Mindfulness has become an impor­tant supportive psychotherapeutic intervention for a variety of psychi­atric conditions,^1-3 regardless of what other modalities the psychiatrist employs (eg, phar­macotherapy, other psychotherapeutic inter­ventions). In general, mindfulness involves engaging in meditation exercises, analogous to working out in the gym, to strengthen “mindfulness muscles.” These exercises increase the patient’s ability to remain in the moment, “as is,” and without judgment.

I think of mindfulness exercises as an “ego gym” for the patient as he (she) gets to exercise the ego functions of agency, atten­tion, awareness, acceptance, and empathy. Advising and helping patients to be present and exist with their thoughts is a psycho-educational approach and form of advice consistent with principles of supportive therapy. In this article, I provide a practical framework for doing and teaching mind­fulness using the mnemonic BREATHE.

Flow is more important than sequence
The 7 elements of mindfulness exercises contained in BREATHE do not need to be done in order. Rather, mindfulness gener­ally involves each of the following elements flowing, or tumbling, into each other, not standing as a distinct entity.

Being in the now, “as is,” without judg­ment (eg, being present/being vs doing; Buddhist origins; diaphragmatic breath­ing/body scans; “breathing-space” medi­tation exercises). In general, mindfulness meditation exercises focus on some sen­sory experience (eg, the physical sensa­tion of breathing or of a difficult emotion, or sounds and smells in the environment). Some mindfulness meditations are called “body scans.”

A patient can shift his (her) focus during mindfulness meditation to a sound or some other stimulus intruding on his original meditative focus, such as an intense emo­tion or pain, that might arise and become the new focus of mindfulness meditation. Ideally, mindfulness exercises are done without the intention of achieving anything (ie, there is no “striving” for anything when being mindful). Striving, after all, is doing; mindfulness is being.

R(AIN). Mindfulness, as operationalized by Kabat-Zinn,⁴ starts with a focus on breath­ing similar to many meditation practices in Buddhism. When the patient wanders into intense emotions, such as suffering, that become the focus of mindfulness, use the mnemonic-within-a-mnemonic RAIN as a guide; typically, this involves first anchoring with a few deep breaths, and then becoming mindful by:
   • Recognizing (and labeling, nam­ing, “tagging”) the emotion (eg, sad, hurt, angry, embarrassed); this engages frontal lobe processes that diminishes amygdaloid limbic system overactivity¹
   • Allowing (ie, accepting suffering)
   • Investigating, with an open and curious attitude, using one’s senses to experience, feel, and explore thoughts and emotions
   • Non-identifying with one’s thoughts, feelings, emotions, or suffering (expressed in the important mindfulness refrain: “You are not your thoughts or emotions. You are the entity that simply is aware of them.”).

Experiencing. The patient stops at the perceived experience or sensation and does not automatically react with thoughts, emo­tions, distress, or judgments. Mindfulness is a psychotherapeutic intervention that is “more experiential than cognitive.” Encourage the patient to stop at the “door of experience” and not enter the doors of thinking, emotion, and feeling.

Accepting without judgment—also called “awarenessing” or “avoid avoiding.” This involves being aware of the experi­ence regardless of what it entails, whether suffering, thoughts, emotions, or pain, and not trying to escape or avoid the difficult experience. Psychodynamic principles help us understand how psychological defenses designed to avoid the experience of the “unbearable affect” often lead to more problems for patients. In mindfulness, only avoiding is to be avoided.

Thoughts. People tend to over-identify with their thoughts and emotions. In mindfulness, you emphasize to the patient that (1) he is not his thoughts or emotions and (2) these cognitive processes do not represent facts.

Heartfulness—or, healthy, happy, free from harm. Mindfulness from the Buddhist tradition also includes “heartfulness” and “loving-kindness” and the development of compassion and kindness for one’s self and others. Mindfulness meditation there­fore also involves development of loving-kindness/compassion toward oneself and others—even one’s enemies (eg, “May I be healthy, happy, and free from harm.”). I have found this aspect of mindfulness useful for patients who feel angry or entitled, with characterological problems.

Empathy for others. As an extension of, or further emphasis on, loving-kindness, medi­tation focuses on understanding the suffer­ing of others. In certain monastic practices, this mindfulness meditation involves “tak­ing on” the suffering of another.

Disclosure
The author reports no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.

Mindfulness has become an impor­tant supportive psychotherapeutic intervention for a variety of psychi­atric conditions,^1-3 regardless of what other modalities the psychiatrist employs (eg, phar­macotherapy, other psychotherapeutic inter­ventions). In general, mindfulness involves engaging in meditation exercises, analogous to working out in the gym, to strengthen “mindfulness muscles.” These exercises increase the patient’s ability to remain in the moment, “as is,” and without judgment.

I think of mindfulness exercises as an “ego gym” for the patient as he (she) gets to exercise the ego functions of agency, atten­tion, awareness, acceptance, and empathy. Advising and helping patients to be present and exist with their thoughts is a psycho-educational approach and form of advice consistent with principles of supportive therapy. In this article, I provide a practical framework for doing and teaching mind­fulness using the mnemonic BREATHE.

Flow is more important than sequence
The 7 elements of mindfulness exercises contained in BREATHE do not need to be done in order. Rather, mindfulness gener­ally involves each of the following elements flowing, or tumbling, into each other, not standing as a distinct entity.

Being in the now, “as is,” without judg­ment (eg, being present/being vs doing; Buddhist origins; diaphragmatic breath­ing/body scans; “breathing-space” medi­tation exercises). In general, mindfulness meditation exercises focus on some sen­sory experience (eg, the physical sensa­tion of breathing or of a difficult emotion, or sounds and smells in the environment). Some mindfulness meditations are called “body scans.”

A patient can shift his (her) focus during mindfulness meditation to a sound or some other stimulus intruding on his original meditative focus, such as an intense emo­tion or pain, that might arise and become the new focus of mindfulness meditation. Ideally, mindfulness exercises are done without the intention of achieving anything (ie, there is no “striving” for anything when being mindful). Striving, after all, is doing; mindfulness is being.

R(AIN). Mindfulness, as operationalized by Kabat-Zinn,⁴ starts with a focus on breath­ing similar to many meditation practices in Buddhism. When the patient wanders into intense emotions, such as suffering, that become the focus of mindfulness, use the mnemonic-within-a-mnemonic RAIN as a guide; typically, this involves first anchoring with a few deep breaths, and then becoming mindful by:
   • Recognizing (and labeling, nam­ing, “tagging”) the emotion (eg, sad, hurt, angry, embarrassed); this engages frontal lobe processes that diminishes amygdaloid limbic system overactivity¹
   • Allowing (ie, accepting suffering)
   • Investigating, with an open and curious attitude, using one’s senses to experience, feel, and explore thoughts and emotions
   • Non-identifying with one’s thoughts, feelings, emotions, or suffering (expressed in the important mindfulness refrain: “You are not your thoughts or emotions. You are the entity that simply is aware of them.”).

Experiencing. The patient stops at the perceived experience or sensation and does not automatically react with thoughts, emo­tions, distress, or judgments. Mindfulness is a psychotherapeutic intervention that is “more experiential than cognitive.” Encourage the patient to stop at the “door of experience” and not enter the doors of thinking, emotion, and feeling.

Accepting without judgment—also called “awarenessing” or “avoid avoiding.” This involves being aware of the experi­ence regardless of what it entails, whether suffering, thoughts, emotions, or pain, and not trying to escape or avoid the difficult experience. Psychodynamic principles help us understand how psychological defenses designed to avoid the experience of the “unbearable affect” often lead to more problems for patients. In mindfulness, only avoiding is to be avoided.

Thoughts. People tend to over-identify with their thoughts and emotions. In mindfulness, you emphasize to the patient that (1) he is not his thoughts or emotions and (2) these cognitive processes do not represent facts.

Heartfulness—or, healthy, happy, free from harm. Mindfulness from the Buddhist tradition also includes “heartfulness” and “loving-kindness” and the development of compassion and kindness for one’s self and others. Mindfulness meditation there­fore also involves development of loving-kindness/compassion toward oneself and others—even one’s enemies (eg, “May I be healthy, happy, and free from harm.”). I have found this aspect of mindfulness useful for patients who feel angry or entitled, with characterological problems.

Empathy for others. As an extension of, or further emphasis on, loving-kindness, medi­tation focuses on understanding the suffer­ing of others. In certain monastic practices, this mindfulness meditation involves “tak­ing on” the suffering of another.

Disclosure
The author reports no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.

Mindfulness has become an impor­tant supportive psychotherapeutic intervention for a variety of psychi­atric conditions,^1-3 regardless of what other modalities the psychiatrist employs (eg, phar­macotherapy, other psychotherapeutic inter­ventions). In general, mindfulness involves engaging in meditation exercises, analogous to working out in the gym, to strengthen “mindfulness muscles.” These exercises increase the patient’s ability to remain in the moment, “as is,” and without judgment.

I think of mindfulness exercises as an “ego gym” for the patient as he (she) gets to exercise the ego functions of agency, atten­tion, awareness, acceptance, and empathy. Advising and helping patients to be present and exist with their thoughts is a psycho-educational approach and form of advice consistent with principles of supportive therapy. In this article, I provide a practical framework for doing and teaching mind­fulness using the mnemonic BREATHE.

Flow is more important than sequence
The 7 elements of mindfulness exercises contained in BREATHE do not need to be done in order. Rather, mindfulness gener­ally involves each of the following elements flowing, or tumbling, into each other, not standing as a distinct entity.

Being in the now, “as is,” without judg­ment (eg, being present/being vs doing; Buddhist origins; diaphragmatic breath­ing/body scans; “breathing-space” medi­tation exercises). In general, mindfulness meditation exercises focus on some sen­sory experience (eg, the physical sensa­tion of breathing or of a difficult emotion, or sounds and smells in the environment). Some mindfulness meditations are called “body scans.”

A patient can shift his (her) focus during mindfulness meditation to a sound or some other stimulus intruding on his original meditative focus, such as an intense emo­tion or pain, that might arise and become the new focus of mindfulness meditation. Ideally, mindfulness exercises are done without the intention of achieving anything (ie, there is no “striving” for anything when being mindful). Striving, after all, is doing; mindfulness is being.

R(AIN). Mindfulness, as operationalized by Kabat-Zinn,⁴ starts with a focus on breath­ing similar to many meditation practices in Buddhism. When the patient wanders into intense emotions, such as suffering, that become the focus of mindfulness, use the mnemonic-within-a-mnemonic RAIN as a guide; typically, this involves first anchoring with a few deep breaths, and then becoming mindful by:
   • Recognizing (and labeling, nam­ing, “tagging”) the emotion (eg, sad, hurt, angry, embarrassed); this engages frontal lobe processes that diminishes amygdaloid limbic system overactivity¹
   • Allowing (ie, accepting suffering)
   • Investigating, with an open and curious attitude, using one’s senses to experience, feel, and explore thoughts and emotions
   • Non-identifying with one’s thoughts, feelings, emotions, or suffering (expressed in the important mindfulness refrain: “You are not your thoughts or emotions. You are the entity that simply is aware of them.”).

Experiencing. The patient stops at the perceived experience or sensation and does not automatically react with thoughts, emo­tions, distress, or judgments. Mindfulness is a psychotherapeutic intervention that is “more experiential than cognitive.” Encourage the patient to stop at the “door of experience” and not enter the doors of thinking, emotion, and feeling.

Accepting without judgment—also called “awarenessing” or “avoid avoiding.” This involves being aware of the experi­ence regardless of what it entails, whether suffering, thoughts, emotions, or pain, and not trying to escape or avoid the difficult experience. Psychodynamic principles help us understand how psychological defenses designed to avoid the experience of the “unbearable affect” often lead to more problems for patients. In mindfulness, only avoiding is to be avoided.

Thoughts. People tend to over-identify with their thoughts and emotions. In mindfulness, you emphasize to the patient that (1) he is not his thoughts or emotions and (2) these cognitive processes do not represent facts.

Heartfulness—or, healthy, happy, free from harm. Mindfulness from the Buddhist tradition also includes “heartfulness” and “loving-kindness” and the development of compassion and kindness for one’s self and others. Mindfulness meditation there­fore also involves development of loving-kindness/compassion toward oneself and others—even one’s enemies (eg, “May I be healthy, happy, and free from harm.”). I have found this aspect of mindfulness useful for patients who feel angry or entitled, with characterological problems.

Empathy for others. As an extension of, or further emphasis on, loving-kindness, medi­tation focuses on understanding the suffer­ing of others. In certain monastic practices, this mindfulness meditation involves “tak­ing on” the suffering of another.

Disclosure
The author reports no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.

Asenapine an atypical antipsychotic sold under the brand name Saphris, was granted a second, pediatric indi­cation by the FDA in March 2015 as mono­therapy for acute treatment of manic or mixed episodes of bipolar I disorder in chil­dren and adolescents age 10 to 17 (Table 1).¹ (Asenapine was first approved in August 2009 as monotherapy or adjunctive therapy to lithium or valproate in adults for schizo­phrenia and bipolar I disorder.^1,2)

Dosage and administration
Asenapine is available as 2.5-, 5-, and 10-mg sublingual tablets, the only atypical anti­psychotic with this formulation.¹ The rec­ommended dosage for the new indication is 2.5 mg twice daily for 3 days, titrated to 5 mg twice daily, titrated again to 10 mg twice daily after 3 days.³ In a phase I study, pedi­atric patients appeared to be more sensitive to dystonia when the recommended dosage escalation schedule was not followed.³

In clinical trials, drinking water 2 to 5 minutes after taking asenapine decreased exposure to the drug. Instruct patients not to swallow the tablet and to avoid eating and drinking for 10 minutes after administration.³

For full prescribing information for pediat­ric and adult patients, see Reference 3.

Safety and efficacy
In a 3-week, placebo-controlled, double-blind trial of 403 patients, 302 children and adolescents age 10 to 17 received asenap­ine at fixed dosages of 2.5 to 10 mg twice daily; the remainder were given placebo. The Young Mania Rating Scale (YMRS) total score and Clinical Global Impressions Severity of Illness scores of patients who received asenapine improved significantly compared with those who received placebo, as measured by change from baseline to week 3 (Table 2).¹

Asenapine was not shown to be effective in pediatric patients with schizophrenia in an 8-week, placebo-controlled, double-blind trial.

The pharmacokinetics of asenapine in pediatric patients are similar to those seen in adults.

Adverse effects
In pediatric patients, the most common reported adverse effects of asenapine are:
   • dizziness
   • dysgeusia
   • fatigue
   • increased appetite
   • increased weight
   • nausea
   • oral paresthesia
   • somnolence.

Similar adverse effects were reported in the pediatric bipolar disorder and adult bipolar disorder clinical trials (Table 3).³ A complete list of reported adverse effects is given in the package insert.³

When treating pediatric patients, moni­tor the child’s weight gain against expected normal weight gain.

Asenapine is contraindicated in patients with hepatic impairment and those who have a hypersensitivity to asenapine or any components in its formulation.³

Asenapine an atypical antipsychotic sold under the brand name Saphris, was granted a second, pediatric indi­cation by the FDA in March 2015 as mono­therapy for acute treatment of manic or mixed episodes of bipolar I disorder in chil­dren and adolescents age 10 to 17 (Table 1).¹ (Asenapine was first approved in August 2009 as monotherapy or adjunctive therapy to lithium or valproate in adults for schizo­phrenia and bipolar I disorder.^1,2)

Dosage and administration
Asenapine is available as 2.5-, 5-, and 10-mg sublingual tablets, the only atypical anti­psychotic with this formulation.¹ The rec­ommended dosage for the new indication is 2.5 mg twice daily for 3 days, titrated to 5 mg twice daily, titrated again to 10 mg twice daily after 3 days.³ In a phase I study, pedi­atric patients appeared to be more sensitive to dystonia when the recommended dosage escalation schedule was not followed.³

In clinical trials, drinking water 2 to 5 minutes after taking asenapine decreased exposure to the drug. Instruct patients not to swallow the tablet and to avoid eating and drinking for 10 minutes after administration.³

For full prescribing information for pediat­ric and adult patients, see Reference 3.

Safety and efficacy
In a 3-week, placebo-controlled, double-blind trial of 403 patients, 302 children and adolescents age 10 to 17 received asenap­ine at fixed dosages of 2.5 to 10 mg twice daily; the remainder were given placebo. The Young Mania Rating Scale (YMRS) total score and Clinical Global Impressions Severity of Illness scores of patients who received asenapine improved significantly compared with those who received placebo, as measured by change from baseline to week 3 (Table 2).¹

Asenapine was not shown to be effective in pediatric patients with schizophrenia in an 8-week, placebo-controlled, double-blind trial.

The pharmacokinetics of asenapine in pediatric patients are similar to those seen in adults.

Adverse effects
In pediatric patients, the most common reported adverse effects of asenapine are:
   • dizziness
   • dysgeusia
   • fatigue
   • increased appetite
   • increased weight
   • nausea
   • oral paresthesia
   • somnolence.

Similar adverse effects were reported in the pediatric bipolar disorder and adult bipolar disorder clinical trials (Table 3).³ A complete list of reported adverse effects is given in the package insert.³

When treating pediatric patients, moni­tor the child’s weight gain against expected normal weight gain.

Asenapine is contraindicated in patients with hepatic impairment and those who have a hypersensitivity to asenapine or any components in its formulation.³

Asenapine an atypical antipsychotic sold under the brand name Saphris, was granted a second, pediatric indi­cation by the FDA in March 2015 as mono­therapy for acute treatment of manic or mixed episodes of bipolar I disorder in chil­dren and adolescents age 10 to 17 (Table 1).¹ (Asenapine was first approved in August 2009 as monotherapy or adjunctive therapy to lithium or valproate in adults for schizo­phrenia and bipolar I disorder.^1,2)

Dosage and administration
Asenapine is available as 2.5-, 5-, and 10-mg sublingual tablets, the only atypical anti­psychotic with this formulation.¹ The rec­ommended dosage for the new indication is 2.5 mg twice daily for 3 days, titrated to 5 mg twice daily, titrated again to 10 mg twice daily after 3 days.³ In a phase I study, pedi­atric patients appeared to be more sensitive to dystonia when the recommended dosage escalation schedule was not followed.³

In clinical trials, drinking water 2 to 5 minutes after taking asenapine decreased exposure to the drug. Instruct patients not to swallow the tablet and to avoid eating and drinking for 10 minutes after administration.³

For full prescribing information for pediat­ric and adult patients, see Reference 3.

Safety and efficacy
In a 3-week, placebo-controlled, double-blind trial of 403 patients, 302 children and adolescents age 10 to 17 received asenap­ine at fixed dosages of 2.5 to 10 mg twice daily; the remainder were given placebo. The Young Mania Rating Scale (YMRS) total score and Clinical Global Impressions Severity of Illness scores of patients who received asenapine improved significantly compared with those who received placebo, as measured by change from baseline to week 3 (Table 2).¹

Asenapine was not shown to be effective in pediatric patients with schizophrenia in an 8-week, placebo-controlled, double-blind trial.

The pharmacokinetics of asenapine in pediatric patients are similar to those seen in adults.

Adverse effects
In pediatric patients, the most common reported adverse effects of asenapine are:
   • dizziness
   • dysgeusia
   • fatigue
   • increased appetite
   • increased weight
   • nausea
   • oral paresthesia
   • somnolence.

Similar adverse effects were reported in the pediatric bipolar disorder and adult bipolar disorder clinical trials (Table 3).³ A complete list of reported adverse effects is given in the package insert.³

When treating pediatric patients, moni­tor the child’s weight gain against expected normal weight gain.

Asenapine is contraindicated in patients with hepatic impairment and those who have a hypersensitivity to asenapine or any components in its formulation.³

Young adult cancer survivors will continue to have high hospitalization rates over time, a Canadian study shows.

In five-year cancer survivors diagnosed between ages 20 and 44, hospitalization rates were elevated for at least 20 years, compared to rates in age- and sex-matched controls, according to Dr. Nancy N. Baxter at St. Michael's Hospital in Toronto and colleagues.

For all malignancies except melanoma and testicular cancer, the adjusted relative rate (ARR) of hospitalizations was significantly higher among survivors than controls.

"Late effects and complications of cancer treatments are experienced by many survivors for the rest of their lives," Dr. Baxter told Reuters Health via e-mail. The patients in this population-based study were treated from 1992-1999. "Therapies have changed, she said. "In some cases there may be fewer late effects, but in others, they may be worse."

The study cohort included 20,275 survivors of young adult cancers who were recurrence-free for at least five years, and 101,344 controls. The authors observed survivors for a median of 9.93 years (range 0-16 years), according to their report online July 13 in the Journal of Clinical Oncology. During this period, 34.3% had at least one hospitalization,

vs. 27.3% for controls. The rate per 100 person-years was similar between male and female survivors.

Overall, the ARR of hospitalization in survivors compared with controls was 1.51. At all-time periods, survivors were more likely to be hospitalized than controls. The rate of hospitalization (per 100-person years) among survivors was 0.22 during years 5 to 8, 9 to11, and 12 to14. It decreased significantly during years 15 to 17 and 18 to 20, falling to 0.17 and 0.15, respectively (P<0.0001). Among controls, the hospitalization rate was relatively constant during all time periods, ranging from 0.13 at 5 to 8 years to 0.12 at years 18 to 20.

The ARR of hospitalizations in survivors compared with controls was also relatively constant during for the first three3 time periods: 1.67, 1.55, and 1.57 at years 5 to 8, 9 to

11, and 12 to 14, respectively. It decreased to 1.36 at 15 to 17 years and 1.22 at years 18 to 20. Those who survived gastrointestinal, urologic, colorectal, or brain cancers, or leukemia or lymphoma, had an ARR of hospitalization at least twice that of controls.

"We only looked at hospital admissions, not visits to the family doctor or medical conditions and disabilities that didn't require inpatient care," Dr. Baxter said, explaining that this likely underestimated the long-term impact of intense treatments that include surgery, chemotherapy, radiation, and hormonal therapy.

"Understanding the late effects of cancer treatment will help us design better treatments, counsel patients, and improve symptom management."

Young adult cancer survivors will continue to have high hospitalization rates over time, a Canadian study shows.

In five-year cancer survivors diagnosed between ages 20 and 44, hospitalization rates were elevated for at least 20 years, compared to rates in age- and sex-matched controls, according to Dr. Nancy N. Baxter at St. Michael's Hospital in Toronto and colleagues.

For all malignancies except melanoma and testicular cancer, the adjusted relative rate (ARR) of hospitalizations was significantly higher among survivors than controls.

"Late effects and complications of cancer treatments are experienced by many survivors for the rest of their lives," Dr. Baxter told Reuters Health via e-mail. The patients in this population-based study were treated from 1992-1999. "Therapies have changed, she said. "In some cases there may be fewer late effects, but in others, they may be worse."

The study cohort included 20,275 survivors of young adult cancers who were recurrence-free for at least five years, and 101,344 controls. The authors observed survivors for a median of 9.93 years (range 0-16 years), according to their report online July 13 in the Journal of Clinical Oncology. During this period, 34.3% had at least one hospitalization,

vs. 27.3% for controls. The rate per 100 person-years was similar between male and female survivors.

Overall, the ARR of hospitalization in survivors compared with controls was 1.51. At all-time periods, survivors were more likely to be hospitalized than controls. The rate of hospitalization (per 100-person years) among survivors was 0.22 during years 5 to 8, 9 to11, and 12 to14. It decreased significantly during years 15 to 17 and 18 to 20, falling to 0.17 and 0.15, respectively (P<0.0001). Among controls, the hospitalization rate was relatively constant during all time periods, ranging from 0.13 at 5 to 8 years to 0.12 at years 18 to 20.

The ARR of hospitalizations in survivors compared with controls was also relatively constant during for the first three3 time periods: 1.67, 1.55, and 1.57 at years 5 to 8, 9 to

11, and 12 to 14, respectively. It decreased to 1.36 at 15 to 17 years and 1.22 at years 18 to 20. Those who survived gastrointestinal, urologic, colorectal, or brain cancers, or leukemia or lymphoma, had an ARR of hospitalization at least twice that of controls.

"We only looked at hospital admissions, not visits to the family doctor or medical conditions and disabilities that didn't require inpatient care," Dr. Baxter said, explaining that this likely underestimated the long-term impact of intense treatments that include surgery, chemotherapy, radiation, and hormonal therapy.

"Understanding the late effects of cancer treatment will help us design better treatments, counsel patients, and improve symptom management."

Young adult cancer survivors will continue to have high hospitalization rates over time, a Canadian study shows.

In five-year cancer survivors diagnosed between ages 20 and 44, hospitalization rates were elevated for at least 20 years, compared to rates in age- and sex-matched controls, according to Dr. Nancy N. Baxter at St. Michael's Hospital in Toronto and colleagues.

For all malignancies except melanoma and testicular cancer, the adjusted relative rate (ARR) of hospitalizations was significantly higher among survivors than controls.

"Late effects and complications of cancer treatments are experienced by many survivors for the rest of their lives," Dr. Baxter told Reuters Health via e-mail. The patients in this population-based study were treated from 1992-1999. "Therapies have changed, she said. "In some cases there may be fewer late effects, but in others, they may be worse."

The study cohort included 20,275 survivors of young adult cancers who were recurrence-free for at least five years, and 101,344 controls. The authors observed survivors for a median of 9.93 years (range 0-16 years), according to their report online July 13 in the Journal of Clinical Oncology. During this period, 34.3% had at least one hospitalization,

vs. 27.3% for controls. The rate per 100 person-years was similar between male and female survivors.

Overall, the ARR of hospitalization in survivors compared with controls was 1.51. At all-time periods, survivors were more likely to be hospitalized than controls. The rate of hospitalization (per 100-person years) among survivors was 0.22 during years 5 to 8, 9 to11, and 12 to14. It decreased significantly during years 15 to 17 and 18 to 20, falling to 0.17 and 0.15, respectively (P<0.0001). Among controls, the hospitalization rate was relatively constant during all time periods, ranging from 0.13 at 5 to 8 years to 0.12 at years 18 to 20.

The ARR of hospitalizations in survivors compared with controls was also relatively constant during for the first three3 time periods: 1.67, 1.55, and 1.57 at years 5 to 8, 9 to

11, and 12 to 14, respectively. It decreased to 1.36 at 15 to 17 years and 1.22 at years 18 to 20. Those who survived gastrointestinal, urologic, colorectal, or brain cancers, or leukemia or lymphoma, had an ARR of hospitalization at least twice that of controls.

"We only looked at hospital admissions, not visits to the family doctor or medical conditions and disabilities that didn't require inpatient care," Dr. Baxter said, explaining that this likely underestimated the long-term impact of intense treatments that include surgery, chemotherapy, radiation, and hormonal therapy.

"Understanding the late effects of cancer treatment will help us design better treatments, counsel patients, and improve symptom management."

Session: Let’s Measure Our Own Performance: Propose and Evaluate Pediatric Hospital Medicine Quality Indicators

Summary: During this workshop, a staff of multiple, nationally-recognized quality leaders led a group to review, help develop, and help validate quality measures. The workshop was facilitated via the use of interactive survey tools, didactic sessions, and small groups.

Presenters discussed why quality measures are important and relevant. These included:

1. Improved quality of care,
2. Demonstration of value,
3. Third-party pay for performance indicators,
4. Determining our own indicators (versus being chosen for us), and
5. Performance incentives.

As part of the introduction to the workshop, the various quality measure validation methods were reviewed. These consisted of methods such as UCLA/RAND and Delphi Panel, as a means to determine validation and feasibility.

Validation was discussed in terms of what is being measured is the true outcome that was hoped to be achieved. The feasibility component used to make sure that the data used for quality measures, or process to be implemented for improvement, can easily be acquired to determine adherence, and that data is free of error. Facilitators reviewed various examples of validity and feasibility of quality measures with direct examples and discussions with attendees.

During the first breakout session, the groups were separated into teams focused on 1. care transitions, 2. safety, and 3. clinical care. The groups were asked to determine three quality indicators per individual, discuss the top five indicators voted on by the group, and than to review and discuss as a group the validity and feasibility of the measures using a scoring tool of 1-3: Not Valid/Feasible, 4-6: Equivocal, 7-9: Valid/Feasible. At the end, a delegated group speaker was asked to discuss either the pros/cons of one of their measures in regards to validity and feasibility to the total audience. Facilitators assisted on clarifying the reasons of why validity and feasibility metrics were appropriate.

During the final parts of workshop, positive and negatives of quality metrics determination methodology were discussed. The attendees reflected on the process of how quality measures are determined along with how these may be used within their settings.

Key Takeaways

Clearly determining the validity and feasibility of quality metrics for pediatrics has become an important topic. It not only has significant ramifications to the value we provide to our patients, but also the financial sustainability of programs and institutions, especially with the current changes in payment models. The workshop gave a clear and concise way of how to come up with quality metrics and the facilitators greatly added to the understanding of how we can “raise the floor” and “raise the ceiling” of pediatric care. TH

Dr. Alvarez is a pediatric hospitalist and medical director of community hospital services at Children’s National Health System in Washington, D.C.

Session: Let’s Measure Our Own Performance: Propose and Evaluate Pediatric Hospital Medicine Quality Indicators

Summary: During this workshop, a staff of multiple, nationally-recognized quality leaders led a group to review, help develop, and help validate quality measures. The workshop was facilitated via the use of interactive survey tools, didactic sessions, and small groups.

Presenters discussed why quality measures are important and relevant. These included:

1. Improved quality of care,
2. Demonstration of value,
3. Third-party pay for performance indicators,
4. Determining our own indicators (versus being chosen for us), and
5. Performance incentives.

As part of the introduction to the workshop, the various quality measure validation methods were reviewed. These consisted of methods such as UCLA/RAND and Delphi Panel, as a means to determine validation and feasibility.

Validation was discussed in terms of what is being measured is the true outcome that was hoped to be achieved. The feasibility component used to make sure that the data used for quality measures, or process to be implemented for improvement, can easily be acquired to determine adherence, and that data is free of error. Facilitators reviewed various examples of validity and feasibility of quality measures with direct examples and discussions with attendees.

During the first breakout session, the groups were separated into teams focused on 1. care transitions, 2. safety, and 3. clinical care. The groups were asked to determine three quality indicators per individual, discuss the top five indicators voted on by the group, and than to review and discuss as a group the validity and feasibility of the measures using a scoring tool of 1-3: Not Valid/Feasible, 4-6: Equivocal, 7-9: Valid/Feasible. At the end, a delegated group speaker was asked to discuss either the pros/cons of one of their measures in regards to validity and feasibility to the total audience. Facilitators assisted on clarifying the reasons of why validity and feasibility metrics were appropriate.

During the final parts of workshop, positive and negatives of quality metrics determination methodology were discussed. The attendees reflected on the process of how quality measures are determined along with how these may be used within their settings.

Key Takeaways

Clearly determining the validity and feasibility of quality metrics for pediatrics has become an important topic. It not only has significant ramifications to the value we provide to our patients, but also the financial sustainability of programs and institutions, especially with the current changes in payment models. The workshop gave a clear and concise way of how to come up with quality metrics and the facilitators greatly added to the understanding of how we can “raise the floor” and “raise the ceiling” of pediatric care. TH

Dr. Alvarez is a pediatric hospitalist and medical director of community hospital services at Children’s National Health System in Washington, D.C.

Session: Let’s Measure Our Own Performance: Propose and Evaluate Pediatric Hospital Medicine Quality Indicators

Summary: During this workshop, a staff of multiple, nationally-recognized quality leaders led a group to review, help develop, and help validate quality measures. The workshop was facilitated via the use of interactive survey tools, didactic sessions, and small groups.

Presenters discussed why quality measures are important and relevant. These included:

1. Improved quality of care,
2. Demonstration of value,
3. Third-party pay for performance indicators,
4. Determining our own indicators (versus being chosen for us), and
5. Performance incentives.

As part of the introduction to the workshop, the various quality measure validation methods were reviewed. These consisted of methods such as UCLA/RAND and Delphi Panel, as a means to determine validation and feasibility.

Validation was discussed in terms of what is being measured is the true outcome that was hoped to be achieved. The feasibility component used to make sure that the data used for quality measures, or process to be implemented for improvement, can easily be acquired to determine adherence, and that data is free of error. Facilitators reviewed various examples of validity and feasibility of quality measures with direct examples and discussions with attendees.

During the first breakout session, the groups were separated into teams focused on 1. care transitions, 2. safety, and 3. clinical care. The groups were asked to determine three quality indicators per individual, discuss the top five indicators voted on by the group, and than to review and discuss as a group the validity and feasibility of the measures using a scoring tool of 1-3: Not Valid/Feasible, 4-6: Equivocal, 7-9: Valid/Feasible. At the end, a delegated group speaker was asked to discuss either the pros/cons of one of their measures in regards to validity and feasibility to the total audience. Facilitators assisted on clarifying the reasons of why validity and feasibility metrics were appropriate.

During the final parts of workshop, positive and negatives of quality metrics determination methodology were discussed. The attendees reflected on the process of how quality measures are determined along with how these may be used within their settings.

Key Takeaways

Clearly determining the validity and feasibility of quality metrics for pediatrics has become an important topic. It not only has significant ramifications to the value we provide to our patients, but also the financial sustainability of programs and institutions, especially with the current changes in payment models. The workshop gave a clear and concise way of how to come up with quality metrics and the facilitators greatly added to the understanding of how we can “raise the floor” and “raise the ceiling” of pediatric care. TH

Dr. Alvarez is a pediatric hospitalist and medical director of community hospital services at Children’s National Health System in Washington, D.C.

“The Burden of Craft in Arthroscopic Rotator Cuff Repair” is a summary of the annual Neer Lecture that was delivered by Stephen S. Burkhart, MD, at the 2014 annual meeting of American Shoulder and Elbow Surgeons. It is a fascinating personal story of the 35-year evolution of arthroscopic rotator cuff surgery presented by one of the most respected arthroscopic innovators of our times. I especially enjoyed his apt citations of classic leaders—Churchill and Gandhi—but 3 points I believe deserve special comment.

First, Steve describes the challenges he faced bringing new products to market in the 1980s. How do we resolve the inherent conflict between innovation that introduces new technology and the “tried and true” standards of established practice? Do the hard work that Steve has done over the years: pose a hypothesis, design a study to answer the question, publish results in peer-reviewed journals, and embrace the techniques that demonstrate better outcomes for patients.

My second point relates to surgeon–device industry relationships, a subject of great interest to The American Journal of Orthopedics dating back to 2006.^1-3 Dr. Burkhart learned early on that he could not fashion new arthroscopic instruments in his garage. Nor could a company develop useful instruments without a knowledgeable surgeon’s input. Hence, a partnership between the innovator-surgeon and the device industry is essential to bring new and effective “tools” to market. Dr. Burkhart’s partnership with Arthrex has benefited many thousands of patients.

The agreements announced in 2007 between the US Department of Justice and 5 orthopedic device manufacturers (interestingly, current presidential candidate and Governor of New Jersey Chris Christie was the lead US Attorney on the case!) dramatically altered the surgeon–industry interaction and established strict guidelines that governed these relationships.⁴ These were needed reforms. However, the changes did not preclude an entrepreneurial surgeon with great ideas and a device manufacturer from profiting from excellent products that advanced patient care, provided, quoting from my editorial of 2006, “that these partnerships comply with legal and ethical standards” and are transparent as well as fully disclosed.¹

Finally, Steve’s last point focuses on the “burden of craft,” a topic dear to all orthopedic surgeons and our professional societies. All of us are committed to improving our surgical skills and, as a profession, we are consistently engaged in learning from our talented colleagues, who are only too willing to share their expertise. The burden of craft requires eager students and dedicated teachers, all committed to the same goal—better outcomes for our patients. We are indeed fortunate that, as orthopedic surgeons, we fundamentally support a culture of continued learning.

I thank Steve for his eloquent paper on this important principle.

“The Burden of Craft in Arthroscopic Rotator Cuff Repair” is a summary of the annual Neer Lecture that was delivered by Stephen S. Burkhart, MD, at the 2014 annual meeting of American Shoulder and Elbow Surgeons. It is a fascinating personal story of the 35-year evolution of arthroscopic rotator cuff surgery presented by one of the most respected arthroscopic innovators of our times. I especially enjoyed his apt citations of classic leaders—Churchill and Gandhi—but 3 points I believe deserve special comment.

First, Steve describes the challenges he faced bringing new products to market in the 1980s. How do we resolve the inherent conflict between innovation that introduces new technology and the “tried and true” standards of established practice? Do the hard work that Steve has done over the years: pose a hypothesis, design a study to answer the question, publish results in peer-reviewed journals, and embrace the techniques that demonstrate better outcomes for patients.

My second point relates to surgeon–device industry relationships, a subject of great interest to The American Journal of Orthopedics dating back to 2006.^1-3 Dr. Burkhart learned early on that he could not fashion new arthroscopic instruments in his garage. Nor could a company develop useful instruments without a knowledgeable surgeon’s input. Hence, a partnership between the innovator-surgeon and the device industry is essential to bring new and effective “tools” to market. Dr. Burkhart’s partnership with Arthrex has benefited many thousands of patients.

The agreements announced in 2007 between the US Department of Justice and 5 orthopedic device manufacturers (interestingly, current presidential candidate and Governor of New Jersey Chris Christie was the lead US Attorney on the case!) dramatically altered the surgeon–industry interaction and established strict guidelines that governed these relationships.⁴ These were needed reforms. However, the changes did not preclude an entrepreneurial surgeon with great ideas and a device manufacturer from profiting from excellent products that advanced patient care, provided, quoting from my editorial of 2006, “that these partnerships comply with legal and ethical standards” and are transparent as well as fully disclosed.¹

Finally, Steve’s last point focuses on the “burden of craft,” a topic dear to all orthopedic surgeons and our professional societies. All of us are committed to improving our surgical skills and, as a profession, we are consistently engaged in learning from our talented colleagues, who are only too willing to share their expertise. The burden of craft requires eager students and dedicated teachers, all committed to the same goal—better outcomes for our patients. We are indeed fortunate that, as orthopedic surgeons, we fundamentally support a culture of continued learning.

I thank Steve for his eloquent paper on this important principle.

“The Burden of Craft in Arthroscopic Rotator Cuff Repair” is a summary of the annual Neer Lecture that was delivered by Stephen S. Burkhart, MD, at the 2014 annual meeting of American Shoulder and Elbow Surgeons. It is a fascinating personal story of the 35-year evolution of arthroscopic rotator cuff surgery presented by one of the most respected arthroscopic innovators of our times. I especially enjoyed his apt citations of classic leaders—Churchill and Gandhi—but 3 points I believe deserve special comment.

First, Steve describes the challenges he faced bringing new products to market in the 1980s. How do we resolve the inherent conflict between innovation that introduces new technology and the “tried and true” standards of established practice? Do the hard work that Steve has done over the years: pose a hypothesis, design a study to answer the question, publish results in peer-reviewed journals, and embrace the techniques that demonstrate better outcomes for patients.

My second point relates to surgeon–device industry relationships, a subject of great interest to The American Journal of Orthopedics dating back to 2006.^1-3 Dr. Burkhart learned early on that he could not fashion new arthroscopic instruments in his garage. Nor could a company develop useful instruments without a knowledgeable surgeon’s input. Hence, a partnership between the innovator-surgeon and the device industry is essential to bring new and effective “tools” to market. Dr. Burkhart’s partnership with Arthrex has benefited many thousands of patients.

The agreements announced in 2007 between the US Department of Justice and 5 orthopedic device manufacturers (interestingly, current presidential candidate and Governor of New Jersey Chris Christie was the lead US Attorney on the case!) dramatically altered the surgeon–industry interaction and established strict guidelines that governed these relationships.⁴ These were needed reforms. However, the changes did not preclude an entrepreneurial surgeon with great ideas and a device manufacturer from profiting from excellent products that advanced patient care, provided, quoting from my editorial of 2006, “that these partnerships comply with legal and ethical standards” and are transparent as well as fully disclosed.¹

Finally, Steve’s last point focuses on the “burden of craft,” a topic dear to all orthopedic surgeons and our professional societies. All of us are committed to improving our surgical skills and, as a profession, we are consistently engaged in learning from our talented colleagues, who are only too willing to share their expertise. The burden of craft requires eager students and dedicated teachers, all committed to the same goal—better outcomes for our patients. We are indeed fortunate that, as orthopedic surgeons, we fundamentally support a culture of continued learning.

I thank Steve for his eloquent paper on this important principle.

For HIV-positive patients with Burkitt lymphoma, a modified intensive chemotherapy regimen produced overall and progression-free survival rates comparable with those seen in HIV-free patients with Burkitt, with manageable toxicities, reported researchers in a multicenter clinical trial.

The AIDS Malignancy Consortium (AMC) 048 study looked at the use of a modified version of the dose intensive CODOX-M/IVAC regimen, consisting of cyclophosphamide, vincristine, doxorubicin, high-dose methotrexate/ifosfamide, etoposide, and high-dose cytarabine. Compared with the standard regimen, the investigators added rituximab, reduced and/or rescheduled cyclophosphamide and methotrexate, limited the use of vincristine, and used combination intrathecal chemotherapy to prevent central nervous system involvement.

Courtesy Wikimedia Commons/Ed Uthman, MD/Creative Commons License

The study included 34 HIV-positive patients (30 men and 4 women) with Burkitt, 26 of whom were also receiving highly active antiretroviral therapy (HAART). The patients ranged in age from 19-55 (median 42) years. Of the 34 patients, 25 had Ann Arbor stage IV disease, 2 had stage III, 1 had stage IIE, 2 had stage II, and 4 had stage I. Median age was 42 years (range, 19-55 years).

The median CD4 count was 195 cells/mL; five patients had fewer than 100 cells/mL

Progression-free survival at 1 year was 69%, and 1- and 2-year overall survival were 72% and 69%, respectively.

The modified CODOX-M/IVAC regimen was associated with a grade 3 to 4 toxicity rate of 79%, with no grade 3 or 4 mucositis reported. In contrast, virtually all patients who receive the unmodified regimen develop at least one grade 3 or greater toxicity.

In total, there were 20 hematologic, 14 infectious, and 6 metabolic toxicities. Five patients did not complete treatment because of adverse events.

There were 11 deaths, including 1 treatment-related death of a patient with encephalopathy, hepatic failure, hepatitis B, and pneumonia cited as contributing causes. Of the remaining 10 patients, 8 died from systemic disease progression, and 2 died during follow-up, 1 during remission from a fungal infection and 1 from nonmalignant complications of HIV.

The investigators say that the addition of rituximab may have contributed to the favorable outcomes, and that rescheduling and limiting the amount of high-dose methotrexate delivered likely contributed to lower incidences of both severe mucositis and neutropenic fever.

Although a separate trial is evaluating a different regimen (EPOCH-R; etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab) in Burkitt lymphoma, “the modified AMC 048 version of CODOX-M/IVAC-R may better serve patients who present with CNS disease or are at high risk for CNS relapse (e.g., patients with bone marrow, testicular, or multiple extranodal sites), because it contains high-dose cytarabine and methotrexate, drugs that cross the blood-brain barrier. Consequently, AMC048 represents a reasonable treatment option in the appropriate setting, possibly irrespective of HIV status.”

The study by Dr. Ariela Noy from the Memorial Sloan Kettering Cancer Center in New York and her colleagues, is published in Blood.

For HIV-positive patients with Burkitt lymphoma, a modified intensive chemotherapy regimen produced overall and progression-free survival rates comparable with those seen in HIV-free patients with Burkitt, with manageable toxicities, reported researchers in a multicenter clinical trial.

The AIDS Malignancy Consortium (AMC) 048 study looked at the use of a modified version of the dose intensive CODOX-M/IVAC regimen, consisting of cyclophosphamide, vincristine, doxorubicin, high-dose methotrexate/ifosfamide, etoposide, and high-dose cytarabine. Compared with the standard regimen, the investigators added rituximab, reduced and/or rescheduled cyclophosphamide and methotrexate, limited the use of vincristine, and used combination intrathecal chemotherapy to prevent central nervous system involvement.

Courtesy Wikimedia Commons/Ed Uthman, MD/Creative Commons License

The study included 34 HIV-positive patients (30 men and 4 women) with Burkitt, 26 of whom were also receiving highly active antiretroviral therapy (HAART). The patients ranged in age from 19-55 (median 42) years. Of the 34 patients, 25 had Ann Arbor stage IV disease, 2 had stage III, 1 had stage IIE, 2 had stage II, and 4 had stage I. Median age was 42 years (range, 19-55 years).

The median CD4 count was 195 cells/mL; five patients had fewer than 100 cells/mL

Progression-free survival at 1 year was 69%, and 1- and 2-year overall survival were 72% and 69%, respectively.

The modified CODOX-M/IVAC regimen was associated with a grade 3 to 4 toxicity rate of 79%, with no grade 3 or 4 mucositis reported. In contrast, virtually all patients who receive the unmodified regimen develop at least one grade 3 or greater toxicity.

In total, there were 20 hematologic, 14 infectious, and 6 metabolic toxicities. Five patients did not complete treatment because of adverse events.

There were 11 deaths, including 1 treatment-related death of a patient with encephalopathy, hepatic failure, hepatitis B, and pneumonia cited as contributing causes. Of the remaining 10 patients, 8 died from systemic disease progression, and 2 died during follow-up, 1 during remission from a fungal infection and 1 from nonmalignant complications of HIV.

The investigators say that the addition of rituximab may have contributed to the favorable outcomes, and that rescheduling and limiting the amount of high-dose methotrexate delivered likely contributed to lower incidences of both severe mucositis and neutropenic fever.

Although a separate trial is evaluating a different regimen (EPOCH-R; etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab) in Burkitt lymphoma, “the modified AMC 048 version of CODOX-M/IVAC-R may better serve patients who present with CNS disease or are at high risk for CNS relapse (e.g., patients with bone marrow, testicular, or multiple extranodal sites), because it contains high-dose cytarabine and methotrexate, drugs that cross the blood-brain barrier. Consequently, AMC048 represents a reasonable treatment option in the appropriate setting, possibly irrespective of HIV status.”

The study by Dr. Ariela Noy from the Memorial Sloan Kettering Cancer Center in New York and her colleagues, is published in Blood.

For HIV-positive patients with Burkitt lymphoma, a modified intensive chemotherapy regimen produced overall and progression-free survival rates comparable with those seen in HIV-free patients with Burkitt, with manageable toxicities, reported researchers in a multicenter clinical trial.

The AIDS Malignancy Consortium (AMC) 048 study looked at the use of a modified version of the dose intensive CODOX-M/IVAC regimen, consisting of cyclophosphamide, vincristine, doxorubicin, high-dose methotrexate/ifosfamide, etoposide, and high-dose cytarabine. Compared with the standard regimen, the investigators added rituximab, reduced and/or rescheduled cyclophosphamide and methotrexate, limited the use of vincristine, and used combination intrathecal chemotherapy to prevent central nervous system involvement.

Courtesy Wikimedia Commons/Ed Uthman, MD/Creative Commons License

The study included 34 HIV-positive patients (30 men and 4 women) with Burkitt, 26 of whom were also receiving highly active antiretroviral therapy (HAART). The patients ranged in age from 19-55 (median 42) years. Of the 34 patients, 25 had Ann Arbor stage IV disease, 2 had stage III, 1 had stage IIE, 2 had stage II, and 4 had stage I. Median age was 42 years (range, 19-55 years).

The median CD4 count was 195 cells/mL; five patients had fewer than 100 cells/mL

Progression-free survival at 1 year was 69%, and 1- and 2-year overall survival were 72% and 69%, respectively.

The modified CODOX-M/IVAC regimen was associated with a grade 3 to 4 toxicity rate of 79%, with no grade 3 or 4 mucositis reported. In contrast, virtually all patients who receive the unmodified regimen develop at least one grade 3 or greater toxicity.

In total, there were 20 hematologic, 14 infectious, and 6 metabolic toxicities. Five patients did not complete treatment because of adverse events.

There were 11 deaths, including 1 treatment-related death of a patient with encephalopathy, hepatic failure, hepatitis B, and pneumonia cited as contributing causes. Of the remaining 10 patients, 8 died from systemic disease progression, and 2 died during follow-up, 1 during remission from a fungal infection and 1 from nonmalignant complications of HIV.

The investigators say that the addition of rituximab may have contributed to the favorable outcomes, and that rescheduling and limiting the amount of high-dose methotrexate delivered likely contributed to lower incidences of both severe mucositis and neutropenic fever.

Although a separate trial is evaluating a different regimen (EPOCH-R; etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab) in Burkitt lymphoma, “the modified AMC 048 version of CODOX-M/IVAC-R may better serve patients who present with CNS disease or are at high risk for CNS relapse (e.g., patients with bone marrow, testicular, or multiple extranodal sites), because it contains high-dose cytarabine and methotrexate, drugs that cross the blood-brain barrier. Consequently, AMC048 represents a reasonable treatment option in the appropriate setting, possibly irrespective of HIV status.”

The study by Dr. Ariela Noy from the Memorial Sloan Kettering Cancer Center in New York and her colleagues, is published in Blood.

CASE A fainting spell
Ms. A, age 13, is admitted to a pediatric unit after fainting and losing consciousness for 5 minutes in the shower, during which time she was non-responsive. She reports feeling nause­ated and having blurry vision before dropping to the floor.

Ms. A reports intentional self-restriction of calories, self-induced vomiting, and other purg­ing behaviors, such as laxative abuse and exces­sive exercising.

During the mental status examination, Ms. A is lying in bed wearing hospital clothes, legs flexed at the knee, hands on her side, and a fixed gaze at the ceiling with poor eye con­tact. She is of slender stature and tall, seems slightly older than her stated age, and is poorly groomed.

Throughout the interview, Ms. A has sig­nificant psychomotor retardation, reports her mood as tired, and has a blunted affect. She speaks at a low volume and has poverty of speech; she takes deep sighs before answer­ing questions. Her thought process is linear and she cooperates with the interview. She has poor recall, including delayed 3-minute recall and poor sustained attention. Her abstraction capacity is fair and her intellect is average and comparable with her age group. Ms. A is pre­occupied that eating will cause weight gain. She denies hallucinations but reports passive death wishes with self-harm by scratching.

What is the differential diagnosis to explain Ms. A’s presentation?
   a) syncope
   b) seizures
   c) dehydration
   d) hypotension

HISTORY Preoccupied with weight
Ms. A reports vomiting twice a day, while show­ering and at night when no one is around, every day for 2 months. She stopped eating and taking in fluids 3 days before admission to the medical unit. Also, she reports restricting her diet to 700 to 1,000 calories a day, skipping lunch at school, and eating minimally at night. Ms. A uses raspberry ketones and green coffee beans, which are adver­tised to aid weight loss, and laxative pills from her mother’s medicine cabinet once or twice a week when her throat is sore from vomiting. She reports exercising excessively, which includes running, crunches, and lifting weights. She has lost approximately 30 lb in the last 2 months.

Ms. A says she fears gaining weight and feels increased guilt after eating a meal. She said that looking at food induced “anxiety attack” symptoms of increased heart rate, sweaty palms, feeling of choking, nervousness, and shakiness. She adds that she does not want to be “bigger” than her classmates. Her under­standing of the consequences of not eating is, “It will get worse, I will shut down and die. I do not fear death, I only fear getting bigger than others.”

She reports that her fixation on avoiding food started when she realized that she was the tallest girl in her class and the only girl in her class running on the track team, after which she quit athletics. She reports that depression symptoms pre-dated her eating disorder symp­toms; onset of significant depression likely was precipitated by her grandfather’s death a year earlier, and then exacerbated by the recent death of a family pet.

Ms. A’s depressive symptoms are described as anhedonia (avoiding being outside and not enjoying drawing anymore), decreased energy, tearfulness, sadness, decreased con­centration, and passive suicidal thoughts. Her mother is supportive and motivates her daughter to “get better.” Ms. A denies any symptoms of psychosis, other anxiety symp­toms, other mood disorder symptoms, sub­stance abuse, or homicidality.

Ms. A’s mother says she felt that, recently, her daughter has been having some difficulty with confused thoughts and significantly delayed responses. However, the mother reports that her daughter always had some­what delayed responses from what she felt is typical. Her mother adds that Ms. A’s suicidal thoughts have worsened since her daughter started restricting her diet.

Which diagnosis likely accounts for Ms. A’s presentation?
   a) major depressive disorder (MDD)
   b) eating disorder, not otherwise specified (NOS)
   c) anorexia nervosa, purging type
   d) catatonia, unspecified
   e) anxiety disorder NOS
   f) cognitive disorder
   g) psychosis NOS

The authors’ observations
There are many reported causes of catatonia in children and adolescents, including those that are psychiatric, medical, or neurological, as well as drugs (Table 1).^1,2 Affective disor­ders have been associated with catatonia in adults, but has not been widely reported in children and adolescents.^1,3 Organic and neu­rologic causes, such as neurological tumors and cerebral hemorrhage, should be ruled out first because, although rare, they can be fatal (Table 2).² If the cause of catatonia is not recognized quickly (Figure,^1,2) effective treatment could be delayed.⁴

Presentation in adults and adolescents is similar.

An eating disorder could be comorbid with another psychiatric disorder, such as MDD, dysthymia, or panic disorder.⁵ Ms. A’s report of depression before she began restricting food favored a primary diagnosis of MDD. Her depressive symptoms of low appetite or low self-worth could have led to her preoccupation with body image.

There has been evidence that negative self-image and eating disorders are associ­ated, but data are limited and the connection remains unclear.⁶ Ms. A’s self-esteem was very low. Her fixation on restricting food could have been perpetuated by her self-criticism and by being excluded from her peer group in school. Her weight loss could have brought anxiety symptoms to the fore­front because of physiologic changes that accompany extreme weight loss.

The treatment team was concerned about her delayed responses, which could be explained by the catatonic features that reflected the severity of her depression. She had no obvious symptoms of psychosis, but her intrusive thoughts and obsessions with avoiding food did not completely rule out psychosis.

Childhood-onset schizophrenia, although rare, has been associated with catatonia; fol­lowing up with a catatonia rating scale, such as the Catatonia Rating Scale or the Bush- Francis Catatonia Rating Scale (BFCRS), would be useful for tracking symptom prog­ress. In Ms. A’s case, her mood disorder was primary, but did not rule out psychosis-like prodromal symptoms.⁷

Ms. A is diagnosed with MDD, single episode, severe, with catatonic features, and without psychosis, and eating disorder, NOS.

EVALUATION Mostly normal
Ms. A does not have a history of mental ill­ness and was not seeing a psychiatrist or therapist, nor did she have any prior psychi­atric admissions. She denies suicide attempts, but reports self-injurious behavior involving scratching her skin, which started during the current mood episode. She has never taken any psychotropic medications. Ms. A lives at home with her biological mother and father and 17-year-old brother. She attends middle school with average grades and has no his­tory of disciplinary actions. She has no his­tory of bullying or teasing, although she did report some previous difficulty with relational aggression toward her peers in the 5th grade. Her mother has a history of anorexia nervosa that began when she was a teenager, but these symptoms are stable and under control. There is additionally a family history of bipolar disorder.

Ms. A has a family history of coronary artery disease and diabetes in the mother and maternal relatives. Her grandfather died from liver cancer. She was allergic to sulfa drugs and was taking a multivitamin and minocycline for acne.

Physical examination reveals some super­ficial scratches but otherwise was within normal limits. Initial lab results reveal a nor­mal complete blood count and differential. Thyroid-stimulating hormone is 1.29 mIU/L and free T4 is 0.96 mg/dL, both within normal limits. Urinalysis is within normal limits and urine pregnancy test is negative. A compre­hensive metabolic panel shows mild elevation in aspartate aminotransferase (AST) at 60 U/L and alanine aminotransferase (ALT) at 92 U/L, respectively. Phosphorus level is within nor­mal limits. Prealbumin level is slightly low at 15.1 mg/dL.

Which treatment plan would you recommend for Ms. A?
   a) discharge with outpatient psychiatric treatment
   b) recommend medical stabilization with follow-up from the psychosomatic team and then outpatient psychiatric follow-up
   c) admit her to the psychiatric acute inpa­tient hospital with psychiatric outpatient discharge follow-up plan
   d) discharge her home with follow-up with her primary care physician
   e) recommend follow-up from the psycho­somatic team while on medical floor with acute inpatient admission and psychiatric outpatient follow-up at discharge

The authors’ observations
Scarcity of data and reporting of cases of ado­lescent catatonia limits guidance for diagno­sis and treatment.⁸ There are several rating scales with variability in definition, but that overall provide a guiding tool for detecting catatonia. The Brief Cognitive Rating Scale is considered the most versatile because it is more valid, reliable, and requires less time to complete than other rating scales.⁹

Ms. A’s symptoms were a combination of depressive symptoms with severity defined by catatonic features, eating disorder with worsening course, anxiety symptoms, and genetic loading of eating disorder in her mother. The challenge of this case was making an accurate diagnosis and treating Ms. A, which required continuous obser­vation following an eating disorder proto­col, resolution of her catatonia, resuming a normal diet, and decreasing her suicidality. Retrospectively, her scores on the BFCRS were high on screening items 1 to 14, which measure presence or absence and severity of symptoms.

The best option was to admit Ms. A to an inpatient psychiatric facility after she is cleared medically with outpatient services to follow up.

How would you treat Ms. A’s symptoms?
   a) aggressively treat catatonia
   b) address her eating disorder
   c) work to resolve her depression

The authors’ observations
The challenge was to choose the psycho­tropic medication that would target her depression, obsessive, rigid thoughts, and catatonia. Administering an antidepressant with an antipsychotic would have relieved her depressive and obsessive symptoms but would not have improved her catato­nia. The psychosomatic medicine team rec­ommended starting a selective serotonin reuptake inhibitor and a benzodiazepine to target both the depression and the cata­tonic symptoms. Ms. A received sertraline, 12.5 mg/d, which was increased to 25 mg/d on the third day. IV lorazepam, 1 mg, 3 times a day, was recommended but the pediatric team prescribed an oral formulation. The hospital’s eating disorder protocol was insti­tuted on the day of admission.

Treatment options for catatonia
Benzodiazepines are the first line of treat­ment for catatonia and other neurolep­tics, specifically antipsychotics, have been considered dangerous.¹⁰ Benzodiazepine-resistant catatonia, which is sometimes seen in patients with autism, might respond to electroconvulsive therapy (ECT),¹¹ although in some states it cannot be administered to children age <18.¹² Benzodiazepines have shown dramatic improvement within hours, as has ECT.^8,13 Additionally, if patients do not respond to a benzodiazepine or ECT, con­sider other options such as zolpidem, olan­zapine,¹⁴ or sensory integration system (in adolescents with autism).¹⁵

Ms. A did not need ECT or an alternative treatment because she responded well to 3 doses of oral lorazepam. Her amotivation, negativism, and rigidity with prolonged posturing improved. Her psychomotor retardation improved overall, although she reported some dizziness and had some pos­tural hypotension, which was attributed to her eating issues and dehydration.

OUTCOME Feeling motivated
Ms. A is transferred to psychiatric inpatient unit. She tolerates sertraline, which is titrated to 50 mg/d. She is placed on the hospital’s standard eating disorder protocol. She con­tinues to eat well with adequate intake of solids and liquid and exhibits only some anxi­ety associated with meals. During the course of hospitalization, she attends group therapy and her catatonic symptoms completely resolve. She says she thinks that her thoughts are improving and that she is not longer feel­ing confused. She reports being motivated to continue to improve her eating disorder symptoms.

The treatment team holds a family session during which family dynamic issues that are stressful to Ms. A are discussed, such as some conflict with her parents as well as some nega­tive interactions between Ms. A and her father. Repeat comprehensive metabolic panel on admission to the inpatient psychiatric hospital reveals persistent elevation of AST at 92 U/L and ALT at 143 U/L. Ms. A is discharged home with follow-up with a psychiatrist and a thera­pist. The treatment team also recommends that she follow up in a program that special­izes in eating disorders.

4-month follow-up. Ms. A returns to inpa­tient psychiatric hospital after overdose of ser­traline and aripiprazole, which were started by an outpatient psychiatrist. She reports severe depressive symptoms because of school stressors. She denies any problems eating and did not show any symptoms of catato­nia. In her chart, there is a mention of “cloudy thoughts” and quietness. At this admission, her ALT is 17 U/L and AST is 19 U/L. Sertraline is increased to 150 mg/d and aripiprazole is reduced to 2 mg/d and then later increased to 5 mg/d, after which she is discharged home with an outpatient psychiatric follow-up.

1-year follow-up. Ms. A has been follow­ing up with an outpatient psychiatrist and is receiving sertraline, 150 mg/d, aripiprazole, 2.5 mg/d, and extended-release methylphe­nidate, 36 mg/d, along with L-methylfolate, multivitamins, and omega-3 fish oil as adju­vants for her depressive symptoms. Ms. A does not show symptoms of an eating disorder or catatonia, and her depression and psychomo­tor activity have improved, with better overall functionality, after adding the stimulant and adjunctives to the antidepressant.

The authors’ observations
The importance of including catatonia NOS with its various specifiers, such as medi­cal, metabolic, toxic, affective, etc., has been discussed.^16,17 In Ms. A’s case, instead of treating the specific symptoms—affective or eating disorder or obsessive quality of thought content, mimicking psychotic-like symptoms—addressing the catatonia ini­tially had a better outcome. More studies related to chronic and acute catatonia in adolescents are needed because of the risk of increased morbidity and premature death.¹⁸ Early recognition of catatonia is needed¹⁹ because it often is underdiagnosed.²⁰

Eating disorders often become worse over the first 5 years, and close monitoring and assessment is needed for adolescents.²¹ Also, prodromal psychotic symptoms require follow-up because techniques for early detection and intervention for children and adolescents are still in their infancy.²²

Bottom Line
Catatonia in adolescents should be addressed early, when it is treatable and the outcome is favorable. It is important to recognize catatonia in an emergency department or inpatient medical unit setting in a hospital because it is often underdiagnosed or misdiagnosed. The presentation of catatonia is similar in adolescents and adults. Benzodiazepines are first-line treatment for catatonia; consider electroconvulsive therapy if patients do not respond to drug therapy.

Related Resources
• Roberto AJ, Pinnaka S, Mohan A, et al. Adolescent catatonia successfully treated with lorazepam and aripiprazole. Case Rep Psychiatry. 2014;2014:309517. doi: 10.1155/2014/309517.
• Raffin M, Zugaj-Bensaou L, Bodeau N, et al. Treatment use in a prospective naturalistic cohort of children and adolescents with catatonia. Eur Child Adolesc Psychiatry. 2015;24(4):441-449.

Drug Brand Names
Aripiprazole • Abilify                                  Minocycline • Minocin
L-methylfolate • Deplin                              Olanzapine • Zyprexa
Lorazepam • Ativan                                   Sertraline • Zoloft
Methylphenidate • Ritalin,  Concerta          Zolpidem • Ambien, Intermezzo

Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE A fainting spell
Ms. A, age 13, is admitted to a pediatric unit after fainting and losing consciousness for 5 minutes in the shower, during which time she was non-responsive. She reports feeling nause­ated and having blurry vision before dropping to the floor.

Ms. A reports intentional self-restriction of calories, self-induced vomiting, and other purg­ing behaviors, such as laxative abuse and exces­sive exercising.

During the mental status examination, Ms. A is lying in bed wearing hospital clothes, legs flexed at the knee, hands on her side, and a fixed gaze at the ceiling with poor eye con­tact. She is of slender stature and tall, seems slightly older than her stated age, and is poorly groomed.

Throughout the interview, Ms. A has sig­nificant psychomotor retardation, reports her mood as tired, and has a blunted affect. She speaks at a low volume and has poverty of speech; she takes deep sighs before answer­ing questions. Her thought process is linear and she cooperates with the interview. She has poor recall, including delayed 3-minute recall and poor sustained attention. Her abstraction capacity is fair and her intellect is average and comparable with her age group. Ms. A is pre­occupied that eating will cause weight gain. She denies hallucinations but reports passive death wishes with self-harm by scratching.

What is the differential diagnosis to explain Ms. A’s presentation?
   a) syncope
   b) seizures
   c) dehydration
   d) hypotension

HISTORY Preoccupied with weight
Ms. A reports vomiting twice a day, while show­ering and at night when no one is around, every day for 2 months. She stopped eating and taking in fluids 3 days before admission to the medical unit. Also, she reports restricting her diet to 700 to 1,000 calories a day, skipping lunch at school, and eating minimally at night. Ms. A uses raspberry ketones and green coffee beans, which are adver­tised to aid weight loss, and laxative pills from her mother’s medicine cabinet once or twice a week when her throat is sore from vomiting. She reports exercising excessively, which includes running, crunches, and lifting weights. She has lost approximately 30 lb in the last 2 months.

Ms. A says she fears gaining weight and feels increased guilt after eating a meal. She said that looking at food induced “anxiety attack” symptoms of increased heart rate, sweaty palms, feeling of choking, nervousness, and shakiness. She adds that she does not want to be “bigger” than her classmates. Her under­standing of the consequences of not eating is, “It will get worse, I will shut down and die. I do not fear death, I only fear getting bigger than others.”

She reports that her fixation on avoiding food started when she realized that she was the tallest girl in her class and the only girl in her class running on the track team, after which she quit athletics. She reports that depression symptoms pre-dated her eating disorder symp­toms; onset of significant depression likely was precipitated by her grandfather’s death a year earlier, and then exacerbated by the recent death of a family pet.

Ms. A’s depressive symptoms are described as anhedonia (avoiding being outside and not enjoying drawing anymore), decreased energy, tearfulness, sadness, decreased con­centration, and passive suicidal thoughts. Her mother is supportive and motivates her daughter to “get better.” Ms. A denies any symptoms of psychosis, other anxiety symp­toms, other mood disorder symptoms, sub­stance abuse, or homicidality.

Ms. A’s mother says she felt that, recently, her daughter has been having some difficulty with confused thoughts and significantly delayed responses. However, the mother reports that her daughter always had some­what delayed responses from what she felt is typical. Her mother adds that Ms. A’s suicidal thoughts have worsened since her daughter started restricting her diet.

Which diagnosis likely accounts for Ms. A’s presentation?
   a) major depressive disorder (MDD)
   b) eating disorder, not otherwise specified (NOS)
   c) anorexia nervosa, purging type
   d) catatonia, unspecified
   e) anxiety disorder NOS
   f) cognitive disorder
   g) psychosis NOS

The authors’ observations
There are many reported causes of catatonia in children and adolescents, including those that are psychiatric, medical, or neurological, as well as drugs (Table 1).^1,2 Affective disor­ders have been associated with catatonia in adults, but has not been widely reported in children and adolescents.^1,3 Organic and neu­rologic causes, such as neurological tumors and cerebral hemorrhage, should be ruled out first because, although rare, they can be fatal (Table 2).² If the cause of catatonia is not recognized quickly (Figure,^1,2) effective treatment could be delayed.⁴

Presentation in adults and adolescents is similar.

An eating disorder could be comorbid with another psychiatric disorder, such as MDD, dysthymia, or panic disorder.⁵ Ms. A’s report of depression before she began restricting food favored a primary diagnosis of MDD. Her depressive symptoms of low appetite or low self-worth could have led to her preoccupation with body image.

There has been evidence that negative self-image and eating disorders are associ­ated, but data are limited and the connection remains unclear.⁶ Ms. A’s self-esteem was very low. Her fixation on restricting food could have been perpetuated by her self-criticism and by being excluded from her peer group in school. Her weight loss could have brought anxiety symptoms to the fore­front because of physiologic changes that accompany extreme weight loss.

The treatment team was concerned about her delayed responses, which could be explained by the catatonic features that reflected the severity of her depression. She had no obvious symptoms of psychosis, but her intrusive thoughts and obsessions with avoiding food did not completely rule out psychosis.

Childhood-onset schizophrenia, although rare, has been associated with catatonia; fol­lowing up with a catatonia rating scale, such as the Catatonia Rating Scale or the Bush- Francis Catatonia Rating Scale (BFCRS), would be useful for tracking symptom prog­ress. In Ms. A’s case, her mood disorder was primary, but did not rule out psychosis-like prodromal symptoms.⁷

Ms. A is diagnosed with MDD, single episode, severe, with catatonic features, and without psychosis, and eating disorder, NOS.

EVALUATION Mostly normal
Ms. A does not have a history of mental ill­ness and was not seeing a psychiatrist or therapist, nor did she have any prior psychi­atric admissions. She denies suicide attempts, but reports self-injurious behavior involving scratching her skin, which started during the current mood episode. She has never taken any psychotropic medications. Ms. A lives at home with her biological mother and father and 17-year-old brother. She attends middle school with average grades and has no his­tory of disciplinary actions. She has no his­tory of bullying or teasing, although she did report some previous difficulty with relational aggression toward her peers in the 5th grade. Her mother has a history of anorexia nervosa that began when she was a teenager, but these symptoms are stable and under control. There is additionally a family history of bipolar disorder.

Ms. A has a family history of coronary artery disease and diabetes in the mother and maternal relatives. Her grandfather died from liver cancer. She was allergic to sulfa drugs and was taking a multivitamin and minocycline for acne.

Physical examination reveals some super­ficial scratches but otherwise was within normal limits. Initial lab results reveal a nor­mal complete blood count and differential. Thyroid-stimulating hormone is 1.29 mIU/L and free T4 is 0.96 mg/dL, both within normal limits. Urinalysis is within normal limits and urine pregnancy test is negative. A compre­hensive metabolic panel shows mild elevation in aspartate aminotransferase (AST) at 60 U/L and alanine aminotransferase (ALT) at 92 U/L, respectively. Phosphorus level is within nor­mal limits. Prealbumin level is slightly low at 15.1 mg/dL.

Which treatment plan would you recommend for Ms. A?
   a) discharge with outpatient psychiatric treatment
   b) recommend medical stabilization with follow-up from the psychosomatic team and then outpatient psychiatric follow-up
   c) admit her to the psychiatric acute inpa­tient hospital with psychiatric outpatient discharge follow-up plan
   d) discharge her home with follow-up with her primary care physician
   e) recommend follow-up from the psycho­somatic team while on medical floor with acute inpatient admission and psychiatric outpatient follow-up at discharge

The authors’ observations
Scarcity of data and reporting of cases of ado­lescent catatonia limits guidance for diagno­sis and treatment.⁸ There are several rating scales with variability in definition, but that overall provide a guiding tool for detecting catatonia. The Brief Cognitive Rating Scale is considered the most versatile because it is more valid, reliable, and requires less time to complete than other rating scales.⁹

Ms. A’s symptoms were a combination of depressive symptoms with severity defined by catatonic features, eating disorder with worsening course, anxiety symptoms, and genetic loading of eating disorder in her mother. The challenge of this case was making an accurate diagnosis and treating Ms. A, which required continuous obser­vation following an eating disorder proto­col, resolution of her catatonia, resuming a normal diet, and decreasing her suicidality. Retrospectively, her scores on the BFCRS were high on screening items 1 to 14, which measure presence or absence and severity of symptoms.

The best option was to admit Ms. A to an inpatient psychiatric facility after she is cleared medically with outpatient services to follow up.

How would you treat Ms. A’s symptoms?
   a) aggressively treat catatonia
   b) address her eating disorder
   c) work to resolve her depression

The authors’ observations
The challenge was to choose the psycho­tropic medication that would target her depression, obsessive, rigid thoughts, and catatonia. Administering an antidepressant with an antipsychotic would have relieved her depressive and obsessive symptoms but would not have improved her catato­nia. The psychosomatic medicine team rec­ommended starting a selective serotonin reuptake inhibitor and a benzodiazepine to target both the depression and the cata­tonic symptoms. Ms. A received sertraline, 12.5 mg/d, which was increased to 25 mg/d on the third day. IV lorazepam, 1 mg, 3 times a day, was recommended but the pediatric team prescribed an oral formulation. The hospital’s eating disorder protocol was insti­tuted on the day of admission.

Treatment options for catatonia
Benzodiazepines are the first line of treat­ment for catatonia and other neurolep­tics, specifically antipsychotics, have been considered dangerous.¹⁰ Benzodiazepine-resistant catatonia, which is sometimes seen in patients with autism, might respond to electroconvulsive therapy (ECT),¹¹ although in some states it cannot be administered to children age <18.¹² Benzodiazepines have shown dramatic improvement within hours, as has ECT.^8,13 Additionally, if patients do not respond to a benzodiazepine or ECT, con­sider other options such as zolpidem, olan­zapine,¹⁴ or sensory integration system (in adolescents with autism).¹⁵

Ms. A did not need ECT or an alternative treatment because she responded well to 3 doses of oral lorazepam. Her amotivation, negativism, and rigidity with prolonged posturing improved. Her psychomotor retardation improved overall, although she reported some dizziness and had some pos­tural hypotension, which was attributed to her eating issues and dehydration.

OUTCOME Feeling motivated
Ms. A is transferred to psychiatric inpatient unit. She tolerates sertraline, which is titrated to 50 mg/d. She is placed on the hospital’s standard eating disorder protocol. She con­tinues to eat well with adequate intake of solids and liquid and exhibits only some anxi­ety associated with meals. During the course of hospitalization, she attends group therapy and her catatonic symptoms completely resolve. She says she thinks that her thoughts are improving and that she is not longer feel­ing confused. She reports being motivated to continue to improve her eating disorder symptoms.

The treatment team holds a family session during which family dynamic issues that are stressful to Ms. A are discussed, such as some conflict with her parents as well as some nega­tive interactions between Ms. A and her father. Repeat comprehensive metabolic panel on admission to the inpatient psychiatric hospital reveals persistent elevation of AST at 92 U/L and ALT at 143 U/L. Ms. A is discharged home with follow-up with a psychiatrist and a thera­pist. The treatment team also recommends that she follow up in a program that special­izes in eating disorders.

4-month follow-up. Ms. A returns to inpa­tient psychiatric hospital after overdose of ser­traline and aripiprazole, which were started by an outpatient psychiatrist. She reports severe depressive symptoms because of school stressors. She denies any problems eating and did not show any symptoms of catato­nia. In her chart, there is a mention of “cloudy thoughts” and quietness. At this admission, her ALT is 17 U/L and AST is 19 U/L. Sertraline is increased to 150 mg/d and aripiprazole is reduced to 2 mg/d and then later increased to 5 mg/d, after which she is discharged home with an outpatient psychiatric follow-up.

1-year follow-up. Ms. A has been follow­ing up with an outpatient psychiatrist and is receiving sertraline, 150 mg/d, aripiprazole, 2.5 mg/d, and extended-release methylphe­nidate, 36 mg/d, along with L-methylfolate, multivitamins, and omega-3 fish oil as adju­vants for her depressive symptoms. Ms. A does not show symptoms of an eating disorder or catatonia, and her depression and psychomo­tor activity have improved, with better overall functionality, after adding the stimulant and adjunctives to the antidepressant.

The authors’ observations
The importance of including catatonia NOS with its various specifiers, such as medi­cal, metabolic, toxic, affective, etc., has been discussed.^16,17 In Ms. A’s case, instead of treating the specific symptoms—affective or eating disorder or obsessive quality of thought content, mimicking psychotic-like symptoms—addressing the catatonia ini­tially had a better outcome. More studies related to chronic and acute catatonia in adolescents are needed because of the risk of increased morbidity and premature death.¹⁸ Early recognition of catatonia is needed¹⁹ because it often is underdiagnosed.²⁰

Eating disorders often become worse over the first 5 years, and close monitoring and assessment is needed for adolescents.²¹ Also, prodromal psychotic symptoms require follow-up because techniques for early detection and intervention for children and adolescents are still in their infancy.²²

Bottom Line
Catatonia in adolescents should be addressed early, when it is treatable and the outcome is favorable. It is important to recognize catatonia in an emergency department or inpatient medical unit setting in a hospital because it is often underdiagnosed or misdiagnosed. The presentation of catatonia is similar in adolescents and adults. Benzodiazepines are first-line treatment for catatonia; consider electroconvulsive therapy if patients do not respond to drug therapy.

Related Resources
• Roberto AJ, Pinnaka S, Mohan A, et al. Adolescent catatonia successfully treated with lorazepam and aripiprazole. Case Rep Psychiatry. 2014;2014:309517. doi: 10.1155/2014/309517.
• Raffin M, Zugaj-Bensaou L, Bodeau N, et al. Treatment use in a prospective naturalistic cohort of children and adolescents with catatonia. Eur Child Adolesc Psychiatry. 2015;24(4):441-449.

Drug Brand Names
Aripiprazole • Abilify                                  Minocycline • Minocin
L-methylfolate • Deplin                              Olanzapine • Zyprexa
Lorazepam • Ativan                                   Sertraline • Zoloft
Methylphenidate • Ritalin,  Concerta          Zolpidem • Ambien, Intermezzo

Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE A fainting spell
Ms. A, age 13, is admitted to a pediatric unit after fainting and losing consciousness for 5 minutes in the shower, during which time she was non-responsive. She reports feeling nause­ated and having blurry vision before dropping to the floor.

Ms. A reports intentional self-restriction of calories, self-induced vomiting, and other purg­ing behaviors, such as laxative abuse and exces­sive exercising.

During the mental status examination, Ms. A is lying in bed wearing hospital clothes, legs flexed at the knee, hands on her side, and a fixed gaze at the ceiling with poor eye con­tact. She is of slender stature and tall, seems slightly older than her stated age, and is poorly groomed.

Throughout the interview, Ms. A has sig­nificant psychomotor retardation, reports her mood as tired, and has a blunted affect. She speaks at a low volume and has poverty of speech; she takes deep sighs before answer­ing questions. Her thought process is linear and she cooperates with the interview. She has poor recall, including delayed 3-minute recall and poor sustained attention. Her abstraction capacity is fair and her intellect is average and comparable with her age group. Ms. A is pre­occupied that eating will cause weight gain. She denies hallucinations but reports passive death wishes with self-harm by scratching.

What is the differential diagnosis to explain Ms. A’s presentation?
   a) syncope
   b) seizures
   c) dehydration
   d) hypotension

HISTORY Preoccupied with weight
Ms. A reports vomiting twice a day, while show­ering and at night when no one is around, every day for 2 months. She stopped eating and taking in fluids 3 days before admission to the medical unit. Also, she reports restricting her diet to 700 to 1,000 calories a day, skipping lunch at school, and eating minimally at night. Ms. A uses raspberry ketones and green coffee beans, which are adver­tised to aid weight loss, and laxative pills from her mother’s medicine cabinet once or twice a week when her throat is sore from vomiting. She reports exercising excessively, which includes running, crunches, and lifting weights. She has lost approximately 30 lb in the last 2 months.

Ms. A says she fears gaining weight and feels increased guilt after eating a meal. She said that looking at food induced “anxiety attack” symptoms of increased heart rate, sweaty palms, feeling of choking, nervousness, and shakiness. She adds that she does not want to be “bigger” than her classmates. Her under­standing of the consequences of not eating is, “It will get worse, I will shut down and die. I do not fear death, I only fear getting bigger than others.”

She reports that her fixation on avoiding food started when she realized that she was the tallest girl in her class and the only girl in her class running on the track team, after which she quit athletics. She reports that depression symptoms pre-dated her eating disorder symp­toms; onset of significant depression likely was precipitated by her grandfather’s death a year earlier, and then exacerbated by the recent death of a family pet.

Ms. A’s depressive symptoms are described as anhedonia (avoiding being outside and not enjoying drawing anymore), decreased energy, tearfulness, sadness, decreased con­centration, and passive suicidal thoughts. Her mother is supportive and motivates her daughter to “get better.” Ms. A denies any symptoms of psychosis, other anxiety symp­toms, other mood disorder symptoms, sub­stance abuse, or homicidality.

Ms. A’s mother says she felt that, recently, her daughter has been having some difficulty with confused thoughts and significantly delayed responses. However, the mother reports that her daughter always had some­what delayed responses from what she felt is typical. Her mother adds that Ms. A’s suicidal thoughts have worsened since her daughter started restricting her diet.

Which diagnosis likely accounts for Ms. A’s presentation?
   a) major depressive disorder (MDD)
   b) eating disorder, not otherwise specified (NOS)
   c) anorexia nervosa, purging type
   d) catatonia, unspecified
   e) anxiety disorder NOS
   f) cognitive disorder
   g) psychosis NOS

The authors’ observations
There are many reported causes of catatonia in children and adolescents, including those that are psychiatric, medical, or neurological, as well as drugs (Table 1).^1,2 Affective disor­ders have been associated with catatonia in adults, but has not been widely reported in children and adolescents.^1,3 Organic and neu­rologic causes, such as neurological tumors and cerebral hemorrhage, should be ruled out first because, although rare, they can be fatal (Table 2).² If the cause of catatonia is not recognized quickly (Figure,^1,2) effective treatment could be delayed.⁴

Presentation in adults and adolescents is similar.

An eating disorder could be comorbid with another psychiatric disorder, such as MDD, dysthymia, or panic disorder.⁵ Ms. A’s report of depression before she began restricting food favored a primary diagnosis of MDD. Her depressive symptoms of low appetite or low self-worth could have led to her preoccupation with body image.

There has been evidence that negative self-image and eating disorders are associ­ated, but data are limited and the connection remains unclear.⁶ Ms. A’s self-esteem was very low. Her fixation on restricting food could have been perpetuated by her self-criticism and by being excluded from her peer group in school. Her weight loss could have brought anxiety symptoms to the fore­front because of physiologic changes that accompany extreme weight loss.

The treatment team was concerned about her delayed responses, which could be explained by the catatonic features that reflected the severity of her depression. She had no obvious symptoms of psychosis, but her intrusive thoughts and obsessions with avoiding food did not completely rule out psychosis.

Childhood-onset schizophrenia, although rare, has been associated with catatonia; fol­lowing up with a catatonia rating scale, such as the Catatonia Rating Scale or the Bush- Francis Catatonia Rating Scale (BFCRS), would be useful for tracking symptom prog­ress. In Ms. A’s case, her mood disorder was primary, but did not rule out psychosis-like prodromal symptoms.⁷

Ms. A is diagnosed with MDD, single episode, severe, with catatonic features, and without psychosis, and eating disorder, NOS.

EVALUATION Mostly normal
Ms. A does not have a history of mental ill­ness and was not seeing a psychiatrist or therapist, nor did she have any prior psychi­atric admissions. She denies suicide attempts, but reports self-injurious behavior involving scratching her skin, which started during the current mood episode. She has never taken any psychotropic medications. Ms. A lives at home with her biological mother and father and 17-year-old brother. She attends middle school with average grades and has no his­tory of disciplinary actions. She has no his­tory of bullying or teasing, although she did report some previous difficulty with relational aggression toward her peers in the 5th grade. Her mother has a history of anorexia nervosa that began when she was a teenager, but these symptoms are stable and under control. There is additionally a family history of bipolar disorder.

Ms. A has a family history of coronary artery disease and diabetes in the mother and maternal relatives. Her grandfather died from liver cancer. She was allergic to sulfa drugs and was taking a multivitamin and minocycline for acne.

Physical examination reveals some super­ficial scratches but otherwise was within normal limits. Initial lab results reveal a nor­mal complete blood count and differential. Thyroid-stimulating hormone is 1.29 mIU/L and free T4 is 0.96 mg/dL, both within normal limits. Urinalysis is within normal limits and urine pregnancy test is negative. A compre­hensive metabolic panel shows mild elevation in aspartate aminotransferase (AST) at 60 U/L and alanine aminotransferase (ALT) at 92 U/L, respectively. Phosphorus level is within nor­mal limits. Prealbumin level is slightly low at 15.1 mg/dL.

Which treatment plan would you recommend for Ms. A?
   a) discharge with outpatient psychiatric treatment
   b) recommend medical stabilization with follow-up from the psychosomatic team and then outpatient psychiatric follow-up
   c) admit her to the psychiatric acute inpa­tient hospital with psychiatric outpatient discharge follow-up plan
   d) discharge her home with follow-up with her primary care physician
   e) recommend follow-up from the psycho­somatic team while on medical floor with acute inpatient admission and psychiatric outpatient follow-up at discharge

The authors’ observations
Scarcity of data and reporting of cases of ado­lescent catatonia limits guidance for diagno­sis and treatment.⁸ There are several rating scales with variability in definition, but that overall provide a guiding tool for detecting catatonia. The Brief Cognitive Rating Scale is considered the most versatile because it is more valid, reliable, and requires less time to complete than other rating scales.⁹

Ms. A’s symptoms were a combination of depressive symptoms with severity defined by catatonic features, eating disorder with worsening course, anxiety symptoms, and genetic loading of eating disorder in her mother. The challenge of this case was making an accurate diagnosis and treating Ms. A, which required continuous obser­vation following an eating disorder proto­col, resolution of her catatonia, resuming a normal diet, and decreasing her suicidality. Retrospectively, her scores on the BFCRS were high on screening items 1 to 14, which measure presence or absence and severity of symptoms.

The best option was to admit Ms. A to an inpatient psychiatric facility after she is cleared medically with outpatient services to follow up.

How would you treat Ms. A’s symptoms?
   a) aggressively treat catatonia
   b) address her eating disorder
   c) work to resolve her depression

The authors’ observations
The challenge was to choose the psycho­tropic medication that would target her depression, obsessive, rigid thoughts, and catatonia. Administering an antidepressant with an antipsychotic would have relieved her depressive and obsessive symptoms but would not have improved her catato­nia. The psychosomatic medicine team rec­ommended starting a selective serotonin reuptake inhibitor and a benzodiazepine to target both the depression and the cata­tonic symptoms. Ms. A received sertraline, 12.5 mg/d, which was increased to 25 mg/d on the third day. IV lorazepam, 1 mg, 3 times a day, was recommended but the pediatric team prescribed an oral formulation. The hospital’s eating disorder protocol was insti­tuted on the day of admission.

Treatment options for catatonia
Benzodiazepines are the first line of treat­ment for catatonia and other neurolep­tics, specifically antipsychotics, have been considered dangerous.¹⁰ Benzodiazepine-resistant catatonia, which is sometimes seen in patients with autism, might respond to electroconvulsive therapy (ECT),¹¹ although in some states it cannot be administered to children age <18.¹² Benzodiazepines have shown dramatic improvement within hours, as has ECT.^8,13 Additionally, if patients do not respond to a benzodiazepine or ECT, con­sider other options such as zolpidem, olan­zapine,¹⁴ or sensory integration system (in adolescents with autism).¹⁵

Ms. A did not need ECT or an alternative treatment because she responded well to 3 doses of oral lorazepam. Her amotivation, negativism, and rigidity with prolonged posturing improved. Her psychomotor retardation improved overall, although she reported some dizziness and had some pos­tural hypotension, which was attributed to her eating issues and dehydration.

OUTCOME Feeling motivated
Ms. A is transferred to psychiatric inpatient unit. She tolerates sertraline, which is titrated to 50 mg/d. She is placed on the hospital’s standard eating disorder protocol. She con­tinues to eat well with adequate intake of solids and liquid and exhibits only some anxi­ety associated with meals. During the course of hospitalization, she attends group therapy and her catatonic symptoms completely resolve. She says she thinks that her thoughts are improving and that she is not longer feel­ing confused. She reports being motivated to continue to improve her eating disorder symptoms.

The treatment team holds a family session during which family dynamic issues that are stressful to Ms. A are discussed, such as some conflict with her parents as well as some nega­tive interactions between Ms. A and her father. Repeat comprehensive metabolic panel on admission to the inpatient psychiatric hospital reveals persistent elevation of AST at 92 U/L and ALT at 143 U/L. Ms. A is discharged home with follow-up with a psychiatrist and a thera­pist. The treatment team also recommends that she follow up in a program that special­izes in eating disorders.

4-month follow-up. Ms. A returns to inpa­tient psychiatric hospital after overdose of ser­traline and aripiprazole, which were started by an outpatient psychiatrist. She reports severe depressive symptoms because of school stressors. She denies any problems eating and did not show any symptoms of catato­nia. In her chart, there is a mention of “cloudy thoughts” and quietness. At this admission, her ALT is 17 U/L and AST is 19 U/L. Sertraline is increased to 150 mg/d and aripiprazole is reduced to 2 mg/d and then later increased to 5 mg/d, after which she is discharged home with an outpatient psychiatric follow-up.

1-year follow-up. Ms. A has been follow­ing up with an outpatient psychiatrist and is receiving sertraline, 150 mg/d, aripiprazole, 2.5 mg/d, and extended-release methylphe­nidate, 36 mg/d, along with L-methylfolate, multivitamins, and omega-3 fish oil as adju­vants for her depressive symptoms. Ms. A does not show symptoms of an eating disorder or catatonia, and her depression and psychomo­tor activity have improved, with better overall functionality, after adding the stimulant and adjunctives to the antidepressant.

The authors’ observations
The importance of including catatonia NOS with its various specifiers, such as medi­cal, metabolic, toxic, affective, etc., has been discussed.^16,17 In Ms. A’s case, instead of treating the specific symptoms—affective or eating disorder or obsessive quality of thought content, mimicking psychotic-like symptoms—addressing the catatonia ini­tially had a better outcome. More studies related to chronic and acute catatonia in adolescents are needed because of the risk of increased morbidity and premature death.¹⁸ Early recognition of catatonia is needed¹⁹ because it often is underdiagnosed.²⁰

Eating disorders often become worse over the first 5 years, and close monitoring and assessment is needed for adolescents.²¹ Also, prodromal psychotic symptoms require follow-up because techniques for early detection and intervention for children and adolescents are still in their infancy.²²

Bottom Line
Catatonia in adolescents should be addressed early, when it is treatable and the outcome is favorable. It is important to recognize catatonia in an emergency department or inpatient medical unit setting in a hospital because it is often underdiagnosed or misdiagnosed. The presentation of catatonia is similar in adolescents and adults. Benzodiazepines are first-line treatment for catatonia; consider electroconvulsive therapy if patients do not respond to drug therapy.

Related Resources
• Roberto AJ, Pinnaka S, Mohan A, et al. Adolescent catatonia successfully treated with lorazepam and aripiprazole. Case Rep Psychiatry. 2014;2014:309517. doi: 10.1155/2014/309517.
• Raffin M, Zugaj-Bensaou L, Bodeau N, et al. Treatment use in a prospective naturalistic cohort of children and adolescents with catatonia. Eur Child Adolesc Psychiatry. 2015;24(4):441-449.

Drug Brand Names
Aripiprazole • Abilify                                  Minocycline • Minocin
L-methylfolate • Deplin                              Olanzapine • Zyprexa
Lorazepam • Ativan                                   Sertraline • Zoloft
Methylphenidate • Ritalin,  Concerta          Zolpidem • Ambien, Intermezzo

Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.

I am very honored that Dr. Rob Bell, past president of the American Shoulder and Elbow Surgeons, invited me to give last year’s Neer Lecture. Dr. Bell asked me to specifically address my role in the development of arthroscopic rotator cuff repair and to recount the significant resistance that the early arthroscopic shoulder surgeons faced from the shoulder establishment as we struggled to achieve mainstream acceptance for this new technology. Tasked with such a personal topic, I find myself in a position analogous to that of Winston Churchill at the end of World War II. When a journalist asked him to speculate on how historians would portray his role in the war, he replied without hesitation, “History will be kind to me because I intend to write it.”

So let’s start at the beginning. And for me it makes the most sense to travel back to the year I started my practice: 1981. The world then was very different from today’s world. On January 20, 1981, Ronald Reagan was inaugurated President of the United States. The same day, 52 US hostages in Iran were released after having been held captive for 442 days. In March 1981, Reagan survived an assassination attempt; 3 months earlier, John Lennon had not been so lucky. Lennon’s hit song “Starting Over” garnered the highest musical awards posthumously.

The world of shoulder surgery was also very different in 1981. The arthroscope was the “instrument of the devil,” according to Dr. Rockwood. And shoulder surgery was ruled by the Charlies—Dr. Charles Neer, Dr. Charlie Rockwood, and any other Charlie who felt compelled to marginalize shoulder arthroscopy.

My personal world in the early 1980s was daunting as well. I had just completed my residency at the Mayo Clinic and my sports medicine fellowship in Eugene, Oregon. I had a young son, a new daughter, and a new job with the San Antonio Orthopaedic Group. I had a new house with a 21% mortgage loan and a “new” used car with a 23% car loan.

I was simultaneously energized and intimidated by my new job, where I was doing general orthopedics with a “special interest” in shoulder surgery and sports medicine. I was initially very proud and humbled by the fact that my senior partners had entrusted me with the care of the most difficult shoulder cases within the practice. But that pride got cut down to its appropriate size the day after I had thanked one of my partners, Dr. Lamar Collie, for his confidence in my potential as a shoulder surgeon. Dr. Collie replied matter-of-factly, “Sure … but you need to understand that we always make the new guy the shoulder expert because shoulders never do worth a damn.”

For shoulder arthroscopy, the early 1980s were exciting. Most of us who were scoping shoulders had already been doing knee arthroscopy and were trying to adapt knee instruments to the shoulder. This worked for some simple excisional cases. For example, I recall excising the bucket-handle portion of a type III SLAP (superior labral tear from anterior to posterior) lesion in 1983. In general, however, shoulder problems were different from knee problems and usually involved repair rather than excision of damaged tissues. Therefore, the technology used in knee arthroscopy was often not directly transferable to the shoulder. Furthermore, treatment of the rotator cuff necessitated development of arthroscopic techniques in a virtual space, the subacromial space, and this was an entirely new arthroscopic concept.

Development of Arthroscopic Rotator Cuff Repair

A major mind-expanding turning point for me occurred in 1984 when I attended one of Dr. Jim Esch’s early San Diego shoulder courses. During that course, Dr. Harvard Ellman of Los Angeles demonstrated to me on a cadaver shoulder how he created a virtual subacromial working space that allowed enough visualization for an arthroscopic acromioplasty. At that moment, I knew that arthroscopic rotator cuff repair was just around the corner. Up until then, I had not been able to envision complex extra-articular reconstructive surgery, as all previous arthroscopic surgery had been intra-articular. But now, having realized a virtual working space could always be created, I knew it would be relatively straightforward to develop the portals to approach the cuff as well as the implants and the instruments to repair it. But I also knew that progression to all-arthroscopic repair techniques would have to be stepwise and that the final repair constructs would need to be at least as strong as those of open repair in order to be acceptable. With an undergraduate degree in mechanical engineering, I had a reasonably clear idea of the concepts I wanted to apply to the instrumentation and techniques, though I could never have envisioned how circuitous the route to the end result would be.

First Steps

I sketched out my ideas for arthroscopic suture passers and knot-tying instruments and presented them to a couple of the major arthroscopy companies in the United States, but the companies were not interested. They did not believe arthroscopy would have any meaningful applications in the shoulder. So, I enlisted the services of a local San Antonio aircraft machinist to fabricate instruments for me. By 1987, I was doing arthroscopic side-to-side margin convergence¹ cuff repairs for U-shape tears on a regular basis. And I was doing these at the most hostile point in the universe for arthroscopic shoulder surgery: San Antonio, Texas.

Only a few surgeons were doing arthroscopic shoulder surgery in the 1980s and early 1990s, and without exception these surgeons became the leader-pioneers in the new discipline. In general, these were young surgeons who were in private practice and removed from academia and professional organizations, and thus relatively sheltered from the actions of the shoulder rule-makers of the day. They accepted their status as pariahs as they developed their techniques out of the view of mainstream orthopedics. These leaders included Jim Esch, Steve Snyder, Dick Caspari, Lanny Johnson, Gene Wolf, Gary Gartsman, Rob Bell, and Howard Sweeney. We shared our techniques and our ideas with one another, encouraged one another, and generally became good friends.

Thomas Kuhn, in his classic book The Structure of Scientific Revolutions,² observed that paradigm shifts within a given field were usually achieved by practitioners who were either very young (naïve) or outside the established hierarchy in the field. The surgeons who contributed most to the shift of shoulder surgery from open to arthroscopic techniques were generally young men who were in private practice and had little to lose by inciting the disdain of the shoulder establishment. Predictably, resistance from the mainstream open shoulder surgeons increased as arthroscopic techniques became more successful and more threatening to the primacy of the open shoulder surgeons. The disdain yielded to disruption and finally to transformation as the paradigm shift occurred. The conflict between the open shoulder surgeons and the arthroscopic shoulder surgeons passed through all the phases that Mahatma Gandhi had described many years before. “First they ignore you; then they laugh at you; then they fight you; then you win.”

Building a Ship in a Bottle

At the start of the 1990s, I recognized that my progress in arthroscopic rotator cuff repair would be extremely slow unless I could find an industry partner who shared my vision for full-scale conversion to arthroscopic means of repair and would be willing to help make it a reality. In 1991, I happened to meet Reinhold Schmieding, the owner of Arthrex, a small arthroscopic device company in Naples, Florida. Reinhold invited me to visit him to discuss the feasibility of developing arthroscopic repair systems for the shoulder. At the time, the world headquarters of Arthrex was a 20×30-ft storage room in an office service center, and there were 2 employees. One employee, Don Grafton, was a talented engineer without medical experience. By the end of my first day there, Reinhold and Don and I had agreed that developing arthroscopic repair systems for shoulder instability and rotator cuff repair would become a top priority for Arthrex.

My initial bias toward arthroscopic cuff repair was that a transosseous bone tunnel technique not only would be possible but would be superior to suture anchor fixation. In fact, my first 2 patents with Arthrex were for instrumentation for an arthroscopic transosseous repair technique. I tested my hypothesis with 2 successive biomechanical studies. The first examined cyclic loading of bone tunnel repairs, and the second examined cyclic loading of anchor-based repairs.^3,4 Evaluating the data from these 2 studies, I was surprised to find that anchor-based repairs were significantly stronger than bone tunnel repairs. In addition, anchors shifted the weak link from the bone–suture interface to the tendon–suture interface; in essence, anchors optimized bone fixation by shifting the weak link in the construct to the tendon. I was then completely convinced of the superiority of suture anchors over bone tunnels, and that conviction has become even stronger over the years. After these 2 cyclic loading studies, I shifted my focus, and that of Arthrex, toward arthroscopic suture anchor repair of the rotator cuff.

Reconciling Technique and Instrumentation With Anatomy and Biomechanics

Having recognized the importance of the rotator cable attachments both anatomically⁵ and biomechanically,^6,7 I thought it important to reinforce them as a routine part of performing rotator cuff repairs. Our anatomical and biomechanical studies had had great translational implications in the development of our techniques and instrumentation.

As mentioned earlier, Don Grafton was the chief (and for a long time only) engineer at Arthrex. As he had no medical experience, I invited him to come to San Antonio to observe surgery. During Don’s many visits, I showed him pathology in the operating room and pointed out what I could do with the instruments I had and what I could not do. Then in the evening we went to my house and brainstormed how to perform the “missing” surgical manipulations, how to improve manipulations that were suboptimal, and how to optimize final surgical constructs.

Passing suture through tendon was an early challenge. One must remember that, in the early 1990s, it was not possible for machinists to fabricate complex shapes. Therefore, straight tubular retrograde suture passers were the logical first option. We initially developed spring-loaded retrograde hook retrievers (Figure 1) and then curved suture hooks with shuttling wires (Lasso). To me, the most unappealing feature of retrograde suture passage was the oblique angle of approach through the tendon, which caused a length–tension mismatch between the upper fibers and the lower fibers of the muscle–tendon unit. We recognized we could eliminate the mismatch if we passed the suture antegrade, such that it would pass perpendicular to the tendon fibers. These insights and efforts culminated in development of the Viper suture passer and then the FastPass Scorpion suture passer, which has a spring-loaded trapdoor on the upper jaw for ergonomic self-retrieving of the suture once it is passed through the tendon.

To develop a knot pusher that optimized knot tying (yielding the highest knot security and the tightest loop security), we used prototype instruments to tie and test literally thousands of knots in the laboratory. We were thus able to verify that the Surgeon’s Sixth Finger Knot Pusher (Arthrex) reproducibly tied optimized knots^8,9 and also optimized knot fixation and bone fixation. However, our suture was not yet optimized and was prone to breakage, and our suture–tendon interface was not yet optimized. Clearly, improvement was needed in 2 more areas.

Don came up with the idea for a virtually unbreakable suture and developed that idea into FiberWire.¹⁰ Shortly thereafter, I contributed the idea and design for FiberTape, which dramatically enhanced suture pullout strength and footprint compression.

Anchor designs improved rapidly and dramatically. We made the second-generation BioCorkscrew fully threaded, which virtually eliminated anchor failure, even in soft bone.

Optimization of the suture–tendon interface took a giant step forward when Park and colleagues^11,12 introduced linked double-row rotator cuff repair. Much as with a Chinese finger trap, the harder you pull, the stronger it becomes, with yield load approaching ultimate load.

At this point, it seemed we had optimized virtually every segment of the rotator cuff repair construct. Each component was just about as good as it could be. Or was it?

The Accidental Quest for Knotless Fixation

In November 1998, I made my first trip to China as a guest speaker at the Congress of the Hong Kong Orthopaedic Association. My first view of the magnificent Hong Kong skyline across Victoria Harbour was truly breathtaking. As I admired the gleaming glass towers and the concrete canyons of the city, I had no idea that the very next day these modern skyscrapers would reveal an ancient secret that would change my approach to arthroscopic rotator cuff repair.

The day after my arrival, Dr. James Lam took me to lunch. As we approached the restaurant, he pointed across the street to a tall building that was being renovated and had scaffolding supporting workers alongside the first 9 stories of the exterior wall. Dr. Lam said that, after lunch, he would take me to the construction site for a closer look at the scaffolding.

After lunch, we walked to the base of the scaffolding. Dr. Lam told me it was constructed entirely of bamboo poles held together with lashings but no knots (Figure 2). Lashings were secured by turning them back on themselves and wrapping them in an entirely knotless manner.¹³ I found it incredible that this knotless fixation was so secure that it could support the weight of workers many stories above the ground. I resolved to determine how this fixation method worked and see if the same mechanism might help us achieve reliable knotless fixation in surgery.

When I returned home, I broke out my college engineering books and reacquainted myself with the concept of cable friction. As has happened so often in the past, however, it took a practical lesson from the ranch to truly illustrate for me how cable friction works.

Every cowboy knows that a spirited horse cannot be restrained with only one lead rope. However, a cowboy can wrap a lead rope around a “snubbing post” and thereby gain complete control over the animal, despite the horse’s superior size and strength. The cable friction between the rope and the post creates such a large restraining force that the cowboy can easily hold the animal without the help of a knotted rope (Figure 3). In similar fashion in the Hong Kong scaffolding, fixation strength results from the significant amount of cable friction produced when the lashings wrap around one another and around the bamboo poles.

The cable friction concept was pivotal in the development of knotless fixation in arthroscopic rotator cuff repair. In lateral row fixation, the eyelet of the PushLock and SwiveLock suture anchors (Arthrex) produces significant cable friction at the eyelet–suture interface, in addition to frictional force wedging the suture between anchor and bone.

As with so many other devices in shoulder arthroscopy, the SwiveLock suture anchor developed in stages. In the first stage, a chainlike suture with consecutive intersecting links was used (FiberChain). The idea for an adjustable fixation construct came to me because I thought that a forked eyelet on a SwiveLock would provide a firm fixation point when inserted into the appropriate suture link, yet would be totally adjustable simply by choosing a tighter or looser link (Figure 4). Although the system worked very well, it was technically challenging. The process was greatly simplified after Don Grafton and I developed FiberTape and recognized that the power of cable friction was dramatically increased by the larger contact area between the eyelet and the braided FiberTape. The SpeedBridge construct (Arthrex), which enhanced cable friction fixation by means of passing FiberTape through the anchor eyelets, also provided a larger compressive interface at the repair site by using FiberTape rather than conventional suture. These incremental improvements led to what I would characterize as today’s gold standard for arthroscopic rotator cuff repair: a largely knotless linked double-row construct using FiberTape, with cinch-loop sutures at the anterior and posterior margins of the tear to reinforce the cable attachments and simultaneously reduce the dog-ears that typically occur in those locations, and a double-pulley medial mattress if tendon quality is poor (Figure 5).

The Burden of Craft

With all the recent enthusiasm for level I studies, I think we need to examine whether they will accelerate technological advancement in rotator cuff repair. The answer, in my opinion, is a resounding no. This answer is based on a major disconnect I have detected in how we evaluate these studies in rotator cuff disease and repair.

An irony related to technological advancement in surgery is that the more technically advanced the surgery becomes, the more skill is required. This fact is completely at odds with the public’s perception that technological advances make procedures easier. In arthroscopic rotator cuff repair, the surgeon must look, feel, and be aware to a greater degree than in open surgery.

Edward Tenner, in his book Why Things Bite Back, described the burden of the practitioner of any advanced technology as the burden of craft.¹⁴ The burden of craft is the inherent demand on all craftspeople, but particularly surgeons, to “up our game” if we are to be successful in our craft. For arthroscopic rotator cuff repair, the burden of craft requires patience, attention to detail, and the ability to work in a virtual space. Not everyone has these skills. But anyone who wants to practice in this discipline has an obligation to learn the skills required, and then to teach them to others and assess how well they are being applied.

The problem with relying on level I studies to assess the efficacy of a surgical procedure is that they are inherently biased by the surgeons involved. As results depend on surgeons’ skills, and surgeons’ skill levels are not equal, level I studies cannot prove what is possible, cannot demonstrate the limits of a technique, and cannot demonstrate the equivalence of techniques.

Amazingly enough, there are still rotator cuff repair “deniers” who confidently assert from the podium that a large percentage of massive cuff tears cannot be repaired and that, even if they can be repaired, they do not have the biological potential to heal. Given the disparity in surgeons’ skills and results, however, one must ask whether poor results are a consequence of a biological deficit in the patient, or of a skill deficit in the surgeon.

What I know is that we have techniques for predictable arthroscopic repair and healing of the vast majority of rotator cuff tears, even massive tears,^15-17 and patients do very well clinically. Yet, among many orthopedic surgeons, there is a trend to go straight to reverse total shoulder arthroplasty (rTSA) for massive tears—despite the evidence against it. As reported in the literature, rTSA results are not as good as arthroscopic cuff repair results, and the complication rate for rTSA is much higher.

Why has this trend toward rTSA for massive tears gained so much momentum? The only reason I can surmise is that, for the average surgeon, rTSA is easier and quicker than arthroscopic repair for massive tears. But the reason for choosing a specific type of surgery for a given problem should not be that it is easiest for the surgeon; it should be that it is best for the patient.

The surgeon should start by asking what procedure he or she would want if the roles were reversed—if the surgeon were the patient with the massive rotator cuff tear. If a surgeon does not have the skill set for the best procedure for a particular patient, he or she is obligated to send that patient to a surgeon who does have the skills. In addition, given that infection is the most feared complication in most shoulder surgeries, the surgeon should ask which infection rate would be personally acceptable. Arthroscopic rotator cuff repair has a reported infection rate of 1.6 per 1000, or .0016,¹⁸ whereas rTSA has an infection rate about 25 times higher, or .04.¹⁹ Further, the surgeon must consider the relative severity of the consequences of infection. By any measure, an infected arthroscopy is a straightforward treatable complication, but an infected shoulder replacement is a human tragedy. Patients vastly prefer the minimally invasive arthroscopic approach, and through online searches can easily identify who can offer an arthroscopic solution.

To reproducibly achieve successful arthroscopic repair of massive rotator cuff tears, the surgeon must know advanced techniques, including subscapularis repair techniques,^20,21 interval slides,^22,23 and self-reinforcing constructs.^24,25

“It’s a poor carpenter who blames his tools.” This 18th-century English proverb is as true today as it was 300 years ago. The tools for arthroscopic cuff repair exist, and they are excellent. The burden of craft is the surgeon’s burden and obligation. As surgeons, we must accept that obligation and the responsibility of that burden.

As mentioned earlier, Dr. Rob Bell’s charge to me when he invited me to give the Neer Lecture was to sum up my involvement in the development of arthroscopic shoulder surgery. The short version is that I have been doing shoulder arthroscopy for 31 years; have received 28 US patents related to shoulder instruments and implants and have 12 US patents pending; have published 167 peer-reviewed articles, a couple dozen book chapters, and 2 textbooks on shoulder arthroscopy; have trained 25 fellows; and have hosted approximately 3000 visiting surgeons in my operating room. My greatest professional dream was to see the standard of care for rotator cuff repair and shoulder instability transition from open to arthroscopic techniques, and I have been fortunate enough to have observed that paradigm shift during my career.

What do I envision over the next 31 years? As we all know, history runs in both directions, and some things simply have not happened yet. In terms of rotator cuff treatment, I think over the next few years the guiding principle of treatment will be joint preservation. All rotator cuff tears, even massive tears, will be repaired arthroscopically. Patients and insurers will demand arthroscopic repair, and surgeons without the skill set will migrate to other subspecialties. As for the role of arthroplasty in the treatment of rotator cuff tears, rTSA will be indicated only for pseudoparalysis after failed cuff repair in low-demand elderly patients.

In rotator cuff treatment, I envision a standard of care that is almost entirely arthroscopic. This standard will demand that surgeons who treat rotator cuff tears be proficient in arthroscopic repair of the full range of tears. Acquiring the skills for arthroscopic repair may not be easy, but then “there’s the easy way, and there’s the Cowboy Way.” As my dad used to tell me when I complained about working too hard, “No man ever drowned in his own sweat.” We shoulder surgeons must accept the burden of craft that accompanies the new standard of arthroscopic cuff repair, and we must offer our patients the same level of care we would choose for ourselves.

Happy trails!

I am very honored that Dr. Rob Bell, past president of the American Shoulder and Elbow Surgeons, invited me to give last year’s Neer Lecture. Dr. Bell asked me to specifically address my role in the development of arthroscopic rotator cuff repair and to recount the significant resistance that the early arthroscopic shoulder surgeons faced from the shoulder establishment as we struggled to achieve mainstream acceptance for this new technology. Tasked with such a personal topic, I find myself in a position analogous to that of Winston Churchill at the end of World War II. When a journalist asked him to speculate on how historians would portray his role in the war, he replied without hesitation, “History will be kind to me because I intend to write it.”

So let’s start at the beginning. And for me it makes the most sense to travel back to the year I started my practice: 1981. The world then was very different from today’s world. On January 20, 1981, Ronald Reagan was inaugurated President of the United States. The same day, 52 US hostages in Iran were released after having been held captive for 442 days. In March 1981, Reagan survived an assassination attempt; 3 months earlier, John Lennon had not been so lucky. Lennon’s hit song “Starting Over” garnered the highest musical awards posthumously.

The world of shoulder surgery was also very different in 1981. The arthroscope was the “instrument of the devil,” according to Dr. Rockwood. And shoulder surgery was ruled by the Charlies—Dr. Charles Neer, Dr. Charlie Rockwood, and any other Charlie who felt compelled to marginalize shoulder arthroscopy.

My personal world in the early 1980s was daunting as well. I had just completed my residency at the Mayo Clinic and my sports medicine fellowship in Eugene, Oregon. I had a young son, a new daughter, and a new job with the San Antonio Orthopaedic Group. I had a new house with a 21% mortgage loan and a “new” used car with a 23% car loan.

I was simultaneously energized and intimidated by my new job, where I was doing general orthopedics with a “special interest” in shoulder surgery and sports medicine. I was initially very proud and humbled by the fact that my senior partners had entrusted me with the care of the most difficult shoulder cases within the practice. But that pride got cut down to its appropriate size the day after I had thanked one of my partners, Dr. Lamar Collie, for his confidence in my potential as a shoulder surgeon. Dr. Collie replied matter-of-factly, “Sure … but you need to understand that we always make the new guy the shoulder expert because shoulders never do worth a damn.”

For shoulder arthroscopy, the early 1980s were exciting. Most of us who were scoping shoulders had already been doing knee arthroscopy and were trying to adapt knee instruments to the shoulder. This worked for some simple excisional cases. For example, I recall excising the bucket-handle portion of a type III SLAP (superior labral tear from anterior to posterior) lesion in 1983. In general, however, shoulder problems were different from knee problems and usually involved repair rather than excision of damaged tissues. Therefore, the technology used in knee arthroscopy was often not directly transferable to the shoulder. Furthermore, treatment of the rotator cuff necessitated development of arthroscopic techniques in a virtual space, the subacromial space, and this was an entirely new arthroscopic concept.

Development of Arthroscopic Rotator Cuff Repair

A major mind-expanding turning point for me occurred in 1984 when I attended one of Dr. Jim Esch’s early San Diego shoulder courses. During that course, Dr. Harvard Ellman of Los Angeles demonstrated to me on a cadaver shoulder how he created a virtual subacromial working space that allowed enough visualization for an arthroscopic acromioplasty. At that moment, I knew that arthroscopic rotator cuff repair was just around the corner. Up until then, I had not been able to envision complex extra-articular reconstructive surgery, as all previous arthroscopic surgery had been intra-articular. But now, having realized a virtual working space could always be created, I knew it would be relatively straightforward to develop the portals to approach the cuff as well as the implants and the instruments to repair it. But I also knew that progression to all-arthroscopic repair techniques would have to be stepwise and that the final repair constructs would need to be at least as strong as those of open repair in order to be acceptable. With an undergraduate degree in mechanical engineering, I had a reasonably clear idea of the concepts I wanted to apply to the instrumentation and techniques, though I could never have envisioned how circuitous the route to the end result would be.

First Steps

I sketched out my ideas for arthroscopic suture passers and knot-tying instruments and presented them to a couple of the major arthroscopy companies in the United States, but the companies were not interested. They did not believe arthroscopy would have any meaningful applications in the shoulder. So, I enlisted the services of a local San Antonio aircraft machinist to fabricate instruments for me. By 1987, I was doing arthroscopic side-to-side margin convergence¹ cuff repairs for U-shape tears on a regular basis. And I was doing these at the most hostile point in the universe for arthroscopic shoulder surgery: San Antonio, Texas.

Only a few surgeons were doing arthroscopic shoulder surgery in the 1980s and early 1990s, and without exception these surgeons became the leader-pioneers in the new discipline. In general, these were young surgeons who were in private practice and removed from academia and professional organizations, and thus relatively sheltered from the actions of the shoulder rule-makers of the day. They accepted their status as pariahs as they developed their techniques out of the view of mainstream orthopedics. These leaders included Jim Esch, Steve Snyder, Dick Caspari, Lanny Johnson, Gene Wolf, Gary Gartsman, Rob Bell, and Howard Sweeney. We shared our techniques and our ideas with one another, encouraged one another, and generally became good friends.

Thomas Kuhn, in his classic book The Structure of Scientific Revolutions,² observed that paradigm shifts within a given field were usually achieved by practitioners who were either very young (naïve) or outside the established hierarchy in the field. The surgeons who contributed most to the shift of shoulder surgery from open to arthroscopic techniques were generally young men who were in private practice and had little to lose by inciting the disdain of the shoulder establishment. Predictably, resistance from the mainstream open shoulder surgeons increased as arthroscopic techniques became more successful and more threatening to the primacy of the open shoulder surgeons. The disdain yielded to disruption and finally to transformation as the paradigm shift occurred. The conflict between the open shoulder surgeons and the arthroscopic shoulder surgeons passed through all the phases that Mahatma Gandhi had described many years before. “First they ignore you; then they laugh at you; then they fight you; then you win.”

Building a Ship in a Bottle

At the start of the 1990s, I recognized that my progress in arthroscopic rotator cuff repair would be extremely slow unless I could find an industry partner who shared my vision for full-scale conversion to arthroscopic means of repair and would be willing to help make it a reality. In 1991, I happened to meet Reinhold Schmieding, the owner of Arthrex, a small arthroscopic device company in Naples, Florida. Reinhold invited me to visit him to discuss the feasibility of developing arthroscopic repair systems for the shoulder. At the time, the world headquarters of Arthrex was a 20×30-ft storage room in an office service center, and there were 2 employees. One employee, Don Grafton, was a talented engineer without medical experience. By the end of my first day there, Reinhold and Don and I had agreed that developing arthroscopic repair systems for shoulder instability and rotator cuff repair would become a top priority for Arthrex.

My initial bias toward arthroscopic cuff repair was that a transosseous bone tunnel technique not only would be possible but would be superior to suture anchor fixation. In fact, my first 2 patents with Arthrex were for instrumentation for an arthroscopic transosseous repair technique. I tested my hypothesis with 2 successive biomechanical studies. The first examined cyclic loading of bone tunnel repairs, and the second examined cyclic loading of anchor-based repairs.^3,4 Evaluating the data from these 2 studies, I was surprised to find that anchor-based repairs were significantly stronger than bone tunnel repairs. In addition, anchors shifted the weak link from the bone–suture interface to the tendon–suture interface; in essence, anchors optimized bone fixation by shifting the weak link in the construct to the tendon. I was then completely convinced of the superiority of suture anchors over bone tunnels, and that conviction has become even stronger over the years. After these 2 cyclic loading studies, I shifted my focus, and that of Arthrex, toward arthroscopic suture anchor repair of the rotator cuff.

Reconciling Technique and Instrumentation With Anatomy and Biomechanics

Having recognized the importance of the rotator cable attachments both anatomically⁵ and biomechanically,^6,7 I thought it important to reinforce them as a routine part of performing rotator cuff repairs. Our anatomical and biomechanical studies had had great translational implications in the development of our techniques and instrumentation.

As mentioned earlier, Don Grafton was the chief (and for a long time only) engineer at Arthrex. As he had no medical experience, I invited him to come to San Antonio to observe surgery. During Don’s many visits, I showed him pathology in the operating room and pointed out what I could do with the instruments I had and what I could not do. Then in the evening we went to my house and brainstormed how to perform the “missing” surgical manipulations, how to improve manipulations that were suboptimal, and how to optimize final surgical constructs.

Passing suture through tendon was an early challenge. One must remember that, in the early 1990s, it was not possible for machinists to fabricate complex shapes. Therefore, straight tubular retrograde suture passers were the logical first option. We initially developed spring-loaded retrograde hook retrievers (Figure 1) and then curved suture hooks with shuttling wires (Lasso). To me, the most unappealing feature of retrograde suture passage was the oblique angle of approach through the tendon, which caused a length–tension mismatch between the upper fibers and the lower fibers of the muscle–tendon unit. We recognized we could eliminate the mismatch if we passed the suture antegrade, such that it would pass perpendicular to the tendon fibers. These insights and efforts culminated in development of the Viper suture passer and then the FastPass Scorpion suture passer, which has a spring-loaded trapdoor on the upper jaw for ergonomic self-retrieving of the suture once it is passed through the tendon.

To develop a knot pusher that optimized knot tying (yielding the highest knot security and the tightest loop security), we used prototype instruments to tie and test literally thousands of knots in the laboratory. We were thus able to verify that the Surgeon’s Sixth Finger Knot Pusher (Arthrex) reproducibly tied optimized knots^8,9 and also optimized knot fixation and bone fixation. However, our suture was not yet optimized and was prone to breakage, and our suture–tendon interface was not yet optimized. Clearly, improvement was needed in 2 more areas.

Don came up with the idea for a virtually unbreakable suture and developed that idea into FiberWire.¹⁰ Shortly thereafter, I contributed the idea and design for FiberTape, which dramatically enhanced suture pullout strength and footprint compression.

Anchor designs improved rapidly and dramatically. We made the second-generation BioCorkscrew fully threaded, which virtually eliminated anchor failure, even in soft bone.

Optimization of the suture–tendon interface took a giant step forward when Park and colleagues^11,12 introduced linked double-row rotator cuff repair. Much as with a Chinese finger trap, the harder you pull, the stronger it becomes, with yield load approaching ultimate load.

At this point, it seemed we had optimized virtually every segment of the rotator cuff repair construct. Each component was just about as good as it could be. Or was it?

The Accidental Quest for Knotless Fixation

In November 1998, I made my first trip to China as a guest speaker at the Congress of the Hong Kong Orthopaedic Association. My first view of the magnificent Hong Kong skyline across Victoria Harbour was truly breathtaking. As I admired the gleaming glass towers and the concrete canyons of the city, I had no idea that the very next day these modern skyscrapers would reveal an ancient secret that would change my approach to arthroscopic rotator cuff repair.

The day after my arrival, Dr. James Lam took me to lunch. As we approached the restaurant, he pointed across the street to a tall building that was being renovated and had scaffolding supporting workers alongside the first 9 stories of the exterior wall. Dr. Lam said that, after lunch, he would take me to the construction site for a closer look at the scaffolding.

After lunch, we walked to the base of the scaffolding. Dr. Lam told me it was constructed entirely of bamboo poles held together with lashings but no knots (Figure 2). Lashings were secured by turning them back on themselves and wrapping them in an entirely knotless manner.¹³ I found it incredible that this knotless fixation was so secure that it could support the weight of workers many stories above the ground. I resolved to determine how this fixation method worked and see if the same mechanism might help us achieve reliable knotless fixation in surgery.

When I returned home, I broke out my college engineering books and reacquainted myself with the concept of cable friction. As has happened so often in the past, however, it took a practical lesson from the ranch to truly illustrate for me how cable friction works.

Every cowboy knows that a spirited horse cannot be restrained with only one lead rope. However, a cowboy can wrap a lead rope around a “snubbing post” and thereby gain complete control over the animal, despite the horse’s superior size and strength. The cable friction between the rope and the post creates such a large restraining force that the cowboy can easily hold the animal without the help of a knotted rope (Figure 3). In similar fashion in the Hong Kong scaffolding, fixation strength results from the significant amount of cable friction produced when the lashings wrap around one another and around the bamboo poles.

The cable friction concept was pivotal in the development of knotless fixation in arthroscopic rotator cuff repair. In lateral row fixation, the eyelet of the PushLock and SwiveLock suture anchors (Arthrex) produces significant cable friction at the eyelet–suture interface, in addition to frictional force wedging the suture between anchor and bone.

As with so many other devices in shoulder arthroscopy, the SwiveLock suture anchor developed in stages. In the first stage, a chainlike suture with consecutive intersecting links was used (FiberChain). The idea for an adjustable fixation construct came to me because I thought that a forked eyelet on a SwiveLock would provide a firm fixation point when inserted into the appropriate suture link, yet would be totally adjustable simply by choosing a tighter or looser link (Figure 4). Although the system worked very well, it was technically challenging. The process was greatly simplified after Don Grafton and I developed FiberTape and recognized that the power of cable friction was dramatically increased by the larger contact area between the eyelet and the braided FiberTape. The SpeedBridge construct (Arthrex), which enhanced cable friction fixation by means of passing FiberTape through the anchor eyelets, also provided a larger compressive interface at the repair site by using FiberTape rather than conventional suture. These incremental improvements led to what I would characterize as today’s gold standard for arthroscopic rotator cuff repair: a largely knotless linked double-row construct using FiberTape, with cinch-loop sutures at the anterior and posterior margins of the tear to reinforce the cable attachments and simultaneously reduce the dog-ears that typically occur in those locations, and a double-pulley medial mattress if tendon quality is poor (Figure 5).

The Burden of Craft

With all the recent enthusiasm for level I studies, I think we need to examine whether they will accelerate technological advancement in rotator cuff repair. The answer, in my opinion, is a resounding no. This answer is based on a major disconnect I have detected in how we evaluate these studies in rotator cuff disease and repair.

An irony related to technological advancement in surgery is that the more technically advanced the surgery becomes, the more skill is required. This fact is completely at odds with the public’s perception that technological advances make procedures easier. In arthroscopic rotator cuff repair, the surgeon must look, feel, and be aware to a greater degree than in open surgery.

Edward Tenner, in his book Why Things Bite Back, described the burden of the practitioner of any advanced technology as the burden of craft.¹⁴ The burden of craft is the inherent demand on all craftspeople, but particularly surgeons, to “up our game” if we are to be successful in our craft. For arthroscopic rotator cuff repair, the burden of craft requires patience, attention to detail, and the ability to work in a virtual space. Not everyone has these skills. But anyone who wants to practice in this discipline has an obligation to learn the skills required, and then to teach them to others and assess how well they are being applied.

The problem with relying on level I studies to assess the efficacy of a surgical procedure is that they are inherently biased by the surgeons involved. As results depend on surgeons’ skills, and surgeons’ skill levels are not equal, level I studies cannot prove what is possible, cannot demonstrate the limits of a technique, and cannot demonstrate the equivalence of techniques.

Amazingly enough, there are still rotator cuff repair “deniers” who confidently assert from the podium that a large percentage of massive cuff tears cannot be repaired and that, even if they can be repaired, they do not have the biological potential to heal. Given the disparity in surgeons’ skills and results, however, one must ask whether poor results are a consequence of a biological deficit in the patient, or of a skill deficit in the surgeon.

What I know is that we have techniques for predictable arthroscopic repair and healing of the vast majority of rotator cuff tears, even massive tears,^15-17 and patients do very well clinically. Yet, among many orthopedic surgeons, there is a trend to go straight to reverse total shoulder arthroplasty (rTSA) for massive tears—despite the evidence against it. As reported in the literature, rTSA results are not as good as arthroscopic cuff repair results, and the complication rate for rTSA is much higher.

Why has this trend toward rTSA for massive tears gained so much momentum? The only reason I can surmise is that, for the average surgeon, rTSA is easier and quicker than arthroscopic repair for massive tears. But the reason for choosing a specific type of surgery for a given problem should not be that it is easiest for the surgeon; it should be that it is best for the patient.

The surgeon should start by asking what procedure he or she would want if the roles were reversed—if the surgeon were the patient with the massive rotator cuff tear. If a surgeon does not have the skill set for the best procedure for a particular patient, he or she is obligated to send that patient to a surgeon who does have the skills. In addition, given that infection is the most feared complication in most shoulder surgeries, the surgeon should ask which infection rate would be personally acceptable. Arthroscopic rotator cuff repair has a reported infection rate of 1.6 per 1000, or .0016,¹⁸ whereas rTSA has an infection rate about 25 times higher, or .04.¹⁹ Further, the surgeon must consider the relative severity of the consequences of infection. By any measure, an infected arthroscopy is a straightforward treatable complication, but an infected shoulder replacement is a human tragedy. Patients vastly prefer the minimally invasive arthroscopic approach, and through online searches can easily identify who can offer an arthroscopic solution.

To reproducibly achieve successful arthroscopic repair of massive rotator cuff tears, the surgeon must know advanced techniques, including subscapularis repair techniques,^20,21 interval slides,^22,23 and self-reinforcing constructs.^24,25

“It’s a poor carpenter who blames his tools.” This 18th-century English proverb is as true today as it was 300 years ago. The tools for arthroscopic cuff repair exist, and they are excellent. The burden of craft is the surgeon’s burden and obligation. As surgeons, we must accept that obligation and the responsibility of that burden.

As mentioned earlier, Dr. Rob Bell’s charge to me when he invited me to give the Neer Lecture was to sum up my involvement in the development of arthroscopic shoulder surgery. The short version is that I have been doing shoulder arthroscopy for 31 years; have received 28 US patents related to shoulder instruments and implants and have 12 US patents pending; have published 167 peer-reviewed articles, a couple dozen book chapters, and 2 textbooks on shoulder arthroscopy; have trained 25 fellows; and have hosted approximately 3000 visiting surgeons in my operating room. My greatest professional dream was to see the standard of care for rotator cuff repair and shoulder instability transition from open to arthroscopic techniques, and I have been fortunate enough to have observed that paradigm shift during my career.

What do I envision over the next 31 years? As we all know, history runs in both directions, and some things simply have not happened yet. In terms of rotator cuff treatment, I think over the next few years the guiding principle of treatment will be joint preservation. All rotator cuff tears, even massive tears, will be repaired arthroscopically. Patients and insurers will demand arthroscopic repair, and surgeons without the skill set will migrate to other subspecialties. As for the role of arthroplasty in the treatment of rotator cuff tears, rTSA will be indicated only for pseudoparalysis after failed cuff repair in low-demand elderly patients.

In rotator cuff treatment, I envision a standard of care that is almost entirely arthroscopic. This standard will demand that surgeons who treat rotator cuff tears be proficient in arthroscopic repair of the full range of tears. Acquiring the skills for arthroscopic repair may not be easy, but then “there’s the easy way, and there’s the Cowboy Way.” As my dad used to tell me when I complained about working too hard, “No man ever drowned in his own sweat.” We shoulder surgeons must accept the burden of craft that accompanies the new standard of arthroscopic cuff repair, and we must offer our patients the same level of care we would choose for ourselves.

Happy trails!

I am very honored that Dr. Rob Bell, past president of the American Shoulder and Elbow Surgeons, invited me to give last year’s Neer Lecture. Dr. Bell asked me to specifically address my role in the development of arthroscopic rotator cuff repair and to recount the significant resistance that the early arthroscopic shoulder surgeons faced from the shoulder establishment as we struggled to achieve mainstream acceptance for this new technology. Tasked with such a personal topic, I find myself in a position analogous to that of Winston Churchill at the end of World War II. When a journalist asked him to speculate on how historians would portray his role in the war, he replied without hesitation, “History will be kind to me because I intend to write it.”

So let’s start at the beginning. And for me it makes the most sense to travel back to the year I started my practice: 1981. The world then was very different from today’s world. On January 20, 1981, Ronald Reagan was inaugurated President of the United States. The same day, 52 US hostages in Iran were released after having been held captive for 442 days. In March 1981, Reagan survived an assassination attempt; 3 months earlier, John Lennon had not been so lucky. Lennon’s hit song “Starting Over” garnered the highest musical awards posthumously.

The world of shoulder surgery was also very different in 1981. The arthroscope was the “instrument of the devil,” according to Dr. Rockwood. And shoulder surgery was ruled by the Charlies—Dr. Charles Neer, Dr. Charlie Rockwood, and any other Charlie who felt compelled to marginalize shoulder arthroscopy.

My personal world in the early 1980s was daunting as well. I had just completed my residency at the Mayo Clinic and my sports medicine fellowship in Eugene, Oregon. I had a young son, a new daughter, and a new job with the San Antonio Orthopaedic Group. I had a new house with a 21% mortgage loan and a “new” used car with a 23% car loan.

I was simultaneously energized and intimidated by my new job, where I was doing general orthopedics with a “special interest” in shoulder surgery and sports medicine. I was initially very proud and humbled by the fact that my senior partners had entrusted me with the care of the most difficult shoulder cases within the practice. But that pride got cut down to its appropriate size the day after I had thanked one of my partners, Dr. Lamar Collie, for his confidence in my potential as a shoulder surgeon. Dr. Collie replied matter-of-factly, “Sure … but you need to understand that we always make the new guy the shoulder expert because shoulders never do worth a damn.”

For shoulder arthroscopy, the early 1980s were exciting. Most of us who were scoping shoulders had already been doing knee arthroscopy and were trying to adapt knee instruments to the shoulder. This worked for some simple excisional cases. For example, I recall excising the bucket-handle portion of a type III SLAP (superior labral tear from anterior to posterior) lesion in 1983. In general, however, shoulder problems were different from knee problems and usually involved repair rather than excision of damaged tissues. Therefore, the technology used in knee arthroscopy was often not directly transferable to the shoulder. Furthermore, treatment of the rotator cuff necessitated development of arthroscopic techniques in a virtual space, the subacromial space, and this was an entirely new arthroscopic concept.

Development of Arthroscopic Rotator Cuff Repair

A major mind-expanding turning point for me occurred in 1984 when I attended one of Dr. Jim Esch’s early San Diego shoulder courses. During that course, Dr. Harvard Ellman of Los Angeles demonstrated to me on a cadaver shoulder how he created a virtual subacromial working space that allowed enough visualization for an arthroscopic acromioplasty. At that moment, I knew that arthroscopic rotator cuff repair was just around the corner. Up until then, I had not been able to envision complex extra-articular reconstructive surgery, as all previous arthroscopic surgery had been intra-articular. But now, having realized a virtual working space could always be created, I knew it would be relatively straightforward to develop the portals to approach the cuff as well as the implants and the instruments to repair it. But I also knew that progression to all-arthroscopic repair techniques would have to be stepwise and that the final repair constructs would need to be at least as strong as those of open repair in order to be acceptable. With an undergraduate degree in mechanical engineering, I had a reasonably clear idea of the concepts I wanted to apply to the instrumentation and techniques, though I could never have envisioned how circuitous the route to the end result would be.

First Steps

I sketched out my ideas for arthroscopic suture passers and knot-tying instruments and presented them to a couple of the major arthroscopy companies in the United States, but the companies were not interested. They did not believe arthroscopy would have any meaningful applications in the shoulder. So, I enlisted the services of a local San Antonio aircraft machinist to fabricate instruments for me. By 1987, I was doing arthroscopic side-to-side margin convergence¹ cuff repairs for U-shape tears on a regular basis. And I was doing these at the most hostile point in the universe for arthroscopic shoulder surgery: San Antonio, Texas.

Only a few surgeons were doing arthroscopic shoulder surgery in the 1980s and early 1990s, and without exception these surgeons became the leader-pioneers in the new discipline. In general, these were young surgeons who were in private practice and removed from academia and professional organizations, and thus relatively sheltered from the actions of the shoulder rule-makers of the day. They accepted their status as pariahs as they developed their techniques out of the view of mainstream orthopedics. These leaders included Jim Esch, Steve Snyder, Dick Caspari, Lanny Johnson, Gene Wolf, Gary Gartsman, Rob Bell, and Howard Sweeney. We shared our techniques and our ideas with one another, encouraged one another, and generally became good friends.

Thomas Kuhn, in his classic book The Structure of Scientific Revolutions,² observed that paradigm shifts within a given field were usually achieved by practitioners who were either very young (naïve) or outside the established hierarchy in the field. The surgeons who contributed most to the shift of shoulder surgery from open to arthroscopic techniques were generally young men who were in private practice and had little to lose by inciting the disdain of the shoulder establishment. Predictably, resistance from the mainstream open shoulder surgeons increased as arthroscopic techniques became more successful and more threatening to the primacy of the open shoulder surgeons. The disdain yielded to disruption and finally to transformation as the paradigm shift occurred. The conflict between the open shoulder surgeons and the arthroscopic shoulder surgeons passed through all the phases that Mahatma Gandhi had described many years before. “First they ignore you; then they laugh at you; then they fight you; then you win.”

Building a Ship in a Bottle

At the start of the 1990s, I recognized that my progress in arthroscopic rotator cuff repair would be extremely slow unless I could find an industry partner who shared my vision for full-scale conversion to arthroscopic means of repair and would be willing to help make it a reality. In 1991, I happened to meet Reinhold Schmieding, the owner of Arthrex, a small arthroscopic device company in Naples, Florida. Reinhold invited me to visit him to discuss the feasibility of developing arthroscopic repair systems for the shoulder. At the time, the world headquarters of Arthrex was a 20×30-ft storage room in an office service center, and there were 2 employees. One employee, Don Grafton, was a talented engineer without medical experience. By the end of my first day there, Reinhold and Don and I had agreed that developing arthroscopic repair systems for shoulder instability and rotator cuff repair would become a top priority for Arthrex.

My initial bias toward arthroscopic cuff repair was that a transosseous bone tunnel technique not only would be possible but would be superior to suture anchor fixation. In fact, my first 2 patents with Arthrex were for instrumentation for an arthroscopic transosseous repair technique. I tested my hypothesis with 2 successive biomechanical studies. The first examined cyclic loading of bone tunnel repairs, and the second examined cyclic loading of anchor-based repairs.^3,4 Evaluating the data from these 2 studies, I was surprised to find that anchor-based repairs were significantly stronger than bone tunnel repairs. In addition, anchors shifted the weak link from the bone–suture interface to the tendon–suture interface; in essence, anchors optimized bone fixation by shifting the weak link in the construct to the tendon. I was then completely convinced of the superiority of suture anchors over bone tunnels, and that conviction has become even stronger over the years. After these 2 cyclic loading studies, I shifted my focus, and that of Arthrex, toward arthroscopic suture anchor repair of the rotator cuff.

Reconciling Technique and Instrumentation With Anatomy and Biomechanics

Having recognized the importance of the rotator cable attachments both anatomically⁵ and biomechanically,^6,7 I thought it important to reinforce them as a routine part of performing rotator cuff repairs. Our anatomical and biomechanical studies had had great translational implications in the development of our techniques and instrumentation.

As mentioned earlier, Don Grafton was the chief (and for a long time only) engineer at Arthrex. As he had no medical experience, I invited him to come to San Antonio to observe surgery. During Don’s many visits, I showed him pathology in the operating room and pointed out what I could do with the instruments I had and what I could not do. Then in the evening we went to my house and brainstormed how to perform the “missing” surgical manipulations, how to improve manipulations that were suboptimal, and how to optimize final surgical constructs.

Passing suture through tendon was an early challenge. One must remember that, in the early 1990s, it was not possible for machinists to fabricate complex shapes. Therefore, straight tubular retrograde suture passers were the logical first option. We initially developed spring-loaded retrograde hook retrievers (Figure 1) and then curved suture hooks with shuttling wires (Lasso). To me, the most unappealing feature of retrograde suture passage was the oblique angle of approach through the tendon, which caused a length–tension mismatch between the upper fibers and the lower fibers of the muscle–tendon unit. We recognized we could eliminate the mismatch if we passed the suture antegrade, such that it would pass perpendicular to the tendon fibers. These insights and efforts culminated in development of the Viper suture passer and then the FastPass Scorpion suture passer, which has a spring-loaded trapdoor on the upper jaw for ergonomic self-retrieving of the suture once it is passed through the tendon.

To develop a knot pusher that optimized knot tying (yielding the highest knot security and the tightest loop security), we used prototype instruments to tie and test literally thousands of knots in the laboratory. We were thus able to verify that the Surgeon’s Sixth Finger Knot Pusher (Arthrex) reproducibly tied optimized knots^8,9 and also optimized knot fixation and bone fixation. However, our suture was not yet optimized and was prone to breakage, and our suture–tendon interface was not yet optimized. Clearly, improvement was needed in 2 more areas.

Don came up with the idea for a virtually unbreakable suture and developed that idea into FiberWire.¹⁰ Shortly thereafter, I contributed the idea and design for FiberTape, which dramatically enhanced suture pullout strength and footprint compression.

Anchor designs improved rapidly and dramatically. We made the second-generation BioCorkscrew fully threaded, which virtually eliminated anchor failure, even in soft bone.

Optimization of the suture–tendon interface took a giant step forward when Park and colleagues^11,12 introduced linked double-row rotator cuff repair. Much as with a Chinese finger trap, the harder you pull, the stronger it becomes, with yield load approaching ultimate load.

At this point, it seemed we had optimized virtually every segment of the rotator cuff repair construct. Each component was just about as good as it could be. Or was it?

The Accidental Quest for Knotless Fixation

In November 1998, I made my first trip to China as a guest speaker at the Congress of the Hong Kong Orthopaedic Association. My first view of the magnificent Hong Kong skyline across Victoria Harbour was truly breathtaking. As I admired the gleaming glass towers and the concrete canyons of the city, I had no idea that the very next day these modern skyscrapers would reveal an ancient secret that would change my approach to arthroscopic rotator cuff repair.

The day after my arrival, Dr. James Lam took me to lunch. As we approached the restaurant, he pointed across the street to a tall building that was being renovated and had scaffolding supporting workers alongside the first 9 stories of the exterior wall. Dr. Lam said that, after lunch, he would take me to the construction site for a closer look at the scaffolding.

After lunch, we walked to the base of the scaffolding. Dr. Lam told me it was constructed entirely of bamboo poles held together with lashings but no knots (Figure 2). Lashings were secured by turning them back on themselves and wrapping them in an entirely knotless manner.¹³ I found it incredible that this knotless fixation was so secure that it could support the weight of workers many stories above the ground. I resolved to determine how this fixation method worked and see if the same mechanism might help us achieve reliable knotless fixation in surgery.

When I returned home, I broke out my college engineering books and reacquainted myself with the concept of cable friction. As has happened so often in the past, however, it took a practical lesson from the ranch to truly illustrate for me how cable friction works.

Every cowboy knows that a spirited horse cannot be restrained with only one lead rope. However, a cowboy can wrap a lead rope around a “snubbing post” and thereby gain complete control over the animal, despite the horse’s superior size and strength. The cable friction between the rope and the post creates such a large restraining force that the cowboy can easily hold the animal without the help of a knotted rope (Figure 3). In similar fashion in the Hong Kong scaffolding, fixation strength results from the significant amount of cable friction produced when the lashings wrap around one another and around the bamboo poles.

The cable friction concept was pivotal in the development of knotless fixation in arthroscopic rotator cuff repair. In lateral row fixation, the eyelet of the PushLock and SwiveLock suture anchors (Arthrex) produces significant cable friction at the eyelet–suture interface, in addition to frictional force wedging the suture between anchor and bone.

As with so many other devices in shoulder arthroscopy, the SwiveLock suture anchor developed in stages. In the first stage, a chainlike suture with consecutive intersecting links was used (FiberChain). The idea for an adjustable fixation construct came to me because I thought that a forked eyelet on a SwiveLock would provide a firm fixation point when inserted into the appropriate suture link, yet would be totally adjustable simply by choosing a tighter or looser link (Figure 4). Although the system worked very well, it was technically challenging. The process was greatly simplified after Don Grafton and I developed FiberTape and recognized that the power of cable friction was dramatically increased by the larger contact area between the eyelet and the braided FiberTape. The SpeedBridge construct (Arthrex), which enhanced cable friction fixation by means of passing FiberTape through the anchor eyelets, also provided a larger compressive interface at the repair site by using FiberTape rather than conventional suture. These incremental improvements led to what I would characterize as today’s gold standard for arthroscopic rotator cuff repair: a largely knotless linked double-row construct using FiberTape, with cinch-loop sutures at the anterior and posterior margins of the tear to reinforce the cable attachments and simultaneously reduce the dog-ears that typically occur in those locations, and a double-pulley medial mattress if tendon quality is poor (Figure 5).

The Burden of Craft

With all the recent enthusiasm for level I studies, I think we need to examine whether they will accelerate technological advancement in rotator cuff repair. The answer, in my opinion, is a resounding no. This answer is based on a major disconnect I have detected in how we evaluate these studies in rotator cuff disease and repair.

An irony related to technological advancement in surgery is that the more technically advanced the surgery becomes, the more skill is required. This fact is completely at odds with the public’s perception that technological advances make procedures easier. In arthroscopic rotator cuff repair, the surgeon must look, feel, and be aware to a greater degree than in open surgery.

Edward Tenner, in his book Why Things Bite Back, described the burden of the practitioner of any advanced technology as the burden of craft.¹⁴ The burden of craft is the inherent demand on all craftspeople, but particularly surgeons, to “up our game” if we are to be successful in our craft. For arthroscopic rotator cuff repair, the burden of craft requires patience, attention to detail, and the ability to work in a virtual space. Not everyone has these skills. But anyone who wants to practice in this discipline has an obligation to learn the skills required, and then to teach them to others and assess how well they are being applied.

The problem with relying on level I studies to assess the efficacy of a surgical procedure is that they are inherently biased by the surgeons involved. As results depend on surgeons’ skills, and surgeons’ skill levels are not equal, level I studies cannot prove what is possible, cannot demonstrate the limits of a technique, and cannot demonstrate the equivalence of techniques.

Amazingly enough, there are still rotator cuff repair “deniers” who confidently assert from the podium that a large percentage of massive cuff tears cannot be repaired and that, even if they can be repaired, they do not have the biological potential to heal. Given the disparity in surgeons’ skills and results, however, one must ask whether poor results are a consequence of a biological deficit in the patient, or of a skill deficit in the surgeon.

What I know is that we have techniques for predictable arthroscopic repair and healing of the vast majority of rotator cuff tears, even massive tears,^15-17 and patients do very well clinically. Yet, among many orthopedic surgeons, there is a trend to go straight to reverse total shoulder arthroplasty (rTSA) for massive tears—despite the evidence against it. As reported in the literature, rTSA results are not as good as arthroscopic cuff repair results, and the complication rate for rTSA is much higher.

Why has this trend toward rTSA for massive tears gained so much momentum? The only reason I can surmise is that, for the average surgeon, rTSA is easier and quicker than arthroscopic repair for massive tears. But the reason for choosing a specific type of surgery for a given problem should not be that it is easiest for the surgeon; it should be that it is best for the patient.

The surgeon should start by asking what procedure he or she would want if the roles were reversed—if the surgeon were the patient with the massive rotator cuff tear. If a surgeon does not have the skill set for the best procedure for a particular patient, he or she is obligated to send that patient to a surgeon who does have the skills. In addition, given that infection is the most feared complication in most shoulder surgeries, the surgeon should ask which infection rate would be personally acceptable. Arthroscopic rotator cuff repair has a reported infection rate of 1.6 per 1000, or .0016,¹⁸ whereas rTSA has an infection rate about 25 times higher, or .04.¹⁹ Further, the surgeon must consider the relative severity of the consequences of infection. By any measure, an infected arthroscopy is a straightforward treatable complication, but an infected shoulder replacement is a human tragedy. Patients vastly prefer the minimally invasive arthroscopic approach, and through online searches can easily identify who can offer an arthroscopic solution.

To reproducibly achieve successful arthroscopic repair of massive rotator cuff tears, the surgeon must know advanced techniques, including subscapularis repair techniques,^20,21 interval slides,^22,23 and self-reinforcing constructs.^24,25

“It’s a poor carpenter who blames his tools.” This 18th-century English proverb is as true today as it was 300 years ago. The tools for arthroscopic cuff repair exist, and they are excellent. The burden of craft is the surgeon’s burden and obligation. As surgeons, we must accept that obligation and the responsibility of that burden.

As mentioned earlier, Dr. Rob Bell’s charge to me when he invited me to give the Neer Lecture was to sum up my involvement in the development of arthroscopic shoulder surgery. The short version is that I have been doing shoulder arthroscopy for 31 years; have received 28 US patents related to shoulder instruments and implants and have 12 US patents pending; have published 167 peer-reviewed articles, a couple dozen book chapters, and 2 textbooks on shoulder arthroscopy; have trained 25 fellows; and have hosted approximately 3000 visiting surgeons in my operating room. My greatest professional dream was to see the standard of care for rotator cuff repair and shoulder instability transition from open to arthroscopic techniques, and I have been fortunate enough to have observed that paradigm shift during my career.

What do I envision over the next 31 years? As we all know, history runs in both directions, and some things simply have not happened yet. In terms of rotator cuff treatment, I think over the next few years the guiding principle of treatment will be joint preservation. All rotator cuff tears, even massive tears, will be repaired arthroscopically. Patients and insurers will demand arthroscopic repair, and surgeons without the skill set will migrate to other subspecialties. As for the role of arthroplasty in the treatment of rotator cuff tears, rTSA will be indicated only for pseudoparalysis after failed cuff repair in low-demand elderly patients.

In rotator cuff treatment, I envision a standard of care that is almost entirely arthroscopic. This standard will demand that surgeons who treat rotator cuff tears be proficient in arthroscopic repair of the full range of tears. Acquiring the skills for arthroscopic repair may not be easy, but then “there’s the easy way, and there’s the Cowboy Way.” As my dad used to tell me when I complained about working too hard, “No man ever drowned in his own sweat.” We shoulder surgeons must accept the burden of craft that accompanies the new standard of arthroscopic cuff repair, and we must offer our patients the same level of care we would choose for ourselves.

Happy trails!

NEW YORK – Patients with both mitral valve regurgitation and atrial fibrillation who undergo concurrent mitral valve surgery and surgical ablation are more than twice as likely to be free of AF a year after surgery than are their counterparts who have mitral valve surgery alone, according to results of a randomized trial.

“About a quarter to a half of our your patients coming for mitral valve surgery also have AF,” Dr. A. Marc Gillinov said at the 2015 Mitral Valve Conclave sponsored by the American Association for Thoracic Surgery. “A great mitral valve repair is your first priority, but you also want to treat the AF.” Currently, cardiac surgeons perform concurrent mitral valve surgery and surgical ablation about 60% of the time in patients eligible for both procedures, he said.

The American College of Cardiology/American Health Association Guidelines state that surgical ablation in patients with AF having cardiac surgery for other indications is “reasonable” – “not very strong language,” he noted, and the level of evidence for concurrent procedures is C.

That led the Cardiothoracic Surgical Trials Network to pursue the clinical trial. The investigators randomized 260 patients with persistent or long-standing persistent atrial fibrillation who needed mitral valve surgery to also undergo either surgical ablation (133) or no ablation (127). The primary endpoint was freedom from AF at both 6 months and 12 months as assessed by 3-day Holter monitoring.

Almost two-thirds (63%) of patients in the ablation group were free from atrial fibrillation at both 6 and 12 months, compared with 29% of those who had mitral valve surgery only, a highly significant difference. Dr. Gillinov described the trial population as “tougher patients” with persistent AF whose average age was around 70 years, and most had organic mitral valve regurgitation.

Results were similar whether the patients underwent pulmonary vein isolation or biatrial maze procedure (61% and 66%, respectively). One-year mortality was 6.8% in the ablation group and 8.7% in the control group, reported Dr. Gillinov, who is surgical director of the Center for Atrial Fibrillation at Cleveland Clinic.

The trial found no significant differences between the ablation and nonablation groups in major cardiac or cerebrovascular adverse events, overall serious adverse events, or hospital readmissions. The results were published prior to the Dr. Gillinov’s presentation (N. Engl. J. Med. 2015;372:1399-409).

These results debunk findings from a survey a few years ago that found cardiac surgeons avoided doing surgical ablation during mitral valve surgery because it makes the operation too complex, requires longer pump times, and raises the risk of surgery, said Dr. Gillinov. “Does ablation improve rhythm control? Yes. Does ablation increase risk? No. Does ablation improve clinical outcomes? It probably does,” he said.

The trial had some limitations, Dr. Gillinov said. Its endpoint was not a clinical outcome, although looking at stroke risk or mortality would have required thousands of patients. Also, 20% of patients did not have follow-up with the 3-day Holter test. However, previous studies have shown a strong association between surgical ablation and a reduced risk of stroke. When Dr. Jolanda Kluin of Utrecht (the Netherlands) University asked if a patient would be better off with AF or a pacemaker, Dr. Gillinov replied, “I think it’s better to have an AV sequential rhythm, but the truth is no one can answer that question without clinical data.”

The bottom line is, “if you have a patient who’s having mitral valve surgery who also has AF, do an ablation,” he said.

The study was supported by the National Institutes of Health and the Canadian Institutes of Health Research. Dr. Gillinov disclosed relationships with AtriCure, Medtronic, Edwards Lifesciences, On-X Life Technologies, Abbott, Tendyne, and Clear Catheter.

NEW YORK – Patients with both mitral valve regurgitation and atrial fibrillation who undergo concurrent mitral valve surgery and surgical ablation are more than twice as likely to be free of AF a year after surgery than are their counterparts who have mitral valve surgery alone, according to results of a randomized trial.

“About a quarter to a half of our your patients coming for mitral valve surgery also have AF,” Dr. A. Marc Gillinov said at the 2015 Mitral Valve Conclave sponsored by the American Association for Thoracic Surgery. “A great mitral valve repair is your first priority, but you also want to treat the AF.” Currently, cardiac surgeons perform concurrent mitral valve surgery and surgical ablation about 60% of the time in patients eligible for both procedures, he said.

The American College of Cardiology/American Health Association Guidelines state that surgical ablation in patients with AF having cardiac surgery for other indications is “reasonable” – “not very strong language,” he noted, and the level of evidence for concurrent procedures is C.

That led the Cardiothoracic Surgical Trials Network to pursue the clinical trial. The investigators randomized 260 patients with persistent or long-standing persistent atrial fibrillation who needed mitral valve surgery to also undergo either surgical ablation (133) or no ablation (127). The primary endpoint was freedom from AF at both 6 months and 12 months as assessed by 3-day Holter monitoring.

Almost two-thirds (63%) of patients in the ablation group were free from atrial fibrillation at both 6 and 12 months, compared with 29% of those who had mitral valve surgery only, a highly significant difference. Dr. Gillinov described the trial population as “tougher patients” with persistent AF whose average age was around 70 years, and most had organic mitral valve regurgitation.

Results were similar whether the patients underwent pulmonary vein isolation or biatrial maze procedure (61% and 66%, respectively). One-year mortality was 6.8% in the ablation group and 8.7% in the control group, reported Dr. Gillinov, who is surgical director of the Center for Atrial Fibrillation at Cleveland Clinic.

The trial found no significant differences between the ablation and nonablation groups in major cardiac or cerebrovascular adverse events, overall serious adverse events, or hospital readmissions. The results were published prior to the Dr. Gillinov’s presentation (N. Engl. J. Med. 2015;372:1399-409).

These results debunk findings from a survey a few years ago that found cardiac surgeons avoided doing surgical ablation during mitral valve surgery because it makes the operation too complex, requires longer pump times, and raises the risk of surgery, said Dr. Gillinov. “Does ablation improve rhythm control? Yes. Does ablation increase risk? No. Does ablation improve clinical outcomes? It probably does,” he said.

The trial had some limitations, Dr. Gillinov said. Its endpoint was not a clinical outcome, although looking at stroke risk or mortality would have required thousands of patients. Also, 20% of patients did not have follow-up with the 3-day Holter test. However, previous studies have shown a strong association between surgical ablation and a reduced risk of stroke. When Dr. Jolanda Kluin of Utrecht (the Netherlands) University asked if a patient would be better off with AF or a pacemaker, Dr. Gillinov replied, “I think it’s better to have an AV sequential rhythm, but the truth is no one can answer that question without clinical data.”

The bottom line is, “if you have a patient who’s having mitral valve surgery who also has AF, do an ablation,” he said.

The study was supported by the National Institutes of Health and the Canadian Institutes of Health Research. Dr. Gillinov disclosed relationships with AtriCure, Medtronic, Edwards Lifesciences, On-X Life Technologies, Abbott, Tendyne, and Clear Catheter.

NEW YORK – Patients with both mitral valve regurgitation and atrial fibrillation who undergo concurrent mitral valve surgery and surgical ablation are more than twice as likely to be free of AF a year after surgery than are their counterparts who have mitral valve surgery alone, according to results of a randomized trial.

“About a quarter to a half of our your patients coming for mitral valve surgery also have AF,” Dr. A. Marc Gillinov said at the 2015 Mitral Valve Conclave sponsored by the American Association for Thoracic Surgery. “A great mitral valve repair is your first priority, but you also want to treat the AF.” Currently, cardiac surgeons perform concurrent mitral valve surgery and surgical ablation about 60% of the time in patients eligible for both procedures, he said.

The American College of Cardiology/American Health Association Guidelines state that surgical ablation in patients with AF having cardiac surgery for other indications is “reasonable” – “not very strong language,” he noted, and the level of evidence for concurrent procedures is C.

That led the Cardiothoracic Surgical Trials Network to pursue the clinical trial. The investigators randomized 260 patients with persistent or long-standing persistent atrial fibrillation who needed mitral valve surgery to also undergo either surgical ablation (133) or no ablation (127). The primary endpoint was freedom from AF at both 6 months and 12 months as assessed by 3-day Holter monitoring.

Almost two-thirds (63%) of patients in the ablation group were free from atrial fibrillation at both 6 and 12 months, compared with 29% of those who had mitral valve surgery only, a highly significant difference. Dr. Gillinov described the trial population as “tougher patients” with persistent AF whose average age was around 70 years, and most had organic mitral valve regurgitation.

Results were similar whether the patients underwent pulmonary vein isolation or biatrial maze procedure (61% and 66%, respectively). One-year mortality was 6.8% in the ablation group and 8.7% in the control group, reported Dr. Gillinov, who is surgical director of the Center for Atrial Fibrillation at Cleveland Clinic.

The trial found no significant differences between the ablation and nonablation groups in major cardiac or cerebrovascular adverse events, overall serious adverse events, or hospital readmissions. The results were published prior to the Dr. Gillinov’s presentation (N. Engl. J. Med. 2015;372:1399-409).

These results debunk findings from a survey a few years ago that found cardiac surgeons avoided doing surgical ablation during mitral valve surgery because it makes the operation too complex, requires longer pump times, and raises the risk of surgery, said Dr. Gillinov. “Does ablation improve rhythm control? Yes. Does ablation increase risk? No. Does ablation improve clinical outcomes? It probably does,” he said.

The trial had some limitations, Dr. Gillinov said. Its endpoint was not a clinical outcome, although looking at stroke risk or mortality would have required thousands of patients. Also, 20% of patients did not have follow-up with the 3-day Holter test. However, previous studies have shown a strong association between surgical ablation and a reduced risk of stroke. When Dr. Jolanda Kluin of Utrecht (the Netherlands) University asked if a patient would be better off with AF or a pacemaker, Dr. Gillinov replied, “I think it’s better to have an AV sequential rhythm, but the truth is no one can answer that question without clinical data.”

The bottom line is, “if you have a patient who’s having mitral valve surgery who also has AF, do an ablation,” he said.

The study was supported by the National Institutes of Health and the Canadian Institutes of Health Research. Dr. Gillinov disclosed relationships with AtriCure, Medtronic, Edwards Lifesciences, On-X Life Technologies, Abbott, Tendyne, and Clear Catheter.

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

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

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

1. Inspection, palpation, strength testing

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

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

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

2. ROM and GIRD assessment

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

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

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

3. Internal impingement: rotator cuff and labrum

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

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

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

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

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

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

4. Scapulothoracic examination

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

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

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

5. Neurovascular examination

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

Thoracic outlet syndrome

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

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

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

Effort thrombosis

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

Arterial aneurysm

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

Conclusion

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

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

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

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

1. Inspection, palpation, strength testing

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

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

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

2. ROM and GIRD assessment

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

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

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

3. Internal impingement: rotator cuff and labrum

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

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

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

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

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

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

4. Scapulothoracic examination

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

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

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

5. Neurovascular examination

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

Thoracic outlet syndrome

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

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

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

Effort thrombosis

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

Arterial aneurysm

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

Conclusion

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

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

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

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

1. Inspection, palpation, strength testing

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

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

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

2. ROM and GIRD assessment

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

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

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

3. Internal impingement: rotator cuff and labrum

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

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

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

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

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

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

4. Scapulothoracic examination

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

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

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

5. Neurovascular examination

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

Thoracic outlet syndrome

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

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

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

Effort thrombosis

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

Arterial aneurysm

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

Conclusion

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