Clinical Review

Football is an important component of American culture, with approximately 3 million youth athletes, 1.1 million high school athletes, and 100,000 college athletes participating each year.¹ Participation in football provides athletes with physical, social, psychological, and academic benefits. Despite these benefits, widespread focus has been placed on the safety of football due to the risk for sport-related concussion (SRC) and potentially long-term effects; however, little recognition has been given to the advancements in concussion management across time and occurrence of concussions during most life activities. Although it is reasonable for concerns to be presented, it is important to better understand SRC and the current factors leading to prolonged recoveries, increased risk for injury, and potentially long-term effects.

What Is a Concussion?

Concussions occur after sustaining direct or indirect injury to the head or other parts of the body, as long as the injury force is transmitted to the head. Athletes often experience physical, cognitive, emotional, and sleep-related symptoms post-concussion secondary to an “energy crisis” within the brain.² The energy crisis occurs as the result of transient neurological dysfunction triggered by changes in the brain (eg, release of neurotransmitters, impaired axonal function).^2,3 Concussion is undetectable with traditional imaging; however, advanced imaging techniques (eg, diffuse tensor imaging) have shown progress in assessing axonal injury.³ Symptom duration post-concussion is highly variable due to individual differences; a recent study showed recovery took 3 to 4 weeks for memory and symptoms.^4,5

Previous Concussion Management

Identification techniques and return-to-play guidelines for concussion have significantly changed across time. In the past, concussion grading scales were utilized for diagnosis and return to play was possible within the same contest.^6,7 It has since been recognized that initial concussion severity makes it difficult to predict recovery.³ For example, research revealed memory decline and increased symptoms 36 hours post-injury for athletes with a grade 1 concussion (ie, transient confusion, no loss of consciousness, concussion symptoms or mental status changes that resolve within 15 minutes of injury) compared to baseline.⁷ Another study found duration of mental status changes to be related to slower symptom resolution and memory impairment 36 hours to 7 days post-injury.⁶ Consequently, return to play within the same contest was likely too liberal. Guidelines today recommend immediate removal from play with suspected SRC. Nevertheless, the “play through pain” culture has led athletes to continue playing after SRC, contributing to prolonged recoveries and potentially long-term effects.

Current Concussion Management: Continued Concerns and Areas of Improvement

Despite increased awareness of concussions, recent estimates revealed high rates (ie, 27:1 ratio for general players) of underreporting in college football, particularly amongst offensive linemen.⁸ Researchers have studied recovery implications for remaining in play, with one study revealing a 2.2 times greater risk for prolonged recovery in college athletes with delayed vs immediate removal.⁹ Another similar study discovered an 8.8 times greater risk for prolonged recovery in adolescent and young adult athletes not removed vs removed from play.¹⁰ Further analysis found remaining in play to be the greatest risk factor for prolonged recovery compared to other previously studied risk factors (eg, age, sex, posttraumatic migraine).¹⁰ Additionally, significant differences in neurocognitive data were seen between the “removed” and “not removed” groups for verbal memory, visual memory, processing speed, and reaction time at 1 to 7 days and 8 to 30 days.¹⁰ The recovery implications of remaining in play and the additional risk for second impact syndrome (SIS), or repeat concussion when recovering from another injury, emphasizes the need for further education efforts amongst athletes to encourage immediate reporting of injury.¹¹

Sideline Assessment

Sideline assessment has become a vital component of concussion management to rule out concussion and/or significant injury other than concussion. Assessment should include observation, cognitive/balance testing, neurologic examination, and possible exertion testing to ensure a comprehensive evaluation of all areas of potential dysfunction.¹² Indications for emergency department evaluation include suspicion for cervical spine injury, intracranial hemorrhage, or skull fracture as well as prolonged loss of consciousness, high-risk mechanisms, posttraumatic seizure(s), and/or significant worsening of symptoms.¹²

Observation

On the sideline, it is important to identify any immediate signs of injury (ie, loss of consciousness, anterograde/retrograde amnesia, and disorientation/confusion). Since immediate signs are not always present, it is important to be aware of the most commonly reported symptoms, including headache, difficulty concentrating, fatigue, drowsiness, and dizziness.¹³ If symptoms are not reported by the athlete, balance problems, lack of coordination, increased emotionality, and difficulty following instructions may be observed during play.¹²

On-Field Assessment

Cognitive and balance testing are essential in determining if an athlete has sustained a concussion. Immediate declines in memory, concentration abilities, and balance abilities are common. Given limitations in administering long testing batteries on the sideline, brief standardized tests such as the Standardized Assessment of Concussion (SAC), Balance Error Scoring System (BESS), and Sport Concussion Assessment Tool (SCAT) are commonly utilized. Identification of cognitive and/or balance abnormalities can help the athlete recognize deficits following injury.¹² Balance problems are experienced due to abnormalities in sensory organization and generally resolve during the acute recovery period.^14,15 Cognitive difficulties typically persist longer than balance problems, though duration varies widely.

 

Neurologic Evaluation

A neurologic evaluation including cranial nerve testing and evaluation of motor-sensory function (ie, assessment for the strength and sensation of upper and lower extremities) is important to identify focal deficits (ie, sensation changes, loss of fine motor control) indicative of serious intracranial pathology.¹² Additionally, clinicians have suggested inclusion of vestibular and oculomotor assessments due to frequent dysfunction post-concussion.^12,15,16 Examination of the vestibular/oculomotor systems through tools such as the Vestibular/Ocular Motor Screening (VOMS) assessment (assesses both the vestibular and oculomotor systems) and King-Devick Test (primarily assesses saccadic eye movements) can elicit symptoms that may not present immediately. If assessment appears normal, exertion testing can be utilized to determine if symptoms are provoked through physical exercise that should include cardio, dynamic, and sport-specific activities to stress the vestibular system.¹²

Risk Factors for Injury and Prolonged Recovery

Medical professionals must consider the presence of risk factors when managing concussion in order to make appropriate treatment recommendations and return-to-play decisions. Research has demonstrated the role of female gender, learning disability, attention-deficit/hyperactivity disorder, psychiatric history, young age, motion sickness, sleep problems, somatization, concussion history, on-field dizziness, posttraumatic migraine, and fogginess in increased risk for injury and/or prolonged recovery.^17-25 Additionally, athletes with ongoing symptoms from a previous injury are at risk for sustaining another injury.

Acute Home Concussion Management

Although strict rest has been recommended post-concussion, recent research evaluating strict rest vs usual care for adolescents revealed greater symptom reports and longer recovery periods for the strict rest group.²⁶ Based on these findings and emphasis for regulation within the migraine literature (due to the common pathophysiology between migraine and concussion²⁷), we recommend that athletes follow a regulated daily schedule post-concussion including: 1) regular sleep-wake schedule with avoidance of naps, 2) regular meals, 3) adequate fluid hydration, 4) light noncontact physical activity (ie, walking, with progressions recommended by a physician), and 5) stress management techniques. Use of these strategies immediately can help in preventing against increased symptoms and stress, and decreases the need for medication in select cases. Additionally, over-the-counter medications should be limited to 2 to 3 doses per week to avoid rebound headaches.²⁸

In-Office Concussion Management

Athletes diagnosed with SRC will experience different symptoms based on the injury mechanism, risk factors, and management approach. Comprehensive evaluation should include assessment of risk factors, injury details, symptoms, neurocognitive functioning, vestibular/oculomotor dysfunction, tolerance of physical exertion, balance functioning, and cervical spine integrity (if necessary).^29,30 Due to individual differences and the heterogeneous symptom profiles, concussion management must move beyond a “one size fits all” approach to avoid nonspecific treatment strategies and consequently prolonged recoveries.²⁹ Clinicians and researchers at University of Pittsburgh Medical Center have identified 6 concussion clinical profiles (ie, vestibular, ocular, posttraumatic migraine, cervical, anxiety/mood, and cognitive/fatigue) that are generally identifiable 48 hours after injury.^29,30 Identification of the clinical profile(s) through a comprehensive evaluation guides the development of individualized treatment plans and targeted rehabilitation strategies.^29,30

Vestibular. The vestibular system is responsible for stabilizing vision while the head moves and balance control.¹⁵ Athletes can experience central and/or peripheral vestibular dysfunction to include benign paroxysmal positional vertigo (BPPV), visual motion sensitivity, vestibular ocular reflex impairment, and balance impairment.^30,31 Symptoms typically include dizziness, impaired balance, blurry vision, difficulty focusing, and environmental sensitivity.^15,29,30 Potential treatment options include vestibular rehabilitation, exertion therapy, and school/work accommodations.

Ocular. The oculomotor system is responsible for control of eye movements. Athletes can experience many different posttraumatic vision changes, including convergence problems, eye-tracking difficulties, refractive error, difficulty with pursuits/saccades, and accommodation insufficiency. Symptoms typically include light sensitivity, blurred vision, double vision, headaches, fatigue, and memory difficulties.^15,29,30 Potential treatment options include vision therapy, vestibular rehabilitation, and school/work accommodations.³²

Posttraumatic Migraine. Headache, the most common post-concussion symptom, can persist and meet criteria for posttraumatic migraine (ie, unilateral headache with accompanying nausea and/or photophobia and phonophobia).^29,30,33 Implementation of a routine schedule, daily physical activity, exertion therapy, pharmacologic intervention, and school/work accommodations are potential treatment options.

Cervical. The cervical spine can be injured during whiplash-type injuries. Therefore, determining the location, onset, and typical exacerbations of pain can be helpful in identifying cervical involvement.^29,30 Symptoms typically include headaches, neck pain, numbness, and tingling. Evaluation and therapy by a certified physical therapist and pharmacologic intervention (eg, muscle relaxants) are potential treatment options. ^29,30

Anxiety/Mood. Anxiety, or worry and fear about everyday situations, is common post-concussion and can sometimes be related to ongoing vestibular impairment. Symptoms typically include ruminative thoughts, avoidance of specific situations, hypervigilance, feelings of being overwhelmed, and difficulty falling asleep.^29,30 Potential treatment options include implementation of a routine schedule, exposure to provocative situations, psychotherapy, pharmacologic intervention, and school/work accommodations.³⁴

 

Cognitive/Fatigue. A global concussion factor (including cognitive, fatigue, and migraine symptoms) has been identified within 1 to 7 days of injury. Although this factor of symptoms generally resolves during the acute recovery period, it persists in select cases.¹³ Symptoms typically include fatigue, decreased energy levels, nonspecific headaches, potential sleep disruption, increased symptoms towards the end of the day, difficulty concentrating, and increased headache with cognitive activities.^29,30,35 Routine schedule, daily physical activity, exertion therapy, pharmacologic intervention (eg, amantadine), and school/work accommodations are potential treatment options.³⁰

Conclusion

Advancements in SRC management warrant change in the conversations regarding concussion in football. Specifically, conversations should address the current understanding of concussion and improvements in the safety of football through stricter concussion guidelines, detailed sideline evaluations, recognition of risk factors, improved acute management, and identification of concussion profiles that help to direct individualized treatment plans and targeted rehabilitation strategies. The biggest concerns related to concussions in football include underreporting of injury, premature return to play, and receiving routine rather than individualized treatment. Therefore, to further improve the safety of football and management of concussion it is essential that future efforts focus on the following 6 areas:

Education: Improved understanding of concussion is imperative to reducing poor outcomes and widespread concerns.

Immediate reporting: Reporting of concussion must be expected and encouraged through consistent responses by coaches to reduce underreporting and fear of reporting in athletes.

Prevention techniques: Athletes must be taught proper form and playing techniques to reduce the risk for concussion. Proper form and technique should be incentivized.

Targeted treatment: Individualized treatment plans and targeted rehabilitation strategies must be developed based on the identified clinical profile(s) to avoid nonspecific treatment recommendations.

Multidisciplinary treatment teams: Given the heterogeneous symptoms profiles and need for care provided by different medical specialties, multidisciplinary teams are essential.

Remain current: With the progress in understanding concussion, providers must remain vigilant of future advances in concussion management to further improve the safety of football.

Am J Orthop. 2016;45(6):352-356. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Football is an important component of American culture, with approximately 3 million youth athletes, 1.1 million high school athletes, and 100,000 college athletes participating each year.¹ Participation in football provides athletes with physical, social, psychological, and academic benefits. Despite these benefits, widespread focus has been placed on the safety of football due to the risk for sport-related concussion (SRC) and potentially long-term effects; however, little recognition has been given to the advancements in concussion management across time and occurrence of concussions during most life activities. Although it is reasonable for concerns to be presented, it is important to better understand SRC and the current factors leading to prolonged recoveries, increased risk for injury, and potentially long-term effects.

What Is a Concussion?

Concussions occur after sustaining direct or indirect injury to the head or other parts of the body, as long as the injury force is transmitted to the head. Athletes often experience physical, cognitive, emotional, and sleep-related symptoms post-concussion secondary to an “energy crisis” within the brain.² The energy crisis occurs as the result of transient neurological dysfunction triggered by changes in the brain (eg, release of neurotransmitters, impaired axonal function).^2,3 Concussion is undetectable with traditional imaging; however, advanced imaging techniques (eg, diffuse tensor imaging) have shown progress in assessing axonal injury.³ Symptom duration post-concussion is highly variable due to individual differences; a recent study showed recovery took 3 to 4 weeks for memory and symptoms.^4,5

Previous Concussion Management

Identification techniques and return-to-play guidelines for concussion have significantly changed across time. In the past, concussion grading scales were utilized for diagnosis and return to play was possible within the same contest.^6,7 It has since been recognized that initial concussion severity makes it difficult to predict recovery.³ For example, research revealed memory decline and increased symptoms 36 hours post-injury for athletes with a grade 1 concussion (ie, transient confusion, no loss of consciousness, concussion symptoms or mental status changes that resolve within 15 minutes of injury) compared to baseline.⁷ Another study found duration of mental status changes to be related to slower symptom resolution and memory impairment 36 hours to 7 days post-injury.⁶ Consequently, return to play within the same contest was likely too liberal. Guidelines today recommend immediate removal from play with suspected SRC. Nevertheless, the “play through pain” culture has led athletes to continue playing after SRC, contributing to prolonged recoveries and potentially long-term effects.

Current Concussion Management: Continued Concerns and Areas of Improvement

Despite increased awareness of concussions, recent estimates revealed high rates (ie, 27:1 ratio for general players) of underreporting in college football, particularly amongst offensive linemen.⁸ Researchers have studied recovery implications for remaining in play, with one study revealing a 2.2 times greater risk for prolonged recovery in college athletes with delayed vs immediate removal.⁹ Another similar study discovered an 8.8 times greater risk for prolonged recovery in adolescent and young adult athletes not removed vs removed from play.¹⁰ Further analysis found remaining in play to be the greatest risk factor for prolonged recovery compared to other previously studied risk factors (eg, age, sex, posttraumatic migraine).¹⁰ Additionally, significant differences in neurocognitive data were seen between the “removed” and “not removed” groups for verbal memory, visual memory, processing speed, and reaction time at 1 to 7 days and 8 to 30 days.¹⁰ The recovery implications of remaining in play and the additional risk for second impact syndrome (SIS), or repeat concussion when recovering from another injury, emphasizes the need for further education efforts amongst athletes to encourage immediate reporting of injury.¹¹

Sideline Assessment

Sideline assessment has become a vital component of concussion management to rule out concussion and/or significant injury other than concussion. Assessment should include observation, cognitive/balance testing, neurologic examination, and possible exertion testing to ensure a comprehensive evaluation of all areas of potential dysfunction.¹² Indications for emergency department evaluation include suspicion for cervical spine injury, intracranial hemorrhage, or skull fracture as well as prolonged loss of consciousness, high-risk mechanisms, posttraumatic seizure(s), and/or significant worsening of symptoms.¹²

Observation

On the sideline, it is important to identify any immediate signs of injury (ie, loss of consciousness, anterograde/retrograde amnesia, and disorientation/confusion). Since immediate signs are not always present, it is important to be aware of the most commonly reported symptoms, including headache, difficulty concentrating, fatigue, drowsiness, and dizziness.¹³ If symptoms are not reported by the athlete, balance problems, lack of coordination, increased emotionality, and difficulty following instructions may be observed during play.¹²

On-Field Assessment

Cognitive and balance testing are essential in determining if an athlete has sustained a concussion. Immediate declines in memory, concentration abilities, and balance abilities are common. Given limitations in administering long testing batteries on the sideline, brief standardized tests such as the Standardized Assessment of Concussion (SAC), Balance Error Scoring System (BESS), and Sport Concussion Assessment Tool (SCAT) are commonly utilized. Identification of cognitive and/or balance abnormalities can help the athlete recognize deficits following injury.¹² Balance problems are experienced due to abnormalities in sensory organization and generally resolve during the acute recovery period.^14,15 Cognitive difficulties typically persist longer than balance problems, though duration varies widely.

 

Neurologic Evaluation

A neurologic evaluation including cranial nerve testing and evaluation of motor-sensory function (ie, assessment for the strength and sensation of upper and lower extremities) is important to identify focal deficits (ie, sensation changes, loss of fine motor control) indicative of serious intracranial pathology.¹² Additionally, clinicians have suggested inclusion of vestibular and oculomotor assessments due to frequent dysfunction post-concussion.^12,15,16 Examination of the vestibular/oculomotor systems through tools such as the Vestibular/Ocular Motor Screening (VOMS) assessment (assesses both the vestibular and oculomotor systems) and King-Devick Test (primarily assesses saccadic eye movements) can elicit symptoms that may not present immediately. If assessment appears normal, exertion testing can be utilized to determine if symptoms are provoked through physical exercise that should include cardio, dynamic, and sport-specific activities to stress the vestibular system.¹²

Risk Factors for Injury and Prolonged Recovery

Medical professionals must consider the presence of risk factors when managing concussion in order to make appropriate treatment recommendations and return-to-play decisions. Research has demonstrated the role of female gender, learning disability, attention-deficit/hyperactivity disorder, psychiatric history, young age, motion sickness, sleep problems, somatization, concussion history, on-field dizziness, posttraumatic migraine, and fogginess in increased risk for injury and/or prolonged recovery.^17-25 Additionally, athletes with ongoing symptoms from a previous injury are at risk for sustaining another injury.

Acute Home Concussion Management

Although strict rest has been recommended post-concussion, recent research evaluating strict rest vs usual care for adolescents revealed greater symptom reports and longer recovery periods for the strict rest group.²⁶ Based on these findings and emphasis for regulation within the migraine literature (due to the common pathophysiology between migraine and concussion²⁷), we recommend that athletes follow a regulated daily schedule post-concussion including: 1) regular sleep-wake schedule with avoidance of naps, 2) regular meals, 3) adequate fluid hydration, 4) light noncontact physical activity (ie, walking, with progressions recommended by a physician), and 5) stress management techniques. Use of these strategies immediately can help in preventing against increased symptoms and stress, and decreases the need for medication in select cases. Additionally, over-the-counter medications should be limited to 2 to 3 doses per week to avoid rebound headaches.²⁸

In-Office Concussion Management

Athletes diagnosed with SRC will experience different symptoms based on the injury mechanism, risk factors, and management approach. Comprehensive evaluation should include assessment of risk factors, injury details, symptoms, neurocognitive functioning, vestibular/oculomotor dysfunction, tolerance of physical exertion, balance functioning, and cervical spine integrity (if necessary).^29,30 Due to individual differences and the heterogeneous symptom profiles, concussion management must move beyond a “one size fits all” approach to avoid nonspecific treatment strategies and consequently prolonged recoveries.²⁹ Clinicians and researchers at University of Pittsburgh Medical Center have identified 6 concussion clinical profiles (ie, vestibular, ocular, posttraumatic migraine, cervical, anxiety/mood, and cognitive/fatigue) that are generally identifiable 48 hours after injury.^29,30 Identification of the clinical profile(s) through a comprehensive evaluation guides the development of individualized treatment plans and targeted rehabilitation strategies.^29,30

Vestibular. The vestibular system is responsible for stabilizing vision while the head moves and balance control.¹⁵ Athletes can experience central and/or peripheral vestibular dysfunction to include benign paroxysmal positional vertigo (BPPV), visual motion sensitivity, vestibular ocular reflex impairment, and balance impairment.^30,31 Symptoms typically include dizziness, impaired balance, blurry vision, difficulty focusing, and environmental sensitivity.^15,29,30 Potential treatment options include vestibular rehabilitation, exertion therapy, and school/work accommodations.

Ocular. The oculomotor system is responsible for control of eye movements. Athletes can experience many different posttraumatic vision changes, including convergence problems, eye-tracking difficulties, refractive error, difficulty with pursuits/saccades, and accommodation insufficiency. Symptoms typically include light sensitivity, blurred vision, double vision, headaches, fatigue, and memory difficulties.^15,29,30 Potential treatment options include vision therapy, vestibular rehabilitation, and school/work accommodations.³²

Posttraumatic Migraine. Headache, the most common post-concussion symptom, can persist and meet criteria for posttraumatic migraine (ie, unilateral headache with accompanying nausea and/or photophobia and phonophobia).^29,30,33 Implementation of a routine schedule, daily physical activity, exertion therapy, pharmacologic intervention, and school/work accommodations are potential treatment options.

Cervical. The cervical spine can be injured during whiplash-type injuries. Therefore, determining the location, onset, and typical exacerbations of pain can be helpful in identifying cervical involvement.^29,30 Symptoms typically include headaches, neck pain, numbness, and tingling. Evaluation and therapy by a certified physical therapist and pharmacologic intervention (eg, muscle relaxants) are potential treatment options. ^29,30

Anxiety/Mood. Anxiety, or worry and fear about everyday situations, is common post-concussion and can sometimes be related to ongoing vestibular impairment. Symptoms typically include ruminative thoughts, avoidance of specific situations, hypervigilance, feelings of being overwhelmed, and difficulty falling asleep.^29,30 Potential treatment options include implementation of a routine schedule, exposure to provocative situations, psychotherapy, pharmacologic intervention, and school/work accommodations.³⁴

 

Cognitive/Fatigue. A global concussion factor (including cognitive, fatigue, and migraine symptoms) has been identified within 1 to 7 days of injury. Although this factor of symptoms generally resolves during the acute recovery period, it persists in select cases.¹³ Symptoms typically include fatigue, decreased energy levels, nonspecific headaches, potential sleep disruption, increased symptoms towards the end of the day, difficulty concentrating, and increased headache with cognitive activities.^29,30,35 Routine schedule, daily physical activity, exertion therapy, pharmacologic intervention (eg, amantadine), and school/work accommodations are potential treatment options.³⁰

Conclusion

Advancements in SRC management warrant change in the conversations regarding concussion in football. Specifically, conversations should address the current understanding of concussion and improvements in the safety of football through stricter concussion guidelines, detailed sideline evaluations, recognition of risk factors, improved acute management, and identification of concussion profiles that help to direct individualized treatment plans and targeted rehabilitation strategies. The biggest concerns related to concussions in football include underreporting of injury, premature return to play, and receiving routine rather than individualized treatment. Therefore, to further improve the safety of football and management of concussion it is essential that future efforts focus on the following 6 areas:

Education: Improved understanding of concussion is imperative to reducing poor outcomes and widespread concerns.

Immediate reporting: Reporting of concussion must be expected and encouraged through consistent responses by coaches to reduce underreporting and fear of reporting in athletes.

Prevention techniques: Athletes must be taught proper form and playing techniques to reduce the risk for concussion. Proper form and technique should be incentivized.

Targeted treatment: Individualized treatment plans and targeted rehabilitation strategies must be developed based on the identified clinical profile(s) to avoid nonspecific treatment recommendations.

Multidisciplinary treatment teams: Given the heterogeneous symptoms profiles and need for care provided by different medical specialties, multidisciplinary teams are essential.

Remain current: With the progress in understanding concussion, providers must remain vigilant of future advances in concussion management to further improve the safety of football.

Am J Orthop. 2016;45(6):352-356. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Football is an important component of American culture, with approximately 3 million youth athletes, 1.1 million high school athletes, and 100,000 college athletes participating each year.¹ Participation in football provides athletes with physical, social, psychological, and academic benefits. Despite these benefits, widespread focus has been placed on the safety of football due to the risk for sport-related concussion (SRC) and potentially long-term effects; however, little recognition has been given to the advancements in concussion management across time and occurrence of concussions during most life activities. Although it is reasonable for concerns to be presented, it is important to better understand SRC and the current factors leading to prolonged recoveries, increased risk for injury, and potentially long-term effects.

What Is a Concussion?

Concussions occur after sustaining direct or indirect injury to the head or other parts of the body, as long as the injury force is transmitted to the head. Athletes often experience physical, cognitive, emotional, and sleep-related symptoms post-concussion secondary to an “energy crisis” within the brain.² The energy crisis occurs as the result of transient neurological dysfunction triggered by changes in the brain (eg, release of neurotransmitters, impaired axonal function).^2,3 Concussion is undetectable with traditional imaging; however, advanced imaging techniques (eg, diffuse tensor imaging) have shown progress in assessing axonal injury.³ Symptom duration post-concussion is highly variable due to individual differences; a recent study showed recovery took 3 to 4 weeks for memory and symptoms.^4,5

Previous Concussion Management

Identification techniques and return-to-play guidelines for concussion have significantly changed across time. In the past, concussion grading scales were utilized for diagnosis and return to play was possible within the same contest.^6,7 It has since been recognized that initial concussion severity makes it difficult to predict recovery.³ For example, research revealed memory decline and increased symptoms 36 hours post-injury for athletes with a grade 1 concussion (ie, transient confusion, no loss of consciousness, concussion symptoms or mental status changes that resolve within 15 minutes of injury) compared to baseline.⁷ Another study found duration of mental status changes to be related to slower symptom resolution and memory impairment 36 hours to 7 days post-injury.⁶ Consequently, return to play within the same contest was likely too liberal. Guidelines today recommend immediate removal from play with suspected SRC. Nevertheless, the “play through pain” culture has led athletes to continue playing after SRC, contributing to prolonged recoveries and potentially long-term effects.

Current Concussion Management: Continued Concerns and Areas of Improvement

Despite increased awareness of concussions, recent estimates revealed high rates (ie, 27:1 ratio for general players) of underreporting in college football, particularly amongst offensive linemen.⁸ Researchers have studied recovery implications for remaining in play, with one study revealing a 2.2 times greater risk for prolonged recovery in college athletes with delayed vs immediate removal.⁹ Another similar study discovered an 8.8 times greater risk for prolonged recovery in adolescent and young adult athletes not removed vs removed from play.¹⁰ Further analysis found remaining in play to be the greatest risk factor for prolonged recovery compared to other previously studied risk factors (eg, age, sex, posttraumatic migraine).¹⁰ Additionally, significant differences in neurocognitive data were seen between the “removed” and “not removed” groups for verbal memory, visual memory, processing speed, and reaction time at 1 to 7 days and 8 to 30 days.¹⁰ The recovery implications of remaining in play and the additional risk for second impact syndrome (SIS), or repeat concussion when recovering from another injury, emphasizes the need for further education efforts amongst athletes to encourage immediate reporting of injury.¹¹

Sideline Assessment

Sideline assessment has become a vital component of concussion management to rule out concussion and/or significant injury other than concussion. Assessment should include observation, cognitive/balance testing, neurologic examination, and possible exertion testing to ensure a comprehensive evaluation of all areas of potential dysfunction.¹² Indications for emergency department evaluation include suspicion for cervical spine injury, intracranial hemorrhage, or skull fracture as well as prolonged loss of consciousness, high-risk mechanisms, posttraumatic seizure(s), and/or significant worsening of symptoms.¹²

Observation

On the sideline, it is important to identify any immediate signs of injury (ie, loss of consciousness, anterograde/retrograde amnesia, and disorientation/confusion). Since immediate signs are not always present, it is important to be aware of the most commonly reported symptoms, including headache, difficulty concentrating, fatigue, drowsiness, and dizziness.¹³ If symptoms are not reported by the athlete, balance problems, lack of coordination, increased emotionality, and difficulty following instructions may be observed during play.¹²

On-Field Assessment

Cognitive and balance testing are essential in determining if an athlete has sustained a concussion. Immediate declines in memory, concentration abilities, and balance abilities are common. Given limitations in administering long testing batteries on the sideline, brief standardized tests such as the Standardized Assessment of Concussion (SAC), Balance Error Scoring System (BESS), and Sport Concussion Assessment Tool (SCAT) are commonly utilized. Identification of cognitive and/or balance abnormalities can help the athlete recognize deficits following injury.¹² Balance problems are experienced due to abnormalities in sensory organization and generally resolve during the acute recovery period.^14,15 Cognitive difficulties typically persist longer than balance problems, though duration varies widely.

 

Neurologic Evaluation

A neurologic evaluation including cranial nerve testing and evaluation of motor-sensory function (ie, assessment for the strength and sensation of upper and lower extremities) is important to identify focal deficits (ie, sensation changes, loss of fine motor control) indicative of serious intracranial pathology.¹² Additionally, clinicians have suggested inclusion of vestibular and oculomotor assessments due to frequent dysfunction post-concussion.^12,15,16 Examination of the vestibular/oculomotor systems through tools such as the Vestibular/Ocular Motor Screening (VOMS) assessment (assesses both the vestibular and oculomotor systems) and King-Devick Test (primarily assesses saccadic eye movements) can elicit symptoms that may not present immediately. If assessment appears normal, exertion testing can be utilized to determine if symptoms are provoked through physical exercise that should include cardio, dynamic, and sport-specific activities to stress the vestibular system.¹²

Risk Factors for Injury and Prolonged Recovery

Medical professionals must consider the presence of risk factors when managing concussion in order to make appropriate treatment recommendations and return-to-play decisions. Research has demonstrated the role of female gender, learning disability, attention-deficit/hyperactivity disorder, psychiatric history, young age, motion sickness, sleep problems, somatization, concussion history, on-field dizziness, posttraumatic migraine, and fogginess in increased risk for injury and/or prolonged recovery.^17-25 Additionally, athletes with ongoing symptoms from a previous injury are at risk for sustaining another injury.

Acute Home Concussion Management

Although strict rest has been recommended post-concussion, recent research evaluating strict rest vs usual care for adolescents revealed greater symptom reports and longer recovery periods for the strict rest group.²⁶ Based on these findings and emphasis for regulation within the migraine literature (due to the common pathophysiology between migraine and concussion²⁷), we recommend that athletes follow a regulated daily schedule post-concussion including: 1) regular sleep-wake schedule with avoidance of naps, 2) regular meals, 3) adequate fluid hydration, 4) light noncontact physical activity (ie, walking, with progressions recommended by a physician), and 5) stress management techniques. Use of these strategies immediately can help in preventing against increased symptoms and stress, and decreases the need for medication in select cases. Additionally, over-the-counter medications should be limited to 2 to 3 doses per week to avoid rebound headaches.²⁸

In-Office Concussion Management

Athletes diagnosed with SRC will experience different symptoms based on the injury mechanism, risk factors, and management approach. Comprehensive evaluation should include assessment of risk factors, injury details, symptoms, neurocognitive functioning, vestibular/oculomotor dysfunction, tolerance of physical exertion, balance functioning, and cervical spine integrity (if necessary).^29,30 Due to individual differences and the heterogeneous symptom profiles, concussion management must move beyond a “one size fits all” approach to avoid nonspecific treatment strategies and consequently prolonged recoveries.²⁹ Clinicians and researchers at University of Pittsburgh Medical Center have identified 6 concussion clinical profiles (ie, vestibular, ocular, posttraumatic migraine, cervical, anxiety/mood, and cognitive/fatigue) that are generally identifiable 48 hours after injury.^29,30 Identification of the clinical profile(s) through a comprehensive evaluation guides the development of individualized treatment plans and targeted rehabilitation strategies.^29,30

Vestibular. The vestibular system is responsible for stabilizing vision while the head moves and balance control.¹⁵ Athletes can experience central and/or peripheral vestibular dysfunction to include benign paroxysmal positional vertigo (BPPV), visual motion sensitivity, vestibular ocular reflex impairment, and balance impairment.^30,31 Symptoms typically include dizziness, impaired balance, blurry vision, difficulty focusing, and environmental sensitivity.^15,29,30 Potential treatment options include vestibular rehabilitation, exertion therapy, and school/work accommodations.

Ocular. The oculomotor system is responsible for control of eye movements. Athletes can experience many different posttraumatic vision changes, including convergence problems, eye-tracking difficulties, refractive error, difficulty with pursuits/saccades, and accommodation insufficiency. Symptoms typically include light sensitivity, blurred vision, double vision, headaches, fatigue, and memory difficulties.^15,29,30 Potential treatment options include vision therapy, vestibular rehabilitation, and school/work accommodations.³²

Posttraumatic Migraine. Headache, the most common post-concussion symptom, can persist and meet criteria for posttraumatic migraine (ie, unilateral headache with accompanying nausea and/or photophobia and phonophobia).^29,30,33 Implementation of a routine schedule, daily physical activity, exertion therapy, pharmacologic intervention, and school/work accommodations are potential treatment options.

Cervical. The cervical spine can be injured during whiplash-type injuries. Therefore, determining the location, onset, and typical exacerbations of pain can be helpful in identifying cervical involvement.^29,30 Symptoms typically include headaches, neck pain, numbness, and tingling. Evaluation and therapy by a certified physical therapist and pharmacologic intervention (eg, muscle relaxants) are potential treatment options. ^29,30

Anxiety/Mood. Anxiety, or worry and fear about everyday situations, is common post-concussion and can sometimes be related to ongoing vestibular impairment. Symptoms typically include ruminative thoughts, avoidance of specific situations, hypervigilance, feelings of being overwhelmed, and difficulty falling asleep.^29,30 Potential treatment options include implementation of a routine schedule, exposure to provocative situations, psychotherapy, pharmacologic intervention, and school/work accommodations.³⁴

 

Cognitive/Fatigue. A global concussion factor (including cognitive, fatigue, and migraine symptoms) has been identified within 1 to 7 days of injury. Although this factor of symptoms generally resolves during the acute recovery period, it persists in select cases.¹³ Symptoms typically include fatigue, decreased energy levels, nonspecific headaches, potential sleep disruption, increased symptoms towards the end of the day, difficulty concentrating, and increased headache with cognitive activities.^29,30,35 Routine schedule, daily physical activity, exertion therapy, pharmacologic intervention (eg, amantadine), and school/work accommodations are potential treatment options.³⁰

Conclusion

Advancements in SRC management warrant change in the conversations regarding concussion in football. Specifically, conversations should address the current understanding of concussion and improvements in the safety of football through stricter concussion guidelines, detailed sideline evaluations, recognition of risk factors, improved acute management, and identification of concussion profiles that help to direct individualized treatment plans and targeted rehabilitation strategies. The biggest concerns related to concussions in football include underreporting of injury, premature return to play, and receiving routine rather than individualized treatment. Therefore, to further improve the safety of football and management of concussion it is essential that future efforts focus on the following 6 areas:

Education: Improved understanding of concussion is imperative to reducing poor outcomes and widespread concerns.

Immediate reporting: Reporting of concussion must be expected and encouraged through consistent responses by coaches to reduce underreporting and fear of reporting in athletes.

Prevention techniques: Athletes must be taught proper form and playing techniques to reduce the risk for concussion. Proper form and technique should be incentivized.

Targeted treatment: Individualized treatment plans and targeted rehabilitation strategies must be developed based on the identified clinical profile(s) to avoid nonspecific treatment recommendations.

Multidisciplinary treatment teams: Given the heterogeneous symptoms profiles and need for care provided by different medical specialties, multidisciplinary teams are essential.

Remain current: With the progress in understanding concussion, providers must remain vigilant of future advances in concussion management to further improve the safety of football.

Am J Orthop. 2016;45(6):352-356. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Football, one of the most popular sports in the United States, is additionally recognized as a leading contributor to sports injury secondary to the contact collision nature of the endeavor. There are an estimated 1.1 million high school football players with another 100,000 participants combined in the National Football League (NFL), college, junior college, Arena Football League, and semipro levels of play.¹ USA Football estimates that an additional 3 million youth participate in community football leagues.¹ The National Center for Catastrophic Sports Injury Research recently calculated a fatality rate of 0.14 per 100,000 participants in 2014 for the 4.2 million who play football at all levels—and 0.45 per 100,000 in high school.¹ While direct deaths from head and spine injury remain a significant contributor to the number of catastrophic injuries, indirect deaths (systemic failure) predominate. Exertional heat stroke (EHS) has emerged as one of the leading indirect causes of death in high school and collegiate football. Boden and colleagues² reported that high school and college football players sustain approximately 12 fatalities annually, with indirect systemic causes being twice as common as direct blunt trauma.²The most common indirect causes identified included cardiac failure, heat illness, and complications of sickle cell trait (SCT). It was also noted that the risk of SCT, heat-related, and cardiac deaths increased during the second decade of the study, indicating these conditions may require a greater emphasis on diagnosis, treatment, and prevention. This review details for the team physician the unique challenge of exercising in the heat to the football player, and the prevention, diagnosis, management and return-to-play issues pertinent to exertional heat illness (EHI).

The Challenge

EHS represents the most severe manifestation of EHI—a gamut of diseases commonly encountered during the hot summer months when American football season begins. The breadth of EHI includes several important clinical diagnoses: exercise-associated muscle cramps (heat cramps); heat exhaustion with and without syncope; heat injury with evidence of end organ injury (eg, rhabdomyolysis); and EHS. EHS is defined as “a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates.”³ EHS, if left untreated, or even if clinical treatment is delayed, may result in significant end organ morbidity and/or mortality.

During exercise, the human thermoregulatory system mitigates heat gain by increasing skin blood flow and sweating, causing an increased dissipation of heat to the surrounding environment by leveraging conduction, convection, and evaporation.^4,5 Elevated environmental temperatures, increased humidity, and dehydration can impede the body’s ability to dissipate heat at a rate needed to maintain thermoregulation. This imbalance can result in hyperthermia secondary to uncompensated heat stress,⁵ which in turn can lead to EHI. Football players have unique challenges that make them particularly vulnerable to EHI. The summer heat during early-season participation and the requirement for equipment that covers nearly 60% of body surfaces pose increased risk of volume losses and hyperthermia that trigger the onset of EHI.⁶ Football athletes’ body compositions and physical size are additional contributing risk factors; the relatively high muscle and fat content increase thermogenicity, which require their bodies to dissipate more heat.⁷

An estimated 9000 cases of EHI occur annually across all high school sports,⁸ with an incidence of 1.6:100,000 athlete-exposures.^8,9 Studies have demonstrated, however, that EHI occurs in football 11.4 times more often than in all other high school sports combined.¹⁰ The incidence of nonfatal EHI in all levels of football is 4.42-5:100,000.^8,9 Between 2000 and 2014, 41 football players died from EHS.¹ In football, approximately 75% of all EHI events occurred during practices, while only 25% of incidents occurred during games.⁸

Given these potentially deadly consequences, it is important that football team physicians are not only alert to the early symptoms of heat illness and prepared to intervene to prevent the progression to EHS, but are critical leaders in educating coaches and players in evidence-based EHI prevention practices and policies.

Prevention

EHS is a preventable condition, arguably the most common cause of preventable nontraumatic exertional death in young athletes in the United States. Close attention to mitigating risk factors should begin prior to the onset of preseason practice and continue through the early season, where athletes are at the highest risk of developing heat illness.

Primary Prevention

Primary prevention is fundamental to minimizing the occurrences of EHI. It focuses on the following methods: recognition of inherent risk factors, acclimatization, hydration, and avoidance of inciting substances (including supplements).

 

Pre-Participation Examination. The purpose of the pre-participation examination (PPE) is to maximize an athlete’s safety by identifying medical conditions that place the athlete at risk.^11,12 The Preparticipation Physical Evaluation, 4th edition, the most widely used consensus publication, specifically queries if an athlete has a previous history of heat injury. However, it only indirectly addresses intrinsic risk factors that may predispose an athlete to EHI who has never had an EHI before. Therefore, providers should take the opportunity of the PPE to inquire about additional risk factors that may make an athlete high risk for sustaining a heat injury. Common risk factors for EHI are listed in Table 1.

While identifying at-risk athletes is important in mitigating the risk of developing EHI, it will not identify all possible cases: a study of military recruits found that up to 50% of Marines who developed EHI lacked an identifiable risk factor.¹³Wet Bulb Globe Temperature. Humidity can heighten a player’s risk of developing thermogenic dysregulation during hot temperatures. As ambient temperature nears internal body temperature, heat may actually be absorbed by the skin rather than dissipated into the air. As a result, the body must increasingly rely on sweat evaporation to encourage heat loss; this process is hindered in very humid climates. Wet bulb globe temperature (WBGT) is a measure of heat stress that accounts for temperature, humidity, wind speed, and cloud cover. WBGT should be utilized to determine the relative risk of EHI based on local environmental conditions, as there is a direct correlation between elevated WBGT and risk of EHI.^11,14 The greatest risk for EHS is performing high-intensity exercise (>75% VO2max) when WBGT >28°C (82°F).⁷ A study of hyperthermia-related deaths in football found that a majority of fatalities occurred on days classified as high risk (23°C-28°C) or extreme risk (>28°C) by WBGT.¹⁴ Consensus guidelines recommend that activities be modified based on WBGT (Table 2).^7,12

The impact of WBGT does not end solely on the day of practice. Athletes who exercise in elevated WBGT environments on 2 consecutive days are at increased risk of EHI due to cumulative effects of exercise in heat.¹¹Clothing. In football, required protective equipment may cover up to 60% of body surfaces. Studies have shown that wearing full uniform with pads increases internal body temperature and decreases time to exhaustion when compared to light clothing.^5,15 In addition, athletic equipment traps heat close to the body and inhibits evaporation of sweat into the environment, thereby inhibiting radiant and evaporative heat dissipation.^5,11 Likewise, wearing dark clothing encourages radiant absorption of heat, further contributing to potential thermal dysregulation.⁵ Use of a helmet is a specific risk factor for EHI, as significant heat dissipation occurs through the head.¹¹ To mitigate these risk factors, the introduction of padded equipment should occur incrementally over the heat acclimatization period (see below). In addition, athletes should be encouraged to remove their helmets during rest periods to promote added heat dissipation and recovery.

Heat Acclimatization. The risk of EHI escalates significantly when athletes are subjected to multiple stressors during periods of heat exposure, such as sudden increases in intensity or duration of exercise; prolonged new exposures to heat; dehydration; and sleep loss.⁵ When football season begins in late summer, athletes are least conditioned as temperatures reach their seasonal peak, causing increased risk of EHI.¹⁵ Planning for heat acclimatization is vital for all athletes who exercise in hot environments. Acclimatization procedures place progressively mounting physiologic strains on the body to improve athletes’ ability to dissipate heat, diminishing thermoregulatory and cardiovascular exertion.^4,5 Acclimatization begins with expansion of plasma volume on days 3 to 6, causing improvements in cardiac efficiency and resulting in an overall decrease in basal internal body temperature.^4,5,15 This process results in improvements in heat tolerance and exercise performance, evolving over 10 to 14 days of gradual escalation of exercise intensity and duration.^5,10,11,16 However, poor fitness levels and extreme temperatures can prolong this period, requiring up to 2 to 3 months to fully take effect.^5,7

The National Athletic Trainers Association (NATA) and National Collegiate Athletic Association (NCAA) have released consensus guidelines regarding heat acclimatization protocols for football athletes at the high school and college levels (Tables 3 and 4). Each of these guidelines involves an initial period without use of protective equipment, followed by a gradual addition of further equipment.^11,16

Secondary Prevention

Despite physicians’ best efforts to prevent all cases of EHI, athletes will still experience the effects of exercise-induced hyperthermia. The goal of secondary prevention is to slow the progression of this hyperthermia so that it does not progress to more dangerous EHI.

 

Hydration. Dehydration is an important risk factor for EHI. Sweat maintains thermoregulation by dissipating heat generated during exercise; however, it also contributes to body water losses. Furthermore, intravascular depletion decreases stroke volume, thereby increasing cardiovascular strain. It is estimated that for every 1% loss in body mass from dehydration, body temperature rises 0.22°C in comparison to a euhydrated state.⁶ Dehydration occurs more rapidly in hot environments, as fluid is lost through increased sweat production.⁷ After approximately 6% to 10% body weight volume loss, cardiac output cannot be maintained, diminishing sweat production and blood flow to both skin and muscle and causing diminished performance and a significant risk of heat exhaustion.⁷ If left unchecked, these physiologic changes result in further elevations in body temperature and increased cardiovascular strain, ultimately placing the athlete at significant risk for development of EHS.

Adequate hydration to maintain euvolemia is an important step in avoiding possible EHI. Multiple studies have shown that football players experience a baseline hypovolemia during their competition season,⁶ a deficit that is most marked during the first week of practices.¹⁷ This deficit is multifactorial, as football players expend a significant amount of fluid through sweat, are not able to adequately replace these losses during practice, and do not appropriately hydrate off the field.^6,18 Some players, especially linemen, sweat at a higher rate than their teammates, posing a possible risk of significant dehydration.⁶ Coaches and players alike should be educated on the importance of adequate hydration to meet their fluid needs.

The goal of hydration during exercise is to prevent large fluid losses that can adversely affect performance and increase risk of EHI;⁶ it may be unrealistic to replace all fluid losses during the practice period. Instead, athletes should target complete volume replacement over the post-exercise period.⁶ Some recommend hydrating based upon thirst drive; however, thirst is activated following a volume loss of approximately 2% body mass, the same degree of losses that place athletes at an increased risk for performance impairment and EHI.^4,6,11,12 Individuals should have access to fluids throughout practice and competition and be encouraged to hydrate as needed.^6,12,15 Furthermore, staff should modify their practices based upon WBGT and acclimatization status to provide more frequent hydration breaks.

Hyperhydration and Salt Intake. Of note, there are inherent risks to hyperhydration. Athletes with low sweat rates have an increased risk of overhydration and the development of exercise-associated hyponatremia (EAH),⁶ a condition whose presentation is very similar to EHS. In addition, inadequate sodium intake and excessive sweating can also contribute to the development of EAH. EAH has been implicated in the deaths of 2 football players in 2014.^1,6 Establishing team hydration guidelines and educating players and staff on appropriate hydration and dietary salt intake is essential to reduce the risk of both dehydration and hyperhydration and their complications.⁶Intra-Event Cooling. During exercise, team physicians can employ strategies for cooling athletes during exertion to mitigate their risk of EHI by decreasing thermal and cardiovascular strain.^4,19 Cooling during exercise is hypothesized to allow for accelerated heat dissipation, where heat is lost from the body more effectively. This accelerated loss enables athletes to maintain a higher heat storage capacity over the duration of exercise, avoiding uncompensated heat stresses that ultimately cause EHI.¹⁹

Some intra-event cooling strategies include the use of cooling garments, cooling packs, and cold water/slurry ingestion. Cooling garments lower skin temperature, which in turn can decrease thermoregulatory strains;⁴ a recent meta-analysis of intra-event cooling modalities revealed that wearing an ice vest during exercise resulted in the greatest decrease in thermal heat strain.¹⁹ Internal cooling strategies—namely ingestion of cold fluids/ice slurry—have shown some mild benefit in decreasing internal temperatures; however, some studies have demonstrated some decrease in sweat production associated with cold oral intake used in isolation.¹⁹ Overall, studies have shown that combining external (cooling clothing, ice packs, fanning) and internal (cold water, ice slurry) cooling methods result in a greater cooling effect than a use of a single method.⁴

Tertiary Prevention

The goal of tertiary prevention is to mitigate the risk of long-term adverse outcomes following an EHS event. The most effective means of reducing risk for morbidity and mortality is rapid identification and treatment of EHS as well as close evaluation of an athlete’s return to activity in heat. This process is spearheaded by an effective and well-rehearsed emergency action plan.

Diagnosis and Management

Rapid identification and treatment of EHS is crucial to minimizing the risk of poor outcomes.⁷ Any delay in the treatment of EHS can dramatically increase the likelihood of associated morbidity and mortality.²⁰

 

EHS is diagnosed by an elevated rectal temperature ≥40°C (104°F) and associated central nervous system (CNS) dysfunction.²¹ EHS should be strongly suspected in any athlete exercising in heat who exhibits signs of CNS dysfunction, including disorientation, confusion, dizziness, erratic behavior, irritability, headache, loss of coordination, delirium, collapse, or seizures.^7,12,15 EHS may also present with symptoms of heat exhaustion, including fatigue, hyperventilation, tachycardia, vomiting, diarrhea, and hypotension.^7,12,15

Rectal temperature should be taken for any athlete with suspected EHS, as other modalities—oral, skin, axillary, and aural—can be inaccurate and easily modified by ambient confounders such as ambient and skin temperature, athlete hyperventilation, and consumption of liquids.^7,11,12 Athletes exhibiting CNS symptoms with moderately elevated rectal temperatures that do not exceed 40°C should also be assumed to be suffering from EHS and treated with rapid cooling.¹¹ On the other hand, athletes with CNS symptoms who are normothermic should be assumed to have EAH until ruled out by electrolyte assessment; IV fluids should be at no more than keep vein open (KVO) pending this determination.¹¹ In some cases, an athlete may initially present with altered mental status but return to “normal.” However, this improvement may represent a “lucid period”; evaluation should continue with rectal temperature and treatment, as EHS in these cases may progress quickly.¹⁵

Treatment is centered on rapid, whole body cooling initiated at the first sign of heat illness.^7,22 The goal of treatment is to achieve a rectal temperature <38.9°C within 30 minutes of the onset of EHS.¹⁵ Upon diagnosis, the athlete should be quickly placed in a tub of ice water to facilitate cold water immersion (CWI) therapy. Some guidelines suggest the athlete’s clothing be removed to potentiate evaporative cooling during CWI;¹² however, cooling should not be delayed due to difficulties in removing equipment. CWI, where a heat stroke victim is submerged in ice water up to their neck while water is continuously circulated, is generally considered to be the gold standard treatment as it is the modality with the highest recorded cooling rates and the lowest rate of morbidity and mortality.^7,20,21 Multiple studies of CWI have shown that survival nears 100% when aggressive cooling starts within 5 minutes of collapse or identification of EHS.^20,21,22

If whole body CWI is unavailable, alternative methods of rapid cooling should be employed. Partial CWI, with torso immersion being preferable to the extremities, has been shown to achieve an acceptable rate of cooling to achieve sufficient drops in internal body temperature.^20,23 However, one popular treatment—applying ice packs to the whole body, in particular to the groin and axillae—has not been shown to be sufficient to achieve standard cooling goals.²⁰ None of these methods have been shown to be as effective as CWI.²³

Intravenous access should be initiated with fluid resuscitation dictated by the provider’s assessment. Normal saline is recommended as the resuscitative fluid of choice, with the rate dictated by clinical judgment and adjusted as guided by electrolyte determination and clinical response. It cannot be overstated that in normothermic patients with confusion, EAH is the diagnosis of exclusion and aggressive fluid resuscitation should be withheld until electrolyte determination.

Once rectal temperature descends appropriately (~38.9°C), the cooling process should stop and the individual should be transported to a hospital for further observation²⁰ and evaluation of possible sequelae, including rhabdomyolysis and renal injury, cardiac dysfunction and arrhythmia, severe electrolyte abnormalities, acute respiratory distress syndrome, lactic acidosis, and other forms of end-organ failure (Figure).

Rapid cooling is more crucial than transport; transport poses a risk of delayed cooling, which can dramatically increase an individual’s risk of morbidity and mortality.^20,23 In situations where a patient can be cooled on-site, physicians should pursue cooling before transporting the patient to a medical treatment facility.

Emergency Action Plan

Team physicians should be proactive in developing an emergency action plan to address possible EHS events. These plans should be site-specific, addressing procedures for all practice and home competition locations.¹² All competition venues should have a CWI tub on-site in events where there is an increased risk of EHS.^12,15,20 This tub should be set up and functional for all high-risk activities, including practices.¹²

Following recognition of a potential case of EHS, treatment teams should have procedures in place to transport athletes to the treatment area, obtain rectal temperature, initiate rapid cooling, and stabilize the athlete for transport to an emergency department (ED) for further evaluation.^12,15 A written record of treatments and medications provided during athlete stabilization should be maintained and transported with the athlete to the ED.¹⁵ A list of helpful equipment and supplies for treatment of EHS can be found in Table 5.

EHS is a unique life-threatening situation where it is best to treat the patient on the sideline before transport.¹⁵ Those athletes transported before cooling risk spending an increased amount of time above critical temperatures for cell damage, which has been associated with increased morbidity and mortality. This mantra of “cool first, transport second” cannot be overemphasized, as those individuals with EHS who present to the ED with a persisting rectal temperature >41°F may risk up to an 80% mortality rate.²⁴ Conversely, a recent large, retrospective study of 274 EHS events sustained during the Falmouth Road Race found a 100% survival rate when athletes were rapidly identified via rectal thermometry and treated with aggressive, rapid cooling through CWI.²¹

 

Return to Play

Perhaps the most challenging and important role the team physician has is determining an athlete’s return to play following EHI, as there currently are no evidence-based guidelines for return to activity for these athletes.⁷ The decisions surrounding return to play are highly individualized, as recovery from EHS and heat injury is associated with the duration of internal body temperature elevation above the critical level (40°C).^7,20 Guidelines for return to activity following recovery from EHI differ among experts and institutions.^7,25 The general consensus from these guidelines is that, at minimum, athletes should not participate in any physical activity until they are asymptomatic and all blood tests have normalized.¹¹ Following this asymptomatic period, most guidelines advocate for a slow, deliberate return to activity.¹¹ The American College of Sports Medicine (ACSM) offers one reasonable approach to the returning athlete following EHS:⁷

• No exercise for at least 7 days following release from medical care.
• Follow-up with a physician 1 week after release from medical care for physical examination and any warranted lab or radiologic studies (based upon organ systems affected during EHS).
• Once cleared to return to activity, the athlete begins exercise in a cool environment, gradually increasing the duration, intensity, and heat exposure over 2 weeks to demonstrate heat tolerance and acclimatization.
• Athletes who cannot resume vigorous activity due to recurrent symptoms (eg, excessive fatigue) should be reevaluated after 4 weeks. Laboratory exercise-heat tolerance testing may be useful in this setting.
• The athlete may resume full competition once they are able to participate in full training in the heat for 2 to 4 weeks without adverse effects.

Heat tolerance testing (HTT) in these athletes remains controversial.^{5 26} The ACSM recommends that HTT be considered only for those unable to return to vigorous activity after a suitable period (approximately 4 weeks). In contrast, the Israeli Defense Force (IDF) uses HTT to evaluate soldiers following EHS to guide decision-making about return to duty.²⁷ The IDF HTT assumes that individuals will respond differently to heat stresses. They identify individuals who are “heat intolerant” as being unable to tolerate specific heat challenges, indicated by increases in body temperature occurring more rapidly than normal responders under identical environmental and exercise conditions. However, despite being used for more than 30 years, there is no clear evidence that HTT adequately predicts who will experience subsequent episodes of EHS.

Conclusion

While the recognized cornerstone of being a team physician is the provision of medical care, the ACSM Team Physician Consensus Statement²⁸ further delineates the medical and administrative responsibilities as both (1) understanding medical management and prevention of injury and illness in athletes; and (2) awareness of or involvement in the development and rehearsal of an emergency action plan. These tenets are critical for the team physician who accepts the responsibility to cover sports at the high school level or higher. Football team physicians play an essential role in mitigating risk of EHI in their athletes. Through development and execution of both comprehensive prevention strategies and emergency action plans, physicians can work to minimize athletes’ risk of both developing and experiencing significant adverse outcomes from an EHI.

 

Am J Orthop. 2016;45(6):340-348. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Football, one of the most popular sports in the United States, is additionally recognized as a leading contributor to sports injury secondary to the contact collision nature of the endeavor. There are an estimated 1.1 million high school football players with another 100,000 participants combined in the National Football League (NFL), college, junior college, Arena Football League, and semipro levels of play.¹ USA Football estimates that an additional 3 million youth participate in community football leagues.¹ The National Center for Catastrophic Sports Injury Research recently calculated a fatality rate of 0.14 per 100,000 participants in 2014 for the 4.2 million who play football at all levels—and 0.45 per 100,000 in high school.¹ While direct deaths from head and spine injury remain a significant contributor to the number of catastrophic injuries, indirect deaths (systemic failure) predominate. Exertional heat stroke (EHS) has emerged as one of the leading indirect causes of death in high school and collegiate football. Boden and colleagues² reported that high school and college football players sustain approximately 12 fatalities annually, with indirect systemic causes being twice as common as direct blunt trauma.²The most common indirect causes identified included cardiac failure, heat illness, and complications of sickle cell trait (SCT). It was also noted that the risk of SCT, heat-related, and cardiac deaths increased during the second decade of the study, indicating these conditions may require a greater emphasis on diagnosis, treatment, and prevention. This review details for the team physician the unique challenge of exercising in the heat to the football player, and the prevention, diagnosis, management and return-to-play issues pertinent to exertional heat illness (EHI).

The Challenge

EHS represents the most severe manifestation of EHI—a gamut of diseases commonly encountered during the hot summer months when American football season begins. The breadth of EHI includes several important clinical diagnoses: exercise-associated muscle cramps (heat cramps); heat exhaustion with and without syncope; heat injury with evidence of end organ injury (eg, rhabdomyolysis); and EHS. EHS is defined as “a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates.”³ EHS, if left untreated, or even if clinical treatment is delayed, may result in significant end organ morbidity and/or mortality.

During exercise, the human thermoregulatory system mitigates heat gain by increasing skin blood flow and sweating, causing an increased dissipation of heat to the surrounding environment by leveraging conduction, convection, and evaporation.^4,5 Elevated environmental temperatures, increased humidity, and dehydration can impede the body’s ability to dissipate heat at a rate needed to maintain thermoregulation. This imbalance can result in hyperthermia secondary to uncompensated heat stress,⁵ which in turn can lead to EHI. Football players have unique challenges that make them particularly vulnerable to EHI. The summer heat during early-season participation and the requirement for equipment that covers nearly 60% of body surfaces pose increased risk of volume losses and hyperthermia that trigger the onset of EHI.⁶ Football athletes’ body compositions and physical size are additional contributing risk factors; the relatively high muscle and fat content increase thermogenicity, which require their bodies to dissipate more heat.⁷

An estimated 9000 cases of EHI occur annually across all high school sports,⁸ with an incidence of 1.6:100,000 athlete-exposures.^8,9 Studies have demonstrated, however, that EHI occurs in football 11.4 times more often than in all other high school sports combined.¹⁰ The incidence of nonfatal EHI in all levels of football is 4.42-5:100,000.^8,9 Between 2000 and 2014, 41 football players died from EHS.¹ In football, approximately 75% of all EHI events occurred during practices, while only 25% of incidents occurred during games.⁸

Given these potentially deadly consequences, it is important that football team physicians are not only alert to the early symptoms of heat illness and prepared to intervene to prevent the progression to EHS, but are critical leaders in educating coaches and players in evidence-based EHI prevention practices and policies.

Prevention

EHS is a preventable condition, arguably the most common cause of preventable nontraumatic exertional death in young athletes in the United States. Close attention to mitigating risk factors should begin prior to the onset of preseason practice and continue through the early season, where athletes are at the highest risk of developing heat illness.

Primary Prevention

Primary prevention is fundamental to minimizing the occurrences of EHI. It focuses on the following methods: recognition of inherent risk factors, acclimatization, hydration, and avoidance of inciting substances (including supplements).

 

Pre-Participation Examination. The purpose of the pre-participation examination (PPE) is to maximize an athlete’s safety by identifying medical conditions that place the athlete at risk.^11,12 The Preparticipation Physical Evaluation, 4th edition, the most widely used consensus publication, specifically queries if an athlete has a previous history of heat injury. However, it only indirectly addresses intrinsic risk factors that may predispose an athlete to EHI who has never had an EHI before. Therefore, providers should take the opportunity of the PPE to inquire about additional risk factors that may make an athlete high risk for sustaining a heat injury. Common risk factors for EHI are listed in Table 1.

While identifying at-risk athletes is important in mitigating the risk of developing EHI, it will not identify all possible cases: a study of military recruits found that up to 50% of Marines who developed EHI lacked an identifiable risk factor.¹³Wet Bulb Globe Temperature. Humidity can heighten a player’s risk of developing thermogenic dysregulation during hot temperatures. As ambient temperature nears internal body temperature, heat may actually be absorbed by the skin rather than dissipated into the air. As a result, the body must increasingly rely on sweat evaporation to encourage heat loss; this process is hindered in very humid climates. Wet bulb globe temperature (WBGT) is a measure of heat stress that accounts for temperature, humidity, wind speed, and cloud cover. WBGT should be utilized to determine the relative risk of EHI based on local environmental conditions, as there is a direct correlation between elevated WBGT and risk of EHI.^11,14 The greatest risk for EHS is performing high-intensity exercise (>75% VO2max) when WBGT >28°C (82°F).⁷ A study of hyperthermia-related deaths in football found that a majority of fatalities occurred on days classified as high risk (23°C-28°C) or extreme risk (>28°C) by WBGT.¹⁴ Consensus guidelines recommend that activities be modified based on WBGT (Table 2).^7,12

The impact of WBGT does not end solely on the day of practice. Athletes who exercise in elevated WBGT environments on 2 consecutive days are at increased risk of EHI due to cumulative effects of exercise in heat.¹¹Clothing. In football, required protective equipment may cover up to 60% of body surfaces. Studies have shown that wearing full uniform with pads increases internal body temperature and decreases time to exhaustion when compared to light clothing.^5,15 In addition, athletic equipment traps heat close to the body and inhibits evaporation of sweat into the environment, thereby inhibiting radiant and evaporative heat dissipation.^5,11 Likewise, wearing dark clothing encourages radiant absorption of heat, further contributing to potential thermal dysregulation.⁵ Use of a helmet is a specific risk factor for EHI, as significant heat dissipation occurs through the head.¹¹ To mitigate these risk factors, the introduction of padded equipment should occur incrementally over the heat acclimatization period (see below). In addition, athletes should be encouraged to remove their helmets during rest periods to promote added heat dissipation and recovery.

Heat Acclimatization. The risk of EHI escalates significantly when athletes are subjected to multiple stressors during periods of heat exposure, such as sudden increases in intensity or duration of exercise; prolonged new exposures to heat; dehydration; and sleep loss.⁵ When football season begins in late summer, athletes are least conditioned as temperatures reach their seasonal peak, causing increased risk of EHI.¹⁵ Planning for heat acclimatization is vital for all athletes who exercise in hot environments. Acclimatization procedures place progressively mounting physiologic strains on the body to improve athletes’ ability to dissipate heat, diminishing thermoregulatory and cardiovascular exertion.^4,5 Acclimatization begins with expansion of plasma volume on days 3 to 6, causing improvements in cardiac efficiency and resulting in an overall decrease in basal internal body temperature.^4,5,15 This process results in improvements in heat tolerance and exercise performance, evolving over 10 to 14 days of gradual escalation of exercise intensity and duration.^5,10,11,16 However, poor fitness levels and extreme temperatures can prolong this period, requiring up to 2 to 3 months to fully take effect.^5,7

The National Athletic Trainers Association (NATA) and National Collegiate Athletic Association (NCAA) have released consensus guidelines regarding heat acclimatization protocols for football athletes at the high school and college levels (Tables 3 and 4). Each of these guidelines involves an initial period without use of protective equipment, followed by a gradual addition of further equipment.^11,16

Secondary Prevention

Despite physicians’ best efforts to prevent all cases of EHI, athletes will still experience the effects of exercise-induced hyperthermia. The goal of secondary prevention is to slow the progression of this hyperthermia so that it does not progress to more dangerous EHI.

 

Hydration. Dehydration is an important risk factor for EHI. Sweat maintains thermoregulation by dissipating heat generated during exercise; however, it also contributes to body water losses. Furthermore, intravascular depletion decreases stroke volume, thereby increasing cardiovascular strain. It is estimated that for every 1% loss in body mass from dehydration, body temperature rises 0.22°C in comparison to a euhydrated state.⁶ Dehydration occurs more rapidly in hot environments, as fluid is lost through increased sweat production.⁷ After approximately 6% to 10% body weight volume loss, cardiac output cannot be maintained, diminishing sweat production and blood flow to both skin and muscle and causing diminished performance and a significant risk of heat exhaustion.⁷ If left unchecked, these physiologic changes result in further elevations in body temperature and increased cardiovascular strain, ultimately placing the athlete at significant risk for development of EHS.

Adequate hydration to maintain euvolemia is an important step in avoiding possible EHI. Multiple studies have shown that football players experience a baseline hypovolemia during their competition season,⁶ a deficit that is most marked during the first week of practices.¹⁷ This deficit is multifactorial, as football players expend a significant amount of fluid through sweat, are not able to adequately replace these losses during practice, and do not appropriately hydrate off the field.^6,18 Some players, especially linemen, sweat at a higher rate than their teammates, posing a possible risk of significant dehydration.⁶ Coaches and players alike should be educated on the importance of adequate hydration to meet their fluid needs.

The goal of hydration during exercise is to prevent large fluid losses that can adversely affect performance and increase risk of EHI;⁶ it may be unrealistic to replace all fluid losses during the practice period. Instead, athletes should target complete volume replacement over the post-exercise period.⁶ Some recommend hydrating based upon thirst drive; however, thirst is activated following a volume loss of approximately 2% body mass, the same degree of losses that place athletes at an increased risk for performance impairment and EHI.^4,6,11,12 Individuals should have access to fluids throughout practice and competition and be encouraged to hydrate as needed.^6,12,15 Furthermore, staff should modify their practices based upon WBGT and acclimatization status to provide more frequent hydration breaks.

Hyperhydration and Salt Intake. Of note, there are inherent risks to hyperhydration. Athletes with low sweat rates have an increased risk of overhydration and the development of exercise-associated hyponatremia (EAH),⁶ a condition whose presentation is very similar to EHS. In addition, inadequate sodium intake and excessive sweating can also contribute to the development of EAH. EAH has been implicated in the deaths of 2 football players in 2014.^1,6 Establishing team hydration guidelines and educating players and staff on appropriate hydration and dietary salt intake is essential to reduce the risk of both dehydration and hyperhydration and their complications.⁶Intra-Event Cooling. During exercise, team physicians can employ strategies for cooling athletes during exertion to mitigate their risk of EHI by decreasing thermal and cardiovascular strain.^4,19 Cooling during exercise is hypothesized to allow for accelerated heat dissipation, where heat is lost from the body more effectively. This accelerated loss enables athletes to maintain a higher heat storage capacity over the duration of exercise, avoiding uncompensated heat stresses that ultimately cause EHI.¹⁹

Some intra-event cooling strategies include the use of cooling garments, cooling packs, and cold water/slurry ingestion. Cooling garments lower skin temperature, which in turn can decrease thermoregulatory strains;⁴ a recent meta-analysis of intra-event cooling modalities revealed that wearing an ice vest during exercise resulted in the greatest decrease in thermal heat strain.¹⁹ Internal cooling strategies—namely ingestion of cold fluids/ice slurry—have shown some mild benefit in decreasing internal temperatures; however, some studies have demonstrated some decrease in sweat production associated with cold oral intake used in isolation.¹⁹ Overall, studies have shown that combining external (cooling clothing, ice packs, fanning) and internal (cold water, ice slurry) cooling methods result in a greater cooling effect than a use of a single method.⁴

Tertiary Prevention

The goal of tertiary prevention is to mitigate the risk of long-term adverse outcomes following an EHS event. The most effective means of reducing risk for morbidity and mortality is rapid identification and treatment of EHS as well as close evaluation of an athlete’s return to activity in heat. This process is spearheaded by an effective and well-rehearsed emergency action plan.

Diagnosis and Management

Rapid identification and treatment of EHS is crucial to minimizing the risk of poor outcomes.⁷ Any delay in the treatment of EHS can dramatically increase the likelihood of associated morbidity and mortality.²⁰

 

EHS is diagnosed by an elevated rectal temperature ≥40°C (104°F) and associated central nervous system (CNS) dysfunction.²¹ EHS should be strongly suspected in any athlete exercising in heat who exhibits signs of CNS dysfunction, including disorientation, confusion, dizziness, erratic behavior, irritability, headache, loss of coordination, delirium, collapse, or seizures.^7,12,15 EHS may also present with symptoms of heat exhaustion, including fatigue, hyperventilation, tachycardia, vomiting, diarrhea, and hypotension.^7,12,15

Rectal temperature should be taken for any athlete with suspected EHS, as other modalities—oral, skin, axillary, and aural—can be inaccurate and easily modified by ambient confounders such as ambient and skin temperature, athlete hyperventilation, and consumption of liquids.^7,11,12 Athletes exhibiting CNS symptoms with moderately elevated rectal temperatures that do not exceed 40°C should also be assumed to be suffering from EHS and treated with rapid cooling.¹¹ On the other hand, athletes with CNS symptoms who are normothermic should be assumed to have EAH until ruled out by electrolyte assessment; IV fluids should be at no more than keep vein open (KVO) pending this determination.¹¹ In some cases, an athlete may initially present with altered mental status but return to “normal.” However, this improvement may represent a “lucid period”; evaluation should continue with rectal temperature and treatment, as EHS in these cases may progress quickly.¹⁵

Treatment is centered on rapid, whole body cooling initiated at the first sign of heat illness.^7,22 The goal of treatment is to achieve a rectal temperature <38.9°C within 30 minutes of the onset of EHS.¹⁵ Upon diagnosis, the athlete should be quickly placed in a tub of ice water to facilitate cold water immersion (CWI) therapy. Some guidelines suggest the athlete’s clothing be removed to potentiate evaporative cooling during CWI;¹² however, cooling should not be delayed due to difficulties in removing equipment. CWI, where a heat stroke victim is submerged in ice water up to their neck while water is continuously circulated, is generally considered to be the gold standard treatment as it is the modality with the highest recorded cooling rates and the lowest rate of morbidity and mortality.^7,20,21 Multiple studies of CWI have shown that survival nears 100% when aggressive cooling starts within 5 minutes of collapse or identification of EHS.^20,21,22

If whole body CWI is unavailable, alternative methods of rapid cooling should be employed. Partial CWI, with torso immersion being preferable to the extremities, has been shown to achieve an acceptable rate of cooling to achieve sufficient drops in internal body temperature.^20,23 However, one popular treatment—applying ice packs to the whole body, in particular to the groin and axillae—has not been shown to be sufficient to achieve standard cooling goals.²⁰ None of these methods have been shown to be as effective as CWI.²³

Intravenous access should be initiated with fluid resuscitation dictated by the provider’s assessment. Normal saline is recommended as the resuscitative fluid of choice, with the rate dictated by clinical judgment and adjusted as guided by electrolyte determination and clinical response. It cannot be overstated that in normothermic patients with confusion, EAH is the diagnosis of exclusion and aggressive fluid resuscitation should be withheld until electrolyte determination.

Once rectal temperature descends appropriately (~38.9°C), the cooling process should stop and the individual should be transported to a hospital for further observation²⁰ and evaluation of possible sequelae, including rhabdomyolysis and renal injury, cardiac dysfunction and arrhythmia, severe electrolyte abnormalities, acute respiratory distress syndrome, lactic acidosis, and other forms of end-organ failure (Figure).

Rapid cooling is more crucial than transport; transport poses a risk of delayed cooling, which can dramatically increase an individual’s risk of morbidity and mortality.^20,23 In situations where a patient can be cooled on-site, physicians should pursue cooling before transporting the patient to a medical treatment facility.

Emergency Action Plan

Team physicians should be proactive in developing an emergency action plan to address possible EHS events. These plans should be site-specific, addressing procedures for all practice and home competition locations.¹² All competition venues should have a CWI tub on-site in events where there is an increased risk of EHS.^12,15,20 This tub should be set up and functional for all high-risk activities, including practices.¹²

Following recognition of a potential case of EHS, treatment teams should have procedures in place to transport athletes to the treatment area, obtain rectal temperature, initiate rapid cooling, and stabilize the athlete for transport to an emergency department (ED) for further evaluation.^12,15 A written record of treatments and medications provided during athlete stabilization should be maintained and transported with the athlete to the ED.¹⁵ A list of helpful equipment and supplies for treatment of EHS can be found in Table 5.

EHS is a unique life-threatening situation where it is best to treat the patient on the sideline before transport.¹⁵ Those athletes transported before cooling risk spending an increased amount of time above critical temperatures for cell damage, which has been associated with increased morbidity and mortality. This mantra of “cool first, transport second” cannot be overemphasized, as those individuals with EHS who present to the ED with a persisting rectal temperature >41°F may risk up to an 80% mortality rate.²⁴ Conversely, a recent large, retrospective study of 274 EHS events sustained during the Falmouth Road Race found a 100% survival rate when athletes were rapidly identified via rectal thermometry and treated with aggressive, rapid cooling through CWI.²¹

 

Return to Play

Perhaps the most challenging and important role the team physician has is determining an athlete’s return to play following EHI, as there currently are no evidence-based guidelines for return to activity for these athletes.⁷ The decisions surrounding return to play are highly individualized, as recovery from EHS and heat injury is associated with the duration of internal body temperature elevation above the critical level (40°C).^7,20 Guidelines for return to activity following recovery from EHI differ among experts and institutions.^7,25 The general consensus from these guidelines is that, at minimum, athletes should not participate in any physical activity until they are asymptomatic and all blood tests have normalized.¹¹ Following this asymptomatic period, most guidelines advocate for a slow, deliberate return to activity.¹¹ The American College of Sports Medicine (ACSM) offers one reasonable approach to the returning athlete following EHS:⁷

• No exercise for at least 7 days following release from medical care.
• Follow-up with a physician 1 week after release from medical care for physical examination and any warranted lab or radiologic studies (based upon organ systems affected during EHS).
• Once cleared to return to activity, the athlete begins exercise in a cool environment, gradually increasing the duration, intensity, and heat exposure over 2 weeks to demonstrate heat tolerance and acclimatization.
• Athletes who cannot resume vigorous activity due to recurrent symptoms (eg, excessive fatigue) should be reevaluated after 4 weeks. Laboratory exercise-heat tolerance testing may be useful in this setting.
• The athlete may resume full competition once they are able to participate in full training in the heat for 2 to 4 weeks without adverse effects.

Heat tolerance testing (HTT) in these athletes remains controversial.^{5 26} The ACSM recommends that HTT be considered only for those unable to return to vigorous activity after a suitable period (approximately 4 weeks). In contrast, the Israeli Defense Force (IDF) uses HTT to evaluate soldiers following EHS to guide decision-making about return to duty.²⁷ The IDF HTT assumes that individuals will respond differently to heat stresses. They identify individuals who are “heat intolerant” as being unable to tolerate specific heat challenges, indicated by increases in body temperature occurring more rapidly than normal responders under identical environmental and exercise conditions. However, despite being used for more than 30 years, there is no clear evidence that HTT adequately predicts who will experience subsequent episodes of EHS.

Conclusion

While the recognized cornerstone of being a team physician is the provision of medical care, the ACSM Team Physician Consensus Statement²⁸ further delineates the medical and administrative responsibilities as both (1) understanding medical management and prevention of injury and illness in athletes; and (2) awareness of or involvement in the development and rehearsal of an emergency action plan. These tenets are critical for the team physician who accepts the responsibility to cover sports at the high school level or higher. Football team physicians play an essential role in mitigating risk of EHI in their athletes. Through development and execution of both comprehensive prevention strategies and emergency action plans, physicians can work to minimize athletes’ risk of both developing and experiencing significant adverse outcomes from an EHI.

 

Am J Orthop. 2016;45(6):340-348. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Football, one of the most popular sports in the United States, is additionally recognized as a leading contributor to sports injury secondary to the contact collision nature of the endeavor. There are an estimated 1.1 million high school football players with another 100,000 participants combined in the National Football League (NFL), college, junior college, Arena Football League, and semipro levels of play.¹ USA Football estimates that an additional 3 million youth participate in community football leagues.¹ The National Center for Catastrophic Sports Injury Research recently calculated a fatality rate of 0.14 per 100,000 participants in 2014 for the 4.2 million who play football at all levels—and 0.45 per 100,000 in high school.¹ While direct deaths from head and spine injury remain a significant contributor to the number of catastrophic injuries, indirect deaths (systemic failure) predominate. Exertional heat stroke (EHS) has emerged as one of the leading indirect causes of death in high school and collegiate football. Boden and colleagues² reported that high school and college football players sustain approximately 12 fatalities annually, with indirect systemic causes being twice as common as direct blunt trauma.²The most common indirect causes identified included cardiac failure, heat illness, and complications of sickle cell trait (SCT). It was also noted that the risk of SCT, heat-related, and cardiac deaths increased during the second decade of the study, indicating these conditions may require a greater emphasis on diagnosis, treatment, and prevention. This review details for the team physician the unique challenge of exercising in the heat to the football player, and the prevention, diagnosis, management and return-to-play issues pertinent to exertional heat illness (EHI).

The Challenge

EHS represents the most severe manifestation of EHI—a gamut of diseases commonly encountered during the hot summer months when American football season begins. The breadth of EHI includes several important clinical diagnoses: exercise-associated muscle cramps (heat cramps); heat exhaustion with and without syncope; heat injury with evidence of end organ injury (eg, rhabdomyolysis); and EHS. EHS is defined as “a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates.”³ EHS, if left untreated, or even if clinical treatment is delayed, may result in significant end organ morbidity and/or mortality.

During exercise, the human thermoregulatory system mitigates heat gain by increasing skin blood flow and sweating, causing an increased dissipation of heat to the surrounding environment by leveraging conduction, convection, and evaporation.^4,5 Elevated environmental temperatures, increased humidity, and dehydration can impede the body’s ability to dissipate heat at a rate needed to maintain thermoregulation. This imbalance can result in hyperthermia secondary to uncompensated heat stress,⁵ which in turn can lead to EHI. Football players have unique challenges that make them particularly vulnerable to EHI. The summer heat during early-season participation and the requirement for equipment that covers nearly 60% of body surfaces pose increased risk of volume losses and hyperthermia that trigger the onset of EHI.⁶ Football athletes’ body compositions and physical size are additional contributing risk factors; the relatively high muscle and fat content increase thermogenicity, which require their bodies to dissipate more heat.⁷

An estimated 9000 cases of EHI occur annually across all high school sports,⁸ with an incidence of 1.6:100,000 athlete-exposures.^8,9 Studies have demonstrated, however, that EHI occurs in football 11.4 times more often than in all other high school sports combined.¹⁰ The incidence of nonfatal EHI in all levels of football is 4.42-5:100,000.^8,9 Between 2000 and 2014, 41 football players died from EHS.¹ In football, approximately 75% of all EHI events occurred during practices, while only 25% of incidents occurred during games.⁸

Given these potentially deadly consequences, it is important that football team physicians are not only alert to the early symptoms of heat illness and prepared to intervene to prevent the progression to EHS, but are critical leaders in educating coaches and players in evidence-based EHI prevention practices and policies.

Prevention

EHS is a preventable condition, arguably the most common cause of preventable nontraumatic exertional death in young athletes in the United States. Close attention to mitigating risk factors should begin prior to the onset of preseason practice and continue through the early season, where athletes are at the highest risk of developing heat illness.

Primary Prevention

Primary prevention is fundamental to minimizing the occurrences of EHI. It focuses on the following methods: recognition of inherent risk factors, acclimatization, hydration, and avoidance of inciting substances (including supplements).

 

Pre-Participation Examination. The purpose of the pre-participation examination (PPE) is to maximize an athlete’s safety by identifying medical conditions that place the athlete at risk.^11,12 The Preparticipation Physical Evaluation, 4th edition, the most widely used consensus publication, specifically queries if an athlete has a previous history of heat injury. However, it only indirectly addresses intrinsic risk factors that may predispose an athlete to EHI who has never had an EHI before. Therefore, providers should take the opportunity of the PPE to inquire about additional risk factors that may make an athlete high risk for sustaining a heat injury. Common risk factors for EHI are listed in Table 1.

While identifying at-risk athletes is important in mitigating the risk of developing EHI, it will not identify all possible cases: a study of military recruits found that up to 50% of Marines who developed EHI lacked an identifiable risk factor.¹³Wet Bulb Globe Temperature. Humidity can heighten a player’s risk of developing thermogenic dysregulation during hot temperatures. As ambient temperature nears internal body temperature, heat may actually be absorbed by the skin rather than dissipated into the air. As a result, the body must increasingly rely on sweat evaporation to encourage heat loss; this process is hindered in very humid climates. Wet bulb globe temperature (WBGT) is a measure of heat stress that accounts for temperature, humidity, wind speed, and cloud cover. WBGT should be utilized to determine the relative risk of EHI based on local environmental conditions, as there is a direct correlation between elevated WBGT and risk of EHI.^11,14 The greatest risk for EHS is performing high-intensity exercise (>75% VO2max) when WBGT >28°C (82°F).⁷ A study of hyperthermia-related deaths in football found that a majority of fatalities occurred on days classified as high risk (23°C-28°C) or extreme risk (>28°C) by WBGT.¹⁴ Consensus guidelines recommend that activities be modified based on WBGT (Table 2).^7,12

The impact of WBGT does not end solely on the day of practice. Athletes who exercise in elevated WBGT environments on 2 consecutive days are at increased risk of EHI due to cumulative effects of exercise in heat.¹¹Clothing. In football, required protective equipment may cover up to 60% of body surfaces. Studies have shown that wearing full uniform with pads increases internal body temperature and decreases time to exhaustion when compared to light clothing.^5,15 In addition, athletic equipment traps heat close to the body and inhibits evaporation of sweat into the environment, thereby inhibiting radiant and evaporative heat dissipation.^5,11 Likewise, wearing dark clothing encourages radiant absorption of heat, further contributing to potential thermal dysregulation.⁵ Use of a helmet is a specific risk factor for EHI, as significant heat dissipation occurs through the head.¹¹ To mitigate these risk factors, the introduction of padded equipment should occur incrementally over the heat acclimatization period (see below). In addition, athletes should be encouraged to remove their helmets during rest periods to promote added heat dissipation and recovery.

Heat Acclimatization. The risk of EHI escalates significantly when athletes are subjected to multiple stressors during periods of heat exposure, such as sudden increases in intensity or duration of exercise; prolonged new exposures to heat; dehydration; and sleep loss.⁵ When football season begins in late summer, athletes are least conditioned as temperatures reach their seasonal peak, causing increased risk of EHI.¹⁵ Planning for heat acclimatization is vital for all athletes who exercise in hot environments. Acclimatization procedures place progressively mounting physiologic strains on the body to improve athletes’ ability to dissipate heat, diminishing thermoregulatory and cardiovascular exertion.^4,5 Acclimatization begins with expansion of plasma volume on days 3 to 6, causing improvements in cardiac efficiency and resulting in an overall decrease in basal internal body temperature.^4,5,15 This process results in improvements in heat tolerance and exercise performance, evolving over 10 to 14 days of gradual escalation of exercise intensity and duration.^5,10,11,16 However, poor fitness levels and extreme temperatures can prolong this period, requiring up to 2 to 3 months to fully take effect.^5,7

The National Athletic Trainers Association (NATA) and National Collegiate Athletic Association (NCAA) have released consensus guidelines regarding heat acclimatization protocols for football athletes at the high school and college levels (Tables 3 and 4). Each of these guidelines involves an initial period without use of protective equipment, followed by a gradual addition of further equipment.^11,16

Secondary Prevention

Despite physicians’ best efforts to prevent all cases of EHI, athletes will still experience the effects of exercise-induced hyperthermia. The goal of secondary prevention is to slow the progression of this hyperthermia so that it does not progress to more dangerous EHI.

 

Hydration. Dehydration is an important risk factor for EHI. Sweat maintains thermoregulation by dissipating heat generated during exercise; however, it also contributes to body water losses. Furthermore, intravascular depletion decreases stroke volume, thereby increasing cardiovascular strain. It is estimated that for every 1% loss in body mass from dehydration, body temperature rises 0.22°C in comparison to a euhydrated state.⁶ Dehydration occurs more rapidly in hot environments, as fluid is lost through increased sweat production.⁷ After approximately 6% to 10% body weight volume loss, cardiac output cannot be maintained, diminishing sweat production and blood flow to both skin and muscle and causing diminished performance and a significant risk of heat exhaustion.⁷ If left unchecked, these physiologic changes result in further elevations in body temperature and increased cardiovascular strain, ultimately placing the athlete at significant risk for development of EHS.

Adequate hydration to maintain euvolemia is an important step in avoiding possible EHI. Multiple studies have shown that football players experience a baseline hypovolemia during their competition season,⁶ a deficit that is most marked during the first week of practices.¹⁷ This deficit is multifactorial, as football players expend a significant amount of fluid through sweat, are not able to adequately replace these losses during practice, and do not appropriately hydrate off the field.^6,18 Some players, especially linemen, sweat at a higher rate than their teammates, posing a possible risk of significant dehydration.⁶ Coaches and players alike should be educated on the importance of adequate hydration to meet their fluid needs.

The goal of hydration during exercise is to prevent large fluid losses that can adversely affect performance and increase risk of EHI;⁶ it may be unrealistic to replace all fluid losses during the practice period. Instead, athletes should target complete volume replacement over the post-exercise period.⁶ Some recommend hydrating based upon thirst drive; however, thirst is activated following a volume loss of approximately 2% body mass, the same degree of losses that place athletes at an increased risk for performance impairment and EHI.^4,6,11,12 Individuals should have access to fluids throughout practice and competition and be encouraged to hydrate as needed.^6,12,15 Furthermore, staff should modify their practices based upon WBGT and acclimatization status to provide more frequent hydration breaks.

Hyperhydration and Salt Intake. Of note, there are inherent risks to hyperhydration. Athletes with low sweat rates have an increased risk of overhydration and the development of exercise-associated hyponatremia (EAH),⁶ a condition whose presentation is very similar to EHS. In addition, inadequate sodium intake and excessive sweating can also contribute to the development of EAH. EAH has been implicated in the deaths of 2 football players in 2014.^1,6 Establishing team hydration guidelines and educating players and staff on appropriate hydration and dietary salt intake is essential to reduce the risk of both dehydration and hyperhydration and their complications.⁶Intra-Event Cooling. During exercise, team physicians can employ strategies for cooling athletes during exertion to mitigate their risk of EHI by decreasing thermal and cardiovascular strain.^4,19 Cooling during exercise is hypothesized to allow for accelerated heat dissipation, where heat is lost from the body more effectively. This accelerated loss enables athletes to maintain a higher heat storage capacity over the duration of exercise, avoiding uncompensated heat stresses that ultimately cause EHI.¹⁹

Some intra-event cooling strategies include the use of cooling garments, cooling packs, and cold water/slurry ingestion. Cooling garments lower skin temperature, which in turn can decrease thermoregulatory strains;⁴ a recent meta-analysis of intra-event cooling modalities revealed that wearing an ice vest during exercise resulted in the greatest decrease in thermal heat strain.¹⁹ Internal cooling strategies—namely ingestion of cold fluids/ice slurry—have shown some mild benefit in decreasing internal temperatures; however, some studies have demonstrated some decrease in sweat production associated with cold oral intake used in isolation.¹⁹ Overall, studies have shown that combining external (cooling clothing, ice packs, fanning) and internal (cold water, ice slurry) cooling methods result in a greater cooling effect than a use of a single method.⁴

Tertiary Prevention

The goal of tertiary prevention is to mitigate the risk of long-term adverse outcomes following an EHS event. The most effective means of reducing risk for morbidity and mortality is rapid identification and treatment of EHS as well as close evaluation of an athlete’s return to activity in heat. This process is spearheaded by an effective and well-rehearsed emergency action plan.

Diagnosis and Management

Rapid identification and treatment of EHS is crucial to minimizing the risk of poor outcomes.⁷ Any delay in the treatment of EHS can dramatically increase the likelihood of associated morbidity and mortality.²⁰

 

EHS is diagnosed by an elevated rectal temperature ≥40°C (104°F) and associated central nervous system (CNS) dysfunction.²¹ EHS should be strongly suspected in any athlete exercising in heat who exhibits signs of CNS dysfunction, including disorientation, confusion, dizziness, erratic behavior, irritability, headache, loss of coordination, delirium, collapse, or seizures.^7,12,15 EHS may also present with symptoms of heat exhaustion, including fatigue, hyperventilation, tachycardia, vomiting, diarrhea, and hypotension.^7,12,15

Rectal temperature should be taken for any athlete with suspected EHS, as other modalities—oral, skin, axillary, and aural—can be inaccurate and easily modified by ambient confounders such as ambient and skin temperature, athlete hyperventilation, and consumption of liquids.^7,11,12 Athletes exhibiting CNS symptoms with moderately elevated rectal temperatures that do not exceed 40°C should also be assumed to be suffering from EHS and treated with rapid cooling.¹¹ On the other hand, athletes with CNS symptoms who are normothermic should be assumed to have EAH until ruled out by electrolyte assessment; IV fluids should be at no more than keep vein open (KVO) pending this determination.¹¹ In some cases, an athlete may initially present with altered mental status but return to “normal.” However, this improvement may represent a “lucid period”; evaluation should continue with rectal temperature and treatment, as EHS in these cases may progress quickly.¹⁵

Treatment is centered on rapid, whole body cooling initiated at the first sign of heat illness.^7,22 The goal of treatment is to achieve a rectal temperature <38.9°C within 30 minutes of the onset of EHS.¹⁵ Upon diagnosis, the athlete should be quickly placed in a tub of ice water to facilitate cold water immersion (CWI) therapy. Some guidelines suggest the athlete’s clothing be removed to potentiate evaporative cooling during CWI;¹² however, cooling should not be delayed due to difficulties in removing equipment. CWI, where a heat stroke victim is submerged in ice water up to their neck while water is continuously circulated, is generally considered to be the gold standard treatment as it is the modality with the highest recorded cooling rates and the lowest rate of morbidity and mortality.^7,20,21 Multiple studies of CWI have shown that survival nears 100% when aggressive cooling starts within 5 minutes of collapse or identification of EHS.^20,21,22

If whole body CWI is unavailable, alternative methods of rapid cooling should be employed. Partial CWI, with torso immersion being preferable to the extremities, has been shown to achieve an acceptable rate of cooling to achieve sufficient drops in internal body temperature.^20,23 However, one popular treatment—applying ice packs to the whole body, in particular to the groin and axillae—has not been shown to be sufficient to achieve standard cooling goals.²⁰ None of these methods have been shown to be as effective as CWI.²³

Intravenous access should be initiated with fluid resuscitation dictated by the provider’s assessment. Normal saline is recommended as the resuscitative fluid of choice, with the rate dictated by clinical judgment and adjusted as guided by electrolyte determination and clinical response. It cannot be overstated that in normothermic patients with confusion, EAH is the diagnosis of exclusion and aggressive fluid resuscitation should be withheld until electrolyte determination.

Once rectal temperature descends appropriately (~38.9°C), the cooling process should stop and the individual should be transported to a hospital for further observation²⁰ and evaluation of possible sequelae, including rhabdomyolysis and renal injury, cardiac dysfunction and arrhythmia, severe electrolyte abnormalities, acute respiratory distress syndrome, lactic acidosis, and other forms of end-organ failure (Figure).

Rapid cooling is more crucial than transport; transport poses a risk of delayed cooling, which can dramatically increase an individual’s risk of morbidity and mortality.^20,23 In situations where a patient can be cooled on-site, physicians should pursue cooling before transporting the patient to a medical treatment facility.

Emergency Action Plan

Team physicians should be proactive in developing an emergency action plan to address possible EHS events. These plans should be site-specific, addressing procedures for all practice and home competition locations.¹² All competition venues should have a CWI tub on-site in events where there is an increased risk of EHS.^12,15,20 This tub should be set up and functional for all high-risk activities, including practices.¹²

Following recognition of a potential case of EHS, treatment teams should have procedures in place to transport athletes to the treatment area, obtain rectal temperature, initiate rapid cooling, and stabilize the athlete for transport to an emergency department (ED) for further evaluation.^12,15 A written record of treatments and medications provided during athlete stabilization should be maintained and transported with the athlete to the ED.¹⁵ A list of helpful equipment and supplies for treatment of EHS can be found in Table 5.

EHS is a unique life-threatening situation where it is best to treat the patient on the sideline before transport.¹⁵ Those athletes transported before cooling risk spending an increased amount of time above critical temperatures for cell damage, which has been associated with increased morbidity and mortality. This mantra of “cool first, transport second” cannot be overemphasized, as those individuals with EHS who present to the ED with a persisting rectal temperature >41°F may risk up to an 80% mortality rate.²⁴ Conversely, a recent large, retrospective study of 274 EHS events sustained during the Falmouth Road Race found a 100% survival rate when athletes were rapidly identified via rectal thermometry and treated with aggressive, rapid cooling through CWI.²¹

 

Return to Play

Perhaps the most challenging and important role the team physician has is determining an athlete’s return to play following EHI, as there currently are no evidence-based guidelines for return to activity for these athletes.⁷ The decisions surrounding return to play are highly individualized, as recovery from EHS and heat injury is associated with the duration of internal body temperature elevation above the critical level (40°C).^7,20 Guidelines for return to activity following recovery from EHI differ among experts and institutions.^7,25 The general consensus from these guidelines is that, at minimum, athletes should not participate in any physical activity until they are asymptomatic and all blood tests have normalized.¹¹ Following this asymptomatic period, most guidelines advocate for a slow, deliberate return to activity.¹¹ The American College of Sports Medicine (ACSM) offers one reasonable approach to the returning athlete following EHS:⁷

• No exercise for at least 7 days following release from medical care.
• Follow-up with a physician 1 week after release from medical care for physical examination and any warranted lab or radiologic studies (based upon organ systems affected during EHS).
• Once cleared to return to activity, the athlete begins exercise in a cool environment, gradually increasing the duration, intensity, and heat exposure over 2 weeks to demonstrate heat tolerance and acclimatization.
• Athletes who cannot resume vigorous activity due to recurrent symptoms (eg, excessive fatigue) should be reevaluated after 4 weeks. Laboratory exercise-heat tolerance testing may be useful in this setting.
• The athlete may resume full competition once they are able to participate in full training in the heat for 2 to 4 weeks without adverse effects.

Heat tolerance testing (HTT) in these athletes remains controversial.^{5 26} The ACSM recommends that HTT be considered only for those unable to return to vigorous activity after a suitable period (approximately 4 weeks). In contrast, the Israeli Defense Force (IDF) uses HTT to evaluate soldiers following EHS to guide decision-making about return to duty.²⁷ The IDF HTT assumes that individuals will respond differently to heat stresses. They identify individuals who are “heat intolerant” as being unable to tolerate specific heat challenges, indicated by increases in body temperature occurring more rapidly than normal responders under identical environmental and exercise conditions. However, despite being used for more than 30 years, there is no clear evidence that HTT adequately predicts who will experience subsequent episodes of EHS.

Conclusion

While the recognized cornerstone of being a team physician is the provision of medical care, the ACSM Team Physician Consensus Statement²⁸ further delineates the medical and administrative responsibilities as both (1) understanding medical management and prevention of injury and illness in athletes; and (2) awareness of or involvement in the development and rehearsal of an emergency action plan. These tenets are critical for the team physician who accepts the responsibility to cover sports at the high school level or higher. Football team physicians play an essential role in mitigating risk of EHI in their athletes. Through development and execution of both comprehensive prevention strategies and emergency action plans, physicians can work to minimize athletes’ risk of both developing and experiencing significant adverse outcomes from an EHI.

 

Am J Orthop. 2016;45(6):340-348. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

The age-adjusted prevalence of any sexual problem is 43% among US women. A full 22% of these women experience sexually related personal distress.¹ With publication of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition² has come a shift in classification and, at times, management approach for reported female sexual dysfunction. When women report to their clinicians decreased sexual desire or arousal or pain at penetration, the management is no longer guided by a linear model of sexual response (excitation, plateau, orgasm, and resolution) but rather by a more nuanced and complex biopsychosocial approach. In this model, diagnosis and management strategies to address bothersome sexual concerns consider the whole woman in the context of her physical and psychosocial health. The patient’s age, medical history, and relationship status are among the factors that could affect management of the problem. In an effort to explore this management approach, I used this Update on Female Sexual Dysfunction as an opportunity to convene a roundtable of several experts, representing varying backgrounds and practice vantage points, to discuss 5 cases of sexual problems that you as a busy clinician may encounter in your practice.

Genital atrophy in a sexually inactive 61-year-old woman

Barbara S. Levy, MD: Two years after her husband's death, which followed several years of illness, your 61-year-old patient mentions at her well woman visit that she anticipates becoming sexually active again. She has not used systemic or vaginal hormone therapy. During pelvic examination, atrophic external genital changes are present, and use of an ultrathin (thinner than a Pederson) speculum reveals vaginal epithelial atrophic changes. A single-digit bimanual exam can be performed with moderate patient discomfort; the patient cannot tolerate a 2-digit bimanual exam. She expresses concern about being able to engage in penile/vaginal sexual intercourse. 

Dr. Kaunitz, what is important for you to ask this patient, and what concerns you most on her physical exam?

Andrew M. Kaunitz, MD: First, it is important to recognize the patient's expectations and desires. As the case suggests, but further questioning could clarify, she would like to be able to comfortably engage in sexual intercourse with a new partner, but penetration may be difficult (and definitely painful for her) unless treatment is pursued. This combination of mucosal and vestibular atrophic changes (genitourinary syndrome of menopause [GSM], or vulvovaginal atrophy [VVA]) plus the absence of penetration for many years can be a double whammy situation for menopausal women. In this case it has led to extensive contracture of the introitus, and if it is not addressed will cause sexual dysfunction.

Dr. Levy: In addition we need to clarify whether or not a history of breast cancer or some other thing may impact the care we provide. How would you approach talking with this patient in order to manage her care?

Dr. Kaunitz: One step is to see how motivated she is to address this, as it is not something that, as gynecologists, we can snap our fingers and the situation will be resolved. If the patient is motivated to treat the atrophic changes with medical treatment, in the form of low-dose vaginal estrogen, and dilation, either on her own if she's highly motivated to do so, or in my practice more commonly with the support of a women's physical therapist, over time she should be able to comfortably engage in sexual intercourse with penetration. If this is what she wants, we can help steer her in the right direction.

Sheryl Kingsberg, PhD: You know that this woman is motivated by virtue of her initiating the topic herself. Patients are often embarrassed talking about sexual issues, or they are not sure that their gynecologist is comfortable with it. After all, they think, if this is the right place to discuss sexual problems, why didn't he or she ask me?  Clinicians must be aware that it is their responsibility to ask about sexual function and not leave it for the patient to open the door.

Dr. Kaunitz: Great point.

Cheryl B. Iglesia, MD: Gratefully, a lot of the atrophic changes this patient demonstrates are reversible. However, other autoimmune diseases (eg, lichen planus, which can affect the vaginal epithelium, or lichen sclerosus, which can affect the clitoris, labia, and vulva) can also cause constriction, and in severe cases, complete obliteration of the vagina and introitus. Women may not be sexually active, and for each annual exam their clinician uses a smaller and smaller speculum--to the point that they cannot even access the cervix anymore--and the vagina can close off. Clinicians may not realize that you need something other than estrogen; with lichen planus you need steroid suppository treatment, and with lichen sclerosus you need topical steroid treatment. So these autoimmune conditions should also be in the differential and, with appropriate treatment, the sexual effects can be reversible.

Michael Krychman, MD: I agree. The vulva can be a great mimicker and, according to the history and physical exam, at some point a vulvoscopy, and even potential biopsies, may be warranted as clinically indicated.

The concept of a comprehensive approach, as Dr. Kingsberg had previously mentioned, involves not only sexual medicine but also evaluating the patient's biopsychosocial variables that may impact her condition.  We also need to set realistic expectations. Some women may benefit from off-label use of medications besides estrogen, including topical testosterone. Informed consent is very important with these treatments. I also have had much clinical success with intravaginal diazepam/lorazepam for pelvic floor hypertonus.

In addition, certainly I agree that pelvic floor physical therapy (PT) is a vital treatment component for this patient and, not to diminish its importance, but many women cannot afford, nor do they have the time or opportunity, to go to pelvic floor PT. As clinicians, we can develop and implement effective programs, even in the office, to educate the patient to help herself as well.

Dr. Kaunitz: Absolutely. Also, if, in a clinical setting consistent with atrophic changes, an ObGyn physician is comfortable that vulvovaginal changes noted on exam represent GSM/atrophic changes, I do not feel vulvoscopy is warranted.

Dr. Levy: In conclusion, we need to be aware that pelvic floor PT may not be available everywhere and that a woman's own digits and her partner can also be incorporated into this treatment.

Something that we have all talked about in other venues, but have not looked at in the larger sphere here, is whether there is value to seeing women annually and performing pelvic exams. As Dr. Kingsberg mentioned, this is a highly motivated patient. We have many patients out there who are silent sufferers. The physical exam is an opportunity for us to recognize and address this problem.

 

Kimberly Martens for OBG Management

Dyspareunia and low sexual desire in a breast cancer survivor

Dr. Levy: In this case, a 36-year-old woman with BRCA1−positive breast cancer has vaginal dryness, painful intercourse, and lowered sexual interest since her treatment, which included chemotherapy after bilateral mastectomies. She has a bilateral salpingo-oophorectomy(BSO) scheduled for primary prevention of her ovarian cancer risk.

Dr. Kingsberg, what is important for you to know to help guide case management?

Dr. Kingsberg: This woman is actually presenting with 2 sexual problems: dyspareunia, which is probably secondary to VVA or GSM, and low sexual desire. Key questions are: 1) When was symptom onset--acquired after treatment or lifelong? 2) Did she develop the dyspareunia and as a result of having pain during sex lost desire to have sex? Or, did she lose desire and then, without it, had no arousal and therefore pain with penetration developed? It also could be that she has 2 distinct problems, VVA and hypoactive sexual desire disorder (HSDD), in which case you need to think about treating both. Finally, we do not actually know if she is having penetrative intercourse or even if she has a partner.

A vulvovaginal exam would give clues as to whether she has VVA, and hormone levels would indicate if she now has chemo-induced menopause. If she is not in menopause now, she certainly is going to be with her BSO. The hormonal changes due to menopause actually can be primarily responsible for both the dyspareunia and HSDD. Management of both symptoms really needs to be based on shared decision making with the patient--with which treatment for which conditions coming first, based on what is causing her the most distress.

I would encourage this woman to treat her VVA since GSM does have long-term physiologic consequences if untreated. The American College of Obstetricians and Gynecologists (ACOG) recommends nonhormonal treatments as first-line treatments, with vaginal estrogen considered if these therapies fail.³ If lubricants and moisturizers and other nonhormonal options are not sufficient, you could consider local estrogen, even though she is a breast cancer survivor, as well as ospemiphene.

If she is distressed by her loss of sexual desire, you can choose to treat her for HSDD. Flibanserin is the first FDA-approved treatment for HSDD. It is only approved in premenopausal women, so it would be considered off-label use if she is postmenopausal (even though she is quite young). You also could consider exogenous testosterone off-label, after consulting with her oncologist.

In addition to the obvious physiologic etiology of her pain and her low desire, the biopsychosocial aspects to consider are: 1) changes to her body image, as she has had bilateral mastectomies, 2) her anxiety about the cancer diagnosis, and 3) concerns about her relationship if she has one--her partner's reactions to her illness and the quality of the relationship outside the bedroom.

Dr. Iglesia: I am seeing here in our nation's capital a lot of advertisements for laser therapy for GSM. I caution women about this because providers are charging a lot of money for this therapy when we do not have long-term safety and effectiveness data for it.

Our group is currently conducting a randomized controlled trial, looking at vaginal estrogen cream versus laser therapy for GSM here at Medstar Health--one of the first in the country as part of a multisite trial. But the North American Menopause Society (NAMS) has come out with a pretty strong statement,⁴ as has ACOG,⁵ on this therapy, and I caution people about overzealously offering a very costly procedure targeted to a very vulnerable population, especially to women with personal histories of estrogen-sensitive cancers.

Dr. Krychman: I agree. Very often cancer patients are preyed upon by those offering emerging unproven technologies or medications. We have to work as a coordinated comprehensive team, whether it's a sexual medicine expert, psychologist, urogynecologist, gynecologist, or oncologist, and incorporate the patient's needs and expectations and risk tolerance coupled with treatment efficacy and safety.

Dr. Levy: This was a complex case. The biopsychosocial model is critical here. It's important that we are not siloes in our medical management approach and that we try to help this patient embrace the complexity of her situation. It's not only that she has cancer at age 36; there is a possible guilt factor if she has children and passed that gene on.

Another point that we began to talk about is the fact that in this country we tend to be early adopters of new technology. In our discussion with patients, we should focus on what we know and the risk of the unknowns related to some of the treatment options. But let's discuss lasers a little more later on.

 

Diminished arousal and orgasmic intensity in a patient taking SSRIs

Dr. Levy: In this next case, a 44-year-old woman in a 15-year marriage notices a change in her orgasmic intensity and latency. She has a supportive husband, and they are attentive to each other's sexual needs. However, she notices a change in her arousal and orgasmic intensity, which has diminished over the last year. She reports that the time to orgasm or latency has increased and both she and her partner are frustrated and getting concerned. She has a history of depression that has been managed by selective serotonin reuptake inhibitors for the past 5 years and has no depressive symptoms currently.

Dr. Krychman, what are you considering before beginning to talk with this patient?

Dr. Krychman: My approach really is a comprehensive one, looking not only at the underlying medical issues but also at the psychological and dynamic relationship facets. We of course also want to look at medications: Has she changed her dose or the timing of when she takes it? Is this a new onset? Finally, we want to know why this is coming to the forefront now. Is it because it is getting worse, or is it because there is some significant issue that is going on in the relationship?

Regarding the physical exam, it is important to rule out underlying genital pelvic pathology. Young women can get changes in the integrity of the pelvic floor, in what I would call the orgasmic matrix--the clitoral tissue, the body, the crura (or arms of the clitoris)--we want to examine and be reassured that her genital anatomy is normal and that there is no underlying pathology that could signal an underlying abnormal hormonal profile. Young women certainly can get lowered estrogen effects at the genital/pelvic tissues (including the labia and vulva), and intravaginally as well. Sometimes women will have pelvic floor hypertonus, as we see with other urinary issues. A thorough pelvic exam is quite vital.

Let's not forget the body that is attached to the genitals; we want to rule out chronic medical disease that may impact her: hypertension, diabetes, or hypercholesterolemia. Untreated, these conditions may directly impact the arousal physiologic mechanisms.

Dr. Levy: In doing this patient's physical exam I would be looking for significant weight gain, and even asking about her partner's weight. Body image can be a huge issue. If she has a history of depression, if she is suffering from a body image problem, she can be feeling unattractive. In my experience this can be a common thing to affect women in their mid-40s.

How would you manage this case?

Dr. Krychman: It is important to divide it up in terms of a conservative to aggressive approach. We want to find out about the relationship. For instance, is the sexual dynamic scripted (ie, boring and predictable)? Is she distracted and frustrated or is she getting enough of the type of stimulation that she likes and enjoys? There certainly are a lot of new devices that are available, whether a self-stimulator or vibrator, the Fiera, or other stimulating devices, that may be important to incorporate into the sexual repertoire. If there is underlying pathology, we want to evaluate and treat that. She may need to be primed, so to speak, with systemic hormones. And does she have issues related to other effects of hormonal deprivation, even local effects? Does she have clitoral atrophy?

There are neutraceuticals that are currently available, whether topical arousal gels or ointments, and we as clinicians need to be critical and evaluate their benefit/risk and look at the data concerning these products. In addition, women who have changes in arousal and in orgasmic intensity and latency may be very frustrated. They describe it as climbing up to a peak but never getting over the top, and this frustration may lead to participant spectatoring, so incorporating a certified sex therapist or counselor is sometimes very critical.

Finally, there are a lot of snake oils, charmers, and charlatan unproven procedures--injecting fillers or other substances into the clitoris are a few examples. I would be a critical clinician, examine the evidence, look at the benefit/risk before advocating an intervention that does not have good clinical data to support its use--a comprehensive approach of sexual medicine as well as sexual psychology.

Dr. Kingsberg: Additionally, we know she is in a long-term relationship--15 years; we want to acknowledge the partner. We talked about the partner's weight, but what about his erectile function? Does he have changes in sexual function that are affecting her, and she is the one carrying the "symptom"?

Looking at each piece separately helps a clinician from getting overwhelmed by the patient who comes in reporting distress with orgasmic dysfunction. We have no pharmacologic FDA-approved treatments, so it can feel off-putting for a clinician to try to fix the reported issue. Looking at each component to help her figure out the underlying cause can be helpful.

Dr. Iglesia: With aging, there can be changes in blood flow, not to mention the hormonal and even peripheral nerve changes, that require more stimulation in order to achieve the desired response. I echo concern about expensive procedures being offered with no evidence, such as the "O" or "G" shot, that can cost up to thousands of dollars.

The other procedure that gives me a lot of angst is clitoral unhooding. The 3 parts of the clitoris are sensitive in terms of innervation and blood flow, and cutting around that delicate tissue goes against the surgical principles required for preserving nerves and blood flow.

 

New onset pain post−prolapse surgery with TOT sling placement

Dr. Levy: For this case, let's consider a 42-year-old woman (P3) who is 6 months post− vaginal hysterectomy. The surgery included ovarian preservation combined with anterior and posterior repair for prolapse as well as apical uterosacral ligament suspension for stage 2 uterovaginal prolapse. A transobturator sling was used.

Extensive preop evaluation was performed, with confirmed symptomatic prolapse. She had no stress incontinence symptoms but did have confirmed occult stress incontinence.

Surgery was uneventful. She resumed intercourse at 8 weeks, but she now has pain with both initial entry and deep penetration. Lubricants and changes in position have not helped. She is in a stable relationship with her husband of 17 years, and she is worried that the sling mesh might be the culprit. On exam, she has no atrophy, pH is 4.5, vaginal length is 8 cm, and there is no prolapse. There is no mesh exposure noted, although she reports slight tenderness with palpation of the right sling arm beneath the right pubic bone.

Dr. Iglesia, what are the patient history questions important to ask here?
 
Dr. Iglesia: This is not an uncommon scenario--elective surgical correction of  occult or latent stress incontinence after surgical correction for pelvic organ prolapse. Now this patient here has no more prolapse complaints; however, she has a new symptom. There are many different causes of dyspareunia; we cannot just assume it is the sling mesh (although with all the legal representation advertisements for those who have had mesh placed, it can certainly be at the top of the patient's mind, causing anxiety and fear).

Multiple trials have looked at prophylactic surgery for incontinence at the time of prolapse repairs. This woman happened to be one of those patients who did not have incontinence symptoms, and they put a sling in. A recent large trial examined women with vaginal prolapse who underwent hysterectomy and suspension.⁶ (They compared 2 different suspensions.) What is interesting is that 25% of women with prolapse do have baseline pain. However, at 24 months, de novo pain can occur in 10% of women--just from the apical suspension. So, here, it could be the prolapse suspension. Or, in terms of the transobturator sling, long-term data do tell us that the de novo dyspareunia rate ranges on the magnitude of 1% to 9%.⁷ What is important here is figuring out the cause of the dyspareunia.

Dr. Levy: One of the important points you raised already was that 25% of these women have preoperative pain. So figuring out what her functioning was before surgery and incorporating that into our assessment postop would be pretty important I would think.

Dr. Iglesia: Yes, you need to understand what her typical encounter was before the surgery and how things have changed now that the prolapse is not in the way. Changes obviously can occur with scar tissue, which over time will improve. If she is perimenopausal and starts to get epithelial changes, we can fix that. The question then becomes, "Is the pain emanating from the mesh?"

When examining this patient, it is not uncommon for me to be able to feel "banjo" strings if the mesh is too tight or close to the surface. It is not exposed but it's palpable, and the patient may feel a ridge during penetration. You can ask the patient if pain occurs with different penetration positions. In addition, explore associated neurologic symptoms (numbness or muscle pain in the thigh).

Dr. Kingsberg: There were 2 different sources of pain--on initial entry and at deep penetration. You want to make sure you address both. Importantly, did one precede the other? For instance, if women have pain with penetration they can then end up with an arousal disorder (the length of the vagina cannot increase as much as it might otherwise) and dystonia secondary to the pain with penetration. The timing of the pain--did it all happen at the same time, or did she start out with pain at one point and did it move to something else--is another critical piece of the history.

Dr. Iglesia: It does take a detailed history and physical exam to identify myofascial trigger points. In this case there seems to be pinpoint tenderness directly on the part of the mesh that is not exposed on the right. There are people who feel you should remove the whole mesh, including the arms. Others feel, okay, we can work on these trigger points, with injections, physical therapy, extra lubrication, and neuromodulatory medications. Only then would they think about potentially excising the sling or a portion thereof.

Dr. Krychman: Keep in mind that, even if you do remove the sling, her pain may not subside, if it is secondary to an underlying issue. Because of media sensationalism, she could be focusing on the sling. It is important to set realistic expectations. I often see vulvar pathology or even provoked vestibulodynia that can present with a deep dyspareunia. The concept of collision dyspareunia or introital discomfort or pain on insertion has far reaching implications. We need to look at the patient in totality, ruling out underlying issues related to the bladder, even the colon.

 

Patient inquires about the benefits of laser treatment for vaginal health

Dr. Levy: Let's move to this last case: A 47-year-old patient who reports lack of sexual satisfaction and attributes it to a loose vagina says, "I've heard about surgery and laser treatment and radiofrequency devices for vaginal health. What are the benefits and risks of these procedures, and will they correct the issues that I'm experiencing?"

How do you approach this patient?

Dr. Krychman: I want to know why this is of paramount importance to her. Is this her actual complaint or is it society's unrealistic expectation of sexual pleasure and performance placed upon her? Or is this a relationship issue surfacing, compounded by physiologic changes? With good communication techniques, like "ask, tell, ask" or effective use of silence (not interrupting), patients will lead us to the reason and the rationale.

Dr. Levy: I have seen a lot of advertising to women, now showing pictures of genitalia, perhaps creating an expectation that we should look infantile in some way. We are creating a sense of beauty and acceptablevisualization of the vagina and vulva that are completely unrealistic. It's fascinating on one hand but it is also disturbing in that some of the direct-to-consumer marketing going on is creating a sense of unease in women who are otherwise perfectly satisfied. Now they take a look at their sagging skin, maybe after having 2 or 3 children, and although they may not look the same they function not so badly perhaps. I think we are creating a distress and an illness model that is interesting to discuss.

Dr. Iglesia, you are in the midst of a randomized trial, giving an informed consent to participants about the expectations for this potential intervention. How do you explain to women what these laser and radiofrequency devices are expected to do and why they might or might not work?

Dr. Iglesia: We are doing a randomized trial for menopausal women who have GSM. We are comparing estrogen cream with fractional CO2 laser therapy. I also am involved in another randomized trial for lichen sclerosus. I am not involved in the cosmetic use of a laser for people who feel their vaginas are just "loose." Like you, Dr. Levy, I am very concerned about the images that women are seeing of the idealized vulva and vagina, and about the rise of cosmetic gynecology, much of which is being performed by plastic surgeons or dermatologists.

A recent article looked at the number of women who are doing pubic hair grooming; the prevalance is about 80% here in America.⁸ So people have a clear view of what is down there, and then they compare it to what they see in pornographic images on the Internet and want to look like a Barbie doll. That is disturbing because women, particularly young women, do not realize what happens with GSM changes to the vulva and vagina. On the other hand, these laser machines are very expensive, and some doctors are charging thousands of dollars and promising cosmetic and functional results for which we lack long-term, comparative data.

The laser that we are studying is one by Cynosure called Mona Lisa, which works with fractional CO2 and has very low depth of penetration. The concept is that, with microdot therapy (on the order of micrometers), pinpoint destruction will foster regeneration of new collagen and blood flow to the vagina and vulva. We are still in the midst of analyzing this.

Dr. Krychman: I caution people not to lump devices together. There is a significant difference between laser and radiofrequency--especially in the depth of tissue penetration, and level of evidence as well. There are companies performing randomized clinical trials, with well designed sham controls, and have demonstrated clinical efficacy. We need to be cautious of a procedure that is saying it's the best thing since sliced bread, curing interstitial cystitis, dyspareunia, and lichen sclerosus and improving orgasm, lubrication, and arousal. These far reaching, off-label claims are concerning and misleading.

Dr. Levy: I think the important things are 1) shared decision making with the patient and 2) disclosure of what we do not know, which are the long-term results and outcomes and possible downstream negative effects of some of these treatments, since the data we have are so short term.

Dr. Kingsberg: Basics are important. You talked about the pressure for cosmetic appearance, but is that really what is going on for this particular patient? Is she describing a sexual dysfunction when she talks about lack of satisfaction? You need to operationally define that term. Does she have problems with arousal or orgasm or desire and those are what underlie her lack of satisfaction? Is the key to management helping her come to terms with body image issues or to treat a sexual dysfunction? If it truly is a sexual dysfunction, then you can have the shared decision making on preferred treatment approach.

Dr. Levy: This has been an enlightening discussion. Thank all of you for your expertise and clinical acumen.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

The age-adjusted prevalence of any sexual problem is 43% among US women. A full 22% of these women experience sexually related personal distress.¹ With publication of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition² has come a shift in classification and, at times, management approach for reported female sexual dysfunction. When women report to their clinicians decreased sexual desire or arousal or pain at penetration, the management is no longer guided by a linear model of sexual response (excitation, plateau, orgasm, and resolution) but rather by a more nuanced and complex biopsychosocial approach. In this model, diagnosis and management strategies to address bothersome sexual concerns consider the whole woman in the context of her physical and psychosocial health. The patient’s age, medical history, and relationship status are among the factors that could affect management of the problem. In an effort to explore this management approach, I used this Update on Female Sexual Dysfunction as an opportunity to convene a roundtable of several experts, representing varying backgrounds and practice vantage points, to discuss 5 cases of sexual problems that you as a busy clinician may encounter in your practice.

Genital atrophy in a sexually inactive 61-year-old woman

Barbara S. Levy, MD: Two years after her husband's death, which followed several years of illness, your 61-year-old patient mentions at her well woman visit that she anticipates becoming sexually active again. She has not used systemic or vaginal hormone therapy. During pelvic examination, atrophic external genital changes are present, and use of an ultrathin (thinner than a Pederson) speculum reveals vaginal epithelial atrophic changes. A single-digit bimanual exam can be performed with moderate patient discomfort; the patient cannot tolerate a 2-digit bimanual exam. She expresses concern about being able to engage in penile/vaginal sexual intercourse. 

Dr. Kaunitz, what is important for you to ask this patient, and what concerns you most on her physical exam?

Andrew M. Kaunitz, MD: First, it is important to recognize the patient's expectations and desires. As the case suggests, but further questioning could clarify, she would like to be able to comfortably engage in sexual intercourse with a new partner, but penetration may be difficult (and definitely painful for her) unless treatment is pursued. This combination of mucosal and vestibular atrophic changes (genitourinary syndrome of menopause [GSM], or vulvovaginal atrophy [VVA]) plus the absence of penetration for many years can be a double whammy situation for menopausal women. In this case it has led to extensive contracture of the introitus, and if it is not addressed will cause sexual dysfunction.

Dr. Levy: In addition we need to clarify whether or not a history of breast cancer or some other thing may impact the care we provide. How would you approach talking with this patient in order to manage her care?

Dr. Kaunitz: One step is to see how motivated she is to address this, as it is not something that, as gynecologists, we can snap our fingers and the situation will be resolved. If the patient is motivated to treat the atrophic changes with medical treatment, in the form of low-dose vaginal estrogen, and dilation, either on her own if she's highly motivated to do so, or in my practice more commonly with the support of a women's physical therapist, over time she should be able to comfortably engage in sexual intercourse with penetration. If this is what she wants, we can help steer her in the right direction.

Sheryl Kingsberg, PhD: You know that this woman is motivated by virtue of her initiating the topic herself. Patients are often embarrassed talking about sexual issues, or they are not sure that their gynecologist is comfortable with it. After all, they think, if this is the right place to discuss sexual problems, why didn't he or she ask me?  Clinicians must be aware that it is their responsibility to ask about sexual function and not leave it for the patient to open the door.

Dr. Kaunitz: Great point.

Cheryl B. Iglesia, MD: Gratefully, a lot of the atrophic changes this patient demonstrates are reversible. However, other autoimmune diseases (eg, lichen planus, which can affect the vaginal epithelium, or lichen sclerosus, which can affect the clitoris, labia, and vulva) can also cause constriction, and in severe cases, complete obliteration of the vagina and introitus. Women may not be sexually active, and for each annual exam their clinician uses a smaller and smaller speculum--to the point that they cannot even access the cervix anymore--and the vagina can close off. Clinicians may not realize that you need something other than estrogen; with lichen planus you need steroid suppository treatment, and with lichen sclerosus you need topical steroid treatment. So these autoimmune conditions should also be in the differential and, with appropriate treatment, the sexual effects can be reversible.

Michael Krychman, MD: I agree. The vulva can be a great mimicker and, according to the history and physical exam, at some point a vulvoscopy, and even potential biopsies, may be warranted as clinically indicated.

The concept of a comprehensive approach, as Dr. Kingsberg had previously mentioned, involves not only sexual medicine but also evaluating the patient's biopsychosocial variables that may impact her condition.  We also need to set realistic expectations. Some women may benefit from off-label use of medications besides estrogen, including topical testosterone. Informed consent is very important with these treatments. I also have had much clinical success with intravaginal diazepam/lorazepam for pelvic floor hypertonus.

In addition, certainly I agree that pelvic floor physical therapy (PT) is a vital treatment component for this patient and, not to diminish its importance, but many women cannot afford, nor do they have the time or opportunity, to go to pelvic floor PT. As clinicians, we can develop and implement effective programs, even in the office, to educate the patient to help herself as well.

Dr. Kaunitz: Absolutely. Also, if, in a clinical setting consistent with atrophic changes, an ObGyn physician is comfortable that vulvovaginal changes noted on exam represent GSM/atrophic changes, I do not feel vulvoscopy is warranted.

Dr. Levy: In conclusion, we need to be aware that pelvic floor PT may not be available everywhere and that a woman's own digits and her partner can also be incorporated into this treatment.

Something that we have all talked about in other venues, but have not looked at in the larger sphere here, is whether there is value to seeing women annually and performing pelvic exams. As Dr. Kingsberg mentioned, this is a highly motivated patient. We have many patients out there who are silent sufferers. The physical exam is an opportunity for us to recognize and address this problem.

 

Kimberly Martens for OBG Management

Dyspareunia and low sexual desire in a breast cancer survivor

Dr. Levy: In this case, a 36-year-old woman with BRCA1−positive breast cancer has vaginal dryness, painful intercourse, and lowered sexual interest since her treatment, which included chemotherapy after bilateral mastectomies. She has a bilateral salpingo-oophorectomy(BSO) scheduled for primary prevention of her ovarian cancer risk.

Dr. Kingsberg, what is important for you to know to help guide case management?

Dr. Kingsberg: This woman is actually presenting with 2 sexual problems: dyspareunia, which is probably secondary to VVA or GSM, and low sexual desire. Key questions are: 1) When was symptom onset--acquired after treatment or lifelong? 2) Did she develop the dyspareunia and as a result of having pain during sex lost desire to have sex? Or, did she lose desire and then, without it, had no arousal and therefore pain with penetration developed? It also could be that she has 2 distinct problems, VVA and hypoactive sexual desire disorder (HSDD), in which case you need to think about treating both. Finally, we do not actually know if she is having penetrative intercourse or even if she has a partner.

A vulvovaginal exam would give clues as to whether she has VVA, and hormone levels would indicate if she now has chemo-induced menopause. If she is not in menopause now, she certainly is going to be with her BSO. The hormonal changes due to menopause actually can be primarily responsible for both the dyspareunia and HSDD. Management of both symptoms really needs to be based on shared decision making with the patient--with which treatment for which conditions coming first, based on what is causing her the most distress.

I would encourage this woman to treat her VVA since GSM does have long-term physiologic consequences if untreated. The American College of Obstetricians and Gynecologists (ACOG) recommends nonhormonal treatments as first-line treatments, with vaginal estrogen considered if these therapies fail.³ If lubricants and moisturizers and other nonhormonal options are not sufficient, you could consider local estrogen, even though she is a breast cancer survivor, as well as ospemiphene.

If she is distressed by her loss of sexual desire, you can choose to treat her for HSDD. Flibanserin is the first FDA-approved treatment for HSDD. It is only approved in premenopausal women, so it would be considered off-label use if she is postmenopausal (even though she is quite young). You also could consider exogenous testosterone off-label, after consulting with her oncologist.

In addition to the obvious physiologic etiology of her pain and her low desire, the biopsychosocial aspects to consider are: 1) changes to her body image, as she has had bilateral mastectomies, 2) her anxiety about the cancer diagnosis, and 3) concerns about her relationship if she has one--her partner's reactions to her illness and the quality of the relationship outside the bedroom.

Dr. Iglesia: I am seeing here in our nation's capital a lot of advertisements for laser therapy for GSM. I caution women about this because providers are charging a lot of money for this therapy when we do not have long-term safety and effectiveness data for it.

Our group is currently conducting a randomized controlled trial, looking at vaginal estrogen cream versus laser therapy for GSM here at Medstar Health--one of the first in the country as part of a multisite trial. But the North American Menopause Society (NAMS) has come out with a pretty strong statement,⁴ as has ACOG,⁵ on this therapy, and I caution people about overzealously offering a very costly procedure targeted to a very vulnerable population, especially to women with personal histories of estrogen-sensitive cancers.

Dr. Krychman: I agree. Very often cancer patients are preyed upon by those offering emerging unproven technologies or medications. We have to work as a coordinated comprehensive team, whether it's a sexual medicine expert, psychologist, urogynecologist, gynecologist, or oncologist, and incorporate the patient's needs and expectations and risk tolerance coupled with treatment efficacy and safety.

Dr. Levy: This was a complex case. The biopsychosocial model is critical here. It's important that we are not siloes in our medical management approach and that we try to help this patient embrace the complexity of her situation. It's not only that she has cancer at age 36; there is a possible guilt factor if she has children and passed that gene on.

Another point that we began to talk about is the fact that in this country we tend to be early adopters of new technology. In our discussion with patients, we should focus on what we know and the risk of the unknowns related to some of the treatment options. But let's discuss lasers a little more later on.

 

Diminished arousal and orgasmic intensity in a patient taking SSRIs

Dr. Levy: In this next case, a 44-year-old woman in a 15-year marriage notices a change in her orgasmic intensity and latency. She has a supportive husband, and they are attentive to each other's sexual needs. However, she notices a change in her arousal and orgasmic intensity, which has diminished over the last year. She reports that the time to orgasm or latency has increased and both she and her partner are frustrated and getting concerned. She has a history of depression that has been managed by selective serotonin reuptake inhibitors for the past 5 years and has no depressive symptoms currently.

Dr. Krychman, what are you considering before beginning to talk with this patient?

Dr. Krychman: My approach really is a comprehensive one, looking not only at the underlying medical issues but also at the psychological and dynamic relationship facets. We of course also want to look at medications: Has she changed her dose or the timing of when she takes it? Is this a new onset? Finally, we want to know why this is coming to the forefront now. Is it because it is getting worse, or is it because there is some significant issue that is going on in the relationship?

Regarding the physical exam, it is important to rule out underlying genital pelvic pathology. Young women can get changes in the integrity of the pelvic floor, in what I would call the orgasmic matrix--the clitoral tissue, the body, the crura (or arms of the clitoris)--we want to examine and be reassured that her genital anatomy is normal and that there is no underlying pathology that could signal an underlying abnormal hormonal profile. Young women certainly can get lowered estrogen effects at the genital/pelvic tissues (including the labia and vulva), and intravaginally as well. Sometimes women will have pelvic floor hypertonus, as we see with other urinary issues. A thorough pelvic exam is quite vital.

Let's not forget the body that is attached to the genitals; we want to rule out chronic medical disease that may impact her: hypertension, diabetes, or hypercholesterolemia. Untreated, these conditions may directly impact the arousal physiologic mechanisms.

Dr. Levy: In doing this patient's physical exam I would be looking for significant weight gain, and even asking about her partner's weight. Body image can be a huge issue. If she has a history of depression, if she is suffering from a body image problem, she can be feeling unattractive. In my experience this can be a common thing to affect women in their mid-40s.

How would you manage this case?

Dr. Krychman: It is important to divide it up in terms of a conservative to aggressive approach. We want to find out about the relationship. For instance, is the sexual dynamic scripted (ie, boring and predictable)? Is she distracted and frustrated or is she getting enough of the type of stimulation that she likes and enjoys? There certainly are a lot of new devices that are available, whether a self-stimulator or vibrator, the Fiera, or other stimulating devices, that may be important to incorporate into the sexual repertoire. If there is underlying pathology, we want to evaluate and treat that. She may need to be primed, so to speak, with systemic hormones. And does she have issues related to other effects of hormonal deprivation, even local effects? Does she have clitoral atrophy?

There are neutraceuticals that are currently available, whether topical arousal gels or ointments, and we as clinicians need to be critical and evaluate their benefit/risk and look at the data concerning these products. In addition, women who have changes in arousal and in orgasmic intensity and latency may be very frustrated. They describe it as climbing up to a peak but never getting over the top, and this frustration may lead to participant spectatoring, so incorporating a certified sex therapist or counselor is sometimes very critical.

Finally, there are a lot of snake oils, charmers, and charlatan unproven procedures--injecting fillers or other substances into the clitoris are a few examples. I would be a critical clinician, examine the evidence, look at the benefit/risk before advocating an intervention that does not have good clinical data to support its use--a comprehensive approach of sexual medicine as well as sexual psychology.

Dr. Kingsberg: Additionally, we know she is in a long-term relationship--15 years; we want to acknowledge the partner. We talked about the partner's weight, but what about his erectile function? Does he have changes in sexual function that are affecting her, and she is the one carrying the "symptom"?

Looking at each piece separately helps a clinician from getting overwhelmed by the patient who comes in reporting distress with orgasmic dysfunction. We have no pharmacologic FDA-approved treatments, so it can feel off-putting for a clinician to try to fix the reported issue. Looking at each component to help her figure out the underlying cause can be helpful.

Dr. Iglesia: With aging, there can be changes in blood flow, not to mention the hormonal and even peripheral nerve changes, that require more stimulation in order to achieve the desired response. I echo concern about expensive procedures being offered with no evidence, such as the "O" or "G" shot, that can cost up to thousands of dollars.

The other procedure that gives me a lot of angst is clitoral unhooding. The 3 parts of the clitoris are sensitive in terms of innervation and blood flow, and cutting around that delicate tissue goes against the surgical principles required for preserving nerves and blood flow.

 

New onset pain post−prolapse surgery with TOT sling placement

Dr. Levy: For this case, let's consider a 42-year-old woman (P3) who is 6 months post− vaginal hysterectomy. The surgery included ovarian preservation combined with anterior and posterior repair for prolapse as well as apical uterosacral ligament suspension for stage 2 uterovaginal prolapse. A transobturator sling was used.

Extensive preop evaluation was performed, with confirmed symptomatic prolapse. She had no stress incontinence symptoms but did have confirmed occult stress incontinence.

Surgery was uneventful. She resumed intercourse at 8 weeks, but she now has pain with both initial entry and deep penetration. Lubricants and changes in position have not helped. She is in a stable relationship with her husband of 17 years, and she is worried that the sling mesh might be the culprit. On exam, she has no atrophy, pH is 4.5, vaginal length is 8 cm, and there is no prolapse. There is no mesh exposure noted, although she reports slight tenderness with palpation of the right sling arm beneath the right pubic bone.

Dr. Iglesia, what are the patient history questions important to ask here?
 
Dr. Iglesia: This is not an uncommon scenario--elective surgical correction of  occult or latent stress incontinence after surgical correction for pelvic organ prolapse. Now this patient here has no more prolapse complaints; however, she has a new symptom. There are many different causes of dyspareunia; we cannot just assume it is the sling mesh (although with all the legal representation advertisements for those who have had mesh placed, it can certainly be at the top of the patient's mind, causing anxiety and fear).

Multiple trials have looked at prophylactic surgery for incontinence at the time of prolapse repairs. This woman happened to be one of those patients who did not have incontinence symptoms, and they put a sling in. A recent large trial examined women with vaginal prolapse who underwent hysterectomy and suspension.⁶ (They compared 2 different suspensions.) What is interesting is that 25% of women with prolapse do have baseline pain. However, at 24 months, de novo pain can occur in 10% of women--just from the apical suspension. So, here, it could be the prolapse suspension. Or, in terms of the transobturator sling, long-term data do tell us that the de novo dyspareunia rate ranges on the magnitude of 1% to 9%.⁷ What is important here is figuring out the cause of the dyspareunia.

Dr. Levy: One of the important points you raised already was that 25% of these women have preoperative pain. So figuring out what her functioning was before surgery and incorporating that into our assessment postop would be pretty important I would think.

Dr. Iglesia: Yes, you need to understand what her typical encounter was before the surgery and how things have changed now that the prolapse is not in the way. Changes obviously can occur with scar tissue, which over time will improve. If she is perimenopausal and starts to get epithelial changes, we can fix that. The question then becomes, "Is the pain emanating from the mesh?"

When examining this patient, it is not uncommon for me to be able to feel "banjo" strings if the mesh is too tight or close to the surface. It is not exposed but it's palpable, and the patient may feel a ridge during penetration. You can ask the patient if pain occurs with different penetration positions. In addition, explore associated neurologic symptoms (numbness or muscle pain in the thigh).

Dr. Kingsberg: There were 2 different sources of pain--on initial entry and at deep penetration. You want to make sure you address both. Importantly, did one precede the other? For instance, if women have pain with penetration they can then end up with an arousal disorder (the length of the vagina cannot increase as much as it might otherwise) and dystonia secondary to the pain with penetration. The timing of the pain--did it all happen at the same time, or did she start out with pain at one point and did it move to something else--is another critical piece of the history.

Dr. Iglesia: It does take a detailed history and physical exam to identify myofascial trigger points. In this case there seems to be pinpoint tenderness directly on the part of the mesh that is not exposed on the right. There are people who feel you should remove the whole mesh, including the arms. Others feel, okay, we can work on these trigger points, with injections, physical therapy, extra lubrication, and neuromodulatory medications. Only then would they think about potentially excising the sling or a portion thereof.

Dr. Krychman: Keep in mind that, even if you do remove the sling, her pain may not subside, if it is secondary to an underlying issue. Because of media sensationalism, she could be focusing on the sling. It is important to set realistic expectations. I often see vulvar pathology or even provoked vestibulodynia that can present with a deep dyspareunia. The concept of collision dyspareunia or introital discomfort or pain on insertion has far reaching implications. We need to look at the patient in totality, ruling out underlying issues related to the bladder, even the colon.

 

Patient inquires about the benefits of laser treatment for vaginal health

Dr. Levy: Let's move to this last case: A 47-year-old patient who reports lack of sexual satisfaction and attributes it to a loose vagina says, "I've heard about surgery and laser treatment and radiofrequency devices for vaginal health. What are the benefits and risks of these procedures, and will they correct the issues that I'm experiencing?"

How do you approach this patient?

Dr. Krychman: I want to know why this is of paramount importance to her. Is this her actual complaint or is it society's unrealistic expectation of sexual pleasure and performance placed upon her? Or is this a relationship issue surfacing, compounded by physiologic changes? With good communication techniques, like "ask, tell, ask" or effective use of silence (not interrupting), patients will lead us to the reason and the rationale.

Dr. Levy: I have seen a lot of advertising to women, now showing pictures of genitalia, perhaps creating an expectation that we should look infantile in some way. We are creating a sense of beauty and acceptablevisualization of the vagina and vulva that are completely unrealistic. It's fascinating on one hand but it is also disturbing in that some of the direct-to-consumer marketing going on is creating a sense of unease in women who are otherwise perfectly satisfied. Now they take a look at their sagging skin, maybe after having 2 or 3 children, and although they may not look the same they function not so badly perhaps. I think we are creating a distress and an illness model that is interesting to discuss.

Dr. Iglesia, you are in the midst of a randomized trial, giving an informed consent to participants about the expectations for this potential intervention. How do you explain to women what these laser and radiofrequency devices are expected to do and why they might or might not work?

Dr. Iglesia: We are doing a randomized trial for menopausal women who have GSM. We are comparing estrogen cream with fractional CO2 laser therapy. I also am involved in another randomized trial for lichen sclerosus. I am not involved in the cosmetic use of a laser for people who feel their vaginas are just "loose." Like you, Dr. Levy, I am very concerned about the images that women are seeing of the idealized vulva and vagina, and about the rise of cosmetic gynecology, much of which is being performed by plastic surgeons or dermatologists.

A recent article looked at the number of women who are doing pubic hair grooming; the prevalance is about 80% here in America.⁸ So people have a clear view of what is down there, and then they compare it to what they see in pornographic images on the Internet and want to look like a Barbie doll. That is disturbing because women, particularly young women, do not realize what happens with GSM changes to the vulva and vagina. On the other hand, these laser machines are very expensive, and some doctors are charging thousands of dollars and promising cosmetic and functional results for which we lack long-term, comparative data.

The laser that we are studying is one by Cynosure called Mona Lisa, which works with fractional CO2 and has very low depth of penetration. The concept is that, with microdot therapy (on the order of micrometers), pinpoint destruction will foster regeneration of new collagen and blood flow to the vagina and vulva. We are still in the midst of analyzing this.

Dr. Krychman: I caution people not to lump devices together. There is a significant difference between laser and radiofrequency--especially in the depth of tissue penetration, and level of evidence as well. There are companies performing randomized clinical trials, with well designed sham controls, and have demonstrated clinical efficacy. We need to be cautious of a procedure that is saying it's the best thing since sliced bread, curing interstitial cystitis, dyspareunia, and lichen sclerosus and improving orgasm, lubrication, and arousal. These far reaching, off-label claims are concerning and misleading.

Dr. Levy: I think the important things are 1) shared decision making with the patient and 2) disclosure of what we do not know, which are the long-term results and outcomes and possible downstream negative effects of some of these treatments, since the data we have are so short term.

Dr. Kingsberg: Basics are important. You talked about the pressure for cosmetic appearance, but is that really what is going on for this particular patient? Is she describing a sexual dysfunction when she talks about lack of satisfaction? You need to operationally define that term. Does she have problems with arousal or orgasm or desire and those are what underlie her lack of satisfaction? Is the key to management helping her come to terms with body image issues or to treat a sexual dysfunction? If it truly is a sexual dysfunction, then you can have the shared decision making on preferred treatment approach.

Dr. Levy: This has been an enlightening discussion. Thank all of you for your expertise and clinical acumen.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

The age-adjusted prevalence of any sexual problem is 43% among US women. A full 22% of these women experience sexually related personal distress.¹ With publication of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition² has come a shift in classification and, at times, management approach for reported female sexual dysfunction. When women report to their clinicians decreased sexual desire or arousal or pain at penetration, the management is no longer guided by a linear model of sexual response (excitation, plateau, orgasm, and resolution) but rather by a more nuanced and complex biopsychosocial approach. In this model, diagnosis and management strategies to address bothersome sexual concerns consider the whole woman in the context of her physical and psychosocial health. The patient’s age, medical history, and relationship status are among the factors that could affect management of the problem. In an effort to explore this management approach, I used this Update on Female Sexual Dysfunction as an opportunity to convene a roundtable of several experts, representing varying backgrounds and practice vantage points, to discuss 5 cases of sexual problems that you as a busy clinician may encounter in your practice.

Genital atrophy in a sexually inactive 61-year-old woman

Barbara S. Levy, MD: Two years after her husband's death, which followed several years of illness, your 61-year-old patient mentions at her well woman visit that she anticipates becoming sexually active again. She has not used systemic or vaginal hormone therapy. During pelvic examination, atrophic external genital changes are present, and use of an ultrathin (thinner than a Pederson) speculum reveals vaginal epithelial atrophic changes. A single-digit bimanual exam can be performed with moderate patient discomfort; the patient cannot tolerate a 2-digit bimanual exam. She expresses concern about being able to engage in penile/vaginal sexual intercourse. 

Dr. Kaunitz, what is important for you to ask this patient, and what concerns you most on her physical exam?

Andrew M. Kaunitz, MD: First, it is important to recognize the patient's expectations and desires. As the case suggests, but further questioning could clarify, she would like to be able to comfortably engage in sexual intercourse with a new partner, but penetration may be difficult (and definitely painful for her) unless treatment is pursued. This combination of mucosal and vestibular atrophic changes (genitourinary syndrome of menopause [GSM], or vulvovaginal atrophy [VVA]) plus the absence of penetration for many years can be a double whammy situation for menopausal women. In this case it has led to extensive contracture of the introitus, and if it is not addressed will cause sexual dysfunction.

Dr. Levy: In addition we need to clarify whether or not a history of breast cancer or some other thing may impact the care we provide. How would you approach talking with this patient in order to manage her care?

Dr. Kaunitz: One step is to see how motivated she is to address this, as it is not something that, as gynecologists, we can snap our fingers and the situation will be resolved. If the patient is motivated to treat the atrophic changes with medical treatment, in the form of low-dose vaginal estrogen, and dilation, either on her own if she's highly motivated to do so, or in my practice more commonly with the support of a women's physical therapist, over time she should be able to comfortably engage in sexual intercourse with penetration. If this is what she wants, we can help steer her in the right direction.

Sheryl Kingsberg, PhD: You know that this woman is motivated by virtue of her initiating the topic herself. Patients are often embarrassed talking about sexual issues, or they are not sure that their gynecologist is comfortable with it. After all, they think, if this is the right place to discuss sexual problems, why didn't he or she ask me?  Clinicians must be aware that it is their responsibility to ask about sexual function and not leave it for the patient to open the door.

Dr. Kaunitz: Great point.

Cheryl B. Iglesia, MD: Gratefully, a lot of the atrophic changes this patient demonstrates are reversible. However, other autoimmune diseases (eg, lichen planus, which can affect the vaginal epithelium, or lichen sclerosus, which can affect the clitoris, labia, and vulva) can also cause constriction, and in severe cases, complete obliteration of the vagina and introitus. Women may not be sexually active, and for each annual exam their clinician uses a smaller and smaller speculum--to the point that they cannot even access the cervix anymore--and the vagina can close off. Clinicians may not realize that you need something other than estrogen; with lichen planus you need steroid suppository treatment, and with lichen sclerosus you need topical steroid treatment. So these autoimmune conditions should also be in the differential and, with appropriate treatment, the sexual effects can be reversible.

Michael Krychman, MD: I agree. The vulva can be a great mimicker and, according to the history and physical exam, at some point a vulvoscopy, and even potential biopsies, may be warranted as clinically indicated.

The concept of a comprehensive approach, as Dr. Kingsberg had previously mentioned, involves not only sexual medicine but also evaluating the patient's biopsychosocial variables that may impact her condition.  We also need to set realistic expectations. Some women may benefit from off-label use of medications besides estrogen, including topical testosterone. Informed consent is very important with these treatments. I also have had much clinical success with intravaginal diazepam/lorazepam for pelvic floor hypertonus.

In addition, certainly I agree that pelvic floor physical therapy (PT) is a vital treatment component for this patient and, not to diminish its importance, but many women cannot afford, nor do they have the time or opportunity, to go to pelvic floor PT. As clinicians, we can develop and implement effective programs, even in the office, to educate the patient to help herself as well.

Dr. Kaunitz: Absolutely. Also, if, in a clinical setting consistent with atrophic changes, an ObGyn physician is comfortable that vulvovaginal changes noted on exam represent GSM/atrophic changes, I do not feel vulvoscopy is warranted.

Dr. Levy: In conclusion, we need to be aware that pelvic floor PT may not be available everywhere and that a woman's own digits and her partner can also be incorporated into this treatment.

Something that we have all talked about in other venues, but have not looked at in the larger sphere here, is whether there is value to seeing women annually and performing pelvic exams. As Dr. Kingsberg mentioned, this is a highly motivated patient. We have many patients out there who are silent sufferers. The physical exam is an opportunity for us to recognize and address this problem.

 

Kimberly Martens for OBG Management

Dyspareunia and low sexual desire in a breast cancer survivor

Dr. Levy: In this case, a 36-year-old woman with BRCA1−positive breast cancer has vaginal dryness, painful intercourse, and lowered sexual interest since her treatment, which included chemotherapy after bilateral mastectomies. She has a bilateral salpingo-oophorectomy(BSO) scheduled for primary prevention of her ovarian cancer risk.

Dr. Kingsberg, what is important for you to know to help guide case management?

Dr. Kingsberg: This woman is actually presenting with 2 sexual problems: dyspareunia, which is probably secondary to VVA or GSM, and low sexual desire. Key questions are: 1) When was symptom onset--acquired after treatment or lifelong? 2) Did she develop the dyspareunia and as a result of having pain during sex lost desire to have sex? Or, did she lose desire and then, without it, had no arousal and therefore pain with penetration developed? It also could be that she has 2 distinct problems, VVA and hypoactive sexual desire disorder (HSDD), in which case you need to think about treating both. Finally, we do not actually know if she is having penetrative intercourse or even if she has a partner.

A vulvovaginal exam would give clues as to whether she has VVA, and hormone levels would indicate if she now has chemo-induced menopause. If she is not in menopause now, she certainly is going to be with her BSO. The hormonal changes due to menopause actually can be primarily responsible for both the dyspareunia and HSDD. Management of both symptoms really needs to be based on shared decision making with the patient--with which treatment for which conditions coming first, based on what is causing her the most distress.

I would encourage this woman to treat her VVA since GSM does have long-term physiologic consequences if untreated. The American College of Obstetricians and Gynecologists (ACOG) recommends nonhormonal treatments as first-line treatments, with vaginal estrogen considered if these therapies fail.³ If lubricants and moisturizers and other nonhormonal options are not sufficient, you could consider local estrogen, even though she is a breast cancer survivor, as well as ospemiphene.

If she is distressed by her loss of sexual desire, you can choose to treat her for HSDD. Flibanserin is the first FDA-approved treatment for HSDD. It is only approved in premenopausal women, so it would be considered off-label use if she is postmenopausal (even though she is quite young). You also could consider exogenous testosterone off-label, after consulting with her oncologist.

In addition to the obvious physiologic etiology of her pain and her low desire, the biopsychosocial aspects to consider are: 1) changes to her body image, as she has had bilateral mastectomies, 2) her anxiety about the cancer diagnosis, and 3) concerns about her relationship if she has one--her partner's reactions to her illness and the quality of the relationship outside the bedroom.

Dr. Iglesia: I am seeing here in our nation's capital a lot of advertisements for laser therapy for GSM. I caution women about this because providers are charging a lot of money for this therapy when we do not have long-term safety and effectiveness data for it.

Our group is currently conducting a randomized controlled trial, looking at vaginal estrogen cream versus laser therapy for GSM here at Medstar Health--one of the first in the country as part of a multisite trial. But the North American Menopause Society (NAMS) has come out with a pretty strong statement,⁴ as has ACOG,⁵ on this therapy, and I caution people about overzealously offering a very costly procedure targeted to a very vulnerable population, especially to women with personal histories of estrogen-sensitive cancers.

Dr. Krychman: I agree. Very often cancer patients are preyed upon by those offering emerging unproven technologies or medications. We have to work as a coordinated comprehensive team, whether it's a sexual medicine expert, psychologist, urogynecologist, gynecologist, or oncologist, and incorporate the patient's needs and expectations and risk tolerance coupled with treatment efficacy and safety.

Dr. Levy: This was a complex case. The biopsychosocial model is critical here. It's important that we are not siloes in our medical management approach and that we try to help this patient embrace the complexity of her situation. It's not only that she has cancer at age 36; there is a possible guilt factor if she has children and passed that gene on.

Another point that we began to talk about is the fact that in this country we tend to be early adopters of new technology. In our discussion with patients, we should focus on what we know and the risk of the unknowns related to some of the treatment options. But let's discuss lasers a little more later on.

 

Diminished arousal and orgasmic intensity in a patient taking SSRIs

Dr. Levy: In this next case, a 44-year-old woman in a 15-year marriage notices a change in her orgasmic intensity and latency. She has a supportive husband, and they are attentive to each other's sexual needs. However, she notices a change in her arousal and orgasmic intensity, which has diminished over the last year. She reports that the time to orgasm or latency has increased and both she and her partner are frustrated and getting concerned. She has a history of depression that has been managed by selective serotonin reuptake inhibitors for the past 5 years and has no depressive symptoms currently.

Dr. Krychman, what are you considering before beginning to talk with this patient?

Dr. Krychman: My approach really is a comprehensive one, looking not only at the underlying medical issues but also at the psychological and dynamic relationship facets. We of course also want to look at medications: Has she changed her dose or the timing of when she takes it? Is this a new onset? Finally, we want to know why this is coming to the forefront now. Is it because it is getting worse, or is it because there is some significant issue that is going on in the relationship?

Regarding the physical exam, it is important to rule out underlying genital pelvic pathology. Young women can get changes in the integrity of the pelvic floor, in what I would call the orgasmic matrix--the clitoral tissue, the body, the crura (or arms of the clitoris)--we want to examine and be reassured that her genital anatomy is normal and that there is no underlying pathology that could signal an underlying abnormal hormonal profile. Young women certainly can get lowered estrogen effects at the genital/pelvic tissues (including the labia and vulva), and intravaginally as well. Sometimes women will have pelvic floor hypertonus, as we see with other urinary issues. A thorough pelvic exam is quite vital.

Let's not forget the body that is attached to the genitals; we want to rule out chronic medical disease that may impact her: hypertension, diabetes, or hypercholesterolemia. Untreated, these conditions may directly impact the arousal physiologic mechanisms.

Dr. Levy: In doing this patient's physical exam I would be looking for significant weight gain, and even asking about her partner's weight. Body image can be a huge issue. If she has a history of depression, if she is suffering from a body image problem, she can be feeling unattractive. In my experience this can be a common thing to affect women in their mid-40s.

How would you manage this case?

Dr. Krychman: It is important to divide it up in terms of a conservative to aggressive approach. We want to find out about the relationship. For instance, is the sexual dynamic scripted (ie, boring and predictable)? Is she distracted and frustrated or is she getting enough of the type of stimulation that she likes and enjoys? There certainly are a lot of new devices that are available, whether a self-stimulator or vibrator, the Fiera, or other stimulating devices, that may be important to incorporate into the sexual repertoire. If there is underlying pathology, we want to evaluate and treat that. She may need to be primed, so to speak, with systemic hormones. And does she have issues related to other effects of hormonal deprivation, even local effects? Does she have clitoral atrophy?

There are neutraceuticals that are currently available, whether topical arousal gels or ointments, and we as clinicians need to be critical and evaluate their benefit/risk and look at the data concerning these products. In addition, women who have changes in arousal and in orgasmic intensity and latency may be very frustrated. They describe it as climbing up to a peak but never getting over the top, and this frustration may lead to participant spectatoring, so incorporating a certified sex therapist or counselor is sometimes very critical.

Finally, there are a lot of snake oils, charmers, and charlatan unproven procedures--injecting fillers or other substances into the clitoris are a few examples. I would be a critical clinician, examine the evidence, look at the benefit/risk before advocating an intervention that does not have good clinical data to support its use--a comprehensive approach of sexual medicine as well as sexual psychology.

Dr. Kingsberg: Additionally, we know she is in a long-term relationship--15 years; we want to acknowledge the partner. We talked about the partner's weight, but what about his erectile function? Does he have changes in sexual function that are affecting her, and she is the one carrying the "symptom"?

Looking at each piece separately helps a clinician from getting overwhelmed by the patient who comes in reporting distress with orgasmic dysfunction. We have no pharmacologic FDA-approved treatments, so it can feel off-putting for a clinician to try to fix the reported issue. Looking at each component to help her figure out the underlying cause can be helpful.

Dr. Iglesia: With aging, there can be changes in blood flow, not to mention the hormonal and even peripheral nerve changes, that require more stimulation in order to achieve the desired response. I echo concern about expensive procedures being offered with no evidence, such as the "O" or "G" shot, that can cost up to thousands of dollars.

The other procedure that gives me a lot of angst is clitoral unhooding. The 3 parts of the clitoris are sensitive in terms of innervation and blood flow, and cutting around that delicate tissue goes against the surgical principles required for preserving nerves and blood flow.

 

New onset pain post−prolapse surgery with TOT sling placement

Dr. Levy: For this case, let's consider a 42-year-old woman (P3) who is 6 months post− vaginal hysterectomy. The surgery included ovarian preservation combined with anterior and posterior repair for prolapse as well as apical uterosacral ligament suspension for stage 2 uterovaginal prolapse. A transobturator sling was used.

Extensive preop evaluation was performed, with confirmed symptomatic prolapse. She had no stress incontinence symptoms but did have confirmed occult stress incontinence.

Surgery was uneventful. She resumed intercourse at 8 weeks, but she now has pain with both initial entry and deep penetration. Lubricants and changes in position have not helped. She is in a stable relationship with her husband of 17 years, and she is worried that the sling mesh might be the culprit. On exam, she has no atrophy, pH is 4.5, vaginal length is 8 cm, and there is no prolapse. There is no mesh exposure noted, although she reports slight tenderness with palpation of the right sling arm beneath the right pubic bone.

Dr. Iglesia, what are the patient history questions important to ask here?
 
Dr. Iglesia: This is not an uncommon scenario--elective surgical correction of  occult or latent stress incontinence after surgical correction for pelvic organ prolapse. Now this patient here has no more prolapse complaints; however, she has a new symptom. There are many different causes of dyspareunia; we cannot just assume it is the sling mesh (although with all the legal representation advertisements for those who have had mesh placed, it can certainly be at the top of the patient's mind, causing anxiety and fear).

Multiple trials have looked at prophylactic surgery for incontinence at the time of prolapse repairs. This woman happened to be one of those patients who did not have incontinence symptoms, and they put a sling in. A recent large trial examined women with vaginal prolapse who underwent hysterectomy and suspension.⁶ (They compared 2 different suspensions.) What is interesting is that 25% of women with prolapse do have baseline pain. However, at 24 months, de novo pain can occur in 10% of women--just from the apical suspension. So, here, it could be the prolapse suspension. Or, in terms of the transobturator sling, long-term data do tell us that the de novo dyspareunia rate ranges on the magnitude of 1% to 9%.⁷ What is important here is figuring out the cause of the dyspareunia.

Dr. Levy: One of the important points you raised already was that 25% of these women have preoperative pain. So figuring out what her functioning was before surgery and incorporating that into our assessment postop would be pretty important I would think.

Dr. Iglesia: Yes, you need to understand what her typical encounter was before the surgery and how things have changed now that the prolapse is not in the way. Changes obviously can occur with scar tissue, which over time will improve. If she is perimenopausal and starts to get epithelial changes, we can fix that. The question then becomes, "Is the pain emanating from the mesh?"

When examining this patient, it is not uncommon for me to be able to feel "banjo" strings if the mesh is too tight or close to the surface. It is not exposed but it's palpable, and the patient may feel a ridge during penetration. You can ask the patient if pain occurs with different penetration positions. In addition, explore associated neurologic symptoms (numbness or muscle pain in the thigh).

Dr. Kingsberg: There were 2 different sources of pain--on initial entry and at deep penetration. You want to make sure you address both. Importantly, did one precede the other? For instance, if women have pain with penetration they can then end up with an arousal disorder (the length of the vagina cannot increase as much as it might otherwise) and dystonia secondary to the pain with penetration. The timing of the pain--did it all happen at the same time, or did she start out with pain at one point and did it move to something else--is another critical piece of the history.

Dr. Iglesia: It does take a detailed history and physical exam to identify myofascial trigger points. In this case there seems to be pinpoint tenderness directly on the part of the mesh that is not exposed on the right. There are people who feel you should remove the whole mesh, including the arms. Others feel, okay, we can work on these trigger points, with injections, physical therapy, extra lubrication, and neuromodulatory medications. Only then would they think about potentially excising the sling or a portion thereof.

Dr. Krychman: Keep in mind that, even if you do remove the sling, her pain may not subside, if it is secondary to an underlying issue. Because of media sensationalism, she could be focusing on the sling. It is important to set realistic expectations. I often see vulvar pathology or even provoked vestibulodynia that can present with a deep dyspareunia. The concept of collision dyspareunia or introital discomfort or pain on insertion has far reaching implications. We need to look at the patient in totality, ruling out underlying issues related to the bladder, even the colon.

 

Patient inquires about the benefits of laser treatment for vaginal health

Dr. Levy: Let's move to this last case: A 47-year-old patient who reports lack of sexual satisfaction and attributes it to a loose vagina says, "I've heard about surgery and laser treatment and radiofrequency devices for vaginal health. What are the benefits and risks of these procedures, and will they correct the issues that I'm experiencing?"

How do you approach this patient?

Dr. Krychman: I want to know why this is of paramount importance to her. Is this her actual complaint or is it society's unrealistic expectation of sexual pleasure and performance placed upon her? Or is this a relationship issue surfacing, compounded by physiologic changes? With good communication techniques, like "ask, tell, ask" or effective use of silence (not interrupting), patients will lead us to the reason and the rationale.

Dr. Levy: I have seen a lot of advertising to women, now showing pictures of genitalia, perhaps creating an expectation that we should look infantile in some way. We are creating a sense of beauty and acceptablevisualization of the vagina and vulva that are completely unrealistic. It's fascinating on one hand but it is also disturbing in that some of the direct-to-consumer marketing going on is creating a sense of unease in women who are otherwise perfectly satisfied. Now they take a look at their sagging skin, maybe after having 2 or 3 children, and although they may not look the same they function not so badly perhaps. I think we are creating a distress and an illness model that is interesting to discuss.

Dr. Iglesia, you are in the midst of a randomized trial, giving an informed consent to participants about the expectations for this potential intervention. How do you explain to women what these laser and radiofrequency devices are expected to do and why they might or might not work?

Dr. Iglesia: We are doing a randomized trial for menopausal women who have GSM. We are comparing estrogen cream with fractional CO2 laser therapy. I also am involved in another randomized trial for lichen sclerosus. I am not involved in the cosmetic use of a laser for people who feel their vaginas are just "loose." Like you, Dr. Levy, I am very concerned about the images that women are seeing of the idealized vulva and vagina, and about the rise of cosmetic gynecology, much of which is being performed by plastic surgeons or dermatologists.

A recent article looked at the number of women who are doing pubic hair grooming; the prevalance is about 80% here in America.⁸ So people have a clear view of what is down there, and then they compare it to what they see in pornographic images on the Internet and want to look like a Barbie doll. That is disturbing because women, particularly young women, do not realize what happens with GSM changes to the vulva and vagina. On the other hand, these laser machines are very expensive, and some doctors are charging thousands of dollars and promising cosmetic and functional results for which we lack long-term, comparative data.

The laser that we are studying is one by Cynosure called Mona Lisa, which works with fractional CO2 and has very low depth of penetration. The concept is that, with microdot therapy (on the order of micrometers), pinpoint destruction will foster regeneration of new collagen and blood flow to the vagina and vulva. We are still in the midst of analyzing this.

Dr. Krychman: I caution people not to lump devices together. There is a significant difference between laser and radiofrequency--especially in the depth of tissue penetration, and level of evidence as well. There are companies performing randomized clinical trials, with well designed sham controls, and have demonstrated clinical efficacy. We need to be cautious of a procedure that is saying it's the best thing since sliced bread, curing interstitial cystitis, dyspareunia, and lichen sclerosus and improving orgasm, lubrication, and arousal. These far reaching, off-label claims are concerning and misleading.

Dr. Levy: I think the important things are 1) shared decision making with the patient and 2) disclosure of what we do not know, which are the long-term results and outcomes and possible downstream negative effects of some of these treatments, since the data we have are so short term.

Dr. Kingsberg: Basics are important. You talked about the pressure for cosmetic appearance, but is that really what is going on for this particular patient? Is she describing a sexual dysfunction when she talks about lack of satisfaction? You need to operationally define that term. Does she have problems with arousal or orgasm or desire and those are what underlie her lack of satisfaction? Is the key to management helping her come to terms with body image issues or to treat a sexual dysfunction? If it truly is a sexual dysfunction, then you can have the shared decision making on preferred treatment approach.

Dr. Levy: This has been an enlightening discussion. Thank all of you for your expertise and clinical acumen.

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