and working distally along the kinetic chain.

Mechanics. Analysis, correction, and maintenance of proper throwing mechanics is essential throughout the early phases of rehabilitation and ITP. Improper pitching mechanics places increased stress on the throwing arm, potentially leading to re-injury. Therefore, it would be valuable to have a pitching coach available to emphasize proper mechanics throughout the rehabilitation process.

The Interval Throwing Program

For a PDF patient handout that summarizes the phases of this program, see Appendix 1.

Phase 1. We have adopted the ITP as described by Reinold and colleagues.¹² Phase begins with the overhead athlete throwing on flat ground. He or she begins tossing from 45 feet and gradually progresses to 60, 90, 120, 150, and 180 feet.

As discussed earlier, it is critical to use proper mechanics throughout the ITP. The “crow hop” method simulates a throwing act and helps maintain proper pitching mechanics. Crow hop has 3 components: hop, skip, and throw. Using this technique, the pitcher begins warm-up throws at a comfortable distance (generally 30 feet) and then progresses to the distance as indicated on the ITP. The athlete will then need to perform each step 2 times, with 1 day of rest between steps, before advancing to the next step. The ball should be thrown with an arc and have only enough momentum to reach the desired distance.

For example, Step 1 calls for the athlete to perform 2 sets of 25 throws at 45 feet, with adequate rest (5 minutes) between sets. This step will be repeated following 1 day of rest. If the athlete demonstrates the ability to throw at the prescribed distance without pain, he or she can progress to Step 2, which calls for 3 sets of 25 throws at 45 feet. If pain is present at any step, the thrower returns to the previous asymptomatic step and can progress once he is pain-free.

Positional players are instructed to complete Phase 1 prior to starting position-specific drills. Pitchers, on the other hand, are instructed to stop once they reach and complete 120 feet. They will then progress to tossing at progressive distances of 60, 90, and 120 feet, followed by throwing at 60 feet 6 inches with normal pitching mechanics, initiating straight line throws with little to no arc.

Phase II (Throwing off the Mound). Once a pitcher completes Phase 1 without pain or complications, he is ready to begin throwing off the mound. The same principle remains in Phase 2: pitchers must complete each step pain-free before advancing to the next stage. Pitchers should first throw fastballs at 50% effort and progress to 75% and 100% effort. Because athletes often find it difficult to gauge their own effort, it is important to emphasize the importance of strictly adhering to the program. Fleisig and colleagues¹³ studied healthy pitchers’ ability to estimate their throwing effort. When targeting 50% effort, athletes generated ball speeds of 85% with forces and torque approaching 75% of maximum. A radar gun may be valuable in guiding effort control.

As the player advances through Phase 2, he will increase the volume of pitches as well as the effort in a gradual manner. The player may introduce breaking ball pitches once he demonstrates the ability to throw light batting practice. Phase 2 concludes with the pitcher throwing simulated games, progressing by 15 throws per workout.

Hitting

Biomechanics Overview

The mechanics of hitting a baseball can be broken down into 6 phases: the preparatory phase, stance phase, stride phase, drive phase, bat acceleration phase, and follow-through phase.¹⁴ While progressing through a return-to-play protocol, it is important to understand and teach the player proper swing mechanics during each phase in order to minimize the risk of re-injury (Figure 2).

The preparatory phase occurs as the player positions himself into the batter’s box. This phase is highly individualized, depending on each player’s personal preference. Though significant variability in approach exists, there are 3 basic stances a player can take in preparation to bat. In the closed stance, the batter’s front foot is positioned closer to the plate than the back foot. A more popular stance is the open stance, where the player’s back foot is placed closer to the plate than the front foot. The square batting stance is the most common stance. This stance is where both feet are in line with the pitcher and parallel with the edge of the batter’s box. Most authors agree that the square stance is the optimal position because it provides batters the best opportunity to hit pitches anywhere in the strike zone and limits compensatory or extra motion to their swing.¹⁵

Once the player begins the swing, he has entered the loading period, which is divided into the stance, stride, and drive phases. The loading period, also known as coiling or triggering, begins as the athlete eccentrically stretches agonist muscles and rotates the body away from the incoming ball. The elastic energy stored during this stretching is released during the concentric contraction of the same muscles and transferred through the entire kinetic chain as different segments of the body are rotated; it culminates in effort directed at hitting the baseball.¹⁶

In each phase of the loading period, certain critical motions should be monitored and corrected in order to return the player to his previous level of competition. Stride length has been shown to be critical in the timing of a batter’s swing. A short stride length can cause early initiation of the swing, while a longer stride can produce delayed activation of hip rotation. As the player enters the drive phase, he should have increased elbow flexion in the back elbow compared to the front elbow. The bat should be placed at a position approximately 45° in the frontal plane, and the bat should bisect the batter’s helmet. The back elbow should be down, both upper extremities should be positioned close to the hitter’s body, and the proximal interphalangeal joints of the hands should align on the handle of the bat. Athletic trainers and coaches should be aware that subtle compensations due to deficits during these movements could cause injury during the swing by disrupting the body’s natural motion.

The bat acceleration phase occurs from maximal bat loading through striking the ball. In this time, the linear force that has been exerted by the player must be transferred into rotational force through the trunk and upper extremities. When the lead leg contacts the ground, the player has created a closed kinetic chain, where the elastic energy gathered during the loading period is used to produce segmental rotation beginning in the hips and rising through the trunk and out to the arms and hands, finally producing contact with the baseball.¹⁶ To produce effective bat velocity, each segment must rotate in a sequential manner. If the upper extremities reach peak velocity before any lower segment, then the player has lost the ability to efficiently transfer kinetic energy up the kinetic chain.

Finally, the follow-through phase occurs after contact with the baseball and ends with complete deceleration, completing the swing. In order to achieve optimal effort, full hip rotation is needed, which is aided by rotation of the trail foot. Both hips and back laces should face the pitcher upon completion of the swing producing maximum power output.¹⁵

Return to Hitting: Principles

As with the initiation of the ITP, an interval hitting protocol (IHP) is designed to begin only after the player has been assessed on impairment measures, physical performance measures, and self-assessment.¹⁷ The player should have minimum to no pain, have no tenderness to palpation, and show adequate range of motion and strength to meet the demands of performing a full hitting cycle.¹² It is recommended that before beginning a return-to-play protocol, the involved extremity should be at least 80% as strong as the uninvolved extremity.¹⁸ Physical measures challenging an athlete’s ability to perform tasks specific to hitting a baseball must also be considered through standardized examinations of the involved area.¹⁹ Finally, the athlete’s self-perception of functional abilities must be taken into account. This gives a subjective account of what the hitter perceives they are able to perform, providing useful insight into whether they are mentally prepared to participate in the protocol.

Like the ITP, progression through the IHP is also based on the player’s level of pain and soreness rather than following a specific timetable (Table). The program features a 1 day on, 1 day off schedule during which the player completes 1 step per day. The athlete must remain pain-free to progress to the next step and monitor his level of soreness during their workout. If pain or soreness persists, the player should rest for 2 days and be reevaluated upon return.¹⁷

The same principles of proper warm-up and mechanics apply in the IHP. An athlete should jog or cycle for a minimum of 10 minutes and perform stretching exercises focused on both upper and lower extremity muscles, as batting involves whole body movement. As the athlete progresses through the IHP, having a hitting coach to analyze, correct and maintain proper swing mechanics is valuable in enhancing performance as well as decreasing risk of re-injury.

The Interval Hitting Program

For a PDF patient handout that summarizes the phases of this program, see Appendix 2.

Phase 1 (Dry Swings). Only the most basic fundamentals are stressed during this phase. The player should focus on properly moving from one phase of the swing to the next, without the goal of hitting the baseball. Trainers should measure critical points in the swing and correct deficits early.

Phase 2 (Batting Off a Tee). In this phase, the player is reintroduced to batting at low intensity with a fixed position target. The initial steps have the batter swing in a position of greatest comfort and natural movement, while the final steps in this phase test the athlete’s range of motion and confidence in the previous, healed injury.

Phase 3 (Soft Toss). As the player progresses to this phase, a baseball with trajectory is used to simulate differences in placement of pitches used during a game. As the hitter is able to pick up differences in target position, his performance and confidence should both increase.²⁰ The coach should sit about 30 feet away, facing the hitter at an angle of 45°, and toss the ball in an underhand motion.

Phase 4 (Simulated Hitting). In this phase, the player and coach should focus on the timing of sequential body movements in order to elicit proper loading and force production. With the randomized pitch delivery and increased velocity, the hitter will practice against pitches similar to those delivered in competition.

Conclusion

Interval throwing and hitting programs are designed to allow the athlete to return to competition through a gradual, stepwise program. This permits the player to prepare his body for the unique stresses associated with throwing and hitting. The medical personnel should familiarize themselves with the philosophy of the interval throwing and hitting programs and individualize them to each athlete. Emphasis on proper warm-up, mechanics, and effort control is paramount in expediting return to play while preventing re-injury.

Throwing and batting each require repetitive motions that can result in injuries unique to baseball. Fortuantely, advances in operative and nonoperative treatments have allowed players to return to competition after sustaining what previously would have been considered a career-ending injury. Once a player has been deemed ready to return to throwing or hitting, a comprehensive, multiphased approach to rehabilitation is necessary to reintroduce the athlete back to baseball activities and avoid re-injury. This article reviews the biomechanics of both throwing and hitting, and outlines the phases of rehabilitation necessary to allow the athlete to return to competition.

Throwing

Biomechanical Overview

The overhead throwing motion is complex and involves full body coordination from the initial force generation through the follow-through phase of throwing. The “kinetic chain”—the concept that movements in the body are connected through segments culminating with the highest energy in the final segment—is paramount to achieving the force and energy needed for throwing.^1-8 The kinetic chain begins in the lower body and trunk and transmits the energy distally to the shoulder, elbow, and hand, ending with kinetic energy transfer to the ball.^3-5,7 The progression of motion through the kinetic chain during throwing includes stride, pelvis rotation, upper torso rotation, elbow extension, shoulder internal rotation, and wrist flexion. Disruptions in this chain due to muscle imbalance or weakness can lead to injury downstream, particularly in the upper extremity.^3,7,9

The importance of the kinetic chain can be highlighted in the 6 phases of throwing motion. These include wind-up, early arm cocking, late arm cocking, arm acceleration, arm deceleration, and follow-through (Figure 1).^1,2,9,10

The wind-up phase starts with initiation of motion and ends with maximal knee lift of the lead leg; its objective is to place the body in an optimal stance to throw.^3-5,7 There are minimal forces, torques, and muscle activity in the upper extremity during this phase, but up to 50% of throw speed is created through stride and trunk rotation.⁶ During the early cocking phase, the thrower keeps his stance foot planted and drives his lead leg towards the target, while bringing both arms into abduction. This is coupled with internal rotation of the stance hip, external rotation of the lead hip, and external rotation of the throwing shoulder. This creates linear velocity by maximizing the length of the elastic components of the body. Elbow, wrist, and finger extensors are also contracting during this phase to control elbow flexion and wrist hyperextension.³

The late cocking phase begins when the lead foot contacts the ground and ends with maximum shoulder external rotation.^3-5 Lead foot contact is followed by quadriceps contraction to decelerate and stabilize the lead leg. This is followed by rotation of the pelvis and upper torso. The result is energy transfer to the throwing arm with a shear force across the anterior shoulder of 400 N.⁴ The shoulder stays in 90° of abduction, 15° of horizontal adduction, and externally rotates to between 150° and 180°. This produces a maximum horizontal adduction moment of 100 N^.m and internal rotation torque of 70 N^.m.⁴ Simultaneously, the elbow generates maximum flexion and a 65 N^.m varus torque.⁷ Forces about the elbow are generated to resist the large angular velocity experienced (up to 3000°/second). This places an extreme amount of valgus stress along the medial elbow, particularly on the ulnar collateral ligament. The shoulder girdle and rotator cuff muscles simultaneously act to stabilize the scapula and glenohumeral joint.

The arm acceleration phase is from maximal shoulder external rotation until ball release.^3-5 In this phase, the thrower flexes his trunk from an extended position, returning to neutral by the time of ball release while the lead leg straightens. The shoulder stays abducted at 90° throughout while the rotator cuff internal rotators and scapular stabilizers contract to explosively internally rotate the shoulder, creating a maximal internal rotation velocity greater than 7000°/second by ball release.^1,4,7 The elbow also begins to extend, reaching maximum velocity during mid-acceleration phase from a combination of triceps contraction and torque generated from rotation at the shoulder and upper trunk.³ Finally, the wrist flexors contract to move the wrist to a neutral position from hyperextension as the ball is released.

During arm deceleration, the shoulder achieves maximum internal rotation until reaching a neutral position and horizontally adducts across the body. This is controlled by contraction of the shoulder girdle musculature; the teres minor has the highest activity.^3,4 The greatest forces produced during the throwing motion act at the shoulder and elbow during deceleration and can contribute to injury.² These include compressive forces of greater than 1000 N, posterior shear forces of 400 N, and inferior shear forces of 300 N.^4,7

The final phase, the follow-through phase, starts at shoulder maximum internal rotation and ends when the arm assumes a balanced position across the trunk. Lower extremity extension and trunk flexion help distribute forces throughout the body, taking stress away from the throwing arm. The posterior shoulder musculature and scapular protractors contribute to continued deceleration and muscle firing returns to resting levels. This complex motion of throwing fueled by the kinetic chain lasts less than 2 seconds and can result in ball release speeds as high as 100 miles per hour.^3,4

Return to Throwing: Principles

Nonoperative and postoperative rehabilitation programs allow restoration of motion, strength, static and dynamic stability, and neuromuscular control. The initiation of an interval throwing program (ITP) is based on the assumption that tissue healing is complete and a complete physical examination has been conducted to the treating physician’s approval.¹¹ An ITP progressively applies forces along the kinetic chain in a controlled manner through graduated throwing distances, while minimizing the risk of re-injury.

Reinold and colleagues¹² described guidelines that were used in the development of the ITP.¹² These factors include: (1) The act of throwing a baseball involves the transfer of energy from the feet up to the hand and therefore careful attention must be paid along the entire kinetic chain; (2) gradual progression of interval throwing decreases the chance for re-injury; (3) proper warm-up; and (4) proper throwing mechanics minimizes the chance of re-injury.

Variability. Unlike traditional rehabilitation programs that advance an athlete based on a specific timetable, the ITP requires that each level or phase to be completed pain-free or without complications prior to starting the next level. Therefore, an ITP can be used for overhead athletes of varying skill levels because progression will be different from one athlete to another. It is also important to have the athlete adhere strictly to the program, as over-eagerness to complete the ITP as quickly as possible can increase the chance of re-injury and thus slow the rehabilitation process.¹²

Warm-up. An adequate warm-up is recommended prior to initiating ITP. An athlete should jog or cycle to develop a light sweat and then progress to stretching and flexibility exercises. As emphasized before, throwing involves nearly all the muscles in the body. Therefore, all muscle groups should be stretched beginning with the legs and working distally along the kinetic chain.

Mechanics. Analysis, correction, and maintenance of proper throwing mechanics is essential throughout the early phases of rehabilitation and ITP. Improper pitching mechanics places increased stress on the throwing arm, potentially leading to re-injury. Therefore, it would be valuable to have a pitching coach available to emphasize proper mechanics throughout the rehabilitation process.

The Interval Throwing Program

For a PDF patient handout that summarizes the phases of this program, see Appendix 1.

Phase 1. We have adopted the ITP as described by Reinold and colleagues.¹² Phase begins with the overhead athlete throwing on flat ground. He or she begins tossing from 45 feet and gradually progresses to 60, 90, 120, 150, and 180 feet.

As discussed earlier, it is critical to use proper mechanics throughout the ITP. The “crow hop” method simulates a throwing act and helps maintain proper pitching mechanics. Crow hop has 3 components: hop, skip, and throw. Using this technique, the pitcher begins warm-up throws at a comfortable distance (generally 30 feet) and then progresses to the distance as indicated on the ITP. The athlete will then need to perform each step 2 times, with 1 day of rest between steps, before advancing to the next step. The ball should be thrown with an arc and have only enough momentum to reach the desired distance.

For example, Step 1 calls for the athlete to perform 2 sets of 25 throws at 45 feet, with adequate rest (5 minutes) between sets. This step will be repeated following 1 day of rest. If the athlete demonstrates the ability to throw at the prescribed distance without pain, he or she can progress to Step 2, which calls for 3 sets of 25 throws at 45 feet. If pain is present at any step, the thrower returns to the previous asymptomatic step and can progress once he is pain-free.

Positional players are instructed to complete Phase 1 prior to starting position-specific drills. Pitchers, on the other hand, are instructed to stop once they reach and complete 120 feet. They will then progress to tossing at progressive distances of 60, 90, and 120 feet, followed by throwing at 60 feet 6 inches with normal pitching mechanics, initiating straight line throws with little to no arc.

Phase II (Throwing off the Mound). Once a pitcher completes Phase 1 without pain or complications, he is ready to begin throwing off the mound. The same principle remains in Phase 2: pitchers must complete each step pain-free before advancing to the next stage. Pitchers should first throw fastballs at 50% effort and progress to 75% and 100% effort. Because athletes often find it difficult to gauge their own effort, it is important to emphasize the importance of strictly adhering to the program. Fleisig and colleagues¹³ studied healthy pitchers’ ability to estimate their throwing effort. When targeting 50% effort, athletes generated ball speeds of 85% with forces and torque approaching 75% of maximum. A radar gun may be valuable in guiding effort control.

As the player advances through Phase 2, he will increase the volume of pitches as well as the effort in a gradual manner. The player may introduce breaking ball pitches once he demonstrates the ability to throw light batting practice. Phase 2 concludes with the pitcher throwing simulated games, progressing by 15 throws per workout.

Hitting

Biomechanics Overview

The mechanics of hitting a baseball can be broken down into 6 phases: the preparatory phase, stance phase, stride phase, drive phase, bat acceleration phase, and follow-through phase.¹⁴ While progressing through a return-to-play protocol, it is important to understand and teach the player proper swing mechanics during each phase in order to minimize the risk of re-injury (Figure 2).

The preparatory phase occurs as the player positions himself into the batter’s box. This phase is highly individualized, depending on each player’s personal preference. Though significant variability in approach exists, there are 3 basic stances a player can take in preparation to bat. In the closed stance, the batter’s front foot is positioned closer to the plate than the back foot. A more popular stance is the open stance, where the player’s back foot is placed closer to the plate than the front foot. The square batting stance is the most common stance. This stance is where both feet are in line with the pitcher and parallel with the edge of the batter’s box. Most authors agree that the square stance is the optimal position because it provides batters the best opportunity to hit pitches anywhere in the strike zone and limits compensatory or extra motion to their swing.¹⁵

Once the player begins the swing, he has entered the loading period, which is divided into the stance, stride, and drive phases. The loading period, also known as coiling or triggering, begins as the athlete eccentrically stretches agonist muscles and rotates the body away from the incoming ball. The elastic energy stored during this stretching is released during the concentric contraction of the same muscles and transferred through the entire kinetic chain as different segments of the body are rotated; it culminates in effort directed at hitting the baseball.¹⁶

In each phase of the loading period, certain critical motions should be monitored and corrected in order to return the player to his previous level of competition. Stride length has been shown to be critical in the timing of a batter’s swing. A short stride length can cause early initiation of the swing, while a longer stride can produce delayed activation of hip rotation. As the player enters the drive phase, he should have increased elbow flexion in the back elbow compared to the front elbow. The bat should be placed at a position approximately 45° in the frontal plane, and the bat should bisect the batter’s helmet. The back elbow should be down, both upper extremities should be positioned close to the hitter’s body, and the proximal interphalangeal joints of the hands should align on the handle of the bat. Athletic trainers and coaches should be aware that subtle compensations due to deficits during these movements could cause injury during the swing by disrupting the body’s natural motion.

The bat acceleration phase occurs from maximal bat loading through striking the ball. In this time, the linear force that has been exerted by the player must be transferred into rotational force through the trunk and upper extremities. When the lead leg contacts the ground, the player has created a closed kinetic chain, where the elastic energy gathered during the loading period is used to produce segmental rotation beginning in the hips and rising through the trunk and out to the arms and hands, finally producing contact with the baseball.¹⁶ To produce effective bat velocity, each segment must rotate in a sequential manner. If the upper extremities reach peak velocity before any lower segment, then the player has lost the ability to efficiently transfer kinetic energy up the kinetic chain.

Finally, the follow-through phase occurs after contact with the baseball and ends with complete deceleration, completing the swing. In order to achieve optimal effort, full hip rotation is needed, which is aided by rotation of the trail foot. Both hips and back laces should face the pitcher upon completion of the swing producing maximum power output.¹⁵

Return to Hitting: Principles

As with the initiation of the ITP, an interval hitting protocol (IHP) is designed to begin only after the player has been assessed on impairment measures, physical performance measures, and self-assessment.¹⁷ The player should have minimum to no pain, have no tenderness to palpation, and show adequate range of motion and strength to meet the demands of performing a full hitting cycle.¹² It is recommended that before beginning a return-to-play protocol, the involved extremity should be at least 80% as strong as the uninvolved extremity.¹⁸ Physical measures challenging an athlete’s ability to perform tasks specific to hitting a baseball must also be considered through standardized examinations of the involved area.¹⁹ Finally, the athlete’s self-perception of functional abilities must be taken into account. This gives a subjective account of what the hitter perceives they are able to perform, providing useful insight into whether they are mentally prepared to participate in the protocol.

Like the ITP, progression through the IHP is also based on the player’s level of pain and soreness rather than following a specific timetable (Table). The program features a 1 day on, 1 day off schedule during which the player completes 1 step per day. The athlete must remain pain-free to progress to the next step and monitor his level of soreness during their workout. If pain or soreness persists, the player should rest for 2 days and be reevaluated upon return.¹⁷

The same principles of proper warm-up and mechanics apply in the IHP. An athlete should jog or cycle for a minimum of 10 minutes and perform stretching exercises focused on both upper and lower extremity muscles, as batting involves whole body movement. As the athlete progresses through the IHP, having a hitting coach to analyze, correct and maintain proper swing mechanics is valuable in enhancing performance as well as decreasing risk of re-injury.

The Interval Hitting Program

For a PDF patient handout that summarizes the phases of this program, see Appendix 2.

Phase 1 (Dry Swings). Only the most basic fundamentals are stressed during this phase. The player should focus on properly moving from one phase of the swing to the next, without the goal of hitting the baseball. Trainers should measure critical points in the swing and correct deficits early.

Phase 2 (Batting Off a Tee). In this phase, the player is reintroduced to batting at low intensity with a fixed position target. The initial steps have the batter swing in a position of greatest comfort and natural movement, while the final steps in this phase test the athlete’s range of motion and confidence in the previous, healed injury.

Phase 3 (Soft Toss). As the player progresses to this phase, a baseball with trajectory is used to simulate differences in placement of pitches used during a game. As the hitter is able to pick up differences in target position, his performance and confidence should both increase.²⁰ The coach should sit about 30 feet away, facing the hitter at an angle of 45°, and toss the ball in an underhand motion.

Phase 4 (Simulated Hitting). In this phase, the player and coach should focus on the timing of sequential body movements in order to elicit proper loading and force production. With the randomized pitch delivery and increased velocity, the hitter will practice against pitches similar to those delivered in competition.

Conclusion

Interval throwing and hitting programs are designed to allow the athlete to return to competition through a gradual, stepwise program. This permits the player to prepare his body for the unique stresses associated with throwing and hitting. The medical personnel should familiarize themselves with the philosophy of the interval throwing and hitting programs and individualize them to each athlete. Emphasis on proper warm-up, mechanics, and effort control is paramount in expediting return to play while preventing re-injury.

Throwing and batting each require repetitive motions that can result in injuries unique to baseball. Fortuantely, advances in operative and nonoperative treatments have allowed players to return to competition after sustaining what previously would have been considered a career-ending injury. Once a player has been deemed ready to return to throwing or hitting, a comprehensive, multiphased approach to rehabilitation is necessary to reintroduce the athlete back to baseball activities and avoid re-injury. This article reviews the biomechanics of both throwing and hitting, and outlines the phases of rehabilitation necessary to allow the athlete to return to competition.

Throwing

Biomechanical Overview

The overhead throwing motion is complex and involves full body coordination from the initial force generation through the follow-through phase of throwing. The “kinetic chain”—the concept that movements in the body are connected through segments culminating with the highest energy in the final segment—is paramount to achieving the force and energy needed for throwing.^1-8 The kinetic chain begins in the lower body and trunk and transmits the energy distally to the shoulder, elbow, and hand, ending with kinetic energy transfer to the ball.^3-5,7 The progression of motion through the kinetic chain during throwing includes stride, pelvis rotation, upper torso rotation, elbow extension, shoulder internal rotation, and wrist flexion. Disruptions in this chain due to muscle imbalance or weakness can lead to injury downstream, particularly in the upper extremity.^3,7,9

The importance of the kinetic chain can be highlighted in the 6 phases of throwing motion. These include wind-up, early arm cocking, late arm cocking, arm acceleration, arm deceleration, and follow-through (Figure 1).^1,2,9,10

The wind-up phase starts with initiation of motion and ends with maximal knee lift of the lead leg; its objective is to place the body in an optimal stance to throw.^3-5,7 There are minimal forces, torques, and muscle activity in the upper extremity during this phase, but up to 50% of throw speed is created through stride and trunk rotation.⁶ During the early cocking phase, the thrower keeps his stance foot planted and drives his lead leg towards the target, while bringing both arms into abduction. This is coupled with internal rotation of the stance hip, external rotation of the lead hip, and external rotation of the throwing shoulder. This creates linear velocity by maximizing the length of the elastic components of the body. Elbow, wrist, and finger extensors are also contracting during this phase to control elbow flexion and wrist hyperextension.³

The late cocking phase begins when the lead foot contacts the ground and ends with maximum shoulder external rotation.^3-5 Lead foot contact is followed by quadriceps contraction to decelerate and stabilize the lead leg. This is followed by rotation of the pelvis and upper torso. The result is energy transfer to the throwing arm with a shear force across the anterior shoulder of 400 N.⁴ The shoulder stays in 90° of abduction, 15° of horizontal adduction, and externally rotates to between 150° and 180°. This produces a maximum horizontal adduction moment of 100 N^.m and internal rotation torque of 70 N^.m.⁴ Simultaneously, the elbow generates maximum flexion and a 65 N^.m varus torque.⁷ Forces about the elbow are generated to resist the large angular velocity experienced (up to 3000°/second). This places an extreme amount of valgus stress along the medial elbow, particularly on the ulnar collateral ligament. The shoulder girdle and rotator cuff muscles simultaneously act to stabilize the scapula and glenohumeral joint.

The arm acceleration phase is from maximal shoulder external rotation until ball release.^3-5 In this phase, the thrower flexes his trunk from an extended position, returning to neutral by the time of ball release while the lead leg straightens. The shoulder stays abducted at 90° throughout while the rotator cuff internal rotators and scapular stabilizers contract to explosively internally rotate the shoulder, creating a maximal internal rotation velocity greater than 7000°/second by ball release.^1,4,7 The elbow also begins to extend, reaching maximum velocity during mid-acceleration phase from a combination of triceps contraction and torque generated from rotation at the shoulder and upper trunk.³ Finally, the wrist flexors contract to move the wrist to a neutral position from hyperextension as the ball is released.

During arm deceleration, the shoulder achieves maximum internal rotation until reaching a neutral position and horizontally adducts across the body. This is controlled by contraction of the shoulder girdle musculature; the teres minor has the highest activity.^3,4 The greatest forces produced during the throwing motion act at the shoulder and elbow during deceleration and can contribute to injury.² These include compressive forces of greater than 1000 N, posterior shear forces of 400 N, and inferior shear forces of 300 N.^4,7

The final phase, the follow-through phase, starts at shoulder maximum internal rotation and ends when the arm assumes a balanced position across the trunk. Lower extremity extension and trunk flexion help distribute forces throughout the body, taking stress away from the throwing arm. The posterior shoulder musculature and scapular protractors contribute to continued deceleration and muscle firing returns to resting levels. This complex motion of throwing fueled by the kinetic chain lasts less than 2 seconds and can result in ball release speeds as high as 100 miles per hour.^3,4

Return to Throwing: Principles

Nonoperative and postoperative rehabilitation programs allow restoration of motion, strength, static and dynamic stability, and neuromuscular control. The initiation of an interval throwing program (ITP) is based on the assumption that tissue healing is complete and a complete physical examination has been conducted to the treating physician’s approval.¹¹ An ITP progressively applies forces along the kinetic chain in a controlled manner through graduated throwing distances, while minimizing the risk of re-injury.

Reinold and colleagues¹² described guidelines that were used in the development of the ITP.¹² These factors include: (1) The act of throwing a baseball involves the transfer of energy from the feet up to the hand and therefore careful attention must be paid along the entire kinetic chain; (2) gradual progression of interval throwing decreases the chance for re-injury; (3) proper warm-up; and (4) proper throwing mechanics minimizes the chance of re-injury.

Variability. Unlike traditional rehabilitation programs that advance an athlete based on a specific timetable, the ITP requires that each level or phase to be completed pain-free or without complications prior to starting the next level. Therefore, an ITP can be used for overhead athletes of varying skill levels because progression will be different from one athlete to another. It is also important to have the athlete adhere strictly to the program, as over-eagerness to complete the ITP as quickly as possible can increase the chance of re-injury and thus slow the rehabilitation process.¹²

Warm-up. An adequate warm-up is recommended prior to initiating ITP. An athlete should jog or cycle to develop a light sweat and then progress to stretching and flexibility exercises. As emphasized before, throwing involves nearly all the muscles in the body. Therefore, all muscle groups should be stretched beginning with the legs and working distally along the kinetic chain.

Mechanics. Analysis, correction, and maintenance of proper throwing mechanics is essential throughout the early phases of rehabilitation and ITP. Improper pitching mechanics places increased stress on the throwing arm, potentially leading to re-injury. Therefore, it would be valuable to have a pitching coach available to emphasize proper mechanics throughout the rehabilitation process.

The Interval Throwing Program

For a PDF patient handout that summarizes the phases of this program, see Appendix 1.

Phase 1. We have adopted the ITP as described by Reinold and colleagues.¹² Phase begins with the overhead athlete throwing on flat ground. He or she begins tossing from 45 feet and gradually progresses to 60, 90, 120, 150, and 180 feet.

As discussed earlier, it is critical to use proper mechanics throughout the ITP. The “crow hop” method simulates a throwing act and helps maintain proper pitching mechanics. Crow hop has 3 components: hop, skip, and throw. Using this technique, the pitcher begins warm-up throws at a comfortable distance (generally 30 feet) and then progresses to the distance as indicated on the ITP. The athlete will then need to perform each step 2 times, with 1 day of rest between steps, before advancing to the next step. The ball should be thrown with an arc and have only enough momentum to reach the desired distance.

For example, Step 1 calls for the athlete to perform 2 sets of 25 throws at 45 feet, with adequate rest (5 minutes) between sets. This step will be repeated following 1 day of rest. If the athlete demonstrates the ability to throw at the prescribed distance without pain, he or she can progress to Step 2, which calls for 3 sets of 25 throws at 45 feet. If pain is present at any step, the thrower returns to the previous asymptomatic step and can progress once he is pain-free.

Positional players are instructed to complete Phase 1 prior to starting position-specific drills. Pitchers, on the other hand, are instructed to stop once they reach and complete 120 feet. They will then progress to tossing at progressive distances of 60, 90, and 120 feet, followed by throwing at 60 feet 6 inches with normal pitching mechanics, initiating straight line throws with little to no arc.

Phase II (Throwing off the Mound). Once a pitcher completes Phase 1 without pain or complications, he is ready to begin throwing off the mound. The same principle remains in Phase 2: pitchers must complete each step pain-free before advancing to the next stage. Pitchers should first throw fastballs at 50% effort and progress to 75% and 100% effort. Because athletes often find it difficult to gauge their own effort, it is important to emphasize the importance of strictly adhering to the program. Fleisig and colleagues¹³ studied healthy pitchers’ ability to estimate their throwing effort. When targeting 50% effort, athletes generated ball speeds of 85% with forces and torque approaching 75% of maximum. A radar gun may be valuable in guiding effort control.

As the player advances through Phase 2, he will increase the volume of pitches as well as the effort in a gradual manner. The player may introduce breaking ball pitches once he demonstrates the ability to throw light batting practice. Phase 2 concludes with the pitcher throwing simulated games, progressing by 15 throws per workout.

Hitting

Biomechanics Overview

The mechanics of hitting a baseball can be broken down into 6 phases: the preparatory phase, stance phase, stride phase, drive phase, bat acceleration phase, and follow-through phase.¹⁴ While progressing through a return-to-play protocol, it is important to understand and teach the player proper swing mechanics during each phase in order to minimize the risk of re-injury (Figure 2).

The preparatory phase occurs as the player positions himself into the batter’s box. This phase is highly individualized, depending on each player’s personal preference. Though significant variability in approach exists, there are 3 basic stances a player can take in preparation to bat. In the closed stance, the batter’s front foot is positioned closer to the plate than the back foot. A more popular stance is the open stance, where the player’s back foot is placed closer to the plate than the front foot. The square batting stance is the most common stance. This stance is where both feet are in line with the pitcher and parallel with the edge of the batter’s box. Most authors agree that the square stance is the optimal position because it provides batters the best opportunity to hit pitches anywhere in the strike zone and limits compensatory or extra motion to their swing.¹⁵

Once the player begins the swing, he has entered the loading period, which is divided into the stance, stride, and drive phases. The loading period, also known as coiling or triggering, begins as the athlete eccentrically stretches agonist muscles and rotates the body away from the incoming ball. The elastic energy stored during this stretching is released during the concentric contraction of the same muscles and transferred through the entire kinetic chain as different segments of the body are rotated; it culminates in effort directed at hitting the baseball.¹⁶

In each phase of the loading period, certain critical motions should be monitored and corrected in order to return the player to his previous level of competition. Stride length has been shown to be critical in the timing of a batter’s swing. A short stride length can cause early initiation of the swing, while a longer stride can produce delayed activation of hip rotation. As the player enters the drive phase, he should have increased elbow flexion in the back elbow compared to the front elbow. The bat should be placed at a position approximately 45° in the frontal plane, and the bat should bisect the batter’s helmet. The back elbow should be down, both upper extremities should be positioned close to the hitter’s body, and the proximal interphalangeal joints of the hands should align on the handle of the bat. Athletic trainers and coaches should be aware that subtle compensations due to deficits during these movements could cause injury during the swing by disrupting the body’s natural motion.

The bat acceleration phase occurs from maximal bat loading through striking the ball. In this time, the linear force that has been exerted by the player must be transferred into rotational force through the trunk and upper extremities. When the lead leg contacts the ground, the player has created a closed kinetic chain, where the elastic energy gathered during the loading period is used to produce segmental rotation beginning in the hips and rising through the trunk and out to the arms and hands, finally producing contact with the baseball.¹⁶ To produce effective bat velocity, each segment must rotate in a sequential manner. If the upper extremities reach peak velocity before any lower segment, then the player has lost the ability to efficiently transfer kinetic energy up the kinetic chain.

Finally, the follow-through phase occurs after contact with the baseball and ends with complete deceleration, completing the swing. In order to achieve optimal effort, full hip rotation is needed, which is aided by rotation of the trail foot. Both hips and back laces should face the pitcher upon completion of the swing producing maximum power output.¹⁵

Return to Hitting: Principles

As with the initiation of the ITP, an interval hitting protocol (IHP) is designed to begin only after the player has been assessed on impairment measures, physical performance measures, and self-assessment.¹⁷ The player should have minimum to no pain, have no tenderness to palpation, and show adequate range of motion and strength to meet the demands of performing a full hitting cycle.¹² It is recommended that before beginning a return-to-play protocol, the involved extremity should be at least 80% as strong as the uninvolved extremity.¹⁸ Physical measures challenging an athlete’s ability to perform tasks specific to hitting a baseball must also be considered through standardized examinations of the involved area.¹⁹ Finally, the athlete’s self-perception of functional abilities must be taken into account. This gives a subjective account of what the hitter perceives they are able to perform, providing useful insight into whether they are mentally prepared to participate in the protocol.

Like the ITP, progression through the IHP is also based on the player’s level of pain and soreness rather than following a specific timetable (Table). The program features a 1 day on, 1 day off schedule during which the player completes 1 step per day. The athlete must remain pain-free to progress to the next step and monitor his level of soreness during their workout. If pain or soreness persists, the player should rest for 2 days and be reevaluated upon return.¹⁷

The same principles of proper warm-up and mechanics apply in the IHP. An athlete should jog or cycle for a minimum of 10 minutes and perform stretching exercises focused on both upper and lower extremity muscles, as batting involves whole body movement. As the athlete progresses through the IHP, having a hitting coach to analyze, correct and maintain proper swing mechanics is valuable in enhancing performance as well as decreasing risk of re-injury.

The Interval Hitting Program

For a PDF patient handout that summarizes the phases of this program, see Appendix 2.

Phase 1 (Dry Swings). Only the most basic fundamentals are stressed during this phase. The player should focus on properly moving from one phase of the swing to the next, without the goal of hitting the baseball. Trainers should measure critical points in the swing and correct deficits early.

Phase 2 (Batting Off a Tee). In this phase, the player is reintroduced to batting at low intensity with a fixed position target. The initial steps have the batter swing in a position of greatest comfort and natural movement, while the final steps in this phase test the athlete’s range of motion and confidence in the previous, healed injury.

Phase 3 (Soft Toss). As the player progresses to this phase, a baseball with trajectory is used to simulate differences in placement of pitches used during a game. As the hitter is able to pick up differences in target position, his performance and confidence should both increase.²⁰ The coach should sit about 30 feet away, facing the hitter at an angle of 45°, and toss the ball in an underhand motion.

Phase 4 (Simulated Hitting). In this phase, the player and coach should focus on the timing of sequential body movements in order to elicit proper loading and force production. With the randomized pitch delivery and increased velocity, the hitter will practice against pitches similar to those delivered in competition.

Conclusion

Interval throwing and hitting programs are designed to allow the athlete to return to competition through a gradual, stepwise program. This permits the player to prepare his body for the unique stresses associated with throwing and hitting. The medical personnel should familiarize themselves with the philosophy of the interval throwing and hitting programs and individualize them to each athlete. Emphasis on proper warm-up, mechanics, and effort control is paramount in expediting return to play while preventing re-injury.

Major league baseball (MLB) is one of the most popular sports in the United States, with an average annual viewership of 11 million for the All-Star game and almost 14 million for the World Series.¹ MLB has an average annual revenue of almost $10 billion, while the net worth of all 30 MLB teams combined is estimated at $36 billion; an increase of 48% from 1 year ago.² As the sport continues to grow in popularity and receives more social media coverage, several issues, specifically injuries to its players, have come to the forefront of the news. Injuries to MLB players, specifically pitchers, have become a significant concern in recent years. The active and extended rosters in MLB include 750 and 1200 athletes, respectively, with approximately 360 active spots taken up by pitchers.³ Hence, MLB employs a large number of elite athletes within its organization. It is important to understand not only what injuries are occurring in these athletes, but also how these injuries may be prevented.

Epidemiology

Injuries to MLB players, specifically pitchers, have increased over the past several years.⁴ Between 2005 and 2008, there was an overall increase of 37% in total number of injuries, with more injuries occurring in pitchers than any other position.⁵ While position players are more likely to sustain an injury to the lower extremity, pitchers are more likely to sustain an injury to the upper extremity.⁵ The month with the most injuries to MLB players was April, while the fewest number of injuries occurred in September.⁵ One injury that has been in the spotlight due to its dramatically increasing incidence is tear of the ulnar collateral ligament (UCL). Several studies have shown that the number of pitchers undergoing ulnar collateral ligament reconstruction (UCLR), commonly known as Tommy John surgery, has significantly increased over the past 20 years (Figure 1).^4,6 Between 25% to 33% of all MLB pitchers have undergone UCLR.

While the number of primary UCLR in MLB pitchers has become a significant concern, an even more pressing concern is the number of pitchers undergoing revision UCLR, as this number has increased over the past several years.⁷ Currently, there is some debate as to how to best address the UCL during primary UCLR (graft type, exposure, treatment of the ulnar nerve, and graft fixation methods) because no study has shown one fixation method or graft type to be superior to others. Similarly, no study has definitively proven how to best manage the ulnar nerve (transpose in all patients, only transpose if preoperative symptoms of numbness/tingling, subluxation, etc. exist). Unfortunately, the results following revision UCLR are inferior to those following primary UCLR.^4,7,8 Hence, given this information, it is imperative to both determine and implement strategies aimed at minimizing the need for revision.

Risk Factors for Injury

Although MLB has received more media attention than lower levels of baseball competition, there is relatively sparse evidence surrounding injury risk factors among MLB players. The majority of studies performed have evaluated risk factors for injury in younger baseball athletes (adolescent, high school, and college). The number of athletes at these lower levels sustaining injuries has increased over the past several years as well.⁹ Several large prospective studies have evaluated risk factors for shoulder and elbow injuries in adolescent baseball players. The risk factors include pitching year-round, pitching more than 100 innings per year, high pitch counts, pitching for multiple teams, geography, pitching on consecutive days, pitching while fatigued, breaking pitches, higher elbow valgus torque, pitching with higher velocity, pitching with supraspinatus weakness, and pitching with a glenohumeral internal rotation deficit (GIRD).^10-17 The large majority of these risk factors are essentially part of a pitcher’s cumulative work, which consists of number of games pitched, total pitches thrown, total innings pitched, innings pitched per game, and pitches thrown per game. One prior study has evaluated cumulative work as a predictor for injury in MLB pitchers.¹⁸ While there were several issues with the study methodology, the authors found no correlation between a MLB pitcher’s cumulative work and risk for injury.

Given our current understanding of repetitive microtrauma as the pathophysiology behind these injuries, it remains unclear why cumulative work would be predictive of injury in youth pitchers but not in MLB pitchers.¹⁶ Several potential reasons exist as to why cumulative work may relate to risk of injury in youth pitchers and not MLB pitchers. Achieving MLB status may infer the element of natural selection based on technique and talent that supersedes the effect of “cumulative trauma” in many players. In MLB pitchers, cumulative work is closely monitored. In addition, these players are only playing for a single team and are not pitching competitively year-round, while many youth players play for multiple teams and may pitch year-round. To combat youth injuries, MLB Pitch Smart has developed recommendations on pitch counts and days of rest for pitchers of all age groups (Table).¹⁹ While data do not yet exist to clearly demonstrate the effectiveness of these guidelines, given the risk factors previously mentioned, it seems that these recommendations will show some reduction in youth injuries in years to come.

Some studies have evaluated anatomic variation among pitchers as a risk factor for injury. Polster and colleagues²⁰ performed computed tomography (CT) scans with 3-dimensional reconstructions on the humeri of both the throwing and non-throwing arms of 25 MLB pitchers to determine if humeral torsion was related to the incidence and severity of upper extremity injuries in these athletes. The authors defined a severe injury as those which kept the player out for >30 days. Overall, 11 pitchers were injured during the 2-year study period. There was a strong inverse relationship between torsion and injury severity such that lower degrees of dominant humeral torsion correlated with higher injury severity (P = .005). However, neither throwing arm humeral torsion nor the difference in torsion between throwing and non-throwing humeri were predictive of overall injury incidence. While this is a nonmodifiable risk factor, it is important to understand how the pitcher’s anatomy plays a role in risk of injury.²⁰ Understanding nonmodifiable risk factors may be helpful in the future to risk stratify, prognosticate, and modulate modifiable risk factors such as cumulative work.

Elbow

Injuries to the elbow have become more common in recent years amongst MLB players, although the literature regarding risk factors for elbow injuries is sparse.^4,6 Wilk and colleagues²¹ performed a prospective study to determine if deficits in glenohumeral passive range of motion (ROM) increased the risk of elbow injury in MLB pitchers. Between 2005-2012, the authors measured passive shoulder ROM of both the throwing and non-throwing shoulder of 296 major and minor league pitchers and followed them for a median of 53.4 months. In total, 38 players suffered 49 elbow injuries and required 8 surgeries, accounting for a total of 2551 days spent on the disabled list (DL). GIRD and external rotation insufficiency were not correlated with elbow injuries. However, pitchers with deficits of >5° in total rotation between the throwing and non-throwing shoulders had a 2.6 times greater risk for injury (P = .007) and pitchers with deficits of ≥5° in flexion of the throwing shoulder compared to the non-throwing shoulder had a 2.8 times greater risk for injury (P = .008).²¹ Prior studies have demonstrated trends towards increased elbow injury in professional baseball pitchers with an increase in both elbow valgus torque as well as shoulder external rotation torque; maximum pitch velocity was also shown to be an independent risk factor for elbow injury in professional baseball pitchers.^10,11 These injuries typically occur during the late cocking/early acceleration phase of the pitching cycle, when the shoulder and elbow experience the most significant force of any point in time during a pitch (Figure 2).¹⁷ At our institution, there are several ongoing studies to determine the relative contributions of pitch velocity, number, and type to elbow injury rates. Prospective studies are also ongoing at other institutions.

Shoulder

Shoulder injuries are one of the most common injuries seen in MLB players, specifically pitchers. Similar to the prior study, Wilk and colleagues²² recently performed a prospective study to determine if passive ROM of the glenohumeral joint in MLB pitchers was predictive of shoulder injury or shoulder surgery. As in the previous study, the authors’ measured passive shoulder ROM of the throwing and non-throwing shoulder of 296 major and minor league pitchers during spring training between 2005-2012 and obtained an average follow-up of 48.4 months. The authors found a total of 75 shoulder injuries and 20 surgeries among 51 pitchers (17%) that resulted in 5570 days on the DL. While total rotation deficit, GIRD, and flexion deficit had no relation to shoulder injury or surgery, pitchers with <5° greater external rotation in the throwing shoulder compared to the non-throwing shoulder were more than 2 times more likely to be placed on the DL for a shoulder injury (P = .014) and were 4 times more likely to require shoulder surgery (P = .009).²² The authors concluded that an insufficient side-to-side difference in external rotation of the throwing shoulder increased a pitcher’s likelihood of shoulder injury as well as surgery.

Other

One area that has not received as much attention as repetitive use injuries of the shoulder and elbow is acute collision injuries. Collision injuries include concussions, hyperextension injuries to the knees, shoulder dislocations, fractures of the foot and ankle, and others.²³ Catchers and base runners during scoring plays are at a high risk for collision injury. Recent evidence has shown that catchers average approximately 2.75 collision injuries per 1000 athletic exposures (AE), accounting for an average of 39.1 days on the DL per collision injury.²³ However, despite these collision injuries, catchers spend more time on the DL from non-collision injuries (specifically shoulder injuries requiring surgical intervention), as studies have shown 19 different non-collision injuries that accounted for >100 days on the DL for catchers compared to no collision injuries that caused a catcher to be on the DL for >100 days.²³ The position of catcher is not an independent risk factor for sustaining an injury in MLB players.⁵

Preventative Measures

Given that recent evidence has identified certain modifiable risk factors, largely regarding shoulder ROM, for injuries to MLB pitchers, it stands to reason that by modifying these risk factors, the number of injuries to MLB pitchers can be decreased.^21,22 However, to the authors’ knowledge, there have been no studies in the current literature that have clearly demonstrated the ability to prevent injuries in MLB players. Based on the prior studies, it seems logical that lowering peak pitch velocity and ensuring proper shoulder ROM would help prevent injuries in MLB players, but this remains speculative. Stretching techniques that have been shown to increase posterior shoulder soft tissue flexibility, including sleeper stretches and modified cross-body stretches, as well as closely monitoring ROM may be helpful in modifying these risk factors.^24-26

Although the number of collision injuries is significantly lower than non-collision repetitive use injuries, MLB has implemented rule changes in recent years to prevent injuries to catchers and base runners alike.^23,27 The rule change, which went into effect in 2014, prohibits catchers from blocking home plate unless they are actively fielding the ball or are in possession of the ball. Similarly, base runners are not allowed to deviate from their path to collide with the catcher while attempting to score.²⁷ However, no study has analyzed whether this rule change has decreased the number of collision injuries sustained by MLB catchers, so it is unclear if this rule change has accomplished its goal.

Outcomes Following Injuries

One of the driving forces behind injury prevention in MLB players is to allow players to reach and maintain their full potential while minimizing time missed because of injury. Furthermore, as with any sport, the clinical outcomes and return to sport (RTS) rates for MLB players following injuries, especially injuries requiring surgical intervention, can be improved.^4,28,29 Several studies have evaluated MLB pitchers following UCLR and have shown that over 80% of pitchers are able to RTS following surgery.^4,30 When critically evaluated in multiple statistical parameters upon RTS, these players perform better in some areas and worse in others.^4,30 However, the results following revision UCLR are not as encouraging as those following primary UCLR in MLB pitchers.⁷ Following revision UCLR, only 65% of pitchers were able to RTS, and those who were able to RTS pitched, on average, almost 1 year less than matched controls.⁷ Unfortunately, results following surgeries about the shoulder in MLB players have been worse than those about the elbow. Cohen and colleagues28 reported on 22 MLB players who underwent labral repair of the shoulder and found that only 32% were able to return to the same or higher level following surgery, while over 45% retired from baseball following surgery. Hence, it is imperative these injuries are prevented, as the RTS rate following treatment is less than ideal.

Future Directions

Although a concerted effort has been made over the past several years to mitigate the number of injuries sustained by MLB players, there is still significant room for improvement. New products are in development/early stages of use that attempt to determine when a pitcher begins to show signs of fatigue to allow the coach to remove him from the game. The mTHROW sleeve (Motus Global), currently used by several MLB teams, is an elastic sleeve that is worn by pitchers on their dominant arm. The sleeve approximates torque, velocity, and workload based upon an accelerometer positioned at the medial elbow and sends this information to a smart phone in real time. This technology theoretically allows players to be intensively monitored and thus may prevent injuries to the UCL by preventing pitchers from throwing while fatigued. However, elbow kinematic parameters may not change significantly as pitchers fatigue, which suggests that this strategy may be suboptimal. Trunk mechanics do change as pitchers become fatigued, opening up the possibility for shoulder and elbow injury.^17,31,32 Further products that track hip-to-shoulder separation and trunk fatigue may be necessary to truly lower injury rates. However, no study has proven modifying either parameter leads to a decrease in injury rates.

Conclusion

Injuries to MLB pitchers and position players have become a significant concern over the past several years. Several risk factors for injury have been identified, including loss of shoulder ROM and pitch velocity. Further studies are necessary to determine the effectiveness of modifying these parameters on injury prevention.

Major league baseball (MLB) is one of the most popular sports in the United States, with an average annual viewership of 11 million for the All-Star game and almost 14 million for the World Series.¹ MLB has an average annual revenue of almost $10 billion, while the net worth of all 30 MLB teams combined is estimated at $36 billion; an increase of 48% from 1 year ago.² As the sport continues to grow in popularity and receives more social media coverage, several issues, specifically injuries to its players, have come to the forefront of the news. Injuries to MLB players, specifically pitchers, have become a significant concern in recent years. The active and extended rosters in MLB include 750 and 1200 athletes, respectively, with approximately 360 active spots taken up by pitchers.³ Hence, MLB employs a large number of elite athletes within its organization. It is important to understand not only what injuries are occurring in these athletes, but also how these injuries may be prevented.

Epidemiology

Injuries to MLB players, specifically pitchers, have increased over the past several years.⁴ Between 2005 and 2008, there was an overall increase of 37% in total number of injuries, with more injuries occurring in pitchers than any other position.⁵ While position players are more likely to sustain an injury to the lower extremity, pitchers are more likely to sustain an injury to the upper extremity.⁵ The month with the most injuries to MLB players was April, while the fewest number of injuries occurred in September.⁵ One injury that has been in the spotlight due to its dramatically increasing incidence is tear of the ulnar collateral ligament (UCL). Several studies have shown that the number of pitchers undergoing ulnar collateral ligament reconstruction (UCLR), commonly known as Tommy John surgery, has significantly increased over the past 20 years (Figure 1).^4,6 Between 25% to 33% of all MLB pitchers have undergone UCLR.

While the number of primary UCLR in MLB pitchers has become a significant concern, an even more pressing concern is the number of pitchers undergoing revision UCLR, as this number has increased over the past several years.⁷ Currently, there is some debate as to how to best address the UCL during primary UCLR (graft type, exposure, treatment of the ulnar nerve, and graft fixation methods) because no study has shown one fixation method or graft type to be superior to others. Similarly, no study has definitively proven how to best manage the ulnar nerve (transpose in all patients, only transpose if preoperative symptoms of numbness/tingling, subluxation, etc. exist). Unfortunately, the results following revision UCLR are inferior to those following primary UCLR.^4,7,8 Hence, given this information, it is imperative to both determine and implement strategies aimed at minimizing the need for revision.

Risk Factors for Injury

Although MLB has received more media attention than lower levels of baseball competition, there is relatively sparse evidence surrounding injury risk factors among MLB players. The majority of studies performed have evaluated risk factors for injury in younger baseball athletes (adolescent, high school, and college). The number of athletes at these lower levels sustaining injuries has increased over the past several years as well.⁹ Several large prospective studies have evaluated risk factors for shoulder and elbow injuries in adolescent baseball players. The risk factors include pitching year-round, pitching more than 100 innings per year, high pitch counts, pitching for multiple teams, geography, pitching on consecutive days, pitching while fatigued, breaking pitches, higher elbow valgus torque, pitching with higher velocity, pitching with supraspinatus weakness, and pitching with a glenohumeral internal rotation deficit (GIRD).^10-17 The large majority of these risk factors are essentially part of a pitcher’s cumulative work, which consists of number of games pitched, total pitches thrown, total innings pitched, innings pitched per game, and pitches thrown per game. One prior study has evaluated cumulative work as a predictor for injury in MLB pitchers.¹⁸ While there were several issues with the study methodology, the authors found no correlation between a MLB pitcher’s cumulative work and risk for injury.

Given our current understanding of repetitive microtrauma as the pathophysiology behind these injuries, it remains unclear why cumulative work would be predictive of injury in youth pitchers but not in MLB pitchers.¹⁶ Several potential reasons exist as to why cumulative work may relate to risk of injury in youth pitchers and not MLB pitchers. Achieving MLB status may infer the element of natural selection based on technique and talent that supersedes the effect of “cumulative trauma” in many players. In MLB pitchers, cumulative work is closely monitored. In addition, these players are only playing for a single team and are not pitching competitively year-round, while many youth players play for multiple teams and may pitch year-round. To combat youth injuries, MLB Pitch Smart has developed recommendations on pitch counts and days of rest for pitchers of all age groups (Table).¹⁹ While data do not yet exist to clearly demonstrate the effectiveness of these guidelines, given the risk factors previously mentioned, it seems that these recommendations will show some reduction in youth injuries in years to come.

Some studies have evaluated anatomic variation among pitchers as a risk factor for injury. Polster and colleagues²⁰ performed computed tomography (CT) scans with 3-dimensional reconstructions on the humeri of both the throwing and non-throwing arms of 25 MLB pitchers to determine if humeral torsion was related to the incidence and severity of upper extremity injuries in these athletes. The authors defined a severe injury as those which kept the player out for >30 days. Overall, 11 pitchers were injured during the 2-year study period. There was a strong inverse relationship between torsion and injury severity such that lower degrees of dominant humeral torsion correlated with higher injury severity (P = .005). However, neither throwing arm humeral torsion nor the difference in torsion between throwing and non-throwing humeri were predictive of overall injury incidence. While this is a nonmodifiable risk factor, it is important to understand how the pitcher’s anatomy plays a role in risk of injury.²⁰ Understanding nonmodifiable risk factors may be helpful in the future to risk stratify, prognosticate, and modulate modifiable risk factors such as cumulative work.

Elbow

Injuries to the elbow have become more common in recent years amongst MLB players, although the literature regarding risk factors for elbow injuries is sparse.^4,6 Wilk and colleagues²¹ performed a prospective study to determine if deficits in glenohumeral passive range of motion (ROM) increased the risk of elbow injury in MLB pitchers. Between 2005-2012, the authors measured passive shoulder ROM of both the throwing and non-throwing shoulder of 296 major and minor league pitchers and followed them for a median of 53.4 months. In total, 38 players suffered 49 elbow injuries and required 8 surgeries, accounting for a total of 2551 days spent on the disabled list (DL). GIRD and external rotation insufficiency were not correlated with elbow injuries. However, pitchers with deficits of >5° in total rotation between the throwing and non-throwing shoulders had a 2.6 times greater risk for injury (P = .007) and pitchers with deficits of ≥5° in flexion of the throwing shoulder compared to the non-throwing shoulder had a 2.8 times greater risk for injury (P = .008).²¹ Prior studies have demonstrated trends towards increased elbow injury in professional baseball pitchers with an increase in both elbow valgus torque as well as shoulder external rotation torque; maximum pitch velocity was also shown to be an independent risk factor for elbow injury in professional baseball pitchers.^10,11 These injuries typically occur during the late cocking/early acceleration phase of the pitching cycle, when the shoulder and elbow experience the most significant force of any point in time during a pitch (Figure 2).¹⁷ At our institution, there are several ongoing studies to determine the relative contributions of pitch velocity, number, and type to elbow injury rates. Prospective studies are also ongoing at other institutions.

Shoulder

Shoulder injuries are one of the most common injuries seen in MLB players, specifically pitchers. Similar to the prior study, Wilk and colleagues²² recently performed a prospective study to determine if passive ROM of the glenohumeral joint in MLB pitchers was predictive of shoulder injury or shoulder surgery. As in the previous study, the authors’ measured passive shoulder ROM of the throwing and non-throwing shoulder of 296 major and minor league pitchers during spring training between 2005-2012 and obtained an average follow-up of 48.4 months. The authors found a total of 75 shoulder injuries and 20 surgeries among 51 pitchers (17%) that resulted in 5570 days on the DL. While total rotation deficit, GIRD, and flexion deficit had no relation to shoulder injury or surgery, pitchers with <5° greater external rotation in the throwing shoulder compared to the non-throwing shoulder were more than 2 times more likely to be placed on the DL for a shoulder injury (P = .014) and were 4 times more likely to require shoulder surgery (P = .009).²² The authors concluded that an insufficient side-to-side difference in external rotation of the throwing shoulder increased a pitcher’s likelihood of shoulder injury as well as surgery.

Other

One area that has not received as much attention as repetitive use injuries of the shoulder and elbow is acute collision injuries. Collision injuries include concussions, hyperextension injuries to the knees, shoulder dislocations, fractures of the foot and ankle, and others.²³ Catchers and base runners during scoring plays are at a high risk for collision injury. Recent evidence has shown that catchers average approximately 2.75 collision injuries per 1000 athletic exposures (AE), accounting for an average of 39.1 days on the DL per collision injury.²³ However, despite these collision injuries, catchers spend more time on the DL from non-collision injuries (specifically shoulder injuries requiring surgical intervention), as studies have shown 19 different non-collision injuries that accounted for >100 days on the DL for catchers compared to no collision injuries that caused a catcher to be on the DL for >100 days.²³ The position of catcher is not an independent risk factor for sustaining an injury in MLB players.⁵

Preventative Measures

Given that recent evidence has identified certain modifiable risk factors, largely regarding shoulder ROM, for injuries to MLB pitchers, it stands to reason that by modifying these risk factors, the number of injuries to MLB pitchers can be decreased.^21,22 However, to the authors’ knowledge, there have been no studies in the current literature that have clearly demonstrated the ability to prevent injuries in MLB players. Based on the prior studies, it seems logical that lowering peak pitch velocity and ensuring proper shoulder ROM would help prevent injuries in MLB players, but this remains speculative. Stretching techniques that have been shown to increase posterior shoulder soft tissue flexibility, including sleeper stretches and modified cross-body stretches, as well as closely monitoring ROM may be helpful in modifying these risk factors.^24-26

Although the number of collision injuries is significantly lower than non-collision repetitive use injuries, MLB has implemented rule changes in recent years to prevent injuries to catchers and base runners alike.^23,27 The rule change, which went into effect in 2014, prohibits catchers from blocking home plate unless they are actively fielding the ball or are in possession of the ball. Similarly, base runners are not allowed to deviate from their path to collide with the catcher while attempting to score.²⁷ However, no study has analyzed whether this rule change has decreased the number of collision injuries sustained by MLB catchers, so it is unclear if this rule change has accomplished its goal.

Outcomes Following Injuries

One of the driving forces behind injury prevention in MLB players is to allow players to reach and maintain their full potential while minimizing time missed because of injury. Furthermore, as with any sport, the clinical outcomes and return to sport (RTS) rates for MLB players following injuries, especially injuries requiring surgical intervention, can be improved.^4,28,29 Several studies have evaluated MLB pitchers following UCLR and have shown that over 80% of pitchers are able to RTS following surgery.^4,30 When critically evaluated in multiple statistical parameters upon RTS, these players perform better in some areas and worse in others.^4,30 However, the results following revision UCLR are not as encouraging as those following primary UCLR in MLB pitchers.⁷ Following revision UCLR, only 65% of pitchers were able to RTS, and those who were able to RTS pitched, on average, almost 1 year less than matched controls.⁷ Unfortunately, results following surgeries about the shoulder in MLB players have been worse than those about the elbow. Cohen and colleagues28 reported on 22 MLB players who underwent labral repair of the shoulder and found that only 32% were able to return to the same or higher level following surgery, while over 45% retired from baseball following surgery. Hence, it is imperative these injuries are prevented, as the RTS rate following treatment is less than ideal.

Future Directions

Although a concerted effort has been made over the past several years to mitigate the number of injuries sustained by MLB players, there is still significant room for improvement. New products are in development/early stages of use that attempt to determine when a pitcher begins to show signs of fatigue to allow the coach to remove him from the game. The mTHROW sleeve (Motus Global), currently used by several MLB teams, is an elastic sleeve that is worn by pitchers on their dominant arm. The sleeve approximates torque, velocity, and workload based upon an accelerometer positioned at the medial elbow and sends this information to a smart phone in real time. This technology theoretically allows players to be intensively monitored and thus may prevent injuries to the UCL by preventing pitchers from throwing while fatigued. However, elbow kinematic parameters may not change significantly as pitchers fatigue, which suggests that this strategy may be suboptimal. Trunk mechanics do change as pitchers become fatigued, opening up the possibility for shoulder and elbow injury.^17,31,32 Further products that track hip-to-shoulder separation and trunk fatigue may be necessary to truly lower injury rates. However, no study has proven modifying either parameter leads to a decrease in injury rates.

Conclusion

Injuries to MLB pitchers and position players have become a significant concern over the past several years. Several risk factors for injury have been identified, including loss of shoulder ROM and pitch velocity. Further studies are necessary to determine the effectiveness of modifying these parameters on injury prevention.

Major league baseball (MLB) is one of the most popular sports in the United States, with an average annual viewership of 11 million for the All-Star game and almost 14 million for the World Series.¹ MLB has an average annual revenue of almost $10 billion, while the net worth of all 30 MLB teams combined is estimated at $36 billion; an increase of 48% from 1 year ago.² As the sport continues to grow in popularity and receives more social media coverage, several issues, specifically injuries to its players, have come to the forefront of the news. Injuries to MLB players, specifically pitchers, have become a significant concern in recent years. The active and extended rosters in MLB include 750 and 1200 athletes, respectively, with approximately 360 active spots taken up by pitchers.³ Hence, MLB employs a large number of elite athletes within its organization. It is important to understand not only what injuries are occurring in these athletes, but also how these injuries may be prevented.

Epidemiology

Injuries to MLB players, specifically pitchers, have increased over the past several years.⁴ Between 2005 and 2008, there was an overall increase of 37% in total number of injuries, with more injuries occurring in pitchers than any other position.⁵ While position players are more likely to sustain an injury to the lower extremity, pitchers are more likely to sustain an injury to the upper extremity.⁵ The month with the most injuries to MLB players was April, while the fewest number of injuries occurred in September.⁵ One injury that has been in the spotlight due to its dramatically increasing incidence is tear of the ulnar collateral ligament (UCL). Several studies have shown that the number of pitchers undergoing ulnar collateral ligament reconstruction (UCLR), commonly known as Tommy John surgery, has significantly increased over the past 20 years (Figure 1).^4,6 Between 25% to 33% of all MLB pitchers have undergone UCLR.

While the number of primary UCLR in MLB pitchers has become a significant concern, an even more pressing concern is the number of pitchers undergoing revision UCLR, as this number has increased over the past several years.⁷ Currently, there is some debate as to how to best address the UCL during primary UCLR (graft type, exposure, treatment of the ulnar nerve, and graft fixation methods) because no study has shown one fixation method or graft type to be superior to others. Similarly, no study has definitively proven how to best manage the ulnar nerve (transpose in all patients, only transpose if preoperative symptoms of numbness/tingling, subluxation, etc. exist). Unfortunately, the results following revision UCLR are inferior to those following primary UCLR.^4,7,8 Hence, given this information, it is imperative to both determine and implement strategies aimed at minimizing the need for revision.

Risk Factors for Injury

Although MLB has received more media attention than lower levels of baseball competition, there is relatively sparse evidence surrounding injury risk factors among MLB players. The majority of studies performed have evaluated risk factors for injury in younger baseball athletes (adolescent, high school, and college). The number of athletes at these lower levels sustaining injuries has increased over the past several years as well.⁹ Several large prospective studies have evaluated risk factors for shoulder and elbow injuries in adolescent baseball players. The risk factors include pitching year-round, pitching more than 100 innings per year, high pitch counts, pitching for multiple teams, geography, pitching on consecutive days, pitching while fatigued, breaking pitches, higher elbow valgus torque, pitching with higher velocity, pitching with supraspinatus weakness, and pitching with a glenohumeral internal rotation deficit (GIRD).^10-17 The large majority of these risk factors are essentially part of a pitcher’s cumulative work, which consists of number of games pitched, total pitches thrown, total innings pitched, innings pitched per game, and pitches thrown per game. One prior study has evaluated cumulative work as a predictor for injury in MLB pitchers.¹⁸ While there were several issues with the study methodology, the authors found no correlation between a MLB pitcher’s cumulative work and risk for injury.

Given our current understanding of repetitive microtrauma as the pathophysiology behind these injuries, it remains unclear why cumulative work would be predictive of injury in youth pitchers but not in MLB pitchers.¹⁶ Several potential reasons exist as to why cumulative work may relate to risk of injury in youth pitchers and not MLB pitchers. Achieving MLB status may infer the element of natural selection based on technique and talent that supersedes the effect of “cumulative trauma” in many players. In MLB pitchers, cumulative work is closely monitored. In addition, these players are only playing for a single team and are not pitching competitively year-round, while many youth players play for multiple teams and may pitch year-round. To combat youth injuries, MLB Pitch Smart has developed recommendations on pitch counts and days of rest for pitchers of all age groups (Table).¹⁹ While data do not yet exist to clearly demonstrate the effectiveness of these guidelines, given the risk factors previously mentioned, it seems that these recommendations will show some reduction in youth injuries in years to come.

Some studies have evaluated anatomic variation among pitchers as a risk factor for injury. Polster and colleagues²⁰ performed computed tomography (CT) scans with 3-dimensional reconstructions on the humeri of both the throwing and non-throwing arms of 25 MLB pitchers to determine if humeral torsion was related to the incidence and severity of upper extremity injuries in these athletes. The authors defined a severe injury as those which kept the player out for >30 days. Overall, 11 pitchers were injured during the 2-year study period. There was a strong inverse relationship between torsion and injury severity such that lower degrees of dominant humeral torsion correlated with higher injury severity (P = .005). However, neither throwing arm humeral torsion nor the difference in torsion between throwing and non-throwing humeri were predictive of overall injury incidence. While this is a nonmodifiable risk factor, it is important to understand how the pitcher’s anatomy plays a role in risk of injury.²⁰ Understanding nonmodifiable risk factors may be helpful in the future to risk stratify, prognosticate, and modulate modifiable risk factors such as cumulative work.

Elbow

Injuries to the elbow have become more common in recent years amongst MLB players, although the literature regarding risk factors for elbow injuries is sparse.^4,6 Wilk and colleagues²¹ performed a prospective study to determine if deficits in glenohumeral passive range of motion (ROM) increased the risk of elbow injury in MLB pitchers. Between 2005-2012, the authors measured passive shoulder ROM of both the throwing and non-throwing shoulder of 296 major and minor league pitchers and followed them for a median of 53.4 months. In total, 38 players suffered 49 elbow injuries and required 8 surgeries, accounting for a total of 2551 days spent on the disabled list (DL). GIRD and external rotation insufficiency were not correlated with elbow injuries. However, pitchers with deficits of >5° in total rotation between the throwing and non-throwing shoulders had a 2.6 times greater risk for injury (P = .007) and pitchers with deficits of ≥5° in flexion of the throwing shoulder compared to the non-throwing shoulder had a 2.8 times greater risk for injury (P = .008).²¹ Prior studies have demonstrated trends towards increased elbow injury in professional baseball pitchers with an increase in both elbow valgus torque as well as shoulder external rotation torque; maximum pitch velocity was also shown to be an independent risk factor for elbow injury in professional baseball pitchers.^10,11 These injuries typically occur during the late cocking/early acceleration phase of the pitching cycle, when the shoulder and elbow experience the most significant force of any point in time during a pitch (Figure 2).¹⁷ At our institution, there are several ongoing studies to determine the relative contributions of pitch velocity, number, and type to elbow injury rates. Prospective studies are also ongoing at other institutions.

Shoulder

Shoulder injuries are one of the most common injuries seen in MLB players, specifically pitchers. Similar to the prior study, Wilk and colleagues²² recently performed a prospective study to determine if passive ROM of the glenohumeral joint in MLB pitchers was predictive of shoulder injury or shoulder surgery. As in the previous study, the authors’ measured passive shoulder ROM of the throwing and non-throwing shoulder of 296 major and minor league pitchers during spring training between 2005-2012 and obtained an average follow-up of 48.4 months. The authors found a total of 75 shoulder injuries and 20 surgeries among 51 pitchers (17%) that resulted in 5570 days on the DL. While total rotation deficit, GIRD, and flexion deficit had no relation to shoulder injury or surgery, pitchers with <5° greater external rotation in the throwing shoulder compared to the non-throwing shoulder were more than 2 times more likely to be placed on the DL for a shoulder injury (P = .014) and were 4 times more likely to require shoulder surgery (P = .009).²² The authors concluded that an insufficient side-to-side difference in external rotation of the throwing shoulder increased a pitcher’s likelihood of shoulder injury as well as surgery.

Other

One area that has not received as much attention as repetitive use injuries of the shoulder and elbow is acute collision injuries. Collision injuries include concussions, hyperextension injuries to the knees, shoulder dislocations, fractures of the foot and ankle, and others.²³ Catchers and base runners during scoring plays are at a high risk for collision injury. Recent evidence has shown that catchers average approximately 2.75 collision injuries per 1000 athletic exposures (AE), accounting for an average of 39.1 days on the DL per collision injury.²³ However, despite these collision injuries, catchers spend more time on the DL from non-collision injuries (specifically shoulder injuries requiring surgical intervention), as studies have shown 19 different non-collision injuries that accounted for >100 days on the DL for catchers compared to no collision injuries that caused a catcher to be on the DL for >100 days.²³ The position of catcher is not an independent risk factor for sustaining an injury in MLB players.⁵

Preventative Measures

Given that recent evidence has identified certain modifiable risk factors, largely regarding shoulder ROM, for injuries to MLB pitchers, it stands to reason that by modifying these risk factors, the number of injuries to MLB pitchers can be decreased.^21,22 However, to the authors’ knowledge, there have been no studies in the current literature that have clearly demonstrated the ability to prevent injuries in MLB players. Based on the prior studies, it seems logical that lowering peak pitch velocity and ensuring proper shoulder ROM would help prevent injuries in MLB players, but this remains speculative. Stretching techniques that have been shown to increase posterior shoulder soft tissue flexibility, including sleeper stretches and modified cross-body stretches, as well as closely monitoring ROM may be helpful in modifying these risk factors.^24-26

Although the number of collision injuries is significantly lower than non-collision repetitive use injuries, MLB has implemented rule changes in recent years to prevent injuries to catchers and base runners alike.^23,27 The rule change, which went into effect in 2014, prohibits catchers from blocking home plate unless they are actively fielding the ball or are in possession of the ball. Similarly, base runners are not allowed to deviate from their path to collide with the catcher while attempting to score.²⁷ However, no study has analyzed whether this rule change has decreased the number of collision injuries sustained by MLB catchers, so it is unclear if this rule change has accomplished its goal.

Outcomes Following Injuries

One of the driving forces behind injury prevention in MLB players is to allow players to reach and maintain their full potential while minimizing time missed because of injury. Furthermore, as with any sport, the clinical outcomes and return to sport (RTS) rates for MLB players following injuries, especially injuries requiring surgical intervention, can be improved.^4,28,29 Several studies have evaluated MLB pitchers following UCLR and have shown that over 80% of pitchers are able to RTS following surgery.^4,30 When critically evaluated in multiple statistical parameters upon RTS, these players perform better in some areas and worse in others.^4,30 However, the results following revision UCLR are not as encouraging as those following primary UCLR in MLB pitchers.⁷ Following revision UCLR, only 65% of pitchers were able to RTS, and those who were able to RTS pitched, on average, almost 1 year less than matched controls.⁷ Unfortunately, results following surgeries about the shoulder in MLB players have been worse than those about the elbow. Cohen and colleagues28 reported on 22 MLB players who underwent labral repair of the shoulder and found that only 32% were able to return to the same or higher level following surgery, while over 45% retired from baseball following surgery. Hence, it is imperative these injuries are prevented, as the RTS rate following treatment is less than ideal.

Future Directions

Although a concerted effort has been made over the past several years to mitigate the number of injuries sustained by MLB players, there is still significant room for improvement. New products are in development/early stages of use that attempt to determine when a pitcher begins to show signs of fatigue to allow the coach to remove him from the game. The mTHROW sleeve (Motus Global), currently used by several MLB teams, is an elastic sleeve that is worn by pitchers on their dominant arm. The sleeve approximates torque, velocity, and workload based upon an accelerometer positioned at the medial elbow and sends this information to a smart phone in real time. This technology theoretically allows players to be intensively monitored and thus may prevent injuries to the UCL by preventing pitchers from throwing while fatigued. However, elbow kinematic parameters may not change significantly as pitchers fatigue, which suggests that this strategy may be suboptimal. Trunk mechanics do change as pitchers become fatigued, opening up the possibility for shoulder and elbow injury.^17,31,32 Further products that track hip-to-shoulder separation and trunk fatigue may be necessary to truly lower injury rates. However, no study has proven modifying either parameter leads to a decrease in injury rates.

Conclusion

Injuries to MLB pitchers and position players have become a significant concern over the past several years. Several risk factors for injury have been identified, including loss of shoulder ROM and pitch velocity. Further studies are necessary to determine the effectiveness of modifying these parameters on injury prevention.

The supraphysiological demands imposed on the elbow of a throwing athlete result in predictable patterns of injury. This is especially true of baseball pitchers. Knowledge of elbow anatomy, as well as the biomechanics of throwing, assist in making diagnostic and therapeutic decisions and also influence surgical technique when surgery is required. During the late cocking and early acceleration phases of throwing, valgus torque can reach 65 Nm with angular velocities of the forearm reaching 5000°/sec, which is considered the fasted recorded human movment.¹ The valgus torque and rapid extension synergistically create 3 major forces placed on the elbow. The first is a tensile stress along the medial aspect of elbow affecting the ulnar collateral ligament (UCL), flexor pronator mass, and medial epicondyle. Secondly, compression forces affect the lateral aspect of the elbow at the radiocapitellar joint. Finally, a shearing stress occurs in the posterior compartment at the posterior medial tip of the olecranon and the olecranon fossa.

These forces generated on the elbow result in predictable pathology. The recurring tensile forces applied on the medial aspect on the elbow can compromise the integrity of the UCL. It is well known that injury to the UCL leads to valgus instability. Individuals with valgus instability who continue to throw may trigger and/or aggravate injury in the posterior and lateral components of the elbow. Lateral compression forces can often reach 500 N, resulting in radiocapitellar overload syndrome, which occurs in combination with medial ligament instability and valgus extension overload.² Radiocapitellar compression may cause chondral or osteochondral fracture with resulting intra-articular loose bodes. This compression also contributes to the etiology of osteochondritis dissecans (OCD) in skeletally immature athletes. In the posterior elbow, throwing forcefully and repeatedly pushes the olecranon into the olecranon fossa. Shear stress on the medial olecranon tip and fossa, due to combined valgus and extension forces, lead to the development of osteophytes. This collection of injuries in the medial, lateral, and posterior aspects of the elbow is known as “valgus extension overload syndrome” or VEO. Symptoms in VEO can be the result of chondral lesions, loose bodies, and marginal exostosis.³

The aim of this review is to provide understanding regarding both the relevant anatomy and pathomechanics of VEO, key aspects to clinical evaluation, and effective treatment options.

Functional Anatomy

A functional comprehension of elbow anatomy and biomechanics is essential to understanding the constellation of injuries in VEO. The osseous anatomy of the elbow permits a variety of movements. These include flexion-extension and pronation-supination, which are mediated by the ulnohumeral and radiocapitellar articulations. While in full extension, the elbow has a normal valgus carrying angle of 11° to 16°. It is important to know that 50% of the elbow’s stability is attributed to the configuration of the bones.^4-6 This is especially true in varus stress while the elbow is in full extension. The soft tissues, including muscle and ligaments such as the UCL, lateral UCL, and radial UCL complexes, provide the remaining elbow stability.^4-6

The UCL complex is composed of 3 main segments known as the anterior, posterior, and oblique bundles (transverse ligament). Collectively, these bundles are responsible for providing medial elbow stability. However, each of these bundles contributes to medial elbow stability in its own way. The first and arguably the most important bundle is the anterior bundle; its most important function is providing stability against valgus stress.^4,5,7 It is composed of parallel fibers inserting on the medial coronoid process.^4,5,7 Furthermore, its eccentric location with respect to the axis of elbow allows it to provide stability throughout the full range of elbow motion.⁶ The anterior bundle can be further divided into individual anterior and posterior bands that have reciprocal functionality.^5,8,9 The anterior band acts as the chief restraint to valgus stress up to 90° of flexion.⁹ Any flexion beyond 90° renders the anterior band’s role secondary in resisting valgus stress.⁹ The posterior band’s function in resisting valgus stress is most important between 60° and full flexion, while having a secondary role in lesser degrees of flexion.^8,9 Notably, the posterior band is isometric and is more important in the overhead-throwing athlete due to the fact its primary role in resisting valgus stress occurs at higher degrees of flexion.¹⁰

The remaining posterior and oblique bundles of the UCL complex have lesser roles in maintaining elbow stability. The posterior bundle of the UCL complex is fan-shaped, originates from the medial epicondyle, and inserts onto the medial margin the semi-lunar notch. It is more slender and frailer than the anterior bundle. This is reflected in its functionality, as it plays a secondary role in elbow stability during elbow flexion beyond 90°.^4,5,8 In contrast to the anterior and posterior bundles, the oblique bundle, also known as the transverse ligament, does not cross the elbow joint. It is a thickening of the caudal most aspect of the joint capsule, which extends from the medial olecranon to the inferior medial coronoid process and as a result functions in expanding the greater sigmoid notch.⁶

The musculotendinous components of the elbow are essential to providing dynamic functional resistance to valgus stress.¹¹ These components are flexor-pronator musculature that originate from the medial epicondyle. Listed proximally to distally, the flexor-pronator muscles include pronator teres, flexor carpi radialis (FCR), palmaris longus, flexor digitorum superficialis, and the flexor carpi ulnaris (FCU).

Pathomechanics

Once familiarized with the relevant function anatomy, it is crucial to understand the mechanics of throwing in order to understand the pathomechanics of VEO. The action of overhead throwing has been divided into 6 phases.^6,12-16 Phase 4, acceleration, is the most relevant when discussing forces on elbow, since the majority of forces are generated during this state. Phase 4 represents a rapid acceleration of the upper extremity with a large forward-directed force on the arm generated by the shoulder muscles. Additionally, there is internal rotation and adduction of the humerus with rapid elbow extension terminating with ball release. The elbow accelerates up to 600,000°/sec² in a miniscule time frame of 40 to 50 milliseconds.^1,5 Immense valgus forces are exerted on the medial aspect of the elbow. The anterior bundle of the UCL bears the majority of the force, with the flexor pronator mass enabling the transmission.¹¹ The majority of injuries occur during stage 4 as a result of the stress load on the medial elbow structures like the UCL. The proceeding phases 5 (deceleration), and 6 (follow-through) involve eventual dissipation of excess kinetic energy as the elbow completely extends. The deceleration during phase 5 is rapid and powerful, occurring at about 500,000°/sec² in the short span of 50 milliseconds.^1,6,12-16 High-velocity throwing, such as baseball pitching, generates forces in the elbow that are opposed by the articular, ligamentous, and muscular portions of the arm. The ulnohumeral articulation stabilizes motion of the arm from 0° to 20° of flexion and beyond 120° of flexion. Static and dynamic soft tissues maintain stability during the remaining of 100° arc of motion.

During deceleration, the elbow undergoes terminal extension resulting in the posteromedial olecranon contacting the trochlea and the olecranon fossa with subsequent dissipation of the combined valgus force and angular moment (Figure 1). This dissipation of force creates pathologic shear and compressive forces in the posterior elbow. Poor muscular control and the traumatic abutment that occurs in the posterior compartment may further add to the pathologic forces. Reactive bone formation is induced by the repetitive compression and shear, resulting in osteophytes on the posteromedial tip of the olecranon (Figure 2). Consequent “kissing lesions” of chondromalacia may occur in the olecranon fossa and posteromedial trochlea. The subsequent development of loose bodies may also occur. The presence of osteophytes and/or loose bodies may result in posteromedial impingement (PMI).

The association between PMI of the olecranon and valgus instability has been elucidated in both clinical and biomechanical investigations.^17,18,19,20 Conway¹⁸ identified tip exostosis in 24% of lateral radiographs of 135 asymptomatic professional pitchers. Approximately one-fifth (21%) of these pitchers had >1.0 mm increased relative valgus laxity on stress radiographs. Roughly one-third (34%) of players with exostosis had >1.0 mm of increased relative valgus laxity, compared to 16% of players without exostosis formation. These results provide evidence for a probable association between PMI and valgus laxity. In biomechanical research, Ahmad and colleagues¹⁷ studied the effect of partial and full thickness UCL injuries on contact forces of the posterior elbow. Posteromedial compartments of cadaver specimens were subjected to physiologic valgus stresses while placed on pressure-senstive film. Contact area and pressure between posteromedial trochlea and olecranon were altered in the setting of UCL insufficiency, helping explain how posteromedial osteophyte formation occurs.

Additional biomechanical studies have also investigated the posteromedial olecranon’s role in functioning as a stabilizing buttress to medial tensile forces. Treating PMI with aggressive bone removal may increase valgus instability as well as strain on the UCL, leading to UCL injury following olecranon resection.^19,20 Kamineni and colleagues¹⁹ investigated strain on anterior bundle of UCL as a function of increasing applied torque and posteromedial resections of the olecranon. This investigation was done utilizing an electromagnetic tracking placed in cadaver elbows. A nonuniform change in strain was found at 3 mm of resection during flexion and valgus testing. This nonuniform change implied that removal of posteromedial olecranon beyond 3 mm made the UCL more vulnerable to injury. Follow-up investigations looked at kinematic effects of increasing valgus and varus torques and sequential posteromedial olecranon resections.²⁰ Valgus angulation of the elbow increased with all resection levels but no critical amount of olecranon resection was identified. The consensus in the literature indicates that posteromedial articulation of the elbow is a significant stabilizer to valgus stress.^17-22 Thus, normal bone should be preserved and only osteophytes should be removed during treatment.

In addition, VEO may lead to injury in the lateral compartment as well. After attenuation and insufficiency of the UCL due to repetitive stress, excessive force transmission to the lateral aspect of the elbow occurs. Compressive and rotatory forces escalate within the radiocapitellar joint, causing synovitis and osteochondral lesions.^3,23 These osteochondral lesions include osteochondritis dissecans and osteochondral fractures that may fragment and become loose bodies.

Evaluation of VEO

History

Patients will typically have a history of repetitive throwing or other repetitive overhead activity. VEO is most common in baseball pitchers but may also occur in other sports, such as tennis, football, lacrosse, gymnastics, and javelin throwing. In baseball pitchers, clinical presentation is often preceded by a decrease in pitch velocity, control, and early fatigability. It presents with elbow pain localized to the posteromedial aspect of olecranon after release of the ball, when the elbow reaches terminal extension. Patients also report limited extension, due to impinging posterior osteophytes. Also, locking and catching caused by loose bodies and chondromalacia may be present. VEO may also occur in combination with concomitant valgus instability, as well as in a patient with a prior history of valgus instability. Flexor pronator injury, ulnar neuritis, and subluxation may also be present in a patient with VEO.

Physical Examination

VEO may occur in an isolated fashion or with concomitant pathology. Therefore, a comprehensive physical examination includes evaluating the entire kinetic chain of throwing and a focused examination covering VEO and associated valgus instability. Patients may exhibit crepitus and tenderness over the posteromedial olecranon and a loss of extension with a firm end point. The extension impingement test should be performed where the elbow is snapped into terminal extension. This typically elicits pain in the posterior compartment in a patient with VEO. The arm bar test involves positioning the patient’s shoulder at 90° of forward flexion, full internal rotation, with the patient’s hand placed on the examiner’s shoulder.²⁴ The examiner pulls down on the olecranon, simulating forced extension; pain is indicative of a positive test. It is important to note if there are signs of ulnar neuritis or subluxing ulnar nerve, especially if planning to utilize medial portals during arthroscopic treatment.

Examination maneuvers for valgus instability should also be conducted during evaluation of VEO. The physical examination for valgus instability in the elbow is ideally performed with the patient seated. Secure the patient’s wrist between the examiner’s forearm and trunk, and flex the patient’s elbow between 20° and 30° to unlock the olecranon from its fossa. Proceed to apply valgus stress. This stresses the anterior band of the anterior bundle of the UCL.^6,25,26 Palpate the UCL from the medial epicondyle to the proximal ulna as valgus stress is applied. Occasionally, valgus laxity can be appreciated when compared to contralateral side. The milking maneuver is a helpful test to determine UCL injury. Pull on the patient’s thumb while the forearm is supinated, shoulder extended, and the elbow flexed beyond 90°.⁶ The milking maneuver exerts valgus stress on a flexed elbow. A patient with an injured UCL will experience the subjective feeling of apprehension and instability, with medial elbow pain.

The most sensitive test is the moving valgus stress test. This is performed with the patient in the upright position and the shoulder abducted 90°. Starting with the arm in full flexion, the examiner applies a constant valgus torque to the elbow and then rapidly extends the elbow. Reproduction of pain during range of motion from 120° to 70° represents UCL injury, while pain with extension beyond 70° represents chondral injury to the ulnohumeral joint. Be aware that the absence of increased pain with wrist flexion, along with pain localized slightly posterior to the common flexor origin, differentiates a UCL injury from flexor-pronator muscle injury.^6,26,27Examine range of motion in affected and unaffected elbows. Loss of terminal extension may be present, along with secondary to flexion contracture due to repeated attempts at healing and stabilization.²⁵

Imaging

Imaging is essential to the accurate diagnosis of VEO and related conditions. Anterior posterior (AP), lateral, and oblique radiographs of elbow (Figures 3A-3C) may show posteromedial olecranon osteophytes and/or loose bodies. Calcification of ligaments or other soft tissues may also be seen. An AP radiograph with 140° of external rotation may best visualize osteophytes on posteromedial olecranon.18 A computed tomography scan with 2-dimensional sagittal and coronal reconstruction and 3-dimensional surface rendering (Figures 4A, 4B) may best demonstrate morphological abnormalities, loose bodies, and osteophytes. Magnetic resonance imaging (MRI) is essential for assessment of soft tissues and chondral injuries. MRI may detect UCL compromise, synovial plicae, bone edema, olecranon, or stress fractures.

Treatment

Nonoperative Treatment

Treatment consists of both nonoperative and operative modalities. Nonoperative treatment methods are first line in treating VEO. Patients should modify their physical activity and rest from throwing activities. Nonsteroid anti-inflammatory drugs are appropriate to treat pain along with intra-articular corticosteroid injections of the elbow. A wide assessment of pitching mechanics should be performed in an attempt to correct errors in throwing technique and address muscular imbalances. After cessation of the resting period, the patient may initiate a progressive throwing program supervised by an experienced therapist and trainer. A plan for returning to competition should be made upon completion of the throwing program.

Operative Treatment

Surgical treatment is reserved for patients who fail nonoperative treatment. These patients have persistent symptoms of posteromedial impingement and desire to return to pre-injury level of performance. Posteromedial decompression is not recommended when provocative physical examination maneuvers are negative, regardless of presence of olecranon osteophytes on imaging. Osteophytes are an asymptomatic finding typically seen in professional baseball players and do not warrant surgical treatment.^18,28 UCL compromise is a relative contraindication to olecranon debridement as UCL injury could become symptomatic following surgery. Surgical options in the appropriate patient to decompress posterior compartment include arthroscopic olecranon debridement or limited incision arthrotomy. Excessive resection of posteromedial osteophytes must be avoided. Arthroscopy has limited morbidity and allows for complete diagnostic assessment. UCL reconstruction should also be considered in combination with posteromedial debridement when the UCL is torn. More challenging indications for UCL reconstruction occur when the UCL is partially torn or torn and asymptomatic. Isolated posteromedial decompression in this setting risks future development of UCL symptoms that would then need to be addressed.

Surgical Technique

As previously mentioned, elbow arthroscopy or limited excision arthrotomy are the preferred operative methods for decompression of the posterior compartment and thus treatment of VEO. Anesthesia and patient positioning should be selected based on the surgeon’s preference. The patient should be positioned supine, prone, or in lateral decubitis. When a UCL reconstruction is expected, supine position is advantageous to avoid repositioning after completing the arthroscopic portion of the procedure. However, arthroscopy can be performed in the lateral position with subsequent repositioning, repeat prepping, and draping for UCL reconstruction (Figures 5A, 5B).

Prepare for elbow arthroscopy by distending the elbow joint with normal saline to aid in protection of neurovascular structures and simplify the insertion of the scope trocar. Perform diagnostic anterior arthroscopy via the proximal anteromedial portal. Assess for presence of loose bodies and osteochondral lesions of the radiocapitellar joint, as well as osteophytes of the coronoid tip and fossa. Utilizing a spinal needle under direct visualization establish a proximal lateral portal with adequate view of the anterior compartment. Proceed to visualize the medial compartment and assess for UCL injury. Apply valgus stress while in 70° of flexion. Visualize the coronoid process and look for medial trochlea gapping of 3 mm or greater, which indicates UCL insufficiency.³⁰

Establish the posterolateral port for visualization of the posterior compartment. A posterior portal is established through the triceps tendon. Proceed to shave and ablate synovitis in order to create an adequate working space. Inspect the posteromedial olecranon, looking for any osteophytes or chondromalacia in the area (Figure 6). Examine the posterior radiocapitellar joint, looking specifically for loose bodies. The presence of loose bodies may require creating an extra mid lateral portal for removal. The ulnar nerve is located superficial to the elbow capsule and can be damaged by instruments utilized in the posteromedial gutter. As a precaution, be sure to remove suction attached to shaver. Place a curved articulating retractor in an accessory posterolateral portal to assist in protecting the ulnar nerve by retracting the capsule away from the surgical field (Figures 7A, 7B).

The osteophyte may be encased in soft tissue. Using a combination of ablation devices and shavers, the osteophyte can be exposed. The olecranon osteophyte can be removed with a small osteotome located at the border of the osteophyte and the normal olecranon. A motorized shaver or burr may also be introduced through the direct posterior portal or the posterolateral portal to complete the contouring of the olecranon (Figures 8A, 8B). Intraoperative lateral radiographs may be obtained for guidance in adequate bone removal and to ensure no bone debris is left in the soft tissues. It is critical that only pathologic osteophyte is removed and that normal olecranon is not compromised. This prevents an increase in UCL strain during valgus loading.¹⁹ However, in some non-throwing athletes, more aggressive debridement can be performed due to a smaller risk of UCL injury after posterior decompression.

Often, with the presence of osteophytes on the olecranon, there may be associated chondromalacia of the trochlea. These kissing lesions must be addressed after debridement of osteophytes. Loose flaps or frayed edges are carefully debrided and for any significant lesion the edges are contoured to a stable rim using shavers and curettes. Once altered to a well-shouldered lesion, microfracture is performed. Anterograde drilling of the lesion with perforations separated by 2 to 3 mm allow for the release of marrow elements and induction of a fibrocartilage healing response.

For an isolated posteromedial decompression, early rehabilitation begins with simple elbow flexion and extension exercises. It is important to restore flexor-pronator strength. Six weeks postoperatively, a progressive throwing program that includes plyometric exercises, neuromuscular training, and endurance exercises can be initiated. Patients can typically return to competition 3 to 4 months after surgery, if they have successfully regained preoperative range of motion, preoperative strength in the elbow, and there is no pain or tenderness on stress testing or palpation.

Outcomes

Safety and Advances in Arthroscopy

A clearer understanding of portal placement and proximity to neurovasculature in conjunction with advances in equipment have allowed for continual improvements in elbow arthroscopy techniques. There is plenty of literature indicating that arthroscopic posteromedial decompression is a safe, reliable, effective procedure, with a high rate of patient satisfaction.^22,30-34] Andrews and Carson³⁰ published one of the earliest investigations indicating the effectiveness of elbow arthroscopy utilizing objective and subjective outcome scores. They found that preoperative scores indicating patient satisfaction increased from 50% to 83%. Patients who underwent only loose body removal had the best outcomes. Andrews and Timmerman³¹ later evaluated the results of 72 professional baseball players who underwent either arthroscopic or open elbow surgery. They found that posteromedial olecranon osteophytes and intraarticular loose bodies were the most common diagnoses, present in 65% and 54% of players, respectively. In addition, a 41% reoperation rate was reported after posteromedial olecranon resection, along with 25% a rate of valgus instability necessitating UCL reconstruction. Andrews and Timmerman³¹ propose that the incidence of UCL injuries is underestimated and that UCL pathology must be treated prior to treating its secondary effects. Recently, Reddy and colleagues³² reviewed the results of 187 arthroscopic procedures. Posterior impingement, loose bodies, and osteoarthritis were the most common problems, occurring in 51%, 31%, and 22% of patients, respectively. Reported results were encouraging, with 87% good to excellent results and 85% of baseball players returning to preinjury levels.

Conclusion

An understanding of the relevant functional anatomy and the biomechanics of throwing is essential to understanding VEO. Potential concomitant valgus instability and UCL injury must be carefully assessed. Only symptomatic patients who have failed conservative treatment should undergo surgery. It is critical to avoid exacerbating and/or causing valgus instability by surgical excessively removing normal bone from the olecranon. Arthroscopy has been shown to be a safe and effective method to treat refractory cases of VEO.

The supraphysiological demands imposed on the elbow of a throwing athlete result in predictable patterns of injury. This is especially true of baseball pitchers. Knowledge of elbow anatomy, as well as the biomechanics of throwing, assist in making diagnostic and therapeutic decisions and also influence surgical technique when surgery is required. During the late cocking and early acceleration phases of throwing, valgus torque can reach 65 Nm with angular velocities of the forearm reaching 5000°/sec, which is considered the fasted recorded human movment.¹ The valgus torque and rapid extension synergistically create 3 major forces placed on the elbow. The first is a tensile stress along the medial aspect of elbow affecting the ulnar collateral ligament (UCL), flexor pronator mass, and medial epicondyle. Secondly, compression forces affect the lateral aspect of the elbow at the radiocapitellar joint. Finally, a shearing stress occurs in the posterior compartment at the posterior medial tip of the olecranon and the olecranon fossa.

These forces generated on the elbow result in predictable pathology. The recurring tensile forces applied on the medial aspect on the elbow can compromise the integrity of the UCL. It is well known that injury to the UCL leads to valgus instability. Individuals with valgus instability who continue to throw may trigger and/or aggravate injury in the posterior and lateral components of the elbow. Lateral compression forces can often reach 500 N, resulting in radiocapitellar overload syndrome, which occurs in combination with medial ligament instability and valgus extension overload.² Radiocapitellar compression may cause chondral or osteochondral fracture with resulting intra-articular loose bodes. This compression also contributes to the etiology of osteochondritis dissecans (OCD) in skeletally immature athletes. In the posterior elbow, throwing forcefully and repeatedly pushes the olecranon into the olecranon fossa. Shear stress on the medial olecranon tip and fossa, due to combined valgus and extension forces, lead to the development of osteophytes. This collection of injuries in the medial, lateral, and posterior aspects of the elbow is known as “valgus extension overload syndrome” or VEO. Symptoms in VEO can be the result of chondral lesions, loose bodies, and marginal exostosis.³

The aim of this review is to provide understanding regarding both the relevant anatomy and pathomechanics of VEO, key aspects to clinical evaluation, and effective treatment options.

Functional Anatomy

A functional comprehension of elbow anatomy and biomechanics is essential to understanding the constellation of injuries in VEO. The osseous anatomy of the elbow permits a variety of movements. These include flexion-extension and pronation-supination, which are mediated by the ulnohumeral and radiocapitellar articulations. While in full extension, the elbow has a normal valgus carrying angle of 11° to 16°. It is important to know that 50% of the elbow’s stability is attributed to the configuration of the bones.^4-6 This is especially true in varus stress while the elbow is in full extension. The soft tissues, including muscle and ligaments such as the UCL, lateral UCL, and radial UCL complexes, provide the remaining elbow stability.^4-6

The UCL complex is composed of 3 main segments known as the anterior, posterior, and oblique bundles (transverse ligament). Collectively, these bundles are responsible for providing medial elbow stability. However, each of these bundles contributes to medial elbow stability in its own way. The first and arguably the most important bundle is the anterior bundle; its most important function is providing stability against valgus stress.^4,5,7 It is composed of parallel fibers inserting on the medial coronoid process.^4,5,7 Furthermore, its eccentric location with respect to the axis of elbow allows it to provide stability throughout the full range of elbow motion.⁶ The anterior bundle can be further divided into individual anterior and posterior bands that have reciprocal functionality.^5,8,9 The anterior band acts as the chief restraint to valgus stress up to 90° of flexion.⁹ Any flexion beyond 90° renders the anterior band’s role secondary in resisting valgus stress.⁹ The posterior band’s function in resisting valgus stress is most important between 60° and full flexion, while having a secondary role in lesser degrees of flexion.^8,9 Notably, the posterior band is isometric and is more important in the overhead-throwing athlete due to the fact its primary role in resisting valgus stress occurs at higher degrees of flexion.¹⁰

The remaining posterior and oblique bundles of the UCL complex have lesser roles in maintaining elbow stability. The posterior bundle of the UCL complex is fan-shaped, originates from the medial epicondyle, and inserts onto the medial margin the semi-lunar notch. It is more slender and frailer than the anterior bundle. This is reflected in its functionality, as it plays a secondary role in elbow stability during elbow flexion beyond 90°.^4,5,8 In contrast to the anterior and posterior bundles, the oblique bundle, also known as the transverse ligament, does not cross the elbow joint. It is a thickening of the caudal most aspect of the joint capsule, which extends from the medial olecranon to the inferior medial coronoid process and as a result functions in expanding the greater sigmoid notch.⁶

The musculotendinous components of the elbow are essential to providing dynamic functional resistance to valgus stress.¹¹ These components are flexor-pronator musculature that originate from the medial epicondyle. Listed proximally to distally, the flexor-pronator muscles include pronator teres, flexor carpi radialis (FCR), palmaris longus, flexor digitorum superficialis, and the flexor carpi ulnaris (FCU).

Pathomechanics

Once familiarized with the relevant function anatomy, it is crucial to understand the mechanics of throwing in order to understand the pathomechanics of VEO. The action of overhead throwing has been divided into 6 phases.^6,12-16 Phase 4, acceleration, is the most relevant when discussing forces on elbow, since the majority of forces are generated during this state. Phase 4 represents a rapid acceleration of the upper extremity with a large forward-directed force on the arm generated by the shoulder muscles. Additionally, there is internal rotation and adduction of the humerus with rapid elbow extension terminating with ball release. The elbow accelerates up to 600,000°/sec² in a miniscule time frame of 40 to 50 milliseconds.^1,5 Immense valgus forces are exerted on the medial aspect of the elbow. The anterior bundle of the UCL bears the majority of the force, with the flexor pronator mass enabling the transmission.¹¹ The majority of injuries occur during stage 4 as a result of the stress load on the medial elbow structures like the UCL. The proceeding phases 5 (deceleration), and 6 (follow-through) involve eventual dissipation of excess kinetic energy as the elbow completely extends. The deceleration during phase 5 is rapid and powerful, occurring at about 500,000°/sec² in the short span of 50 milliseconds.^1,6,12-16 High-velocity throwing, such as baseball pitching, generates forces in the elbow that are opposed by the articular, ligamentous, and muscular portions of the arm. The ulnohumeral articulation stabilizes motion of the arm from 0° to 20° of flexion and beyond 120° of flexion. Static and dynamic soft tissues maintain stability during the remaining of 100° arc of motion.

During deceleration, the elbow undergoes terminal extension resulting in the posteromedial olecranon contacting the trochlea and the olecranon fossa with subsequent dissipation of the combined valgus force and angular moment (Figure 1). This dissipation of force creates pathologic shear and compressive forces in the posterior elbow. Poor muscular control and the traumatic abutment that occurs in the posterior compartment may further add to the pathologic forces. Reactive bone formation is induced by the repetitive compression and shear, resulting in osteophytes on the posteromedial tip of the olecranon (Figure 2). Consequent “kissing lesions” of chondromalacia may occur in the olecranon fossa and posteromedial trochlea. The subsequent development of loose bodies may also occur. The presence of osteophytes and/or loose bodies may result in posteromedial impingement (PMI).

The association between PMI of the olecranon and valgus instability has been elucidated in both clinical and biomechanical investigations.^17,18,19,20 Conway¹⁸ identified tip exostosis in 24% of lateral radiographs of 135 asymptomatic professional pitchers. Approximately one-fifth (21%) of these pitchers had >1.0 mm increased relative valgus laxity on stress radiographs. Roughly one-third (34%) of players with exostosis had >1.0 mm of increased relative valgus laxity, compared to 16% of players without exostosis formation. These results provide evidence for a probable association between PMI and valgus laxity. In biomechanical research, Ahmad and colleagues¹⁷ studied the effect of partial and full thickness UCL injuries on contact forces of the posterior elbow. Posteromedial compartments of cadaver specimens were subjected to physiologic valgus stresses while placed on pressure-senstive film. Contact area and pressure between posteromedial trochlea and olecranon were altered in the setting of UCL insufficiency, helping explain how posteromedial osteophyte formation occurs.

Additional biomechanical studies have also investigated the posteromedial olecranon’s role in functioning as a stabilizing buttress to medial tensile forces. Treating PMI with aggressive bone removal may increase valgus instability as well as strain on the UCL, leading to UCL injury following olecranon resection.^19,20 Kamineni and colleagues¹⁹ investigated strain on anterior bundle of UCL as a function of increasing applied torque and posteromedial resections of the olecranon. This investigation was done utilizing an electromagnetic tracking placed in cadaver elbows. A nonuniform change in strain was found at 3 mm of resection during flexion and valgus testing. This nonuniform change implied that removal of posteromedial olecranon beyond 3 mm made the UCL more vulnerable to injury. Follow-up investigations looked at kinematic effects of increasing valgus and varus torques and sequential posteromedial olecranon resections.²⁰ Valgus angulation of the elbow increased with all resection levels but no critical amount of olecranon resection was identified. The consensus in the literature indicates that posteromedial articulation of the elbow is a significant stabilizer to valgus stress.^17-22 Thus, normal bone should be preserved and only osteophytes should be removed during treatment.

In addition, VEO may lead to injury in the lateral compartment as well. After attenuation and insufficiency of the UCL due to repetitive stress, excessive force transmission to the lateral aspect of the elbow occurs. Compressive and rotatory forces escalate within the radiocapitellar joint, causing synovitis and osteochondral lesions.^3,23 These osteochondral lesions include osteochondritis dissecans and osteochondral fractures that may fragment and become loose bodies.

Evaluation of VEO

History

Patients will typically have a history of repetitive throwing or other repetitive overhead activity. VEO is most common in baseball pitchers but may also occur in other sports, such as tennis, football, lacrosse, gymnastics, and javelin throwing. In baseball pitchers, clinical presentation is often preceded by a decrease in pitch velocity, control, and early fatigability. It presents with elbow pain localized to the posteromedial aspect of olecranon after release of the ball, when the elbow reaches terminal extension. Patients also report limited extension, due to impinging posterior osteophytes. Also, locking and catching caused by loose bodies and chondromalacia may be present. VEO may also occur in combination with concomitant valgus instability, as well as in a patient with a prior history of valgus instability. Flexor pronator injury, ulnar neuritis, and subluxation may also be present in a patient with VEO.

Physical Examination

VEO may occur in an isolated fashion or with concomitant pathology. Therefore, a comprehensive physical examination includes evaluating the entire kinetic chain of throwing and a focused examination covering VEO and associated valgus instability. Patients may exhibit crepitus and tenderness over the posteromedial olecranon and a loss of extension with a firm end point. The extension impingement test should be performed where the elbow is snapped into terminal extension. This typically elicits pain in the posterior compartment in a patient with VEO. The arm bar test involves positioning the patient’s shoulder at 90° of forward flexion, full internal rotation, with the patient’s hand placed on the examiner’s shoulder.²⁴ The examiner pulls down on the olecranon, simulating forced extension; pain is indicative of a positive test. It is important to note if there are signs of ulnar neuritis or subluxing ulnar nerve, especially if planning to utilize medial portals during arthroscopic treatment.

Examination maneuvers for valgus instability should also be conducted during evaluation of VEO. The physical examination for valgus instability in the elbow is ideally performed with the patient seated. Secure the patient’s wrist between the examiner’s forearm and trunk, and flex the patient’s elbow between 20° and 30° to unlock the olecranon from its fossa. Proceed to apply valgus stress. This stresses the anterior band of the anterior bundle of the UCL.^6,25,26 Palpate the UCL from the medial epicondyle to the proximal ulna as valgus stress is applied. Occasionally, valgus laxity can be appreciated when compared to contralateral side. The milking maneuver is a helpful test to determine UCL injury. Pull on the patient’s thumb while the forearm is supinated, shoulder extended, and the elbow flexed beyond 90°.⁶ The milking maneuver exerts valgus stress on a flexed elbow. A patient with an injured UCL will experience the subjective feeling of apprehension and instability, with medial elbow pain.

The most sensitive test is the moving valgus stress test. This is performed with the patient in the upright position and the shoulder abducted 90°. Starting with the arm in full flexion, the examiner applies a constant valgus torque to the elbow and then rapidly extends the elbow. Reproduction of pain during range of motion from 120° to 70° represents UCL injury, while pain with extension beyond 70° represents chondral injury to the ulnohumeral joint. Be aware that the absence of increased pain with wrist flexion, along with pain localized slightly posterior to the common flexor origin, differentiates a UCL injury from flexor-pronator muscle injury.^6,26,27Examine range of motion in affected and unaffected elbows. Loss of terminal extension may be present, along with secondary to flexion contracture due to repeated attempts at healing and stabilization.²⁵

Imaging

Imaging is essential to the accurate diagnosis of VEO and related conditions. Anterior posterior (AP), lateral, and oblique radiographs of elbow (Figures 3A-3C) may show posteromedial olecranon osteophytes and/or loose bodies. Calcification of ligaments or other soft tissues may also be seen. An AP radiograph with 140° of external rotation may best visualize osteophytes on posteromedial olecranon.18 A computed tomography scan with 2-dimensional sagittal and coronal reconstruction and 3-dimensional surface rendering (Figures 4A, 4B) may best demonstrate morphological abnormalities, loose bodies, and osteophytes. Magnetic resonance imaging (MRI) is essential for assessment of soft tissues and chondral injuries. MRI may detect UCL compromise, synovial plicae, bone edema, olecranon, or stress fractures.

Treatment

Nonoperative Treatment

Treatment consists of both nonoperative and operative modalities. Nonoperative treatment methods are first line in treating VEO. Patients should modify their physical activity and rest from throwing activities. Nonsteroid anti-inflammatory drugs are appropriate to treat pain along with intra-articular corticosteroid injections of the elbow. A wide assessment of pitching mechanics should be performed in an attempt to correct errors in throwing technique and address muscular imbalances. After cessation of the resting period, the patient may initiate a progressive throwing program supervised by an experienced therapist and trainer. A plan for returning to competition should be made upon completion of the throwing program.

Operative Treatment

Surgical treatment is reserved for patients who fail nonoperative treatment. These patients have persistent symptoms of posteromedial impingement and desire to return to pre-injury level of performance. Posteromedial decompression is not recommended when provocative physical examination maneuvers are negative, regardless of presence of olecranon osteophytes on imaging. Osteophytes are an asymptomatic finding typically seen in professional baseball players and do not warrant surgical treatment.^18,28 UCL compromise is a relative contraindication to olecranon debridement as UCL injury could become symptomatic following surgery. Surgical options in the appropriate patient to decompress posterior compartment include arthroscopic olecranon debridement or limited incision arthrotomy. Excessive resection of posteromedial osteophytes must be avoided. Arthroscopy has limited morbidity and allows for complete diagnostic assessment. UCL reconstruction should also be considered in combination with posteromedial debridement when the UCL is torn. More challenging indications for UCL reconstruction occur when the UCL is partially torn or torn and asymptomatic. Isolated posteromedial decompression in this setting risks future development of UCL symptoms that would then need to be addressed.

Surgical Technique

As previously mentioned, elbow arthroscopy or limited excision arthrotomy are the preferred operative methods for decompression of the posterior compartment and thus treatment of VEO. Anesthesia and patient positioning should be selected based on the surgeon’s preference. The patient should be positioned supine, prone, or in lateral decubitis. When a UCL reconstruction is expected, supine position is advantageous to avoid repositioning after completing the arthroscopic portion of the procedure. However, arthroscopy can be performed in the lateral position with subsequent repositioning, repeat prepping, and draping for UCL reconstruction (Figures 5A, 5B).

Prepare for elbow arthroscopy by distending the elbow joint with normal saline to aid in protection of neurovascular structures and simplify the insertion of the scope trocar. Perform diagnostic anterior arthroscopy via the proximal anteromedial portal. Assess for presence of loose bodies and osteochondral lesions of the radiocapitellar joint, as well as osteophytes of the coronoid tip and fossa. Utilizing a spinal needle under direct visualization establish a proximal lateral portal with adequate view of the anterior compartment. Proceed to visualize the medial compartment and assess for UCL injury. Apply valgus stress while in 70° of flexion. Visualize the coronoid process and look for medial trochlea gapping of 3 mm or greater, which indicates UCL insufficiency.³⁰

Establish the posterolateral port for visualization of the posterior compartment. A posterior portal is established through the triceps tendon. Proceed to shave and ablate synovitis in order to create an adequate working space. Inspect the posteromedial olecranon, looking for any osteophytes or chondromalacia in the area (Figure 6). Examine the posterior radiocapitellar joint, looking specifically for loose bodies. The presence of loose bodies may require creating an extra mid lateral portal for removal. The ulnar nerve is located superficial to the elbow capsule and can be damaged by instruments utilized in the posteromedial gutter. As a precaution, be sure to remove suction attached to shaver. Place a curved articulating retractor in an accessory posterolateral portal to assist in protecting the ulnar nerve by retracting the capsule away from the surgical field (Figures 7A, 7B).

The osteophyte may be encased in soft tissue. Using a combination of ablation devices and shavers, the osteophyte can be exposed. The olecranon osteophyte can be removed with a small osteotome located at the border of the osteophyte and the normal olecranon. A motorized shaver or burr may also be introduced through the direct posterior portal or the posterolateral portal to complete the contouring of the olecranon (Figures 8A, 8B). Intraoperative lateral radiographs may be obtained for guidance in adequate bone removal and to ensure no bone debris is left in the soft tissues. It is critical that only pathologic osteophyte is removed and that normal olecranon is not compromised. This prevents an increase in UCL strain during valgus loading.¹⁹ However, in some non-throwing athletes, more aggressive debridement can be performed due to a smaller risk of UCL injury after posterior decompression.

Often, with the presence of osteophytes on the olecranon, there may be associated chondromalacia of the trochlea. These kissing lesions must be addressed after debridement of osteophytes. Loose flaps or frayed edges are carefully debrided and for any significant lesion the edges are contoured to a stable rim using shavers and curettes. Once altered to a well-shouldered lesion, microfracture is performed. Anterograde drilling of the lesion with perforations separated by 2 to 3 mm allow for the release of marrow elements and induction of a fibrocartilage healing response.

For an isolated posteromedial decompression, early rehabilitation begins with simple elbow flexion and extension exercises. It is important to restore flexor-pronator strength. Six weeks postoperatively, a progressive throwing program that includes plyometric exercises, neuromuscular training, and endurance exercises can be initiated. Patients can typically return to competition 3 to 4 months after surgery, if they have successfully regained preoperative range of motion, preoperative strength in the elbow, and there is no pain or tenderness on stress testing or palpation.

Outcomes

Safety and Advances in Arthroscopy

A clearer understanding of portal placement and proximity to neurovasculature in conjunction with advances in equipment have allowed for continual improvements in elbow arthroscopy techniques. There is plenty of literature indicating that arthroscopic posteromedial decompression is a safe, reliable, effective procedure, with a high rate of patient satisfaction.^22,30-34] Andrews and Carson³⁰ published one of the earliest investigations indicating the effectiveness of elbow arthroscopy utilizing objective and subjective outcome scores. They found that preoperative scores indicating patient satisfaction increased from 50% to 83%. Patients who underwent only loose body removal had the best outcomes. Andrews and Timmerman³¹ later evaluated the results of 72 professional baseball players who underwent either arthroscopic or open elbow surgery. They found that posteromedial olecranon osteophytes and intraarticular loose bodies were the most common diagnoses, present in 65% and 54% of players, respectively. In addition, a 41% reoperation rate was reported after posteromedial olecranon resection, along with 25% a rate of valgus instability necessitating UCL reconstruction. Andrews and Timmerman³¹ propose that the incidence of UCL injuries is underestimated and that UCL pathology must be treated prior to treating its secondary effects. Recently, Reddy and colleagues³² reviewed the results of 187 arthroscopic procedures. Posterior impingement, loose bodies, and osteoarthritis were the most common problems, occurring in 51%, 31%, and 22% of patients, respectively. Reported results were encouraging, with 87% good to excellent results and 85% of baseball players returning to preinjury levels.

Conclusion

An understanding of the relevant functional anatomy and the biomechanics of throwing is essential to understanding VEO. Potential concomitant valgus instability and UCL injury must be carefully assessed. Only symptomatic patients who have failed conservative treatment should undergo surgery. It is critical to avoid exacerbating and/or causing valgus instability by surgical excessively removing normal bone from the olecranon. Arthroscopy has been shown to be a safe and effective method to treat refractory cases of VEO.

The supraphysiological demands imposed on the elbow of a throwing athlete result in predictable patterns of injury. This is especially true of baseball pitchers. Knowledge of elbow anatomy, as well as the biomechanics of throwing, assist in making diagnostic and therapeutic decisions and also influence surgical technique when surgery is required. During the late cocking and early acceleration phases of throwing, valgus torque can reach 65 Nm with angular velocities of the forearm reaching 5000°/sec, which is considered the fasted recorded human movment.¹ The valgus torque and rapid extension synergistically create 3 major forces placed on the elbow. The first is a tensile stress along the medial aspect of elbow affecting the ulnar collateral ligament (UCL), flexor pronator mass, and medial epicondyle. Secondly, compression forces affect the lateral aspect of the elbow at the radiocapitellar joint. Finally, a shearing stress occurs in the posterior compartment at the posterior medial tip of the olecranon and the olecranon fossa.

These forces generated on the elbow result in predictable pathology. The recurring tensile forces applied on the medial aspect on the elbow can compromise the integrity of the UCL. It is well known that injury to the UCL leads to valgus instability. Individuals with valgus instability who continue to throw may trigger and/or aggravate injury in the posterior and lateral components of the elbow. Lateral compression forces can often reach 500 N, resulting in radiocapitellar overload syndrome, which occurs in combination with medial ligament instability and valgus extension overload.² Radiocapitellar compression may cause chondral or osteochondral fracture with resulting intra-articular loose bodes. This compression also contributes to the etiology of osteochondritis dissecans (OCD) in skeletally immature athletes. In the posterior elbow, throwing forcefully and repeatedly pushes the olecranon into the olecranon fossa. Shear stress on the medial olecranon tip and fossa, due to combined valgus and extension forces, lead to the development of osteophytes. This collection of injuries in the medial, lateral, and posterior aspects of the elbow is known as “valgus extension overload syndrome” or VEO. Symptoms in VEO can be the result of chondral lesions, loose bodies, and marginal exostosis.³

The aim of this review is to provide understanding regarding both the relevant anatomy and pathomechanics of VEO, key aspects to clinical evaluation, and effective treatment options.

Functional Anatomy

A functional comprehension of elbow anatomy and biomechanics is essential to understanding the constellation of injuries in VEO. The osseous anatomy of the elbow permits a variety of movements. These include flexion-extension and pronation-supination, which are mediated by the ulnohumeral and radiocapitellar articulations. While in full extension, the elbow has a normal valgus carrying angle of 11° to 16°. It is important to know that 50% of the elbow’s stability is attributed to the configuration of the bones.^4-6 This is especially true in varus stress while the elbow is in full extension. The soft tissues, including muscle and ligaments such as the UCL, lateral UCL, and radial UCL complexes, provide the remaining elbow stability.^4-6

The UCL complex is composed of 3 main segments known as the anterior, posterior, and oblique bundles (transverse ligament). Collectively, these bundles are responsible for providing medial elbow stability. However, each of these bundles contributes to medial elbow stability in its own way. The first and arguably the most important bundle is the anterior bundle; its most important function is providing stability against valgus stress.^4,5,7 It is composed of parallel fibers inserting on the medial coronoid process.^4,5,7 Furthermore, its eccentric location with respect to the axis of elbow allows it to provide stability throughout the full range of elbow motion.⁶ The anterior bundle can be further divided into individual anterior and posterior bands that have reciprocal functionality.^5,8,9 The anterior band acts as the chief restraint to valgus stress up to 90° of flexion.⁹ Any flexion beyond 90° renders the anterior band’s role secondary in resisting valgus stress.⁹ The posterior band’s function in resisting valgus stress is most important between 60° and full flexion, while having a secondary role in lesser degrees of flexion.^8,9 Notably, the posterior band is isometric and is more important in the overhead-throwing athlete due to the fact its primary role in resisting valgus stress occurs at higher degrees of flexion.¹⁰

The remaining posterior and oblique bundles of the UCL complex have lesser roles in maintaining elbow stability. The posterior bundle of the UCL complex is fan-shaped, originates from the medial epicondyle, and inserts onto the medial margin the semi-lunar notch. It is more slender and frailer than the anterior bundle. This is reflected in its functionality, as it plays a secondary role in elbow stability during elbow flexion beyond 90°.^4,5,8 In contrast to the anterior and posterior bundles, the oblique bundle, also known as the transverse ligament, does not cross the elbow joint. It is a thickening of the caudal most aspect of the joint capsule, which extends from the medial olecranon to the inferior medial coronoid process and as a result functions in expanding the greater sigmoid notch.⁶

The musculotendinous components of the elbow are essential to providing dynamic functional resistance to valgus stress.¹¹ These components are flexor-pronator musculature that originate from the medial epicondyle. Listed proximally to distally, the flexor-pronator muscles include pronator teres, flexor carpi radialis (FCR), palmaris longus, flexor digitorum superficialis, and the flexor carpi ulnaris (FCU).

Pathomechanics

Once familiarized with the relevant function anatomy, it is crucial to understand the mechanics of throwing in order to understand the pathomechanics of VEO. The action of overhead throwing has been divided into 6 phases.^6,12-16 Phase 4, acceleration, is the most relevant when discussing forces on elbow, since the majority of forces are generated during this state. Phase 4 represents a rapid acceleration of the upper extremity with a large forward-directed force on the arm generated by the shoulder muscles. Additionally, there is internal rotation and adduction of the humerus with rapid elbow extension terminating with ball release. The elbow accelerates up to 600,000°/sec² in a miniscule time frame of 40 to 50 milliseconds.^1,5 Immense valgus forces are exerted on the medial aspect of the elbow. The anterior bundle of the UCL bears the majority of the force, with the flexor pronator mass enabling the transmission.¹¹ The majority of injuries occur during stage 4 as a result of the stress load on the medial elbow structures like the UCL. The proceeding phases 5 (deceleration), and 6 (follow-through) involve eventual dissipation of excess kinetic energy as the elbow completely extends. The deceleration during phase 5 is rapid and powerful, occurring at about 500,000°/sec² in the short span of 50 milliseconds.^1,6,12-16 High-velocity throwing, such as baseball pitching, generates forces in the elbow that are opposed by the articular, ligamentous, and muscular portions of the arm. The ulnohumeral articulation stabilizes motion of the arm from 0° to 20° of flexion and beyond 120° of flexion. Static and dynamic soft tissues maintain stability during the remaining of 100° arc of motion.

During deceleration, the elbow undergoes terminal extension resulting in the posteromedial olecranon contacting the trochlea and the olecranon fossa with subsequent dissipation of the combined valgus force and angular moment (Figure 1). This dissipation of force creates pathologic shear and compressive forces in the posterior elbow. Poor muscular control and the traumatic abutment that occurs in the posterior compartment may further add to the pathologic forces. Reactive bone formation is induced by the repetitive compression and shear, resulting in osteophytes on the posteromedial tip of the olecranon (Figure 2). Consequent “kissing lesions” of chondromalacia may occur in the olecranon fossa and posteromedial trochlea. The subsequent development of loose bodies may also occur. The presence of osteophytes and/or loose bodies may result in posteromedial impingement (PMI).

The association between PMI of the olecranon and valgus instability has been elucidated in both clinical and biomechanical investigations.^17,18,19,20 Conway¹⁸ identified tip exostosis in 24% of lateral radiographs of 135 asymptomatic professional pitchers. Approximately one-fifth (21%) of these pitchers had >1.0 mm increased relative valgus laxity on stress radiographs. Roughly one-third (34%) of players with exostosis had >1.0 mm of increased relative valgus laxity, compared to 16% of players without exostosis formation. These results provide evidence for a probable association between PMI and valgus laxity. In biomechanical research, Ahmad and colleagues¹⁷ studied the effect of partial and full thickness UCL injuries on contact forces of the posterior elbow. Posteromedial compartments of cadaver specimens were subjected to physiologic valgus stresses while placed on pressure-senstive film. Contact area and pressure between posteromedial trochlea and olecranon were altered in the setting of UCL insufficiency, helping explain how posteromedial osteophyte formation occurs.

Additional biomechanical studies have also investigated the posteromedial olecranon’s role in functioning as a stabilizing buttress to medial tensile forces. Treating PMI with aggressive bone removal may increase valgus instability as well as strain on the UCL, leading to UCL injury following olecranon resection.^19,20 Kamineni and colleagues¹⁹ investigated strain on anterior bundle of UCL as a function of increasing applied torque and posteromedial resections of the olecranon. This investigation was done utilizing an electromagnetic tracking placed in cadaver elbows. A nonuniform change in strain was found at 3 mm of resection during flexion and valgus testing. This nonuniform change implied that removal of posteromedial olecranon beyond 3 mm made the UCL more vulnerable to injury. Follow-up investigations looked at kinematic effects of increasing valgus and varus torques and sequential posteromedial olecranon resections.²⁰ Valgus angulation of the elbow increased with all resection levels but no critical amount of olecranon resection was identified. The consensus in the literature indicates that posteromedial articulation of the elbow is a significant stabilizer to valgus stress.^17-22 Thus, normal bone should be preserved and only osteophytes should be removed during treatment.

In addition, VEO may lead to injury in the lateral compartment as well. After attenuation and insufficiency of the UCL due to repetitive stress, excessive force transmission to the lateral aspect of the elbow occurs. Compressive and rotatory forces escalate within the radiocapitellar joint, causing synovitis and osteochondral lesions.^3,23 These osteochondral lesions include osteochondritis dissecans and osteochondral fractures that may fragment and become loose bodies.

Evaluation of VEO

History

Patients will typically have a history of repetitive throwing or other repetitive overhead activity. VEO is most common in baseball pitchers but may also occur in other sports, such as tennis, football, lacrosse, gymnastics, and javelin throwing. In baseball pitchers, clinical presentation is often preceded by a decrease in pitch velocity, control, and early fatigability. It presents with elbow pain localized to the posteromedial aspect of olecranon after release of the ball, when the elbow reaches terminal extension. Patients also report limited extension, due to impinging posterior osteophytes. Also, locking and catching caused by loose bodies and chondromalacia may be present. VEO may also occur in combination with concomitant valgus instability, as well as in a patient with a prior history of valgus instability. Flexor pronator injury, ulnar neuritis, and subluxation may also be present in a patient with VEO.

Physical Examination

VEO may occur in an isolated fashion or with concomitant pathology. Therefore, a comprehensive physical examination includes evaluating the entire kinetic chain of throwing and a focused examination covering VEO and associated valgus instability. Patients may exhibit crepitus and tenderness over the posteromedial olecranon and a loss of extension with a firm end point. The extension impingement test should be performed where the elbow is snapped into terminal extension. This typically elicits pain in the posterior compartment in a patient with VEO. The arm bar test involves positioning the patient’s shoulder at 90° of forward flexion, full internal rotation, with the patient’s hand placed on the examiner’s shoulder.²⁴ The examiner pulls down on the olecranon, simulating forced extension; pain is indicative of a positive test. It is important to note if there are signs of ulnar neuritis or subluxing ulnar nerve, especially if planning to utilize medial portals during arthroscopic treatment.

Examination maneuvers for valgus instability should also be conducted during evaluation of VEO. The physical examination for valgus instability in the elbow is ideally performed with the patient seated. Secure the patient’s wrist between the examiner’s forearm and trunk, and flex the patient’s elbow between 20° and 30° to unlock the olecranon from its fossa. Proceed to apply valgus stress. This stresses the anterior band of the anterior bundle of the UCL.^6,25,26 Palpate the UCL from the medial epicondyle to the proximal ulna as valgus stress is applied. Occasionally, valgus laxity can be appreciated when compared to contralateral side. The milking maneuver is a helpful test to determine UCL injury. Pull on the patient’s thumb while the forearm is supinated, shoulder extended, and the elbow flexed beyond 90°.⁶ The milking maneuver exerts valgus stress on a flexed elbow. A patient with an injured UCL will experience the subjective feeling of apprehension and instability, with medial elbow pain.

The most sensitive test is the moving valgus stress test. This is performed with the patient in the upright position and the shoulder abducted 90°. Starting with the arm in full flexion, the examiner applies a constant valgus torque to the elbow and then rapidly extends the elbow. Reproduction of pain during range of motion from 120° to 70° represents UCL injury, while pain with extension beyond 70° represents chondral injury to the ulnohumeral joint. Be aware that the absence of increased pain with wrist flexion, along with pain localized slightly posterior to the common flexor origin, differentiates a UCL injury from flexor-pronator muscle injury.^6,26,27Examine range of motion in affected and unaffected elbows. Loss of terminal extension may be present, along with secondary to flexion contracture due to repeated attempts at healing and stabilization.²⁵

Imaging

Imaging is essential to the accurate diagnosis of VEO and related conditions. Anterior posterior (AP), lateral, and oblique radiographs of elbow (Figures 3A-3C) may show posteromedial olecranon osteophytes and/or loose bodies. Calcification of ligaments or other soft tissues may also be seen. An AP radiograph with 140° of external rotation may best visualize osteophytes on posteromedial olecranon.18 A computed tomography scan with 2-dimensional sagittal and coronal reconstruction and 3-dimensional surface rendering (Figures 4A, 4B) may best demonstrate morphological abnormalities, loose bodies, and osteophytes. Magnetic resonance imaging (MRI) is essential for assessment of soft tissues and chondral injuries. MRI may detect UCL compromise, synovial plicae, bone edema, olecranon, or stress fractures.

Treatment

Nonoperative Treatment

Treatment consists of both nonoperative and operative modalities. Nonoperative treatment methods are first line in treating VEO. Patients should modify their physical activity and rest from throwing activities. Nonsteroid anti-inflammatory drugs are appropriate to treat pain along with intra-articular corticosteroid injections of the elbow. A wide assessment of pitching mechanics should be performed in an attempt to correct errors in throwing technique and address muscular imbalances. After cessation of the resting period, the patient may initiate a progressive throwing program supervised by an experienced therapist and trainer. A plan for returning to competition should be made upon completion of the throwing program.

Operative Treatment

Surgical treatment is reserved for patients who fail nonoperative treatment. These patients have persistent symptoms of posteromedial impingement and desire to return to pre-injury level of performance. Posteromedial decompression is not recommended when provocative physical examination maneuvers are negative, regardless of presence of olecranon osteophytes on imaging. Osteophytes are an asymptomatic finding typically seen in professional baseball players and do not warrant surgical treatment.^18,28 UCL compromise is a relative contraindication to olecranon debridement as UCL injury could become symptomatic following surgery. Surgical options in the appropriate patient to decompress posterior compartment include arthroscopic olecranon debridement or limited incision arthrotomy. Excessive resection of posteromedial osteophytes must be avoided. Arthroscopy has limited morbidity and allows for complete diagnostic assessment. UCL reconstruction should also be considered in combination with posteromedial debridement when the UCL is torn. More challenging indications for UCL reconstruction occur when the UCL is partially torn or torn and asymptomatic. Isolated posteromedial decompression in this setting risks future development of UCL symptoms that would then need to be addressed.

Surgical Technique

As previously mentioned, elbow arthroscopy or limited excision arthrotomy are the preferred operative methods for decompression of the posterior compartment and thus treatment of VEO. Anesthesia and patient positioning should be selected based on the surgeon’s preference. The patient should be positioned supine, prone, or in lateral decubitis. When a UCL reconstruction is expected, supine position is advantageous to avoid repositioning after completing the arthroscopic portion of the procedure. However, arthroscopy can be performed in the lateral position with subsequent repositioning, repeat prepping, and draping for UCL reconstruction (Figures 5A, 5B).

Prepare for elbow arthroscopy by distending the elbow joint with normal saline to aid in protection of neurovascular structures and simplify the insertion of the scope trocar. Perform diagnostic anterior arthroscopy via the proximal anteromedial portal. Assess for presence of loose bodies and osteochondral lesions of the radiocapitellar joint, as well as osteophytes of the coronoid tip and fossa. Utilizing a spinal needle under direct visualization establish a proximal lateral portal with adequate view of the anterior compartment. Proceed to visualize the medial compartment and assess for UCL injury. Apply valgus stress while in 70° of flexion. Visualize the coronoid process and look for medial trochlea gapping of 3 mm or greater, which indicates UCL insufficiency.³⁰

Establish the posterolateral port for visualization of the posterior compartment. A posterior portal is established through the triceps tendon. Proceed to shave and ablate synovitis in order to create an adequate working space. Inspect the posteromedial olecranon, looking for any osteophytes or chondromalacia in the area (Figure 6). Examine the posterior radiocapitellar joint, looking specifically for loose bodies. The presence of loose bodies may require creating an extra mid lateral portal for removal. The ulnar nerve is located superficial to the elbow capsule and can be damaged by instruments utilized in the posteromedial gutter. As a precaution, be sure to remove suction attached to shaver. Place a curved articulating retractor in an accessory posterolateral portal to assist in protecting the ulnar nerve by retracting the capsule away from the surgical field (Figures 7A, 7B).

The osteophyte may be encased in soft tissue. Using a combination of ablation devices and shavers, the osteophyte can be exposed. The olecranon osteophyte can be removed with a small osteotome located at the border of the osteophyte and the normal olecranon. A motorized shaver or burr may also be introduced through the direct posterior portal or the posterolateral portal to complete the contouring of the olecranon (Figures 8A, 8B). Intraoperative lateral radiographs may be obtained for guidance in adequate bone removal and to ensure no bone debris is left in the soft tissues. It is critical that only pathologic osteophyte is removed and that normal olecranon is not compromised. This prevents an increase in UCL strain during valgus loading.¹⁹ However, in some non-throwing athletes, more aggressive debridement can be performed due to a smaller risk of UCL injury after posterior decompression.

Often, with the presence of osteophytes on the olecranon, there may be associated chondromalacia of the trochlea. These kissing lesions must be addressed after debridement of osteophytes. Loose flaps or frayed edges are carefully debrided and for any significant lesion the edges are contoured to a stable rim using shavers and curettes. Once altered to a well-shouldered lesion, microfracture is performed. Anterograde drilling of the lesion with perforations separated by 2 to 3 mm allow for the release of marrow elements and induction of a fibrocartilage healing response.

For an isolated posteromedial decompression, early rehabilitation begins with simple elbow flexion and extension exercises. It is important to restore flexor-pronator strength. Six weeks postoperatively, a progressive throwing program that includes plyometric exercises, neuromuscular training, and endurance exercises can be initiated. Patients can typically return to competition 3 to 4 months after surgery, if they have successfully regained preoperative range of motion, preoperative strength in the elbow, and there is no pain or tenderness on stress testing or palpation.

Outcomes

Safety and Advances in Arthroscopy

A clearer understanding of portal placement and proximity to neurovasculature in conjunction with advances in equipment have allowed for continual improvements in elbow arthroscopy techniques. There is plenty of literature indicating that arthroscopic posteromedial decompression is a safe, reliable, effective procedure, with a high rate of patient satisfaction.^22,30-34] Andrews and Carson³⁰ published one of the earliest investigations indicating the effectiveness of elbow arthroscopy utilizing objective and subjective outcome scores. They found that preoperative scores indicating patient satisfaction increased from 50% to 83%. Patients who underwent only loose body removal had the best outcomes. Andrews and Timmerman³¹ later evaluated the results of 72 professional baseball players who underwent either arthroscopic or open elbow surgery. They found that posteromedial olecranon osteophytes and intraarticular loose bodies were the most common diagnoses, present in 65% and 54% of players, respectively. In addition, a 41% reoperation rate was reported after posteromedial olecranon resection, along with 25% a rate of valgus instability necessitating UCL reconstruction. Andrews and Timmerman³¹ propose that the incidence of UCL injuries is underestimated and that UCL pathology must be treated prior to treating its secondary effects. Recently, Reddy and colleagues³² reviewed the results of 187 arthroscopic procedures. Posterior impingement, loose bodies, and osteoarthritis were the most common problems, occurring in 51%, 31%, and 22% of patients, respectively. Reported results were encouraging, with 87% good to excellent results and 85% of baseball players returning to preinjury levels.

Conclusion

An understanding of the relevant functional anatomy and the biomechanics of throwing is essential to understanding VEO. Potential concomitant valgus instability and UCL injury must be carefully assessed. Only symptomatic patients who have failed conservative treatment should undergo surgery. It is critical to avoid exacerbating and/or causing valgus instability by surgical excessively removing normal bone from the olecranon. Arthroscopy has been shown to be a safe and effective method to treat refractory cases of VEO.

For the last 20 years, injuries resulting in time out of play have been on the rise in Major League Baseball (MLB), and those affecting the back are no exception.^1,2 In the first comprehensive report on injuries in MLB players, back injuries resulted in a mean of 1016 disabled list days per season from 1995 to 1999.¹ Similarly, core and back injuries were responsible for 359 disabled list designations from 2002 to 2008. This represented 11.7% of all injuries resulting in time out of play during that time span.² During that time, back injury prevalence ranked 6th highest of all possible body regions (out of 17), and both position players and pitchers were similarly affected (7.8% and 7.4% of all injuries, respectively).² These injuries often result in a significant time out of play and can have a tremendous impact on player health. A healthy, stable, and well-functioning lumbar spine is a prerequisite for nearly all baseball-related activities, including pitching, throwing, batting, and running. Accordingly, even minor lumbar spine injuries may profoundly influence baseball performance. Despite this, less is currently known about the true epidemiology and impact of back injuries in professional baseball compared to other professional sporting organizations.³

The most common causes of low back pain and injury in elite baseball players include muscle strains, stress fractures (spondylolysis), annular tears, disc herniation, stenosis, transverse process fractures, facetogenic pain, and sacroiliac (SI) joint arthropathy.^4-8 These injuries present in a variety of ways with varying symptomatology. Accordingly, a thorough understanding and comprehensive approach to the diagnosis and treatment of these injuries is necessary. The purpose of this article is to discuss the current state of lumbar spine injuries in professional baseball players. Specifically, we will discuss the critical role of the spine in baseball activities, common causes of injury, tips for making the diagnosis, treatment options, outcomes, and injury prevention and rehabilitation strategies.

Role of the Spine in Baseball

The spine and core musculature are responsible for positioning the head, shoulders, and upper extremities in space over the hips and lower extremities. Proper maintenance of this relationship is required during all phases of throwing, pitching, running, and hitting. During these activities, the spine may dynamically flex, extend, rotate, and laterally bend as needed to keep the body balanced with the head centered over the trunk.

Pitching and Throwing

Whether pitching from the wind-up or the stretch, the head begins centered over the hips and pelvis. As the pitching motion progresses, the hips undergo rotation, flexion, extension, abduction, and circumduction. While this is occurring, the shoulders and upper truck must bend, rotate, and translate toward home plate with the body. Just prior to front foot contact, trunk rotation averages 55 ± 6° with a maximal mean angular acceleration of 11,600 ± 3100°/s². ⁹ In order for the body to remain balanced, controlled, and synchronized throughout this delivery, the lumbar spine and core musculature must work diligently to stabilize the entire kinetic chain. Of all the trunk muscles (paraspinal, rectus abdominis, obliques, and glutei), the lumbar paraspinal muscles often work the hardest during the pitching motion, demonstrating activity increases ranging from 100% to 400%.¹⁰ Accordingly, it is not uncommon for pitchers to develop SI joint or lumbar facet joint pain due to this high degree of torsional strain exerted on the low back.⁴ Poor lumbopelvic control has been shown to be a predictor of subsequent injury, and the degree of lumbopelvic dysfunction is proportional to injury severity in MLB pitchers.⁵

Hitting

Similar to pitching, hitting involves a complex combination of movements from the upper and lower extremities that must be balanced by the core and spine. Although numerous movements occur simultaneously, rotational motion is primarily responsible for generating power. The trunk rotates an average of 46 ± 9° during the swing and reaches a maximal angular acceleration of 7200 ± 2800°/s² just after contact.⁹ During this period of rapid torsion, the spine must rotate in conjunction with the hips and shoulders to create a stable cylinder and axis of rotation. The spine and core are responsible for synchronizing rotation to ensure that hip and shoulder parallelism is maintained from swing initiation to ball contact. If the body does not rotate as a unit, the position of the head is affected and the batter’s ability to see the ball may be compromised. Additionally, if delivery of the shoulders lags too far behind that of the hips, the position of the hands (and bat) in space is adversely affected. The entire kinetic chain must remain balanced, coordinated, precisely timed, and standardized throughout the entire swing from initial trigger to final follow-through. The lumbar spine plays a critical role in each of these steps. If lumbar spine mechanics are not sound, this can have significant adverse effects on batting performance and may predispose hitters to injury.⁴

Common Etiologies for Spinal Injury

The vast majority of baseball players who experience lumbar pain will have injuries that can be classified as mechanical back pain (ie, spondylolysis, annular tears, facetogenic pain, SI joint arthropathy, or muscle injuries) (Table). Although less likely to occur, nerve entrapment or impingement syndromes (ie, disc herniation, stenosis, and peripheral nerve entrapment) have been observed in professional baseball players. Finally, more concerning pathologies such as infection and tumor are extremely rare, but they must not be overlooked in this high-demand patient population.

Stress Fracture or Spondylolysis

In young athletic patients, up to one-third of those with low back pain may have evidence of a lumbar stress fracture on bone scan.^11,12 This is particularly true for athletes who undergo repetitive lumbar extension and rotation, such as linemen, gymnasts, wrestlers, weight lifters, and baseball players.^4,13 Although the majority of lumbar stress fractures occur at the pars interarticularis, they can occur in the pedicle or articular process (Figure 1). Most spondylolytic lesions do not progress to spondylolisthesis, especially once patients reach skeletal maturity. Because the fifth lumbar vertebra represents the transition from the lumbar to the sacral spine, most stress fractures occur at L5. These typically present as localized low back pain that worsens with flexion, extension, and rotation.

Muscle Injury

One of the most common causes of low back pain in athletes is muscle strains and spasms. Because the lumbar paraspinal muscles are extremely active during throwing and hitting,¹⁰ they are particularly susceptible to injury. This is particularly true in deconditioned athletes or those who report to spring training having not adequately maintained strength and flexibility through the off-season.^4,5 These injuries typically present in an acute fashion with an obvious inciting incident. Players may have a history of similar muscle injuries in the past. On examination, they tend to have difficulty maintaining normal posture or ranging the spine through a full arc of motion. Localized, superficial tenderness to palpation in the injured muscle is a key component of the diagnosis.

Annular Tears and Disc Herniation

These injuries typically occur as the result of a combination of compressive and rotary forces on the lumbar spine that overcome the ability of the annulus fibrosus to resist hoop stresses. Patients with annular tears typically present with severe lower back pain that may be accompanied by spasm and pain radiation into the buttock or lower extremities. Pain is usually worsened by valsalva, coughing, sneezing, or bearing down.⁴ Although annular tears can occur in isolation, they can also lead to herniation of the nucleus pulposus into the spinal canal (Figure 2). Depending on the location and severity of the herniation, nerve entrapment or impingement can occur. This may initially present as pain that radiates into the lower extremities in a dermatomal fashion. As the herniation progresses, decreased sensation and weakness may develop.

Facet Joint Pain

Facetogenic pain can occur as the result of degenerative changes, trauma, or joint inflammation. Facet injury typically occurs during rotation while the back is extended.⁴ This results in localized pain and tenderness that can be reproduced by loading the facet joint (lumbar extension) during the examination, and patients will often demonstrate discomfort and altered motion when extending the flexed back.

Sacroiliac Joint Pain

Although pain in the region of the SI joint is very common, much of this may actually be referred from more centrally located neuromotion segments.⁴ SI joint pathology can occur as a result of trauma, degeneration, or inflammatory processes as is seen in ankylosing spondylitis (AS). Patients with AS typically present with a gradual onset of progressive stiffness and pain in the low back and hips that is worse in the morning or following periods of inactivity. It is most common in Caucasian males in their second to fourth decades.¹⁴ Although 80% to 95% of patients with AS will test positive for human leukocyte antigen B27 (HLA-B27), it is important to note that the vast majority of people with HLA-B27 do not go on to develop AS.¹⁴ Regardless of the cause, SI joint pain can be very debilitating and negatively impact all baseball-related activities.

Stenosis

Lumbar stenosis may develop from arthritic changes, disc protrusion, facet hypertrophy, or ligament ossification. In this young, athletic population, congenital stenosis should also be a consideration. Patients with congenital stenosis at baseline are at increased risk for developing neurologic symptoms from disc protrusion or other acquired spinal pathology. Lumbar stenosis generally manifests as a gradual onset of progressive low back pain with radicular symptoms or neurogenic claudication.⁴

Making the Diagnosis

History

When identifying the cause of any musculoskeletal complaint, the diagnosis begins with a thorough history. In addition to the standard components of the history, such as timing, severity, relation to activity, exacerbating factors, associated symptoms, and prior treatments, Watkins and colleagues4 have outlined a number of key factors that should be determined when specifically evaluating the athlete with low back pain.These include quantification of the morbidity, identification of contributing psychosocial factors, ruling out of urgent diagnoses (ie, neoplasm, infection, rapidly progressive neurologic deficits, cauda equina, and paralysis), determination of injury type and duration, identification of the clinical syndrome/etiology, pinpointing the location of the pathology (what nerve at what level?), and quantification of back versus leg symptoms. Answers to these questions will set the framework for an appropriately directed physical examination, imaging, and diagnostic tests.

Physical Examination

The physical examination begins by observing the patient or player walk across the playing field, training room, or examination room, paying attention to posture, gait, and overall body movement. Many patients with lumbar injuries will demonstrate adaptive patterns of motion in an attempt to accommodate their pain. This may be seen during baseball-related activities such as throwing, batting, or running. The spine should be visualized and palpated for malalignment while standing erect and during forward bending. If possible, motion should be assessed in rotation, lateral bending, and the flexion and extension planes. Special attention should be paid to any positions or maneuvers that reproduce pain or neurologic symptoms. Areas of tenderness and radiating pain should be fully palpated. A full neurologic examination consisting of manual muscle testing, sensory examination, and reflex evaluation of both the upper and lower extremities should be performed. Numerous special tests and neurologic stretch maneuvers that assess specific lumbar nerve roots have been described.¹⁵

Imaging and Diagnostic Tests

Depending on the history and physical examination, imaging of the lumbar spine is not always warranted in the acute setting. This is especially the case if muscle injury, herniation, or annular tears are suspected. In cases of persistent pain, trauma, or suspected neoplasia, imaging is generally warranted. When x-rays are negative and spondylolysis is suspected, bone scan with lumbar single photon emission computed tomography (SPECT) is the most sensitive test.¹⁶ SPECT scans are positive in active spondylolysis because the radio-nucleotide is taken up by active, bone-forming osteoblasts. Quiescent stress fractures that are not apparent on SPECT scans are generally chronic and painless.⁴ If the SPECT scan is positive, the injury can be further characterized by computed tomography (CT) (Figure 1), which can distinguish between spondylolysis, osteoid osteoma, osteoblastoma, acute fracture, or arthritic degeneration. When the SPECT is negative, or if neural impingement is suspected, magnetic resonance imaging (MRI) (Figure 2) is likely the best diagnostic imaging tool. MRI allows identification of bone edema, disc herniation, annular disruption, disc desiccation, stenosis, and nerve entrapment. Finally, when attempting to distinguish between central and peripheral nerve entrapment syndromes, an electromyogram (EMG) or nerve conduction study (NCS) is a reliable way to identify the location of injury.

Treatment and Outcomes

The approach to a patient with low back pain begins with identification of the etiology and discontinuation of the activities that reproduce pain.⁴ Trunk stabilization exercises and anti-inflammatory medications are the mainstays of treatment regardless of the cause of the lumbar spinal injury in the baseball player.⁴

Stress Fracture or Spondylolysis

Management of symptomatic spondylolysis or spondylolisthesis in the athlete initially consists of conservative treatment, which achieves good to excellent long-term outcomes and return to play in 70% to 90% of athletes, especially for acute injuries.^17-19 After stopping the activity that causes the pain, trunk stabilization exercises should be started as soon as tolerated with the use of non-steroidal anti-inflammatory medications (NSAIDs), oral steroids, and spinal injections to control symptoms and permit initiation of the rehabilitation program.⁴ Although bracing is a commonly used adjunctive treatment, a recent meta-analysis did not demonstrate any difference in clinical outcomes between patients treated with a brace compared to non-braced controls.²⁰

Surgical indications for the treatment of spondylolysis or spondylolisthesis are limited; however, failure of nonoperative treatment after 6 months is a reasonable time to consider surgery.17 The spondylolytic defect can often be repaired directly using hook screws, translaminar screws, wiring, pedicle screws, or image-guided lag screws across the lesion with grafting.4 Lumbar spinal fusion is less successful in professional athletes due to the high demands placed on adjacent levels as well as the time required for the fusion to heal.4 Bony union can be determined by a CT scan at 6 months postoperatively if the patient has met appropriate return to play criteria.4

Muscle Injury

Management of lumbar sprains and strains typically includes restricting painful postures and a rehabilitation program that focuses on core strengthening within a pain-free arc of motion.²¹ Because acute injuries typically resolve quickly and spontaneously, a short interval of decreased activity, icing, NSAIDs, and stretching followed by focused strength training is appropriate before return to sports activity.²²

Annular Tears and Disc Herniation

Initial management of baseball players with acute lumbar disc herniation and/or annular tears consists of rest for up to 5 days followed by physical therapy and NSAIDs, Medrol Dose pak, or epidural injections.⁴ Professional baseball players return to play at high rates following a herniated lumbar disc.⁶ Earhart and colleagues6 found that 97.1% of players returned to play at an average time of 6.6 months from the time of injury. When stratified by position, all pitchers (29 of 29) returned to competitive play after operative or nonoperative management, while 38 of 40 hitters returned.⁶ The average career length after lumbar disc herniation in the professional baseball player is between 4.1 and 5.3 years or between 256 and 471 games.^6,23 Other work has suggested that players undergoing operative treatment for lumbar herniation had shorter career lengths; however, patients in the operative group tended to be older at the time of injury.²³

Emphasis should be placed on nonoperative management of baseball players with disc pathology except in cases of cauda equina syndrome.⁴ Hitters and pitchers who require surgery have demonstrated decreased 1-year and 3-year postoperative statistical performance compared to preinjury levels.⁶ No significant changes in any performance statistic were seen in baseball following nonoperative management.⁶ Consequently, indications for surgery in the baseball player with lumbar disc pathology includes cauda equina syndrome, progressive neurologic deficit, sufficient morbidity, failure of conservative care, a lesion that can be corrected safely with surgery, and the ability for the patient to comply with a comprehensive postoperative rehabilitation program.⁴ Operative treatment typically consists of a lumbar microdiscectomy and/or laminotomy. ^4,6

Facet Joint Pain

The mainstay of therapy in patients with facet joint pain consists of analgesia and a trunk stabilization program.²⁴ Lumbar zygapophysial joint injections and radiofrequency denervation can be considered if the patient fails 4 weeks of directed conservative treatment.^24,25 Injections may be useful in select patients; however, the literature supporting the use of lumbar facet joint injections or radiofrequency denervation for facetogenic pain is limited.^24,25

Sacroiliac Joint Pain

Acute injury of the SI joint can be treated with NSAIDs, icing, and relative rest.²⁶ Mobilization of the SI joint in addition to correcting any asymmetries in muscle length or stiffness should be started and progressed as soon as tolerated within a pain-free range of motion.²⁶ Rehabilitation should correct biomechanical deficits and maladaptation with a special focus on agonist and antagonist muscle groups across the sacrum and ilium.²⁶ Treatment of AS in the athlete should emphasize symptom control, as there is no definite treatment. For patients with AS, other long-term therapeutic options include sulfasalazine, methotrexate, thalidomide, and anti-tumor necrosis factor therapies.¹⁴

Stenosis

Lumbar spinal stenosis, whether congenital or acquired, should initially be managed conservatively.²⁷ Although they do not alter the progression of the disease, epidural steroids and local injections may temporarily decrease symptoms in approximately 40% of cases.²⁷ Those who fail conservative therapy after 3 months may be candidates for surgical decompression and/or fusion.^27,28 However, surgical treatment for lumbar spinal stenosis in elite baseball players has not been thoroughly studied, so the long-term prognosis is not well documented.²⁷

Rehabilitation and Prevention of Injuries

After an appropriate diagnosis has been made, a structured rehabilitation process should commence. During rehabilitation, it is of primary importance that deep core stabilization is established. As an initial step in this process, athletes are trained to initiate deep core stabilization with breathing techniques in a static, supine position.²⁹ Proper diaphragm activation with co-contractions of the transverse abdominis (TA) and pelvic floor has been shown to increase lumbar spine stability.³⁰ This will allow for an increase in intra-abdominal pressure (IAP) and improved stabilization of the lumbar spine, creating a muscular cylinder between the bottom of the rib cage and top of the pelvis. These activities are initiated in the supine position but are soon advanced as upper and lower extremity movement against resistance is added. It is important to make sure IAP and contraction of the TA is maintained throughout this sequence of progression.

Once deep core stabilization has been established, athletes are progressed to global muscle training and kinetic linking in all 3 planes of movement. This is an important phase, as lumbar stability is a result of coordinated muscle activation involving many muscles.³¹ This program progresses from supine breathing exercises to a modified side bridge position to enhance core activation along with frontal plane stability. Next, athletes are progressed to a half kneeling position and then on to standing. Rotational activities are introduced starting with isometric holds progressing to chops/lifts and rotational medicine ball toss. During these tasks, focus should be on quality of movement and maintenance of core activation. Endurance of these muscles should be trained during this process. Appropriate pain-free and safe cardiovascular exercise, such as walking, biking, swimming, and jogging, should be performed throughout each stage in the rehabilitation process. Activities should be halted with any increase in pain. At the completion of the rehabilitation process, it is important to observe the athlete while performing sport-specific tasks. Spinal stabilization must be translational and monitored by observing maintenance of the “cylinder” from the training room to sports specific movements.

Since poor lumbar control has been associated with increased amount of time on the disabled list,⁵ it would be ideal to identify those at risk of injury before problems arise. Conte and colleagues32 have shown that core muscle strains could be a result of muscle imbalance or improper pitching or hitting technique. Other work has demonstrated that pitchers with poor lumbopelvic control did not perform as well as those with superior control.³³ By assessing spinal stability and biomechanics at baseline, we may be able to identify those at risk. Pitchers with suboptimal spinal stabilization can present with an unstable balance phase, increased amounts of hyperextension of the lumbar spine from the moment of max cocking through ball release, as well as increased lateral trunk tilt at ball release. Correcting these flaws and increasing deep core stabilization can prevent injuries and improve performance.

Summary

A stable, well-functioning lumbar spine is vital to nearly every baseball-related activity, including pitching, throwing, batting, fielding, and running. The spine serves as a critical link in the kinetic chain between the upper and lower extremities. Due to the high demand on the lumbar spine, injuries to this area represent a significant amount of time out of play in MLB. Initial treatment typically consists of a comprehensive nonoperative rehabilitation process involving analgesics, rest, and therapy focusing on core stabilization. Because poor lumbopelvic control and mechanics have been demonstrated to increase injury risk, preemptive spinal and core stabilization is likely an appropriate step towards injury prevention.

For the last 20 years, injuries resulting in time out of play have been on the rise in Major League Baseball (MLB), and those affecting the back are no exception.^1,2 In the first comprehensive report on injuries in MLB players, back injuries resulted in a mean of 1016 disabled list days per season from 1995 to 1999.¹ Similarly, core and back injuries were responsible for 359 disabled list designations from 2002 to 2008. This represented 11.7% of all injuries resulting in time out of play during that time span.² During that time, back injury prevalence ranked 6th highest of all possible body regions (out of 17), and both position players and pitchers were similarly affected (7.8% and 7.4% of all injuries, respectively).² These injuries often result in a significant time out of play and can have a tremendous impact on player health. A healthy, stable, and well-functioning lumbar spine is a prerequisite for nearly all baseball-related activities, including pitching, throwing, batting, and running. Accordingly, even minor lumbar spine injuries may profoundly influence baseball performance. Despite this, less is currently known about the true epidemiology and impact of back injuries in professional baseball compared to other professional sporting organizations.³

The most common causes of low back pain and injury in elite baseball players include muscle strains, stress fractures (spondylolysis), annular tears, disc herniation, stenosis, transverse process fractures, facetogenic pain, and sacroiliac (SI) joint arthropathy.^4-8 These injuries present in a variety of ways with varying symptomatology. Accordingly, a thorough understanding and comprehensive approach to the diagnosis and treatment of these injuries is necessary. The purpose of this article is to discuss the current state of lumbar spine injuries in professional baseball players. Specifically, we will discuss the critical role of the spine in baseball activities, common causes of injury, tips for making the diagnosis, treatment options, outcomes, and injury prevention and rehabilitation strategies.

Role of the Spine in Baseball

The spine and core musculature are responsible for positioning the head, shoulders, and upper extremities in space over the hips and lower extremities. Proper maintenance of this relationship is required during all phases of throwing, pitching, running, and hitting. During these activities, the spine may dynamically flex, extend, rotate, and laterally bend as needed to keep the body balanced with the head centered over the trunk.

Pitching and Throwing

Whether pitching from the wind-up or the stretch, the head begins centered over the hips and pelvis. As the pitching motion progresses, the hips undergo rotation, flexion, extension, abduction, and circumduction. While this is occurring, the shoulders and upper truck must bend, rotate, and translate toward home plate with the body. Just prior to front foot contact, trunk rotation averages 55 ± 6° with a maximal mean angular acceleration of 11,600 ± 3100°/s². ⁹ In order for the body to remain balanced, controlled, and synchronized throughout this delivery, the lumbar spine and core musculature must work diligently to stabilize the entire kinetic chain. Of all the trunk muscles (paraspinal, rectus abdominis, obliques, and glutei), the lumbar paraspinal muscles often work the hardest during the pitching motion, demonstrating activity increases ranging from 100% to 400%.¹⁰ Accordingly, it is not uncommon for pitchers to develop SI joint or lumbar facet joint pain due to this high degree of torsional strain exerted on the low back.⁴ Poor lumbopelvic control has been shown to be a predictor of subsequent injury, and the degree of lumbopelvic dysfunction is proportional to injury severity in MLB pitchers.⁵

Hitting

Similar to pitching, hitting involves a complex combination of movements from the upper and lower extremities that must be balanced by the core and spine. Although numerous movements occur simultaneously, rotational motion is primarily responsible for generating power. The trunk rotates an average of 46 ± 9° during the swing and reaches a maximal angular acceleration of 7200 ± 2800°/s² just after contact.⁹ During this period of rapid torsion, the spine must rotate in conjunction with the hips and shoulders to create a stable cylinder and axis of rotation. The spine and core are responsible for synchronizing rotation to ensure that hip and shoulder parallelism is maintained from swing initiation to ball contact. If the body does not rotate as a unit, the position of the head is affected and the batter’s ability to see the ball may be compromised. Additionally, if delivery of the shoulders lags too far behind that of the hips, the position of the hands (and bat) in space is adversely affected. The entire kinetic chain must remain balanced, coordinated, precisely timed, and standardized throughout the entire swing from initial trigger to final follow-through. The lumbar spine plays a critical role in each of these steps. If lumbar spine mechanics are not sound, this can have significant adverse effects on batting performance and may predispose hitters to injury.⁴

Common Etiologies for Spinal Injury

The vast majority of baseball players who experience lumbar pain will have injuries that can be classified as mechanical back pain (ie, spondylolysis, annular tears, facetogenic pain, SI joint arthropathy, or muscle injuries) (Table). Although less likely to occur, nerve entrapment or impingement syndromes (ie, disc herniation, stenosis, and peripheral nerve entrapment) have been observed in professional baseball players. Finally, more concerning pathologies such as infection and tumor are extremely rare, but they must not be overlooked in this high-demand patient population.

Stress Fracture or Spondylolysis

In young athletic patients, up to one-third of those with low back pain may have evidence of a lumbar stress fracture on bone scan.^11,12 This is particularly true for athletes who undergo repetitive lumbar extension and rotation, such as linemen, gymnasts, wrestlers, weight lifters, and baseball players.^4,13 Although the majority of lumbar stress fractures occur at the pars interarticularis, they can occur in the pedicle or articular process (Figure 1). Most spondylolytic lesions do not progress to spondylolisthesis, especially once patients reach skeletal maturity. Because the fifth lumbar vertebra represents the transition from the lumbar to the sacral spine, most stress fractures occur at L5. These typically present as localized low back pain that worsens with flexion, extension, and rotation.

Muscle Injury

One of the most common causes of low back pain in athletes is muscle strains and spasms. Because the lumbar paraspinal muscles are extremely active during throwing and hitting,¹⁰ they are particularly susceptible to injury. This is particularly true in deconditioned athletes or those who report to spring training having not adequately maintained strength and flexibility through the off-season.^4,5 These injuries typically present in an acute fashion with an obvious inciting incident. Players may have a history of similar muscle injuries in the past. On examination, they tend to have difficulty maintaining normal posture or ranging the spine through a full arc of motion. Localized, superficial tenderness to palpation in the injured muscle is a key component of the diagnosis.

Annular Tears and Disc Herniation

These injuries typically occur as the result of a combination of compressive and rotary forces on the lumbar spine that overcome the ability of the annulus fibrosus to resist hoop stresses. Patients with annular tears typically present with severe lower back pain that may be accompanied by spasm and pain radiation into the buttock or lower extremities. Pain is usually worsened by valsalva, coughing, sneezing, or bearing down.⁴ Although annular tears can occur in isolation, they can also lead to herniation of the nucleus pulposus into the spinal canal (Figure 2). Depending on the location and severity of the herniation, nerve entrapment or impingement can occur. This may initially present as pain that radiates into the lower extremities in a dermatomal fashion. As the herniation progresses, decreased sensation and weakness may develop.

Facet Joint Pain

Facetogenic pain can occur as the result of degenerative changes, trauma, or joint inflammation. Facet injury typically occurs during rotation while the back is extended.⁴ This results in localized pain and tenderness that can be reproduced by loading the facet joint (lumbar extension) during the examination, and patients will often demonstrate discomfort and altered motion when extending the flexed back.

Sacroiliac Joint Pain

Although pain in the region of the SI joint is very common, much of this may actually be referred from more centrally located neuromotion segments.⁴ SI joint pathology can occur as a result of trauma, degeneration, or inflammatory processes as is seen in ankylosing spondylitis (AS). Patients with AS typically present with a gradual onset of progressive stiffness and pain in the low back and hips that is worse in the morning or following periods of inactivity. It is most common in Caucasian males in their second to fourth decades.¹⁴ Although 80% to 95% of patients with AS will test positive for human leukocyte antigen B27 (HLA-B27), it is important to note that the vast majority of people with HLA-B27 do not go on to develop AS.¹⁴ Regardless of the cause, SI joint pain can be very debilitating and negatively impact all baseball-related activities.

Stenosis

Lumbar stenosis may develop from arthritic changes, disc protrusion, facet hypertrophy, or ligament ossification. In this young, athletic population, congenital stenosis should also be a consideration. Patients with congenital stenosis at baseline are at increased risk for developing neurologic symptoms from disc protrusion or other acquired spinal pathology. Lumbar stenosis generally manifests as a gradual onset of progressive low back pain with radicular symptoms or neurogenic claudication.⁴

Making the Diagnosis

History

When identifying the cause of any musculoskeletal complaint, the diagnosis begins with a thorough history. In addition to the standard components of the history, such as timing, severity, relation to activity, exacerbating factors, associated symptoms, and prior treatments, Watkins and colleagues4 have outlined a number of key factors that should be determined when specifically evaluating the athlete with low back pain.These include quantification of the morbidity, identification of contributing psychosocial factors, ruling out of urgent diagnoses (ie, neoplasm, infection, rapidly progressive neurologic deficits, cauda equina, and paralysis), determination of injury type and duration, identification of the clinical syndrome/etiology, pinpointing the location of the pathology (what nerve at what level?), and quantification of back versus leg symptoms. Answers to these questions will set the framework for an appropriately directed physical examination, imaging, and diagnostic tests.

Physical Examination

The physical examination begins by observing the patient or player walk across the playing field, training room, or examination room, paying attention to posture, gait, and overall body movement. Many patients with lumbar injuries will demonstrate adaptive patterns of motion in an attempt to accommodate their pain. This may be seen during baseball-related activities such as throwing, batting, or running. The spine should be visualized and palpated for malalignment while standing erect and during forward bending. If possible, motion should be assessed in rotation, lateral bending, and the flexion and extension planes. Special attention should be paid to any positions or maneuvers that reproduce pain or neurologic symptoms. Areas of tenderness and radiating pain should be fully palpated. A full neurologic examination consisting of manual muscle testing, sensory examination, and reflex evaluation of both the upper and lower extremities should be performed. Numerous special tests and neurologic stretch maneuvers that assess specific lumbar nerve roots have been described.¹⁵

Imaging and Diagnostic Tests

Depending on the history and physical examination, imaging of the lumbar spine is not always warranted in the acute setting. This is especially the case if muscle injury, herniation, or annular tears are suspected. In cases of persistent pain, trauma, or suspected neoplasia, imaging is generally warranted. When x-rays are negative and spondylolysis is suspected, bone scan with lumbar single photon emission computed tomography (SPECT) is the most sensitive test.¹⁶ SPECT scans are positive in active spondylolysis because the radio-nucleotide is taken up by active, bone-forming osteoblasts. Quiescent stress fractures that are not apparent on SPECT scans are generally chronic and painless.⁴ If the SPECT scan is positive, the injury can be further characterized by computed tomography (CT) (Figure 1), which can distinguish between spondylolysis, osteoid osteoma, osteoblastoma, acute fracture, or arthritic degeneration. When the SPECT is negative, or if neural impingement is suspected, magnetic resonance imaging (MRI) (Figure 2) is likely the best diagnostic imaging tool. MRI allows identification of bone edema, disc herniation, annular disruption, disc desiccation, stenosis, and nerve entrapment. Finally, when attempting to distinguish between central and peripheral nerve entrapment syndromes, an electromyogram (EMG) or nerve conduction study (NCS) is a reliable way to identify the location of injury.

Treatment and Outcomes

The approach to a patient with low back pain begins with identification of the etiology and discontinuation of the activities that reproduce pain.⁴ Trunk stabilization exercises and anti-inflammatory medications are the mainstays of treatment regardless of the cause of the lumbar spinal injury in the baseball player.⁴

Stress Fracture or Spondylolysis

Management of symptomatic spondylolysis or spondylolisthesis in the athlete initially consists of conservative treatment, which achieves good to excellent long-term outcomes and return to play in 70% to 90% of athletes, especially for acute injuries.^17-19 After stopping the activity that causes the pain, trunk stabilization exercises should be started as soon as tolerated with the use of non-steroidal anti-inflammatory medications (NSAIDs), oral steroids, and spinal injections to control symptoms and permit initiation of the rehabilitation program.⁴ Although bracing is a commonly used adjunctive treatment, a recent meta-analysis did not demonstrate any difference in clinical outcomes between patients treated with a brace compared to non-braced controls.²⁰

Surgical indications for the treatment of spondylolysis or spondylolisthesis are limited; however, failure of nonoperative treatment after 6 months is a reasonable time to consider surgery.17 The spondylolytic defect can often be repaired directly using hook screws, translaminar screws, wiring, pedicle screws, or image-guided lag screws across the lesion with grafting.4 Lumbar spinal fusion is less successful in professional athletes due to the high demands placed on adjacent levels as well as the time required for the fusion to heal.4 Bony union can be determined by a CT scan at 6 months postoperatively if the patient has met appropriate return to play criteria.4

Muscle Injury

Management of lumbar sprains and strains typically includes restricting painful postures and a rehabilitation program that focuses on core strengthening within a pain-free arc of motion.²¹ Because acute injuries typically resolve quickly and spontaneously, a short interval of decreased activity, icing, NSAIDs, and stretching followed by focused strength training is appropriate before return to sports activity.²²

Annular Tears and Disc Herniation

Initial management of baseball players with acute lumbar disc herniation and/or annular tears consists of rest for up to 5 days followed by physical therapy and NSAIDs, Medrol Dose pak, or epidural injections.⁴ Professional baseball players return to play at high rates following a herniated lumbar disc.⁶ Earhart and colleagues6 found that 97.1% of players returned to play at an average time of 6.6 months from the time of injury. When stratified by position, all pitchers (29 of 29) returned to competitive play after operative or nonoperative management, while 38 of 40 hitters returned.⁶ The average career length after lumbar disc herniation in the professional baseball player is between 4.1 and 5.3 years or between 256 and 471 games.^6,23 Other work has suggested that players undergoing operative treatment for lumbar herniation had shorter career lengths; however, patients in the operative group tended to be older at the time of injury.²³

Emphasis should be placed on nonoperative management of baseball players with disc pathology except in cases of cauda equina syndrome.⁴ Hitters and pitchers who require surgery have demonstrated decreased 1-year and 3-year postoperative statistical performance compared to preinjury levels.⁶ No significant changes in any performance statistic were seen in baseball following nonoperative management.⁶ Consequently, indications for surgery in the baseball player with lumbar disc pathology includes cauda equina syndrome, progressive neurologic deficit, sufficient morbidity, failure of conservative care, a lesion that can be corrected safely with surgery, and the ability for the patient to comply with a comprehensive postoperative rehabilitation program.⁴ Operative treatment typically consists of a lumbar microdiscectomy and/or laminotomy. ^4,6

Facet Joint Pain

The mainstay of therapy in patients with facet joint pain consists of analgesia and a trunk stabilization program.²⁴ Lumbar zygapophysial joint injections and radiofrequency denervation can be considered if the patient fails 4 weeks of directed conservative treatment.^24,25 Injections may be useful in select patients; however, the literature supporting the use of lumbar facet joint injections or radiofrequency denervation for facetogenic pain is limited.^24,25

Sacroiliac Joint Pain

Acute injury of the SI joint can be treated with NSAIDs, icing, and relative rest.²⁶ Mobilization of the SI joint in addition to correcting any asymmetries in muscle length or stiffness should be started and progressed as soon as tolerated within a pain-free range of motion.²⁶ Rehabilitation should correct biomechanical deficits and maladaptation with a special focus on agonist and antagonist muscle groups across the sacrum and ilium.²⁶ Treatment of AS in the athlete should emphasize symptom control, as there is no definite treatment. For patients with AS, other long-term therapeutic options include sulfasalazine, methotrexate, thalidomide, and anti-tumor necrosis factor therapies.¹⁴

Stenosis

Lumbar spinal stenosis, whether congenital or acquired, should initially be managed conservatively.²⁷ Although they do not alter the progression of the disease, epidural steroids and local injections may temporarily decrease symptoms in approximately 40% of cases.²⁷ Those who fail conservative therapy after 3 months may be candidates for surgical decompression and/or fusion.^27,28 However, surgical treatment for lumbar spinal stenosis in elite baseball players has not been thoroughly studied, so the long-term prognosis is not well documented.²⁷

Rehabilitation and Prevention of Injuries

After an appropriate diagnosis has been made, a structured rehabilitation process should commence. During rehabilitation, it is of primary importance that deep core stabilization is established. As an initial step in this process, athletes are trained to initiate deep core stabilization with breathing techniques in a static, supine position.²⁹ Proper diaphragm activation with co-contractions of the transverse abdominis (TA) and pelvic floor has been shown to increase lumbar spine stability.³⁰ This will allow for an increase in intra-abdominal pressure (IAP) and improved stabilization of the lumbar spine, creating a muscular cylinder between the bottom of the rib cage and top of the pelvis. These activities are initiated in the supine position but are soon advanced as upper and lower extremity movement against resistance is added. It is important to make sure IAP and contraction of the TA is maintained throughout this sequence of progression.

Once deep core stabilization has been established, athletes are progressed to global muscle training and kinetic linking in all 3 planes of movement. This is an important phase, as lumbar stability is a result of coordinated muscle activation involving many muscles.³¹ This program progresses from supine breathing exercises to a modified side bridge position to enhance core activation along with frontal plane stability. Next, athletes are progressed to a half kneeling position and then on to standing. Rotational activities are introduced starting with isometric holds progressing to chops/lifts and rotational medicine ball toss. During these tasks, focus should be on quality of movement and maintenance of core activation. Endurance of these muscles should be trained during this process. Appropriate pain-free and safe cardiovascular exercise, such as walking, biking, swimming, and jogging, should be performed throughout each stage in the rehabilitation process. Activities should be halted with any increase in pain. At the completion of the rehabilitation process, it is important to observe the athlete while performing sport-specific tasks. Spinal stabilization must be translational and monitored by observing maintenance of the “cylinder” from the training room to sports specific movements.

Since poor lumbar control has been associated with increased amount of time on the disabled list,⁵ it would be ideal to identify those at risk of injury before problems arise. Conte and colleagues32 have shown that core muscle strains could be a result of muscle imbalance or improper pitching or hitting technique. Other work has demonstrated that pitchers with poor lumbopelvic control did not perform as well as those with superior control.³³ By assessing spinal stability and biomechanics at baseline, we may be able to identify those at risk. Pitchers with suboptimal spinal stabilization can present with an unstable balance phase, increased amounts of hyperextension of the lumbar spine from the moment of max cocking through ball release, as well as increased lateral trunk tilt at ball release. Correcting these flaws and increasing deep core stabilization can prevent injuries and improve performance.

Summary

A stable, well-functioning lumbar spine is vital to nearly every baseball-related activity, including pitching, throwing, batting, fielding, and running. The spine serves as a critical link in the kinetic chain between the upper and lower extremities. Due to the high demand on the lumbar spine, injuries to this area represent a significant amount of time out of play in MLB. Initial treatment typically consists of a comprehensive nonoperative rehabilitation process involving analgesics, rest, and therapy focusing on core stabilization. Because poor lumbopelvic control and mechanics have been demonstrated to increase injury risk, preemptive spinal and core stabilization is likely an appropriate step towards injury prevention.

For the last 20 years, injuries resulting in time out of play have been on the rise in Major League Baseball (MLB), and those affecting the back are no exception.^1,2 In the first comprehensive report on injuries in MLB players, back injuries resulted in a mean of 1016 disabled list days per season from 1995 to 1999.¹ Similarly, core and back injuries were responsible for 359 disabled list designations from 2002 to 2008. This represented 11.7% of all injuries resulting in time out of play during that time span.² During that time, back injury prevalence ranked 6th highest of all possible body regions (out of 17), and both position players and pitchers were similarly affected (7.8% and 7.4% of all injuries, respectively).² These injuries often result in a significant time out of play and can have a tremendous impact on player health. A healthy, stable, and well-functioning lumbar spine is a prerequisite for nearly all baseball-related activities, including pitching, throwing, batting, and running. Accordingly, even minor lumbar spine injuries may profoundly influence baseball performance. Despite this, less is currently known about the true epidemiology and impact of back injuries in professional baseball compared to other professional sporting organizations.³

The most common causes of low back pain and injury in elite baseball players include muscle strains, stress fractures (spondylolysis), annular tears, disc herniation, stenosis, transverse process fractures, facetogenic pain, and sacroiliac (SI) joint arthropathy.^4-8 These injuries present in a variety of ways with varying symptomatology. Accordingly, a thorough understanding and comprehensive approach to the diagnosis and treatment of these injuries is necessary. The purpose of this article is to discuss the current state of lumbar spine injuries in professional baseball players. Specifically, we will discuss the critical role of the spine in baseball activities, common causes of injury, tips for making the diagnosis, treatment options, outcomes, and injury prevention and rehabilitation strategies.

Role of the Spine in Baseball

The spine and core musculature are responsible for positioning the head, shoulders, and upper extremities in space over the hips and lower extremities. Proper maintenance of this relationship is required during all phases of throwing, pitching, running, and hitting. During these activities, the spine may dynamically flex, extend, rotate, and laterally bend as needed to keep the body balanced with the head centered over the trunk.

Pitching and Throwing

Whether pitching from the wind-up or the stretch, the head begins centered over the hips and pelvis. As the pitching motion progresses, the hips undergo rotation, flexion, extension, abduction, and circumduction. While this is occurring, the shoulders and upper truck must bend, rotate, and translate toward home plate with the body. Just prior to front foot contact, trunk rotation averages 55 ± 6° with a maximal mean angular acceleration of 11,600 ± 3100°/s². ⁹ In order for the body to remain balanced, controlled, and synchronized throughout this delivery, the lumbar spine and core musculature must work diligently to stabilize the entire kinetic chain. Of all the trunk muscles (paraspinal, rectus abdominis, obliques, and glutei), the lumbar paraspinal muscles often work the hardest during the pitching motion, demonstrating activity increases ranging from 100% to 400%.¹⁰ Accordingly, it is not uncommon for pitchers to develop SI joint or lumbar facet joint pain due to this high degree of torsional strain exerted on the low back.⁴ Poor lumbopelvic control has been shown to be a predictor of subsequent injury, and the degree of lumbopelvic dysfunction is proportional to injury severity in MLB pitchers.⁵

Hitting

Similar to pitching, hitting involves a complex combination of movements from the upper and lower extremities that must be balanced by the core and spine. Although numerous movements occur simultaneously, rotational motion is primarily responsible for generating power. The trunk rotates an average of 46 ± 9° during the swing and reaches a maximal angular acceleration of 7200 ± 2800°/s² just after contact.⁹ During this period of rapid torsion, the spine must rotate in conjunction with the hips and shoulders to create a stable cylinder and axis of rotation. The spine and core are responsible for synchronizing rotation to ensure that hip and shoulder parallelism is maintained from swing initiation to ball contact. If the body does not rotate as a unit, the position of the head is affected and the batter’s ability to see the ball may be compromised. Additionally, if delivery of the shoulders lags too far behind that of the hips, the position of the hands (and bat) in space is adversely affected. The entire kinetic chain must remain balanced, coordinated, precisely timed, and standardized throughout the entire swing from initial trigger to final follow-through. The lumbar spine plays a critical role in each of these steps. If lumbar spine mechanics are not sound, this can have significant adverse effects on batting performance and may predispose hitters to injury.⁴

Common Etiologies for Spinal Injury

The vast majority of baseball players who experience lumbar pain will have injuries that can be classified as mechanical back pain (ie, spondylolysis, annular tears, facetogenic pain, SI joint arthropathy, or muscle injuries) (Table). Although less likely to occur, nerve entrapment or impingement syndromes (ie, disc herniation, stenosis, and peripheral nerve entrapment) have been observed in professional baseball players. Finally, more concerning pathologies such as infection and tumor are extremely rare, but they must not be overlooked in this high-demand patient population.

Stress Fracture or Spondylolysis

In young athletic patients, up to one-third of those with low back pain may have evidence of a lumbar stress fracture on bone scan.^11,12 This is particularly true for athletes who undergo repetitive lumbar extension and rotation, such as linemen, gymnasts, wrestlers, weight lifters, and baseball players.^4,13 Although the majority of lumbar stress fractures occur at the pars interarticularis, they can occur in the pedicle or articular process (Figure 1). Most spondylolytic lesions do not progress to spondylolisthesis, especially once patients reach skeletal maturity. Because the fifth lumbar vertebra represents the transition from the lumbar to the sacral spine, most stress fractures occur at L5. These typically present as localized low back pain that worsens with flexion, extension, and rotation.

Muscle Injury

One of the most common causes of low back pain in athletes is muscle strains and spasms. Because the lumbar paraspinal muscles are extremely active during throwing and hitting,¹⁰ they are particularly susceptible to injury. This is particularly true in deconditioned athletes or those who report to spring training having not adequately maintained strength and flexibility through the off-season.^4,5 These injuries typically present in an acute fashion with an obvious inciting incident. Players may have a history of similar muscle injuries in the past. On examination, they tend to have difficulty maintaining normal posture or ranging the spine through a full arc of motion. Localized, superficial tenderness to palpation in the injured muscle is a key component of the diagnosis.

Annular Tears and Disc Herniation

These injuries typically occur as the result of a combination of compressive and rotary forces on the lumbar spine that overcome the ability of the annulus fibrosus to resist hoop stresses. Patients with annular tears typically present with severe lower back pain that may be accompanied by spasm and pain radiation into the buttock or lower extremities. Pain is usually worsened by valsalva, coughing, sneezing, or bearing down.⁴ Although annular tears can occur in isolation, they can also lead to herniation of the nucleus pulposus into the spinal canal (Figure 2). Depending on the location and severity of the herniation, nerve entrapment or impingement can occur. This may initially present as pain that radiates into the lower extremities in a dermatomal fashion. As the herniation progresses, decreased sensation and weakness may develop.

Facet Joint Pain

Facetogenic pain can occur as the result of degenerative changes, trauma, or joint inflammation. Facet injury typically occurs during rotation while the back is extended.⁴ This results in localized pain and tenderness that can be reproduced by loading the facet joint (lumbar extension) during the examination, and patients will often demonstrate discomfort and altered motion when extending the flexed back.

Sacroiliac Joint Pain

Although pain in the region of the SI joint is very common, much of this may actually be referred from more centrally located neuromotion segments.⁴ SI joint pathology can occur as a result of trauma, degeneration, or inflammatory processes as is seen in ankylosing spondylitis (AS). Patients with AS typically present with a gradual onset of progressive stiffness and pain in the low back and hips that is worse in the morning or following periods of inactivity. It is most common in Caucasian males in their second to fourth decades.¹⁴ Although 80% to 95% of patients with AS will test positive for human leukocyte antigen B27 (HLA-B27), it is important to note that the vast majority of people with HLA-B27 do not go on to develop AS.¹⁴ Regardless of the cause, SI joint pain can be very debilitating and negatively impact all baseball-related activities.

Stenosis

Lumbar stenosis may develop from arthritic changes, disc protrusion, facet hypertrophy, or ligament ossification. In this young, athletic population, congenital stenosis should also be a consideration. Patients with congenital stenosis at baseline are at increased risk for developing neurologic symptoms from disc protrusion or other acquired spinal pathology. Lumbar stenosis generally manifests as a gradual onset of progressive low back pain with radicular symptoms or neurogenic claudication.⁴

Making the Diagnosis

History

When identifying the cause of any musculoskeletal complaint, the diagnosis begins with a thorough history. In addition to the standard components of the history, such as timing, severity, relation to activity, exacerbating factors, associated symptoms, and prior treatments, Watkins and colleagues4 have outlined a number of key factors that should be determined when specifically evaluating the athlete with low back pain.These include quantification of the morbidity, identification of contributing psychosocial factors, ruling out of urgent diagnoses (ie, neoplasm, infection, rapidly progressive neurologic deficits, cauda equina, and paralysis), determination of injury type and duration, identification of the clinical syndrome/etiology, pinpointing the location of the pathology (what nerve at what level?), and quantification of back versus leg symptoms. Answers to these questions will set the framework for an appropriately directed physical examination, imaging, and diagnostic tests.

Physical Examination

The physical examination begins by observing the patient or player walk across the playing field, training room, or examination room, paying attention to posture, gait, and overall body movement. Many patients with lumbar injuries will demonstrate adaptive patterns of motion in an attempt to accommodate their pain. This may be seen during baseball-related activities such as throwing, batting, or running. The spine should be visualized and palpated for malalignment while standing erect and during forward bending. If possible, motion should be assessed in rotation, lateral bending, and the flexion and extension planes. Special attention should be paid to any positions or maneuvers that reproduce pain or neurologic symptoms. Areas of tenderness and radiating pain should be fully palpated. A full neurologic examination consisting of manual muscle testing, sensory examination, and reflex evaluation of both the upper and lower extremities should be performed. Numerous special tests and neurologic stretch maneuvers that assess specific lumbar nerve roots have been described.¹⁵

Imaging and Diagnostic Tests

Depending on the history and physical examination, imaging of the lumbar spine is not always warranted in the acute setting. This is especially the case if muscle injury, herniation, or annular tears are suspected. In cases of persistent pain, trauma, or suspected neoplasia, imaging is generally warranted. When x-rays are negative and spondylolysis is suspected, bone scan with lumbar single photon emission computed tomography (SPECT) is the most sensitive test.¹⁶ SPECT scans are positive in active spondylolysis because the radio-nucleotide is taken up by active, bone-forming osteoblasts. Quiescent stress fractures that are not apparent on SPECT scans are generally chronic and painless.⁴ If the SPECT scan is positive, the injury can be further characterized by computed tomography (CT) (Figure 1), which can distinguish between spondylolysis, osteoid osteoma, osteoblastoma, acute fracture, or arthritic degeneration. When the SPECT is negative, or if neural impingement is suspected, magnetic resonance imaging (MRI) (Figure 2) is likely the best diagnostic imaging tool. MRI allows identification of bone edema, disc herniation, annular disruption, disc desiccation, stenosis, and nerve entrapment. Finally, when attempting to distinguish between central and peripheral nerve entrapment syndromes, an electromyogram (EMG) or nerve conduction study (NCS) is a reliable way to identify the location of injury.

Treatment and Outcomes

The approach to a patient with low back pain begins with identification of the etiology and discontinuation of the activities that reproduce pain.⁴ Trunk stabilization exercises and anti-inflammatory medications are the mainstays of treatment regardless of the cause of the lumbar spinal injury in the baseball player.⁴

Stress Fracture or Spondylolysis

Management of symptomatic spondylolysis or spondylolisthesis in the athlete initially consists of conservative treatment, which achieves good to excellent long-term outcomes and return to play in 70% to 90% of athletes, especially for acute injuries.^17-19 After stopping the activity that causes the pain, trunk stabilization exercises should be started as soon as tolerated with the use of non-steroidal anti-inflammatory medications (NSAIDs), oral steroids, and spinal injections to control symptoms and permit initiation of the rehabilitation program.⁴ Although bracing is a commonly used adjunctive treatment, a recent meta-analysis did not demonstrate any difference in clinical outcomes between patients treated with a brace compared to non-braced controls.²⁰

Surgical indications for the treatment of spondylolysis or spondylolisthesis are limited; however, failure of nonoperative treatment after 6 months is a reasonable time to consider surgery.17 The spondylolytic defect can often be repaired directly using hook screws, translaminar screws, wiring, pedicle screws, or image-guided lag screws across the lesion with grafting.4 Lumbar spinal fusion is less successful in professional athletes due to the high demands placed on adjacent levels as well as the time required for the fusion to heal.4 Bony union can be determined by a CT scan at 6 months postoperatively if the patient has met appropriate return to play criteria.4

Muscle Injury

Management of lumbar sprains and strains typically includes restricting painful postures and a rehabilitation program that focuses on core strengthening within a pain-free arc of motion.²¹ Because acute injuries typically resolve quickly and spontaneously, a short interval of decreased activity, icing, NSAIDs, and stretching followed by focused strength training is appropriate before return to sports activity.²²

Annular Tears and Disc Herniation

Initial management of baseball players with acute lumbar disc herniation and/or annular tears consists of rest for up to 5 days followed by physical therapy and NSAIDs, Medrol Dose pak, or epidural injections.⁴ Professional baseball players return to play at high rates following a herniated lumbar disc.⁶ Earhart and colleagues6 found that 97.1% of players returned to play at an average time of 6.6 months from the time of injury. When stratified by position, all pitchers (29 of 29) returned to competitive play after operative or nonoperative management, while 38 of 40 hitters returned.⁶ The average career length after lumbar disc herniation in the professional baseball player is between 4.1 and 5.3 years or between 256 and 471 games.^6,23 Other work has suggested that players undergoing operative treatment for lumbar herniation had shorter career lengths; however, patients in the operative group tended to be older at the time of injury.²³

Emphasis should be placed on nonoperative management of baseball players with disc pathology except in cases of cauda equina syndrome.⁴ Hitters and pitchers who require surgery have demonstrated decreased 1-year and 3-year postoperative statistical performance compared to preinjury levels.⁶ No significant changes in any performance statistic were seen in baseball following nonoperative management.⁶ Consequently, indications for surgery in the baseball player with lumbar disc pathology includes cauda equina syndrome, progressive neurologic deficit, sufficient morbidity, failure of conservative care, a lesion that can be corrected safely with surgery, and the ability for the patient to comply with a comprehensive postoperative rehabilitation program.⁴ Operative treatment typically consists of a lumbar microdiscectomy and/or laminotomy. ^4,6

Facet Joint Pain

The mainstay of therapy in patients with facet joint pain consists of analgesia and a trunk stabilization program.²⁴ Lumbar zygapophysial joint injections and radiofrequency denervation can be considered if the patient fails 4 weeks of directed conservative treatment.^24,25 Injections may be useful in select patients; however, the literature supporting the use of lumbar facet joint injections or radiofrequency denervation for facetogenic pain is limited.^24,25

Sacroiliac Joint Pain

Acute injury of the SI joint can be treated with NSAIDs, icing, and relative rest.²⁶ Mobilization of the SI joint in addition to correcting any asymmetries in muscle length or stiffness should be started and progressed as soon as tolerated within a pain-free range of motion.²⁶ Rehabilitation should correct biomechanical deficits and maladaptation with a special focus on agonist and antagonist muscle groups across the sacrum and ilium.²⁶ Treatment of AS in the athlete should emphasize symptom control, as there is no definite treatment. For patients with AS, other long-term therapeutic options include sulfasalazine, methotrexate, thalidomide, and anti-tumor necrosis factor therapies.¹⁴

Stenosis

Lumbar spinal stenosis, whether congenital or acquired, should initially be managed conservatively.²⁷ Although they do not alter the progression of the disease, epidural steroids and local injections may temporarily decrease symptoms in approximately 40% of cases.²⁷ Those who fail conservative therapy after 3 months may be candidates for surgical decompression and/or fusion.^27,28 However, surgical treatment for lumbar spinal stenosis in elite baseball players has not been thoroughly studied, so the long-term prognosis is not well documented.²⁷

Rehabilitation and Prevention of Injuries

After an appropriate diagnosis has been made, a structured rehabilitation process should commence. During rehabilitation, it is of primary importance that deep core stabilization is established. As an initial step in this process, athletes are trained to initiate deep core stabilization with breathing techniques in a static, supine position.²⁹ Proper diaphragm activation with co-contractions of the transverse abdominis (TA) and pelvic floor has been shown to increase lumbar spine stability.³⁰ This will allow for an increase in intra-abdominal pressure (IAP) and improved stabilization of the lumbar spine, creating a muscular cylinder between the bottom of the rib cage and top of the pelvis. These activities are initiated in the supine position but are soon advanced as upper and lower extremity movement against resistance is added. It is important to make sure IAP and contraction of the TA is maintained throughout this sequence of progression.

Once deep core stabilization has been established, athletes are progressed to global muscle training and kinetic linking in all 3 planes of movement. This is an important phase, as lumbar stability is a result of coordinated muscle activation involving many muscles.³¹ This program progresses from supine breathing exercises to a modified side bridge position to enhance core activation along with frontal plane stability. Next, athletes are progressed to a half kneeling position and then on to standing. Rotational activities are introduced starting with isometric holds progressing to chops/lifts and rotational medicine ball toss. During these tasks, focus should be on quality of movement and maintenance of core activation. Endurance of these muscles should be trained during this process. Appropriate pain-free and safe cardiovascular exercise, such as walking, biking, swimming, and jogging, should be performed throughout each stage in the rehabilitation process. Activities should be halted with any increase in pain. At the completion of the rehabilitation process, it is important to observe the athlete while performing sport-specific tasks. Spinal stabilization must be translational and monitored by observing maintenance of the “cylinder” from the training room to sports specific movements.

Since poor lumbar control has been associated with increased amount of time on the disabled list,⁵ it would be ideal to identify those at risk of injury before problems arise. Conte and colleagues32 have shown that core muscle strains could be a result of muscle imbalance or improper pitching or hitting technique. Other work has demonstrated that pitchers with poor lumbopelvic control did not perform as well as those with superior control.³³ By assessing spinal stability and biomechanics at baseline, we may be able to identify those at risk. Pitchers with suboptimal spinal stabilization can present with an unstable balance phase, increased amounts of hyperextension of the lumbar spine from the moment of max cocking through ball release, as well as increased lateral trunk tilt at ball release. Correcting these flaws and increasing deep core stabilization can prevent injuries and improve performance.

Summary

A stable, well-functioning lumbar spine is vital to nearly every baseball-related activity, including pitching, throwing, batting, fielding, and running. The spine serves as a critical link in the kinetic chain between the upper and lower extremities. Due to the high demand on the lumbar spine, injuries to this area represent a significant amount of time out of play in MLB. Initial treatment typically consists of a comprehensive nonoperative rehabilitation process involving analgesics, rest, and therapy focusing on core stabilization. Because poor lumbopelvic control and mechanics have been demonstrated to increase injury risk, preemptive spinal and core stabilization is likely an appropriate step towards injury prevention.

Friction blisters result from repetitive friction and strain forces that develop between the skin and various objects. Blisters form in areas where the stratum corneum and stratum granulosum are sufficiently robust (Figure), such as the palmar and plantar surfaces of the hand and feet. Thus, these layers are capable of transmitting the surface forces to the underlying layer, the stratum spinosum. In areas without strong stratum corneum and stratum granulosum layers, an abrasion forms instead.¹

It has been shown that the transmitted frictional forces disrupt the stratum spinosum, with the blister roof being composed of the 2 upper epidermal layers as well as prickle cells of the traumatically disrupted stratum spinosum. The basal cell layer typically shows little damage and the dermal-epidermal junction remains intact.¹

Early experimental studies in humans using repeatedly cycled probes demonstrated the pathologic sequence of events in blister formation. First, there is slight exfoliation of the stratum corneum layer, accompanied by a reddened area in the zone of rubbing (erythroderma). This is followed by a pale, narrow demarcation, which forms around the reddened region. Subsequently, this pale area fills in toward the center to occupy the entire affected area, which becomes the blister lesion.^1,2

Hydrostatic pressure then causes blister fluid to accumulate within 1 to 2 hours following the trauma. Compared to plasma, the blister fluid has a lower protein level and similar electrolyte content.^3,4 Cells in the blister cavity continue to degrade for about 4 hours following the injury, with resumption of cellular activity beginning at 6 hours. Mitotic activity is increased after 24 to 30 hours, and at 48 hours, a new granular layer is present. By 120 hours post-injury, a new stratum corneum is formed.^5,6

A number of factors have been found to affect blister formation. Frictional force magnitude and number of cycles play the most obvious role. There is an inverse relationship between the two: as the frictional force increases, fewer cycles are required for blister formation.⁷ This is likely the reason blisters occur most commonly in areas where the fingertips are in contact with a seam, as opposed to the smoother surface of a baseball.

Many authors have examined moisture’s effect on frictional forces, and found that very dry and very wet skin produce low frictional forces, whereas moist skin produces the highest frictional force.^1,2,8-10 In the case of dry skin, this is thought to be due to exfoliation and sloughing of cells from the stratum corneum, which produces a dry lubrication similar to graphite. Very wet skin has a fluid layer that lubricates the 2 surfaces. In the case of moist skin, however, it is hypothesized that surface tension impedes the movement of squamous cells, increasing the frictional forces.^2,9 This moist environment is most commonly produced by sweating.

Other factors include skin temperature, which, when elevated, mildly predisposes the skin to blister formation. Some studies have shown temperatures as high as 50°C in rubbing experiments^2,7,8,11; however, it should be noted that friction blisters do not resemble second-degree burns, either histologically or clinically.^12,13

Blisters in Baseball Pitchers

Blisters in baseball pitchers are a well-known and frequently publicized problem; however, there is a paucity of literature describing the incidence or treatment of such blisters.^14,15 The digital pulp experiences frictional forces from the baseball stiches as well as from the distal margin of the nail plate during release of the ball. Forces are transmitted to the ball predominately through the thumb, index, and long fingers. While the thumb acts mainly as a post, the index and long fingers impart the “action” on the ball. Not surprisingly, blisters form most commonly on these 2 fingers. While relatively small in size and significance, the impact of such a blister on a pitcher’s ability to maintain the fine control of his pitches cannot be overlooked. Biomechanical studies have shown that maximum gripping strength is attained when the fingers grasp a dynamometer handle at the level of the distal interphalangeal joint.¹⁶ Contact pressure mapping during gripping of a cylindrical object has shown that phalanges 2, 3, and 4 experience the highest forces in gripping and pulling activities.¹⁷ No study has specifically addressed phalangeal pressure generation in pitchers, however.

Blister Prevention

Blister prevention and treatment methods in baseball pitchers are steeped in folklore and tradition. Methods for drying out blisters and hardening calluses have included the use of pickle juice, urine, bags of rice, and superglue.^14,15 Superglue, surgical glue, or any other foreign substance is not allowed during a game on the finger or hands of pitchers by Major League Baseball rules. Other anecdotal options include the use of compounded medicines that are marketed as creams and sprays designed to toughen skin.

As with other injuries, it is important to recognize any predisposing factors and ways to avoid them. Dampness and temperature (>104°F) have been identified as chief factors that substantially increase the friction coefficient and increase blister incidence.¹⁸ While temperature and perspiration are impossible to avoid during competition, steps can be taken to keep the pitcher’s hand dry on the mound as well as between innings, such as a rosin bag, a dry towel, and a rice bucket.

Maintaining fingernail length plays an important role in preventing blister formation. The nail can both protect the adjacent skin by decreasing the frictional force on the skin as well as lead to the development of blisters on the other fingers by repetitive abrasion. Nail length and contour need to be tailored to each pitcher specifically. The length of the nail can protect the finger pulp by minimally “elevating” the ball off of the finger itself. However, too long of a nail may come at the cost of abrading the abutting finger as the spin is imparted onto the ball. The shape of the nail is generally kept well contoured to avoid any sharp edges, which can act as local irritants. In the instance of soft, cracked, or torn nails, some pitchers have used acrylic nails. Maintaining proper fingernail shape and length is an essential preventive measure that requires regular use of clippers and emery boards.

Callus care is also paramount in preventing blister formation. It is believed that development of a callus is inevitable with repetitive throwing and likely protective of the underlying skin. The size and shape of the callus, like that of the nail, needs to be carefully monitored. A callus that becomes overly prominent can lead to increased friction with a baseball seam. This can lead to blister development. A small, smooth callus without edges or loose borders is the goal. The free edges of a callus can be trimmed with clean clippers. Contouring is best performed with careful use of an emery board.

Treatment of Finger Blisters

Blister management is determined by the size of the blister as well as the integrity of the overlying callus. Small blisters with intact skin coverage can be sterilely drained with a needle or a No. 11 blade.^6,19-21 This allows apposition of the skin layers and quicker healing. The free edge of the blister can then be repaired with surgical glue. In these instances, a starting pitcher may be required to miss a start to allow further healing. In most cases, there is no need to place the player on the disabled list (DL).

Larger blisters, or those that traumatically open, represent a more concerning issue. The loose layers of skin can be removed, and the raw bed can then be treated with antibiotic ointment for the first 2 to 3 days. Subsequently, benzoin tincture, a commonly used paste of benzoin and alum, can be utilized to toughen the raw skin. Bulky dressings can be applied early in treatment but should then be discouraged, as the underlying skin softens due to the presence of moisture. These instances generally lead to lost time on the field. It is not uncommon that the pitcher requires placement on the 15-day DL.

Summary

Blisters on the fingertips of professional baseball players can lead to significant pain and decreased performance. Prevention of blister formation represents the goal of the player and the medical staff. Skin and nail care requires daily evaluation. When blisters do form, appropriate management can minimize lost time.

Friction blisters result from repetitive friction and strain forces that develop between the skin and various objects. Blisters form in areas where the stratum corneum and stratum granulosum are sufficiently robust (Figure), such as the palmar and plantar surfaces of the hand and feet. Thus, these layers are capable of transmitting the surface forces to the underlying layer, the stratum spinosum. In areas without strong stratum corneum and stratum granulosum layers, an abrasion forms instead.¹

It has been shown that the transmitted frictional forces disrupt the stratum spinosum, with the blister roof being composed of the 2 upper epidermal layers as well as prickle cells of the traumatically disrupted stratum spinosum. The basal cell layer typically shows little damage and the dermal-epidermal junction remains intact.¹

Early experimental studies in humans using repeatedly cycled probes demonstrated the pathologic sequence of events in blister formation. First, there is slight exfoliation of the stratum corneum layer, accompanied by a reddened area in the zone of rubbing (erythroderma). This is followed by a pale, narrow demarcation, which forms around the reddened region. Subsequently, this pale area fills in toward the center to occupy the entire affected area, which becomes the blister lesion.^1,2

Hydrostatic pressure then causes blister fluid to accumulate within 1 to 2 hours following the trauma. Compared to plasma, the blister fluid has a lower protein level and similar electrolyte content.^3,4 Cells in the blister cavity continue to degrade for about 4 hours following the injury, with resumption of cellular activity beginning at 6 hours. Mitotic activity is increased after 24 to 30 hours, and at 48 hours, a new granular layer is present. By 120 hours post-injury, a new stratum corneum is formed.^5,6

A number of factors have been found to affect blister formation. Frictional force magnitude and number of cycles play the most obvious role. There is an inverse relationship between the two: as the frictional force increases, fewer cycles are required for blister formation.⁷ This is likely the reason blisters occur most commonly in areas where the fingertips are in contact with a seam, as opposed to the smoother surface of a baseball.

Many authors have examined moisture’s effect on frictional forces, and found that very dry and very wet skin produce low frictional forces, whereas moist skin produces the highest frictional force.^1,2,8-10 In the case of dry skin, this is thought to be due to exfoliation and sloughing of cells from the stratum corneum, which produces a dry lubrication similar to graphite. Very wet skin has a fluid layer that lubricates the 2 surfaces. In the case of moist skin, however, it is hypothesized that surface tension impedes the movement of squamous cells, increasing the frictional forces.^2,9 This moist environment is most commonly produced by sweating.

Other factors include skin temperature, which, when elevated, mildly predisposes the skin to blister formation. Some studies have shown temperatures as high as 50°C in rubbing experiments^2,7,8,11; however, it should be noted that friction blisters do not resemble second-degree burns, either histologically or clinically.^12,13

Blisters in Baseball Pitchers

Blisters in baseball pitchers are a well-known and frequently publicized problem; however, there is a paucity of literature describing the incidence or treatment of such blisters.^14,15 The digital pulp experiences frictional forces from the baseball stiches as well as from the distal margin of the nail plate during release of the ball. Forces are transmitted to the ball predominately through the thumb, index, and long fingers. While the thumb acts mainly as a post, the index and long fingers impart the “action” on the ball. Not surprisingly, blisters form most commonly on these 2 fingers. While relatively small in size and significance, the impact of such a blister on a pitcher’s ability to maintain the fine control of his pitches cannot be overlooked. Biomechanical studies have shown that maximum gripping strength is attained when the fingers grasp a dynamometer handle at the level of the distal interphalangeal joint.¹⁶ Contact pressure mapping during gripping of a cylindrical object has shown that phalanges 2, 3, and 4 experience the highest forces in gripping and pulling activities.¹⁷ No study has specifically addressed phalangeal pressure generation in pitchers, however.

Blister Prevention

Blister prevention and treatment methods in baseball pitchers are steeped in folklore and tradition. Methods for drying out blisters and hardening calluses have included the use of pickle juice, urine, bags of rice, and superglue.^14,15 Superglue, surgical glue, or any other foreign substance is not allowed during a game on the finger or hands of pitchers by Major League Baseball rules. Other anecdotal options include the use of compounded medicines that are marketed as creams and sprays designed to toughen skin.

As with other injuries, it is important to recognize any predisposing factors and ways to avoid them. Dampness and temperature (>104°F) have been identified as chief factors that substantially increase the friction coefficient and increase blister incidence.¹⁸ While temperature and perspiration are impossible to avoid during competition, steps can be taken to keep the pitcher’s hand dry on the mound as well as between innings, such as a rosin bag, a dry towel, and a rice bucket.

Maintaining fingernail length plays an important role in preventing blister formation. The nail can both protect the adjacent skin by decreasing the frictional force on the skin as well as lead to the development of blisters on the other fingers by repetitive abrasion. Nail length and contour need to be tailored to each pitcher specifically. The length of the nail can protect the finger pulp by minimally “elevating” the ball off of the finger itself. However, too long of a nail may come at the cost of abrading the abutting finger as the spin is imparted onto the ball. The shape of the nail is generally kept well contoured to avoid any sharp edges, which can act as local irritants. In the instance of soft, cracked, or torn nails, some pitchers have used acrylic nails. Maintaining proper fingernail shape and length is an essential preventive measure that requires regular use of clippers and emery boards.

Callus care is also paramount in preventing blister formation. It is believed that development of a callus is inevitable with repetitive throwing and likely protective of the underlying skin. The size and shape of the callus, like that of the nail, needs to be carefully monitored. A callus that becomes overly prominent can lead to increased friction with a baseball seam. This can lead to blister development. A small, smooth callus without edges or loose borders is the goal. The free edges of a callus can be trimmed with clean clippers. Contouring is best performed with careful use of an emery board.

Treatment of Finger Blisters

Blister management is determined by the size of the blister as well as the integrity of the overlying callus. Small blisters with intact skin coverage can be sterilely drained with a needle or a No. 11 blade.^6,19-21 This allows apposition of the skin layers and quicker healing. The free edge of the blister can then be repaired with surgical glue. In these instances, a starting pitcher may be required to miss a start to allow further healing. In most cases, there is no need to place the player on the disabled list (DL).

Larger blisters, or those that traumatically open, represent a more concerning issue. The loose layers of skin can be removed, and the raw bed can then be treated with antibiotic ointment for the first 2 to 3 days. Subsequently, benzoin tincture, a commonly used paste of benzoin and alum, can be utilized to toughen the raw skin. Bulky dressings can be applied early in treatment but should then be discouraged, as the underlying skin softens due to the presence of moisture. These instances generally lead to lost time on the field. It is not uncommon that the pitcher requires placement on the 15-day DL.

Summary

Blisters on the fingertips of professional baseball players can lead to significant pain and decreased performance. Prevention of blister formation represents the goal of the player and the medical staff. Skin and nail care requires daily evaluation. When blisters do form, appropriate management can minimize lost time.

Friction blisters result from repetitive friction and strain forces that develop between the skin and various objects. Blisters form in areas where the stratum corneum and stratum granulosum are sufficiently robust (Figure), such as the palmar and plantar surfaces of the hand and feet. Thus, these layers are capable of transmitting the surface forces to the underlying layer, the stratum spinosum. In areas without strong stratum corneum and stratum granulosum layers, an abrasion forms instead.¹

It has been shown that the transmitted frictional forces disrupt the stratum spinosum, with the blister roof being composed of the 2 upper epidermal layers as well as prickle cells of the traumatically disrupted stratum spinosum. The basal cell layer typically shows little damage and the dermal-epidermal junction remains intact.¹

Early experimental studies in humans using repeatedly cycled probes demonstrated the pathologic sequence of events in blister formation. First, there is slight exfoliation of the stratum corneum layer, accompanied by a reddened area in the zone of rubbing (erythroderma). This is followed by a pale, narrow demarcation, which forms around the reddened region. Subsequently, this pale area fills in toward the center to occupy the entire affected area, which becomes the blister lesion.^1,2

Hydrostatic pressure then causes blister fluid to accumulate within 1 to 2 hours following the trauma. Compared to plasma, the blister fluid has a lower protein level and similar electrolyte content.^3,4 Cells in the blister cavity continue to degrade for about 4 hours following the injury, with resumption of cellular activity beginning at 6 hours. Mitotic activity is increased after 24 to 30 hours, and at 48 hours, a new granular layer is present. By 120 hours post-injury, a new stratum corneum is formed.^5,6

A number of factors have been found to affect blister formation. Frictional force magnitude and number of cycles play the most obvious role. There is an inverse relationship between the two: as the frictional force increases, fewer cycles are required for blister formation.⁷ This is likely the reason blisters occur most commonly in areas where the fingertips are in contact with a seam, as opposed to the smoother surface of a baseball.

Many authors have examined moisture’s effect on frictional forces, and found that very dry and very wet skin produce low frictional forces, whereas moist skin produces the highest frictional force.^1,2,8-10 In the case of dry skin, this is thought to be due to exfoliation and sloughing of cells from the stratum corneum, which produces a dry lubrication similar to graphite. Very wet skin has a fluid layer that lubricates the 2 surfaces. In the case of moist skin, however, it is hypothesized that surface tension impedes the movement of squamous cells, increasing the frictional forces.^2,9 This moist environment is most commonly produced by sweating.

Other factors include skin temperature, which, when elevated, mildly predisposes the skin to blister formation. Some studies have shown temperatures as high as 50°C in rubbing experiments^2,7,8,11; however, it should be noted that friction blisters do not resemble second-degree burns, either histologically or clinically.^12,13

Blisters in Baseball Pitchers

Blisters in baseball pitchers are a well-known and frequently publicized problem; however, there is a paucity of literature describing the incidence or treatment of such blisters.^14,15 The digital pulp experiences frictional forces from the baseball stiches as well as from the distal margin of the nail plate during release of the ball. Forces are transmitted to the ball predominately through the thumb, index, and long fingers. While the thumb acts mainly as a post, the index and long fingers impart the “action” on the ball. Not surprisingly, blisters form most commonly on these 2 fingers. While relatively small in size and significance, the impact of such a blister on a pitcher’s ability to maintain the fine control of his pitches cannot be overlooked. Biomechanical studies have shown that maximum gripping strength is attained when the fingers grasp a dynamometer handle at the level of the distal interphalangeal joint.¹⁶ Contact pressure mapping during gripping of a cylindrical object has shown that phalanges 2, 3, and 4 experience the highest forces in gripping and pulling activities.¹⁷ No study has specifically addressed phalangeal pressure generation in pitchers, however.

Blister Prevention

Blister prevention and treatment methods in baseball pitchers are steeped in folklore and tradition. Methods for drying out blisters and hardening calluses have included the use of pickle juice, urine, bags of rice, and superglue.^14,15 Superglue, surgical glue, or any other foreign substance is not allowed during a game on the finger or hands of pitchers by Major League Baseball rules. Other anecdotal options include the use of compounded medicines that are marketed as creams and sprays designed to toughen skin.

As with other injuries, it is important to recognize any predisposing factors and ways to avoid them. Dampness and temperature (>104°F) have been identified as chief factors that substantially increase the friction coefficient and increase blister incidence.¹⁸ While temperature and perspiration are impossible to avoid during competition, steps can be taken to keep the pitcher’s hand dry on the mound as well as between innings, such as a rosin bag, a dry towel, and a rice bucket.

Maintaining fingernail length plays an important role in preventing blister formation. The nail can both protect the adjacent skin by decreasing the frictional force on the skin as well as lead to the development of blisters on the other fingers by repetitive abrasion. Nail length and contour need to be tailored to each pitcher specifically. The length of the nail can protect the finger pulp by minimally “elevating” the ball off of the finger itself. However, too long of a nail may come at the cost of abrading the abutting finger as the spin is imparted onto the ball. The shape of the nail is generally kept well contoured to avoid any sharp edges, which can act as local irritants. In the instance of soft, cracked, or torn nails, some pitchers have used acrylic nails. Maintaining proper fingernail shape and length is an essential preventive measure that requires regular use of clippers and emery boards.

Callus care is also paramount in preventing blister formation. It is believed that development of a callus is inevitable with repetitive throwing and likely protective of the underlying skin. The size and shape of the callus, like that of the nail, needs to be carefully monitored. A callus that becomes overly prominent can lead to increased friction with a baseball seam. This can lead to blister development. A small, smooth callus without edges or loose borders is the goal. The free edges of a callus can be trimmed with clean clippers. Contouring is best performed with careful use of an emery board.

Treatment of Finger Blisters

Blister management is determined by the size of the blister as well as the integrity of the overlying callus. Small blisters with intact skin coverage can be sterilely drained with a needle or a No. 11 blade.^6,19-21 This allows apposition of the skin layers and quicker healing. The free edge of the blister can then be repaired with surgical glue. In these instances, a starting pitcher may be required to miss a start to allow further healing. In most cases, there is no need to place the player on the disabled list (DL).

Larger blisters, or those that traumatically open, represent a more concerning issue. The loose layers of skin can be removed, and the raw bed can then be treated with antibiotic ointment for the first 2 to 3 days. Subsequently, benzoin tincture, a commonly used paste of benzoin and alum, can be utilized to toughen the raw skin. Bulky dressings can be applied early in treatment but should then be discouraged, as the underlying skin softens due to the presence of moisture. These instances generally lead to lost time on the field. It is not uncommon that the pitcher requires placement on the 15-day DL.

Summary

Blisters on the fingertips of professional baseball players can lead to significant pain and decreased performance. Prevention of blister formation represents the goal of the player and the medical staff. Skin and nail care requires daily evaluation. When blisters do form, appropriate management can minimize lost time.