Commentary

The horrors faced by migrant families forced to separate under the new U.S. “zero tolerance” policy continue to unfold. Tragic emblems of this policy include tapes of crying children and the reported suicide of a father who had been separated from his children.

A federal judge had issued an injunction requiring the reunification of thousands of families by July 26. Despite that deadline, hundreds of adults are no longer in the United States, and hundreds of children are scattered in shelters across the country.

In response to those events, mental health and medical organizations have released powerful statements. The American Psychological Association stated: “The administration’s policy ... is not only needless and cruel, it threatens the mental and physical health of both the children and their caregivers.” The American Medical Association issued a call asserting that separating children from their parents “will do great harm” and “create negative health impacts that will last an individual’s entire lifespan.” Meanwhile, the American Psychiatric Association’s president, Altha J. Stewart, MD, released a statement affirming that “any forced separation is highly stressful for children and can cause lifelong trauma, as well as an increased risk of other mental illnesses, such as depression, anxiety, and posttraumatic stress disorder.”

As forensic experts who testify about the mental well-being of immigration detainees, we applaud those powerful and unambiguous messages from the leaders in our fields. Yet, their statements also underscore the limitations of our diagnostic models: Our field is caught in the difficult position of either applying ill-fitting diagnostic labels or overpathologizing a normal reaction to horrific circumstances. While not applying diagnoses potentially minimizes the enormous psychological burden of separation, diagnosing depression or PTSD as catchalls for suffering incorrectly defines the experience of many survivors of ongoing trauma.

Currently, most providers, in trying to communicate the effects of ongoing trauma, rely on the diagnoses of depression or PTSD. Both of these diagnoses, however, are problematic. The diagnosis of major depressive disorder, for example, is useful in communicating a loss of hope, and the inability to enjoy pleasurable things. However, depression is an episodic illness, often part of a larger chronic disorder.¹ Depression often has a genetic-hereditary component. On the other hand, children suffering from childhood traumas often present lifelong and wide-ranging problems, which may be triggered by reminders but are not episodic. For example, children experiencing parental separation have difficulty forming attachments, which, in turn, leads to subsequent difficulty forming meaningful interpersonal relationships.

The diagnosis of PTSD is useful in communicating a myriad of possible symptoms, which may accompany the trauma. However, PTSD implies a traumatic event as described in criteria A of the DSM-5: “exposure to actual or threatened death, serious injury, or sexual violence.” As such, PTSD poorly encompasses the wide array of smaller yet repetitive traumas experienced by victims of ongoing trauma, such as those youth separated from their parents at the U.S. border. Furthermore, PTSD is a disorder with specific symptoms that, based on a vast body of research,^2,3 inadequately describes the multitude of interpersonal, psychological, and physical consequences associated with the type of trauma caused by family separations.

Our understanding of the long-term sequelae of childhood trauma has been greatly influenced by the adverse childhood experiences (ACE) study. The ACE study, one of the largest investigations ever conducted to assess associations between childhood maltreatment and later-life health and well-being, collected the life histories of more than 17,000 patients in a collaborative effort between the Centers for Disease Control and Prevention and Kaiser Permanente’s Health Appraisal Clinic.

The ACE study identified 10 forms of childhood trauma, including: abuse, neglect, abandonment, household dysfunction, and exposure to violence, that were strongly associated with negative psychological outcomes such as depression, suicide attempts, and engagement in high-risk behaviors, as well as significant medical consequences, including higher incidence of heart disease, diabetes, and stroke. Ultimately, having four or more ACEs was associated with early death.

In response to the emerging body of research on childhood trauma, various terms, including complex trauma, type-II trauma, and complex PTSD, have entered our professional lexicon as a means of communicating the wide-ranging consequences of developmental trauma. On the one hand, the less defined and rigid nature of these terms permits mental health providers to develop a rich narrative of a patient’s background, encompassing the patient’s behavior, character, and symptoms. However, the absence of formal terminology also has its drawbacks: Courts and juries have grown accustomed to diagnoses, labels, and syndromes. Most forensic mental health providers who testify about developmental trauma in court can predict the question: “So doctor, you are saying that the individual’s presentation is not severe enough to be considered PTSD, am I correct?” Disorders justify treatment, can explain disability, and warrant empathy; concomitantly, “complex trauma” runs the risk of being considered an academic explanation for trauma victims’ lifelong problems, rather than a societal failure that merits care.

Recognizing the limitations of our current diagnoses, the forthcoming update to the International Classification of Diseases (ICD-11) will add a new category: complex PTSD. The ICD-11 will attempt to widen the concept of trauma to include “conditions of prolonged adversity, in the form of sustained, repeated, or multiple forms of traumatic exposure.” Trauma exposure examples include genocide campaigns, childhood sexual abuse, child soldiering, severe domestic violence, torture, or slavery. The ICD-11 also expands our understanding of the consequences of trauma to include “affective dysregulation,” “negative self-concept,” and “disturbances in relationships” as part of a concept called “disturbances in self-organization.” Those are important steps in acknowledging the consequences of different forms of trauma as well as noticing a richer array of damages from those incidents.⁴

While the World Health Organization’s latest iteration of the ICD takes an important step in widening the scope of our diagnostic tools, we are cognizant that our field’s obsessional search for diagnoses, labels, and nomenclature reinforces a detrimental focus on symptoms over stories. However, as forensic mental health providers, we also are keenly aware that a failure to adopt common definitions impedes forensic evaluations, patient advocacy, public policy, and most importantly, patient care.

In the end, we have trained society to understand pathology through narrow lenses, and therefore, in the face of tragic events such as family separations, we need the appropriate language to clearly define and communicate the experiences of our patients. So, despite the limitations of labels, let’s be encouraged by the World Health Organization’s efforts and continue in that direction.

 Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Lehman is a licensed clinical and forensic psychologist in San Diego. Her practice consists of conducting forensic psychological evaluations for the courts with children, adolescents, and adults. Dr. Lehman has been qualified as an expert witness in California as well as in the federal courts. She previously was a supervisor at Sharper Future, a forensic rehabilitation program, and previously served as an adjunct faculty member at Alliant International University, San Diego. Dr. Lehman can be reached at [email protected].

References

1. Am J Psychiatry. 2000 Sep;157(9):1501-4.

2. Psychiatr Ann. 2005;35(5):390-8.

3. Psychiatr Ann. 2005;35(5):401-8.

4. Eur J Psychotraumatol. 2018 Jan 15. doi: 10.1080/20008198.2017.1418103.

The horrors faced by migrant families forced to separate under the new U.S. “zero tolerance” policy continue to unfold. Tragic emblems of this policy include tapes of crying children and the reported suicide of a father who had been separated from his children.

A federal judge had issued an injunction requiring the reunification of thousands of families by July 26. Despite that deadline, hundreds of adults are no longer in the United States, and hundreds of children are scattered in shelters across the country.

In response to those events, mental health and medical organizations have released powerful statements. The American Psychological Association stated: “The administration’s policy ... is not only needless and cruel, it threatens the mental and physical health of both the children and their caregivers.” The American Medical Association issued a call asserting that separating children from their parents “will do great harm” and “create negative health impacts that will last an individual’s entire lifespan.” Meanwhile, the American Psychiatric Association’s president, Altha J. Stewart, MD, released a statement affirming that “any forced separation is highly stressful for children and can cause lifelong trauma, as well as an increased risk of other mental illnesses, such as depression, anxiety, and posttraumatic stress disorder.”

As forensic experts who testify about the mental well-being of immigration detainees, we applaud those powerful and unambiguous messages from the leaders in our fields. Yet, their statements also underscore the limitations of our diagnostic models: Our field is caught in the difficult position of either applying ill-fitting diagnostic labels or overpathologizing a normal reaction to horrific circumstances. While not applying diagnoses potentially minimizes the enormous psychological burden of separation, diagnosing depression or PTSD as catchalls for suffering incorrectly defines the experience of many survivors of ongoing trauma.

Currently, most providers, in trying to communicate the effects of ongoing trauma, rely on the diagnoses of depression or PTSD. Both of these diagnoses, however, are problematic. The diagnosis of major depressive disorder, for example, is useful in communicating a loss of hope, and the inability to enjoy pleasurable things. However, depression is an episodic illness, often part of a larger chronic disorder.¹ Depression often has a genetic-hereditary component. On the other hand, children suffering from childhood traumas often present lifelong and wide-ranging problems, which may be triggered by reminders but are not episodic. For example, children experiencing parental separation have difficulty forming attachments, which, in turn, leads to subsequent difficulty forming meaningful interpersonal relationships.

The diagnosis of PTSD is useful in communicating a myriad of possible symptoms, which may accompany the trauma. However, PTSD implies a traumatic event as described in criteria A of the DSM-5: “exposure to actual or threatened death, serious injury, or sexual violence.” As such, PTSD poorly encompasses the wide array of smaller yet repetitive traumas experienced by victims of ongoing trauma, such as those youth separated from their parents at the U.S. border. Furthermore, PTSD is a disorder with specific symptoms that, based on a vast body of research,^2,3 inadequately describes the multitude of interpersonal, psychological, and physical consequences associated with the type of trauma caused by family separations.

Our understanding of the long-term sequelae of childhood trauma has been greatly influenced by the adverse childhood experiences (ACE) study. The ACE study, one of the largest investigations ever conducted to assess associations between childhood maltreatment and later-life health and well-being, collected the life histories of more than 17,000 patients in a collaborative effort between the Centers for Disease Control and Prevention and Kaiser Permanente’s Health Appraisal Clinic.

The ACE study identified 10 forms of childhood trauma, including: abuse, neglect, abandonment, household dysfunction, and exposure to violence, that were strongly associated with negative psychological outcomes such as depression, suicide attempts, and engagement in high-risk behaviors, as well as significant medical consequences, including higher incidence of heart disease, diabetes, and stroke. Ultimately, having four or more ACEs was associated with early death.

In response to the emerging body of research on childhood trauma, various terms, including complex trauma, type-II trauma, and complex PTSD, have entered our professional lexicon as a means of communicating the wide-ranging consequences of developmental trauma. On the one hand, the less defined and rigid nature of these terms permits mental health providers to develop a rich narrative of a patient’s background, encompassing the patient’s behavior, character, and symptoms. However, the absence of formal terminology also has its drawbacks: Courts and juries have grown accustomed to diagnoses, labels, and syndromes. Most forensic mental health providers who testify about developmental trauma in court can predict the question: “So doctor, you are saying that the individual’s presentation is not severe enough to be considered PTSD, am I correct?” Disorders justify treatment, can explain disability, and warrant empathy; concomitantly, “complex trauma” runs the risk of being considered an academic explanation for trauma victims’ lifelong problems, rather than a societal failure that merits care.

Recognizing the limitations of our current diagnoses, the forthcoming update to the International Classification of Diseases (ICD-11) will add a new category: complex PTSD. The ICD-11 will attempt to widen the concept of trauma to include “conditions of prolonged adversity, in the form of sustained, repeated, or multiple forms of traumatic exposure.” Trauma exposure examples include genocide campaigns, childhood sexual abuse, child soldiering, severe domestic violence, torture, or slavery. The ICD-11 also expands our understanding of the consequences of trauma to include “affective dysregulation,” “negative self-concept,” and “disturbances in relationships” as part of a concept called “disturbances in self-organization.” Those are important steps in acknowledging the consequences of different forms of trauma as well as noticing a richer array of damages from those incidents.⁴

While the World Health Organization’s latest iteration of the ICD takes an important step in widening the scope of our diagnostic tools, we are cognizant that our field’s obsessional search for diagnoses, labels, and nomenclature reinforces a detrimental focus on symptoms over stories. However, as forensic mental health providers, we also are keenly aware that a failure to adopt common definitions impedes forensic evaluations, patient advocacy, public policy, and most importantly, patient care.

In the end, we have trained society to understand pathology through narrow lenses, and therefore, in the face of tragic events such as family separations, we need the appropriate language to clearly define and communicate the experiences of our patients. So, despite the limitations of labels, let’s be encouraged by the World Health Organization’s efforts and continue in that direction.

 Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Lehman is a licensed clinical and forensic psychologist in San Diego. Her practice consists of conducting forensic psychological evaluations for the courts with children, adolescents, and adults. Dr. Lehman has been qualified as an expert witness in California as well as in the federal courts. She previously was a supervisor at Sharper Future, a forensic rehabilitation program, and previously served as an adjunct faculty member at Alliant International University, San Diego. Dr. Lehman can be reached at [email protected].

References

1. Am J Psychiatry. 2000 Sep;157(9):1501-4.

2. Psychiatr Ann. 2005;35(5):390-8.

3. Psychiatr Ann. 2005;35(5):401-8.

4. Eur J Psychotraumatol. 2018 Jan 15. doi: 10.1080/20008198.2017.1418103.

The horrors faced by migrant families forced to separate under the new U.S. “zero tolerance” policy continue to unfold. Tragic emblems of this policy include tapes of crying children and the reported suicide of a father who had been separated from his children.

A federal judge had issued an injunction requiring the reunification of thousands of families by July 26. Despite that deadline, hundreds of adults are no longer in the United States, and hundreds of children are scattered in shelters across the country.

In response to those events, mental health and medical organizations have released powerful statements. The American Psychological Association stated: “The administration’s policy ... is not only needless and cruel, it threatens the mental and physical health of both the children and their caregivers.” The American Medical Association issued a call asserting that separating children from their parents “will do great harm” and “create negative health impacts that will last an individual’s entire lifespan.” Meanwhile, the American Psychiatric Association’s president, Altha J. Stewart, MD, released a statement affirming that “any forced separation is highly stressful for children and can cause lifelong trauma, as well as an increased risk of other mental illnesses, such as depression, anxiety, and posttraumatic stress disorder.”

As forensic experts who testify about the mental well-being of immigration detainees, we applaud those powerful and unambiguous messages from the leaders in our fields. Yet, their statements also underscore the limitations of our diagnostic models: Our field is caught in the difficult position of either applying ill-fitting diagnostic labels or overpathologizing a normal reaction to horrific circumstances. While not applying diagnoses potentially minimizes the enormous psychological burden of separation, diagnosing depression or PTSD as catchalls for suffering incorrectly defines the experience of many survivors of ongoing trauma.

Currently, most providers, in trying to communicate the effects of ongoing trauma, rely on the diagnoses of depression or PTSD. Both of these diagnoses, however, are problematic. The diagnosis of major depressive disorder, for example, is useful in communicating a loss of hope, and the inability to enjoy pleasurable things. However, depression is an episodic illness, often part of a larger chronic disorder.¹ Depression often has a genetic-hereditary component. On the other hand, children suffering from childhood traumas often present lifelong and wide-ranging problems, which may be triggered by reminders but are not episodic. For example, children experiencing parental separation have difficulty forming attachments, which, in turn, leads to subsequent difficulty forming meaningful interpersonal relationships.

The diagnosis of PTSD is useful in communicating a myriad of possible symptoms, which may accompany the trauma. However, PTSD implies a traumatic event as described in criteria A of the DSM-5: “exposure to actual or threatened death, serious injury, or sexual violence.” As such, PTSD poorly encompasses the wide array of smaller yet repetitive traumas experienced by victims of ongoing trauma, such as those youth separated from their parents at the U.S. border. Furthermore, PTSD is a disorder with specific symptoms that, based on a vast body of research,^2,3 inadequately describes the multitude of interpersonal, psychological, and physical consequences associated with the type of trauma caused by family separations.

Our understanding of the long-term sequelae of childhood trauma has been greatly influenced by the adverse childhood experiences (ACE) study. The ACE study, one of the largest investigations ever conducted to assess associations between childhood maltreatment and later-life health and well-being, collected the life histories of more than 17,000 patients in a collaborative effort between the Centers for Disease Control and Prevention and Kaiser Permanente’s Health Appraisal Clinic.

The ACE study identified 10 forms of childhood trauma, including: abuse, neglect, abandonment, household dysfunction, and exposure to violence, that were strongly associated with negative psychological outcomes such as depression, suicide attempts, and engagement in high-risk behaviors, as well as significant medical consequences, including higher incidence of heart disease, diabetes, and stroke. Ultimately, having four or more ACEs was associated with early death.

In response to the emerging body of research on childhood trauma, various terms, including complex trauma, type-II trauma, and complex PTSD, have entered our professional lexicon as a means of communicating the wide-ranging consequences of developmental trauma. On the one hand, the less defined and rigid nature of these terms permits mental health providers to develop a rich narrative of a patient’s background, encompassing the patient’s behavior, character, and symptoms. However, the absence of formal terminology also has its drawbacks: Courts and juries have grown accustomed to diagnoses, labels, and syndromes. Most forensic mental health providers who testify about developmental trauma in court can predict the question: “So doctor, you are saying that the individual’s presentation is not severe enough to be considered PTSD, am I correct?” Disorders justify treatment, can explain disability, and warrant empathy; concomitantly, “complex trauma” runs the risk of being considered an academic explanation for trauma victims’ lifelong problems, rather than a societal failure that merits care.

Recognizing the limitations of our current diagnoses, the forthcoming update to the International Classification of Diseases (ICD-11) will add a new category: complex PTSD. The ICD-11 will attempt to widen the concept of trauma to include “conditions of prolonged adversity, in the form of sustained, repeated, or multiple forms of traumatic exposure.” Trauma exposure examples include genocide campaigns, childhood sexual abuse, child soldiering, severe domestic violence, torture, or slavery. The ICD-11 also expands our understanding of the consequences of trauma to include “affective dysregulation,” “negative self-concept,” and “disturbances in relationships” as part of a concept called “disturbances in self-organization.” Those are important steps in acknowledging the consequences of different forms of trauma as well as noticing a richer array of damages from those incidents.⁴

While the World Health Organization’s latest iteration of the ICD takes an important step in widening the scope of our diagnostic tools, we are cognizant that our field’s obsessional search for diagnoses, labels, and nomenclature reinforces a detrimental focus on symptoms over stories. However, as forensic mental health providers, we also are keenly aware that a failure to adopt common definitions impedes forensic evaluations, patient advocacy, public policy, and most importantly, patient care.

In the end, we have trained society to understand pathology through narrow lenses, and therefore, in the face of tragic events such as family separations, we need the appropriate language to clearly define and communicate the experiences of our patients. So, despite the limitations of labels, let’s be encouraged by the World Health Organization’s efforts and continue in that direction.

 Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Lehman is a licensed clinical and forensic psychologist in San Diego. Her practice consists of conducting forensic psychological evaluations for the courts with children, adolescents, and adults. Dr. Lehman has been qualified as an expert witness in California as well as in the federal courts. She previously was a supervisor at Sharper Future, a forensic rehabilitation program, and previously served as an adjunct faculty member at Alliant International University, San Diego. Dr. Lehman can be reached at [email protected].

References

1. Am J Psychiatry. 2000 Sep;157(9):1501-4.

2. Psychiatr Ann. 2005;35(5):390-8.

3. Psychiatr Ann. 2005;35(5):401-8.

4. Eur J Psychotraumatol. 2018 Jan 15. doi: 10.1080/20008198.2017.1418103.

By 2025, it is estimated that the annual cost of treating osteoporosis-related fractures in the United States will be 25 billion dollars, which is 10 billion dollars more than was spent in 2010.¹ As healthcare costs in the United States continue to skyrocket, it is imperative that orthopedic surgeons take an active role in avoiding preventable injury and disease. For orthopedic surgeons, preventative medicine will include promoting bone health and educating patients on injury prevention. By incorporating these principles into residency and fellowship education, and by leveraging the electronic medical record to support preventive care through systematic reminders, orthopedic surgeons have a critical opportunity to take a leading role in promoting prevention to our patients.

In 2009, the American Orthopaedic Association (AOA) launched a “Own the Bone” campaign, a national quality improvement program designed to optimize the treatment of osteoporosis.² This program came about following the Surgeon General’s call, in 2004, for orthopedic surgeons to take a more active role in treating osteoporosis. The program primarily aims to improve treatment of osteoporosis after a fragility fracture in an inpatient setting. Early results from a 2010 follow-up study showed that the new emphasis on prevention inspired by this program is effective. As compared with patients who had osteoporosis work-up and treatment initiated during their hospital admission, the group of patients who were referred for osteoporosis treatment after discharge were found to have a significantly lower rate of diagnosis and treatment.³ The loss of aftercare for patients who do not obtain immediate diagnosis and treatment for osteoporosis can and should be avoided. Many hospitals now have hip fracture services with multidisciplinary input. The successful outcomes of these programs include shorter times to the operating room, shorter hospital stays, decreased readmission, and decreased 30-day mortality.^4-6 These services provide an excellent opportunity to ensure that each patient has initiated management of osteoporosis before discharge. Ideally, patients would be scheduled for bone mineral density testing prior to leaving the hospital, when applicable, and would begin calcium and vitamin D supplementation or bisphosphonate treatment in the hospital, when appropriate. As part of these hip fracture services, a goal of clearly initiating or managing treatment for osteoporosis should be routinely addressed.

While patients presenting with hip fractures are an easily identifiable high-risk population, other patients present in an outpatient setting following fragility fractures, such as distal radius or vertebral compression fractures. These patients should be considered for osteoporosis work-up and counseled accordingly. A recent study compared the efficacy of the orthopedic surgeon initiating bone mineral density testing after a distal radius fracture, compared with referring the patient back to their primary care physician for testing. The study found a significantly higher rate of patients going on to bone mineral density testing when the surgeon initiated this process.⁷ In the era of improved digital communication, the outpatient setting offers an opportunity for clinicians to communicate with patients’ primary care physicians and initiate a multidisciplinary approach to bone health and prevention. In the outpatient setting, the orthopedist can address nutritional issues and screening on a repeated basis. Studies have demonstrated that physician counseling can be very effective in changing behavior and helping patients to stop using tobacco.⁸ In this vein, efforts by the physician to encourage calcium and vitamin D intake and weight-bearing exercise have the potential to be very effective.

Programs such as “Own the Bone” are crucial to orthopedists’ treatment of osteoporosis, but prevention of bone disease and fragility fracture must extend even further. Individual practitioners must be cognizant that many patients may benefit from outpatient diagnosis of osteoporosis and initiation of appropriate treatment, before fragility fractures occur. Moreover, although patients at high risk include post-menopausal women, orthopedists need to be consistently aware of osteoporosis as a disease of both genders. An estimated 2.8 million men in the United States have osteoporosis.⁹ A 2012 study published out of Washington, DC found a significant disparity in the rate of osteoporosis screening between men and women. Among the elderly men and women in their patient population, 60% of women underwent screening compared with only 18.4% of men.¹⁰ This gender disparity potentially represents significant physician bias regarding the risk of osteoporosis and offers an important opportunity for orthopedic surgeons to improve preventative care for this population.

Preventative care in terms of advocating for bone health should not be limited to patients presenting with fragility fractures. Education regarding smoking cessation, resistance exercise, and calcium intake are relevant to many orthopedic patients. With the advent of the electronic medical record system, a simple intervention could easily ensure that patients report on their calcium intake. A trial published in 2006 found that a simple reminder from the electronic medical record improved osteoporosis management following a fragility fracture.¹¹ This type of intervention could certainly be expanded to include counseling on calcium and vitamin D for any orthopedic patient.

Another area in which orthopedic surgeons have an opportunity to practice good preventative care is injury prevention. Several studies examining fall prevention among the elderly have shown that physical therapy or exercise may decrease the rate of falls.¹² Promotion of activity and therapy among high-risk patients by orthopedic surgeons may help to reduce fracture incidence. Injury prevention is also relevant to young, healthy patients. It is well established that neuromuscular training helps to prevent anterior cruciate ligament injuries.¹³ Orthopedic surgeons have an opportunity during sports physicals or as team physicians to help promote injury prevention strategies. Discussion of training regimens may prevent overuse injuries among athletes. Moreover, faced with many patients who present with significant musculoskeletal trauma, orthopedic surgeons have the opportunity to offer education regarding motorcycle helmets, seatbelt use, and avoidance of drunk driving.

New orthopedic residency educational goals were recently published to include core competencies in resident education. Among these goals is to educate residents on care of a patient with hip fracture, including counseling and management of osteoporosis.¹⁴ These milestones could be expanded to include a thorough understanding of bone health. Residents should be able to make nutritional recommendations for any patient seen as an inpatient or outpatient, identify when a referral to an endocrinologist is needed, and educate patients regarding injury and fall prevention.

As healthcare expenditures rise, so does the impetus for physicians to work to improve efficiency in the healthcare system. Furthermore, the best possible care for our patients is to prevent injury and disability before it arises, rather than to depend on our ability to intervene after the fact. Residencies and training programs should work to incorporate preventative strategies into trainee education. Hospitals and outpatient settings should include a basic bone health questionnaire in the electronic medical record. The identification and management of risk factors for injury has the potential to help our patients and to help our healthcare system, but such intervention needs to start with the clinician.

By 2025, it is estimated that the annual cost of treating osteoporosis-related fractures in the United States will be 25 billion dollars, which is 10 billion dollars more than was spent in 2010.¹ As healthcare costs in the United States continue to skyrocket, it is imperative that orthopedic surgeons take an active role in avoiding preventable injury and disease. For orthopedic surgeons, preventative medicine will include promoting bone health and educating patients on injury prevention. By incorporating these principles into residency and fellowship education, and by leveraging the electronic medical record to support preventive care through systematic reminders, orthopedic surgeons have a critical opportunity to take a leading role in promoting prevention to our patients.

In 2009, the American Orthopaedic Association (AOA) launched a “Own the Bone” campaign, a national quality improvement program designed to optimize the treatment of osteoporosis.² This program came about following the Surgeon General’s call, in 2004, for orthopedic surgeons to take a more active role in treating osteoporosis. The program primarily aims to improve treatment of osteoporosis after a fragility fracture in an inpatient setting. Early results from a 2010 follow-up study showed that the new emphasis on prevention inspired by this program is effective. As compared with patients who had osteoporosis work-up and treatment initiated during their hospital admission, the group of patients who were referred for osteoporosis treatment after discharge were found to have a significantly lower rate of diagnosis and treatment.³ The loss of aftercare for patients who do not obtain immediate diagnosis and treatment for osteoporosis can and should be avoided. Many hospitals now have hip fracture services with multidisciplinary input. The successful outcomes of these programs include shorter times to the operating room, shorter hospital stays, decreased readmission, and decreased 30-day mortality.^4-6 These services provide an excellent opportunity to ensure that each patient has initiated management of osteoporosis before discharge. Ideally, patients would be scheduled for bone mineral density testing prior to leaving the hospital, when applicable, and would begin calcium and vitamin D supplementation or bisphosphonate treatment in the hospital, when appropriate. As part of these hip fracture services, a goal of clearly initiating or managing treatment for osteoporosis should be routinely addressed.

While patients presenting with hip fractures are an easily identifiable high-risk population, other patients present in an outpatient setting following fragility fractures, such as distal radius or vertebral compression fractures. These patients should be considered for osteoporosis work-up and counseled accordingly. A recent study compared the efficacy of the orthopedic surgeon initiating bone mineral density testing after a distal radius fracture, compared with referring the patient back to their primary care physician for testing. The study found a significantly higher rate of patients going on to bone mineral density testing when the surgeon initiated this process.⁷ In the era of improved digital communication, the outpatient setting offers an opportunity for clinicians to communicate with patients’ primary care physicians and initiate a multidisciplinary approach to bone health and prevention. In the outpatient setting, the orthopedist can address nutritional issues and screening on a repeated basis. Studies have demonstrated that physician counseling can be very effective in changing behavior and helping patients to stop using tobacco.⁸ In this vein, efforts by the physician to encourage calcium and vitamin D intake and weight-bearing exercise have the potential to be very effective.

Programs such as “Own the Bone” are crucial to orthopedists’ treatment of osteoporosis, but prevention of bone disease and fragility fracture must extend even further. Individual practitioners must be cognizant that many patients may benefit from outpatient diagnosis of osteoporosis and initiation of appropriate treatment, before fragility fractures occur. Moreover, although patients at high risk include post-menopausal women, orthopedists need to be consistently aware of osteoporosis as a disease of both genders. An estimated 2.8 million men in the United States have osteoporosis.⁹ A 2012 study published out of Washington, DC found a significant disparity in the rate of osteoporosis screening between men and women. Among the elderly men and women in their patient population, 60% of women underwent screening compared with only 18.4% of men.¹⁰ This gender disparity potentially represents significant physician bias regarding the risk of osteoporosis and offers an important opportunity for orthopedic surgeons to improve preventative care for this population.

Preventative care in terms of advocating for bone health should not be limited to patients presenting with fragility fractures. Education regarding smoking cessation, resistance exercise, and calcium intake are relevant to many orthopedic patients. With the advent of the electronic medical record system, a simple intervention could easily ensure that patients report on their calcium intake. A trial published in 2006 found that a simple reminder from the electronic medical record improved osteoporosis management following a fragility fracture.¹¹ This type of intervention could certainly be expanded to include counseling on calcium and vitamin D for any orthopedic patient.

Another area in which orthopedic surgeons have an opportunity to practice good preventative care is injury prevention. Several studies examining fall prevention among the elderly have shown that physical therapy or exercise may decrease the rate of falls.¹² Promotion of activity and therapy among high-risk patients by orthopedic surgeons may help to reduce fracture incidence. Injury prevention is also relevant to young, healthy patients. It is well established that neuromuscular training helps to prevent anterior cruciate ligament injuries.¹³ Orthopedic surgeons have an opportunity during sports physicals or as team physicians to help promote injury prevention strategies. Discussion of training regimens may prevent overuse injuries among athletes. Moreover, faced with many patients who present with significant musculoskeletal trauma, orthopedic surgeons have the opportunity to offer education regarding motorcycle helmets, seatbelt use, and avoidance of drunk driving.

New orthopedic residency educational goals were recently published to include core competencies in resident education. Among these goals is to educate residents on care of a patient with hip fracture, including counseling and management of osteoporosis.¹⁴ These milestones could be expanded to include a thorough understanding of bone health. Residents should be able to make nutritional recommendations for any patient seen as an inpatient or outpatient, identify when a referral to an endocrinologist is needed, and educate patients regarding injury and fall prevention.

As healthcare expenditures rise, so does the impetus for physicians to work to improve efficiency in the healthcare system. Furthermore, the best possible care for our patients is to prevent injury and disability before it arises, rather than to depend on our ability to intervene after the fact. Residencies and training programs should work to incorporate preventative strategies into trainee education. Hospitals and outpatient settings should include a basic bone health questionnaire in the electronic medical record. The identification and management of risk factors for injury has the potential to help our patients and to help our healthcare system, but such intervention needs to start with the clinician.

By 2025, it is estimated that the annual cost of treating osteoporosis-related fractures in the United States will be 25 billion dollars, which is 10 billion dollars more than was spent in 2010.¹ As healthcare costs in the United States continue to skyrocket, it is imperative that orthopedic surgeons take an active role in avoiding preventable injury and disease. For orthopedic surgeons, preventative medicine will include promoting bone health and educating patients on injury prevention. By incorporating these principles into residency and fellowship education, and by leveraging the electronic medical record to support preventive care through systematic reminders, orthopedic surgeons have a critical opportunity to take a leading role in promoting prevention to our patients.

In 2009, the American Orthopaedic Association (AOA) launched a “Own the Bone” campaign, a national quality improvement program designed to optimize the treatment of osteoporosis.² This program came about following the Surgeon General’s call, in 2004, for orthopedic surgeons to take a more active role in treating osteoporosis. The program primarily aims to improve treatment of osteoporosis after a fragility fracture in an inpatient setting. Early results from a 2010 follow-up study showed that the new emphasis on prevention inspired by this program is effective. As compared with patients who had osteoporosis work-up and treatment initiated during their hospital admission, the group of patients who were referred for osteoporosis treatment after discharge were found to have a significantly lower rate of diagnosis and treatment.³ The loss of aftercare for patients who do not obtain immediate diagnosis and treatment for osteoporosis can and should be avoided. Many hospitals now have hip fracture services with multidisciplinary input. The successful outcomes of these programs include shorter times to the operating room, shorter hospital stays, decreased readmission, and decreased 30-day mortality.^4-6 These services provide an excellent opportunity to ensure that each patient has initiated management of osteoporosis before discharge. Ideally, patients would be scheduled for bone mineral density testing prior to leaving the hospital, when applicable, and would begin calcium and vitamin D supplementation or bisphosphonate treatment in the hospital, when appropriate. As part of these hip fracture services, a goal of clearly initiating or managing treatment for osteoporosis should be routinely addressed.

While patients presenting with hip fractures are an easily identifiable high-risk population, other patients present in an outpatient setting following fragility fractures, such as distal radius or vertebral compression fractures. These patients should be considered for osteoporosis work-up and counseled accordingly. A recent study compared the efficacy of the orthopedic surgeon initiating bone mineral density testing after a distal radius fracture, compared with referring the patient back to their primary care physician for testing. The study found a significantly higher rate of patients going on to bone mineral density testing when the surgeon initiated this process.⁷ In the era of improved digital communication, the outpatient setting offers an opportunity for clinicians to communicate with patients’ primary care physicians and initiate a multidisciplinary approach to bone health and prevention. In the outpatient setting, the orthopedist can address nutritional issues and screening on a repeated basis. Studies have demonstrated that physician counseling can be very effective in changing behavior and helping patients to stop using tobacco.⁸ In this vein, efforts by the physician to encourage calcium and vitamin D intake and weight-bearing exercise have the potential to be very effective.

Programs such as “Own the Bone” are crucial to orthopedists’ treatment of osteoporosis, but prevention of bone disease and fragility fracture must extend even further. Individual practitioners must be cognizant that many patients may benefit from outpatient diagnosis of osteoporosis and initiation of appropriate treatment, before fragility fractures occur. Moreover, although patients at high risk include post-menopausal women, orthopedists need to be consistently aware of osteoporosis as a disease of both genders. An estimated 2.8 million men in the United States have osteoporosis.⁹ A 2012 study published out of Washington, DC found a significant disparity in the rate of osteoporosis screening between men and women. Among the elderly men and women in their patient population, 60% of women underwent screening compared with only 18.4% of men.¹⁰ This gender disparity potentially represents significant physician bias regarding the risk of osteoporosis and offers an important opportunity for orthopedic surgeons to improve preventative care for this population.

Preventative care in terms of advocating for bone health should not be limited to patients presenting with fragility fractures. Education regarding smoking cessation, resistance exercise, and calcium intake are relevant to many orthopedic patients. With the advent of the electronic medical record system, a simple intervention could easily ensure that patients report on their calcium intake. A trial published in 2006 found that a simple reminder from the electronic medical record improved osteoporosis management following a fragility fracture.¹¹ This type of intervention could certainly be expanded to include counseling on calcium and vitamin D for any orthopedic patient.

Another area in which orthopedic surgeons have an opportunity to practice good preventative care is injury prevention. Several studies examining fall prevention among the elderly have shown that physical therapy or exercise may decrease the rate of falls.¹² Promotion of activity and therapy among high-risk patients by orthopedic surgeons may help to reduce fracture incidence. Injury prevention is also relevant to young, healthy patients. It is well established that neuromuscular training helps to prevent anterior cruciate ligament injuries.¹³ Orthopedic surgeons have an opportunity during sports physicals or as team physicians to help promote injury prevention strategies. Discussion of training regimens may prevent overuse injuries among athletes. Moreover, faced with many patients who present with significant musculoskeletal trauma, orthopedic surgeons have the opportunity to offer education regarding motorcycle helmets, seatbelt use, and avoidance of drunk driving.

New orthopedic residency educational goals were recently published to include core competencies in resident education. Among these goals is to educate residents on care of a patient with hip fracture, including counseling and management of osteoporosis.¹⁴ These milestones could be expanded to include a thorough understanding of bone health. Residents should be able to make nutritional recommendations for any patient seen as an inpatient or outpatient, identify when a referral to an endocrinologist is needed, and educate patients regarding injury and fall prevention.

As healthcare expenditures rise, so does the impetus for physicians to work to improve efficiency in the healthcare system. Furthermore, the best possible care for our patients is to prevent injury and disability before it arises, rather than to depend on our ability to intervene after the fact. Residencies and training programs should work to incorporate preventative strategies into trainee education. Hospitals and outpatient settings should include a basic bone health questionnaire in the electronic medical record. The identification and management of risk factors for injury has the potential to help our patients and to help our healthcare system, but such intervention needs to start with the clinician.

Benzodiazepines’ potential antidepressant properties and their role in the treatment of depression were fairly extensively examined during the 1980s and early 1990s. There were various reasons for this investigation—from the adverse effects of available antidepressants (tricyclic antidepressants [TCAs] and monoamine oxidase inhibitors) to the delay of action of the existing antidepressants and treatment resistance of a significant portion of depressed patients. Benzodiazepines had already been used in the treatment of depressive disorders for decades, but not as monotherapy or main treatment agents, but rather in combination with existing antidepressants to alleviate initial or persistent anxiety, and to help with insomnia. Some authors¹ felt that specific benzodiazepines, such as alprazolam, were effective in mild and moderate depression, although not as effective as TCAs for patients with endogenous or melancholic depression. Others² proposed that benzodiazepines, particularly alprazolam, may be a useful treatment option for patients for whom antidepressants are contraindicated, poorly tolerated, or ineffective. Petty et al² suggested that the antidepressant efficacy of benzodiazepines was consistent with the then-entertained γ-aminobutyric acid theory of depression.

A shift from benzodiazepines to antidepressants

The evidence for using benzodiazepines in anxious depression was based on results of several studies, but it has not been adequately analyzed, summarized, and promoted. Then, after the arrival of the selective serotonin reuptake inhibitors (SSRIs) (fluoxetine arrived in the United States in 1987, and paroxetine and sertraline arrived in 1992), interest in benzodiazepines gradually waned. Within a few years, the SSRIs were also approved for various anxiety disorders. The SSRIs were heavily promoted not only for the treatment of depressive disorders, but also anxiety disorders, and were touted as well-tolerated medications without abuse potential. Benzodiazepines, on the other hand, were frequently described as less effective and having a substantial abuse potential.

Looking back, these claims were not properly substantiated. Berney et al³ concluded in a systematic review that comparative data of a high level of proof for using newer antidepressants in anxiety disorders rather that benzodiazepines were not available. Then, 5 years later, Offidani et al⁴ demonstrated in a systematic review and meta-analysis that benzodiazepines were more effective and better tolerated in the treatment of various anxiety disorders than TCAs. In addition, in a few studies comparing benzodiazepines with newer antidepressants such as paroxetine and venlafaxine, benzodiazepines were either comparable or showed greater improvement and fewer adverse effects that these antidepressants. Similarly to Berney et al,³ Offidani et al⁴ concluded that the change in the prescribing pattern favoring newer antidepressants over benzodiazepines for the treatment of anxiety disorders occurred without supporting evidence.

As far as abuse potential, the American Psychiatric Association Task Force on Benzodiazepine Dependency concluded that benzodiazepines do not strongly reinforce their own use and are not widely abused.⁵ When abuse occurs, it is almost always in the context of abusing other substances. The Task Force also noted that physiological dependence develops when benzodiazepines are used chronically; dependence being defined mostly in terms of symptoms of discontinuance.⁵ Thus, benzodiazepines need to be used appropriately, not in extremely high doses, and under medical supervision.

Nevertheless, the judgment, right or wrong, was out—benzodiazepines were deemed problematic and to be avoided. This has become, unfortunately, a pattern of many prescribing psychiatrists’ practice.

What about benzodiazepines for anxious depression?

Recently Benasi et al⁶ filled the void by investigating data from studies using benzodiazepines as monotherapy in depressive disorders (I was one of the co-authors of this study). They conducted a systematic review of 38 published randomized controlled trials that used benzodiazepines as a monotherapy vs placebo, antidepressants, or both. Patients in these trials were primarily diagnosed with depressive disorder or anxious depression. The majority of these studies used alprazolam as the benzodiazepine (other benzodiazepines used were adinazolam, bromazepam, chlordiazepoxide, and lorazepam) and imipramine or amitriptyline as the antidepressant comparator (other antidepressants used were desipramine, dothiepin, doxepin, and only one newer antidepressant, fluvoxamine, in one study). There was a lack of significant differences in response rate between benzodiazepines and placebo, and between benzodiazepines and TCAs.

In more than half of the studies comparing benzodiazepines with TCAs and/or placebo, benzodiazepines were significantly more effective than placebo and as effective as TCAs. In 11 studies, TCAs were better than benzodiazepines, while benzodiazepines were better than TCAs in one study. In 12 studies, benzodiazepines were associated with a faster onset of action than TCAs. Adverse effects occurred more frequently with TCAs, with the exception of drowsiness and cognitive impairment, which occurred more frequently with benzodiazepines. The findings of the meta-analysis (22 studies) confirmed the low response of anxious depression to psychotropic medications, whether TCAs or benzodiazepines. There was no demonstrated superiority of antidepressants over benzodiazepines for anxious depression. Thus, clearly, benzodiazepines are a bona fide therapeutic option for anxious depression and so far, there is no indication that antidepressants are preferable for this indication.

Continue to: However, it is important to note...

However, it is important to note that there are almost no studies comparing benzodiazepines to newer antidepressants for anxious depression. One double-blind 6-week study of 112 patients⁷ compared fluvoxamine with lorazepam for mixed anxiety and depression in general practice. There were no significant differences between treatments at any point in the study. Lorazepam produced more sedation, while fluvoxamine produced more nausea and vomiting.

We clearly need randomized controlled trials comparing benzodiazepines with newer antidepressants in anxious depression. However, as in the case with anxiety disorders, these types of trials are strikingly missing.

Any clinical wisdom?

Anxiety could be a serious clinical problem in the treatment of patients with depressive disorder(s). We have not always paid enough attention to anxiety and related issues in depressed patients. Interestingly, anxiety has not been listed among symptoms of major depression disorder (MDD) in several editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM). Only and finally did DSM-5⁸ add a specifier “with anxious distress” for both MDD and persistent depressive disorder (dysthymia), although this specifier still avoids the word “anxiety” in the description of its symptomatology.

It is difficult to disentangle whether the anxiety is part of depressive disorder symptomatology or whether it is a comorbid anxiety disorder. As I noted in a previous article,⁹ psychiatric comorbidity is a confusing phenomenon. Nevertheless, anxiety and depression are highly comorbid or co-symptomatologic. In a study by Kessler et al,¹⁰ 45.7% of survey responders with lifetime MDD had ≥1 lifetime anxiety disorder. Similarly, in a STAR*D study,¹¹ in Level 1, 53.2% of patients had anxious depression.

Kessler et al¹⁰ raised an interesting question about the importance of temporally primary anxiety disorders as risk markers vs causal risk factors for the onset and persistence of subsequent MDD, including the possibility that anxiety disorders might primarily be risk markers for MDD onset and causal risk factors for MDD persistence. As is well-known, mood disorders should be treated as soon as possible after they are diagnosed, and should be treated vigorously, addressing the major symptomatology.

Continue to: These findings emphasize the need to...

These findings emphasize the need to pay more attention to anxiety in depressed patients (especially those newly diagnosed) and for forceful treatment of anxious depression. Importantly, in the STAR*D study,¹¹ remission in anxious Level 1 (treated with citalopram) depressed patients was significantly less likely and took longer to occur than in patients with nonanxious depression. In addition, ratings of adverse effects frequency, intensity, and burden, as well as the number of serious adverse events, were significantly greater in the anxious depression group. Similarly, in Level 2 (either switched to bupropion, sertraline or venlafaxine, or citalopram augmented with bupropion or buspirone), patients with anxious depression fared significantly worse in both the switching and augmentation options. One wonders if Level 1 patients treated with benzodiazepines, and Level 2 patients switched to benzodiazepines or offered augmentation with them would not have fared better, especially in view of the fact that many old and new antidepressants have significant adverse effects and are difficult to discontinue due to withdrawal symptoms such as dizziness, vertigo, and, in case of newer antidepressants, brain “zaps.” Benzodiazepines certainly have serious withdrawal symptoms, including anxiety, rebound insomnia, and withdrawal seizures, especially when discontinued abruptly and when the dose was high. Thus, as is the case for many other medications (eg, steroids, anticoagulants, and some antidepressants), benzodiazepines must be tapered carefully in order to avoid discontinuance signs and symptoms. Because benzodiazepines have been involved in nearly one-third of overdose-related deaths (either separately or in combination with opioids), and the FDA strongly warns against co-prescribing benzodiazepines and opioids, they need to be prescribed appropriately, carefully weighing their risks and benefits.¹²

Because the analysis by Benasi et al⁶ demonstrated that benzodiazepines seem comparably effective as antidepressants in anxious depression, we should be considering using benzodiazepines as monotherapy for this indication more frequently and vigorously, considering their similar efficacy, faster onset of action, and better tolerability, while also considering their risks. Clinicians use them in combinations anyway. We also need rigorous trials comparing benzodiazepines with newer antidepressants for anxious depression.

Benzodiazepines’ potential antidepressant properties and their role in the treatment of depression were fairly extensively examined during the 1980s and early 1990s. There were various reasons for this investigation—from the adverse effects of available antidepressants (tricyclic antidepressants [TCAs] and monoamine oxidase inhibitors) to the delay of action of the existing antidepressants and treatment resistance of a significant portion of depressed patients. Benzodiazepines had already been used in the treatment of depressive disorders for decades, but not as monotherapy or main treatment agents, but rather in combination with existing antidepressants to alleviate initial or persistent anxiety, and to help with insomnia. Some authors¹ felt that specific benzodiazepines, such as alprazolam, were effective in mild and moderate depression, although not as effective as TCAs for patients with endogenous or melancholic depression. Others² proposed that benzodiazepines, particularly alprazolam, may be a useful treatment option for patients for whom antidepressants are contraindicated, poorly tolerated, or ineffective. Petty et al² suggested that the antidepressant efficacy of benzodiazepines was consistent with the then-entertained γ-aminobutyric acid theory of depression.

A shift from benzodiazepines to antidepressants

The evidence for using benzodiazepines in anxious depression was based on results of several studies, but it has not been adequately analyzed, summarized, and promoted. Then, after the arrival of the selective serotonin reuptake inhibitors (SSRIs) (fluoxetine arrived in the United States in 1987, and paroxetine and sertraline arrived in 1992), interest in benzodiazepines gradually waned. Within a few years, the SSRIs were also approved for various anxiety disorders. The SSRIs were heavily promoted not only for the treatment of depressive disorders, but also anxiety disorders, and were touted as well-tolerated medications without abuse potential. Benzodiazepines, on the other hand, were frequently described as less effective and having a substantial abuse potential.

Looking back, these claims were not properly substantiated. Berney et al³ concluded in a systematic review that comparative data of a high level of proof for using newer antidepressants in anxiety disorders rather that benzodiazepines were not available. Then, 5 years later, Offidani et al⁴ demonstrated in a systematic review and meta-analysis that benzodiazepines were more effective and better tolerated in the treatment of various anxiety disorders than TCAs. In addition, in a few studies comparing benzodiazepines with newer antidepressants such as paroxetine and venlafaxine, benzodiazepines were either comparable or showed greater improvement and fewer adverse effects that these antidepressants. Similarly to Berney et al,³ Offidani et al⁴ concluded that the change in the prescribing pattern favoring newer antidepressants over benzodiazepines for the treatment of anxiety disorders occurred without supporting evidence.

As far as abuse potential, the American Psychiatric Association Task Force on Benzodiazepine Dependency concluded that benzodiazepines do not strongly reinforce their own use and are not widely abused.⁵ When abuse occurs, it is almost always in the context of abusing other substances. The Task Force also noted that physiological dependence develops when benzodiazepines are used chronically; dependence being defined mostly in terms of symptoms of discontinuance.⁵ Thus, benzodiazepines need to be used appropriately, not in extremely high doses, and under medical supervision.

Nevertheless, the judgment, right or wrong, was out—benzodiazepines were deemed problematic and to be avoided. This has become, unfortunately, a pattern of many prescribing psychiatrists’ practice.

What about benzodiazepines for anxious depression?

Recently Benasi et al⁶ filled the void by investigating data from studies using benzodiazepines as monotherapy in depressive disorders (I was one of the co-authors of this study). They conducted a systematic review of 38 published randomized controlled trials that used benzodiazepines as a monotherapy vs placebo, antidepressants, or both. Patients in these trials were primarily diagnosed with depressive disorder or anxious depression. The majority of these studies used alprazolam as the benzodiazepine (other benzodiazepines used were adinazolam, bromazepam, chlordiazepoxide, and lorazepam) and imipramine or amitriptyline as the antidepressant comparator (other antidepressants used were desipramine, dothiepin, doxepin, and only one newer antidepressant, fluvoxamine, in one study). There was a lack of significant differences in response rate between benzodiazepines and placebo, and between benzodiazepines and TCAs.

In more than half of the studies comparing benzodiazepines with TCAs and/or placebo, benzodiazepines were significantly more effective than placebo and as effective as TCAs. In 11 studies, TCAs were better than benzodiazepines, while benzodiazepines were better than TCAs in one study. In 12 studies, benzodiazepines were associated with a faster onset of action than TCAs. Adverse effects occurred more frequently with TCAs, with the exception of drowsiness and cognitive impairment, which occurred more frequently with benzodiazepines. The findings of the meta-analysis (22 studies) confirmed the low response of anxious depression to psychotropic medications, whether TCAs or benzodiazepines. There was no demonstrated superiority of antidepressants over benzodiazepines for anxious depression. Thus, clearly, benzodiazepines are a bona fide therapeutic option for anxious depression and so far, there is no indication that antidepressants are preferable for this indication.

Continue to: However, it is important to note...

However, it is important to note that there are almost no studies comparing benzodiazepines to newer antidepressants for anxious depression. One double-blind 6-week study of 112 patients⁷ compared fluvoxamine with lorazepam for mixed anxiety and depression in general practice. There were no significant differences between treatments at any point in the study. Lorazepam produced more sedation, while fluvoxamine produced more nausea and vomiting.

We clearly need randomized controlled trials comparing benzodiazepines with newer antidepressants in anxious depression. However, as in the case with anxiety disorders, these types of trials are strikingly missing.

Any clinical wisdom?

Anxiety could be a serious clinical problem in the treatment of patients with depressive disorder(s). We have not always paid enough attention to anxiety and related issues in depressed patients. Interestingly, anxiety has not been listed among symptoms of major depression disorder (MDD) in several editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM). Only and finally did DSM-5⁸ add a specifier “with anxious distress” for both MDD and persistent depressive disorder (dysthymia), although this specifier still avoids the word “anxiety” in the description of its symptomatology.

It is difficult to disentangle whether the anxiety is part of depressive disorder symptomatology or whether it is a comorbid anxiety disorder. As I noted in a previous article,⁹ psychiatric comorbidity is a confusing phenomenon. Nevertheless, anxiety and depression are highly comorbid or co-symptomatologic. In a study by Kessler et al,¹⁰ 45.7% of survey responders with lifetime MDD had ≥1 lifetime anxiety disorder. Similarly, in a STAR*D study,¹¹ in Level 1, 53.2% of patients had anxious depression.

Kessler et al¹⁰ raised an interesting question about the importance of temporally primary anxiety disorders as risk markers vs causal risk factors for the onset and persistence of subsequent MDD, including the possibility that anxiety disorders might primarily be risk markers for MDD onset and causal risk factors for MDD persistence. As is well-known, mood disorders should be treated as soon as possible after they are diagnosed, and should be treated vigorously, addressing the major symptomatology.

Continue to: These findings emphasize the need to...

These findings emphasize the need to pay more attention to anxiety in depressed patients (especially those newly diagnosed) and for forceful treatment of anxious depression. Importantly, in the STAR*D study,¹¹ remission in anxious Level 1 (treated with citalopram) depressed patients was significantly less likely and took longer to occur than in patients with nonanxious depression. In addition, ratings of adverse effects frequency, intensity, and burden, as well as the number of serious adverse events, were significantly greater in the anxious depression group. Similarly, in Level 2 (either switched to bupropion, sertraline or venlafaxine, or citalopram augmented with bupropion or buspirone), patients with anxious depression fared significantly worse in both the switching and augmentation options. One wonders if Level 1 patients treated with benzodiazepines, and Level 2 patients switched to benzodiazepines or offered augmentation with them would not have fared better, especially in view of the fact that many old and new antidepressants have significant adverse effects and are difficult to discontinue due to withdrawal symptoms such as dizziness, vertigo, and, in case of newer antidepressants, brain “zaps.” Benzodiazepines certainly have serious withdrawal symptoms, including anxiety, rebound insomnia, and withdrawal seizures, especially when discontinued abruptly and when the dose was high. Thus, as is the case for many other medications (eg, steroids, anticoagulants, and some antidepressants), benzodiazepines must be tapered carefully in order to avoid discontinuance signs and symptoms. Because benzodiazepines have been involved in nearly one-third of overdose-related deaths (either separately or in combination with opioids), and the FDA strongly warns against co-prescribing benzodiazepines and opioids, they need to be prescribed appropriately, carefully weighing their risks and benefits.¹²

Because the analysis by Benasi et al⁶ demonstrated that benzodiazepines seem comparably effective as antidepressants in anxious depression, we should be considering using benzodiazepines as monotherapy for this indication more frequently and vigorously, considering their similar efficacy, faster onset of action, and better tolerability, while also considering their risks. Clinicians use them in combinations anyway. We also need rigorous trials comparing benzodiazepines with newer antidepressants for anxious depression.

Benzodiazepines’ potential antidepressant properties and their role in the treatment of depression were fairly extensively examined during the 1980s and early 1990s. There were various reasons for this investigation—from the adverse effects of available antidepressants (tricyclic antidepressants [TCAs] and monoamine oxidase inhibitors) to the delay of action of the existing antidepressants and treatment resistance of a significant portion of depressed patients. Benzodiazepines had already been used in the treatment of depressive disorders for decades, but not as monotherapy or main treatment agents, but rather in combination with existing antidepressants to alleviate initial or persistent anxiety, and to help with insomnia. Some authors¹ felt that specific benzodiazepines, such as alprazolam, were effective in mild and moderate depression, although not as effective as TCAs for patients with endogenous or melancholic depression. Others² proposed that benzodiazepines, particularly alprazolam, may be a useful treatment option for patients for whom antidepressants are contraindicated, poorly tolerated, or ineffective. Petty et al² suggested that the antidepressant efficacy of benzodiazepines was consistent with the then-entertained γ-aminobutyric acid theory of depression.

A shift from benzodiazepines to antidepressants

The evidence for using benzodiazepines in anxious depression was based on results of several studies, but it has not been adequately analyzed, summarized, and promoted. Then, after the arrival of the selective serotonin reuptake inhibitors (SSRIs) (fluoxetine arrived in the United States in 1987, and paroxetine and sertraline arrived in 1992), interest in benzodiazepines gradually waned. Within a few years, the SSRIs were also approved for various anxiety disorders. The SSRIs were heavily promoted not only for the treatment of depressive disorders, but also anxiety disorders, and were touted as well-tolerated medications without abuse potential. Benzodiazepines, on the other hand, were frequently described as less effective and having a substantial abuse potential.

Looking back, these claims were not properly substantiated. Berney et al³ concluded in a systematic review that comparative data of a high level of proof for using newer antidepressants in anxiety disorders rather that benzodiazepines were not available. Then, 5 years later, Offidani et al⁴ demonstrated in a systematic review and meta-analysis that benzodiazepines were more effective and better tolerated in the treatment of various anxiety disorders than TCAs. In addition, in a few studies comparing benzodiazepines with newer antidepressants such as paroxetine and venlafaxine, benzodiazepines were either comparable or showed greater improvement and fewer adverse effects that these antidepressants. Similarly to Berney et al,³ Offidani et al⁴ concluded that the change in the prescribing pattern favoring newer antidepressants over benzodiazepines for the treatment of anxiety disorders occurred without supporting evidence.

As far as abuse potential, the American Psychiatric Association Task Force on Benzodiazepine Dependency concluded that benzodiazepines do not strongly reinforce their own use and are not widely abused.⁵ When abuse occurs, it is almost always in the context of abusing other substances. The Task Force also noted that physiological dependence develops when benzodiazepines are used chronically; dependence being defined mostly in terms of symptoms of discontinuance.⁵ Thus, benzodiazepines need to be used appropriately, not in extremely high doses, and under medical supervision.

Nevertheless, the judgment, right or wrong, was out—benzodiazepines were deemed problematic and to be avoided. This has become, unfortunately, a pattern of many prescribing psychiatrists’ practice.

What about benzodiazepines for anxious depression?

Recently Benasi et al⁶ filled the void by investigating data from studies using benzodiazepines as monotherapy in depressive disorders (I was one of the co-authors of this study). They conducted a systematic review of 38 published randomized controlled trials that used benzodiazepines as a monotherapy vs placebo, antidepressants, or both. Patients in these trials were primarily diagnosed with depressive disorder or anxious depression. The majority of these studies used alprazolam as the benzodiazepine (other benzodiazepines used were adinazolam, bromazepam, chlordiazepoxide, and lorazepam) and imipramine or amitriptyline as the antidepressant comparator (other antidepressants used were desipramine, dothiepin, doxepin, and only one newer antidepressant, fluvoxamine, in one study). There was a lack of significant differences in response rate between benzodiazepines and placebo, and between benzodiazepines and TCAs.

In more than half of the studies comparing benzodiazepines with TCAs and/or placebo, benzodiazepines were significantly more effective than placebo and as effective as TCAs. In 11 studies, TCAs were better than benzodiazepines, while benzodiazepines were better than TCAs in one study. In 12 studies, benzodiazepines were associated with a faster onset of action than TCAs. Adverse effects occurred more frequently with TCAs, with the exception of drowsiness and cognitive impairment, which occurred more frequently with benzodiazepines. The findings of the meta-analysis (22 studies) confirmed the low response of anxious depression to psychotropic medications, whether TCAs or benzodiazepines. There was no demonstrated superiority of antidepressants over benzodiazepines for anxious depression. Thus, clearly, benzodiazepines are a bona fide therapeutic option for anxious depression and so far, there is no indication that antidepressants are preferable for this indication.

Continue to: However, it is important to note...

However, it is important to note that there are almost no studies comparing benzodiazepines to newer antidepressants for anxious depression. One double-blind 6-week study of 112 patients⁷ compared fluvoxamine with lorazepam for mixed anxiety and depression in general practice. There were no significant differences between treatments at any point in the study. Lorazepam produced more sedation, while fluvoxamine produced more nausea and vomiting.

We clearly need randomized controlled trials comparing benzodiazepines with newer antidepressants in anxious depression. However, as in the case with anxiety disorders, these types of trials are strikingly missing.

Any clinical wisdom?

Anxiety could be a serious clinical problem in the treatment of patients with depressive disorder(s). We have not always paid enough attention to anxiety and related issues in depressed patients. Interestingly, anxiety has not been listed among symptoms of major depression disorder (MDD) in several editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM). Only and finally did DSM-5⁸ add a specifier “with anxious distress” for both MDD and persistent depressive disorder (dysthymia), although this specifier still avoids the word “anxiety” in the description of its symptomatology.

It is difficult to disentangle whether the anxiety is part of depressive disorder symptomatology or whether it is a comorbid anxiety disorder. As I noted in a previous article,⁹ psychiatric comorbidity is a confusing phenomenon. Nevertheless, anxiety and depression are highly comorbid or co-symptomatologic. In a study by Kessler et al,¹⁰ 45.7% of survey responders with lifetime MDD had ≥1 lifetime anxiety disorder. Similarly, in a STAR*D study,¹¹ in Level 1, 53.2% of patients had anxious depression.

Kessler et al¹⁰ raised an interesting question about the importance of temporally primary anxiety disorders as risk markers vs causal risk factors for the onset and persistence of subsequent MDD, including the possibility that anxiety disorders might primarily be risk markers for MDD onset and causal risk factors for MDD persistence. As is well-known, mood disorders should be treated as soon as possible after they are diagnosed, and should be treated vigorously, addressing the major symptomatology.

Continue to: These findings emphasize the need to...

These findings emphasize the need to pay more attention to anxiety in depressed patients (especially those newly diagnosed) and for forceful treatment of anxious depression. Importantly, in the STAR*D study,¹¹ remission in anxious Level 1 (treated with citalopram) depressed patients was significantly less likely and took longer to occur than in patients with nonanxious depression. In addition, ratings of adverse effects frequency, intensity, and burden, as well as the number of serious adverse events, were significantly greater in the anxious depression group. Similarly, in Level 2 (either switched to bupropion, sertraline or venlafaxine, or citalopram augmented with bupropion or buspirone), patients with anxious depression fared significantly worse in both the switching and augmentation options. One wonders if Level 1 patients treated with benzodiazepines, and Level 2 patients switched to benzodiazepines or offered augmentation with them would not have fared better, especially in view of the fact that many old and new antidepressants have significant adverse effects and are difficult to discontinue due to withdrawal symptoms such as dizziness, vertigo, and, in case of newer antidepressants, brain “zaps.” Benzodiazepines certainly have serious withdrawal symptoms, including anxiety, rebound insomnia, and withdrawal seizures, especially when discontinued abruptly and when the dose was high. Thus, as is the case for many other medications (eg, steroids, anticoagulants, and some antidepressants), benzodiazepines must be tapered carefully in order to avoid discontinuance signs and symptoms. Because benzodiazepines have been involved in nearly one-third of overdose-related deaths (either separately or in combination with opioids), and the FDA strongly warns against co-prescribing benzodiazepines and opioids, they need to be prescribed appropriately, carefully weighing their risks and benefits.¹²

Because the analysis by Benasi et al⁶ demonstrated that benzodiazepines seem comparably effective as antidepressants in anxious depression, we should be considering using benzodiazepines as monotherapy for this indication more frequently and vigorously, considering their similar efficacy, faster onset of action, and better tolerability, while also considering their risks. Clinicians use them in combinations anyway. We also need rigorous trials comparing benzodiazepines with newer antidepressants for anxious depression.

Pseudotumor cerebri, benign intracranial hypertension, and idiopathic intracranial hypertension are all terms to describe a syndrome of increased intracranial pressure, headaches, vision loss, or changes without an associated mass lesion.¹ The condition was considered relatively rare, presenting most commonly in obese women in childbearing years. Surprisingly, with the obesity rates increasing among children and adolescents, rates of pseudotumor cerebri also are rising sharply in these populations.²

Obesity is the fastest growing morbidity among adolescents. The Centers for Disease Control and Prevention reported 32% of children 2-19 years were obese.¹ This reality is impacting many areas of an adolescent’s health, but it also is changing the landscape of diseases that present in this age group. Although pediatric and adult pseudotumor cerebri always have had slightly varied features, many features were similar such as the papilledema, vision loss, headaches, and sixth nerve palsy. Obesity and female predominance tended to present more in the adult population, as many pediatric patients were not obese,² and had fewer associated symptoms at the time of diagnosis, and the cause was thought to idiopathic.

Now, with the increase in obesity, more adolescents and more male patients are presenting with pseudotumor cerebri as a cause for their headache, and 57%-100% are obese, making it a compounding factor.³

Pediatric populations also are at risk of secondary pseudotumor cerebri, which is an increase in intracranial pressure from the use of medication, or other disease states such as anemia, kidney disease, or Down syndrome. Minocycline use is the most common medication cause and usually presents 1-2 months after normal use.⁴ Discontinuing the drug does lead to resolution. Retinoids, vitamin A products, growth hormone, and steroids also have been implicated. Given that acne is a common complaint amongst teens, knowledge of these side effects is important.⁴

In 2013, the criteria for diagnosis of pseudotumor cerebri was revised. Currently, the presence of papilledema, normal neurologic exam except for abnormal sixth cranial nerve, normal cerebral spinal fluid, elevated lumbar opening pressure, and normal imaging are needed for a definitive diagnosis. A probable diagnosis can be made if papilledema is not present but there abducens nerve palsy.²

In a routine physical exam, when I questioned a patient on any medication that was used daily, she replied she took ibuprofen daily for headaches and that she had been doing this for several months. Headaches were not in her chief complaints as she had learned to live with and ignore this symptom. Upon further evaluation, she was slightly overweight and has a questionable fundoscopic exam. After further evaluation by an ophthalmologist and a neurologist, pseudotumor cerebri was diagnosed.

Index of suspicion is key in correctly diagnosing patients, and understanding the changing landscape of medicine will lead to more thoughtful questioning during routine health exams and better outcomes for your patients.
 

Dr. Pearce is a pediatrician in Frankfort, Ill. She said she had no relevant financial disclosures. Email her at [email protected].

References

1. Am J Ophthalmol. 2015 Feb;159(2):344-52.e1.

2. Horm Res Paediatr. 2014;81(4):217-25.

3. Clin Imaging. 2018 May 24. doi: 10.1016/j.clinimag.2018.05.020.

4. Am J Ophthalmol. 1998 Jul;126(1):116-21.

5. Glob Pediatr Health. 2018. doi:10.1177/2333794X18785550.

Pseudotumor cerebri, benign intracranial hypertension, and idiopathic intracranial hypertension are all terms to describe a syndrome of increased intracranial pressure, headaches, vision loss, or changes without an associated mass lesion.¹ The condition was considered relatively rare, presenting most commonly in obese women in childbearing years. Surprisingly, with the obesity rates increasing among children and adolescents, rates of pseudotumor cerebri also are rising sharply in these populations.²

Obesity is the fastest growing morbidity among adolescents. The Centers for Disease Control and Prevention reported 32% of children 2-19 years were obese.¹ This reality is impacting many areas of an adolescent’s health, but it also is changing the landscape of diseases that present in this age group. Although pediatric and adult pseudotumor cerebri always have had slightly varied features, many features were similar such as the papilledema, vision loss, headaches, and sixth nerve palsy. Obesity and female predominance tended to present more in the adult population, as many pediatric patients were not obese,² and had fewer associated symptoms at the time of diagnosis, and the cause was thought to idiopathic.

Now, with the increase in obesity, more adolescents and more male patients are presenting with pseudotumor cerebri as a cause for their headache, and 57%-100% are obese, making it a compounding factor.³

Pediatric populations also are at risk of secondary pseudotumor cerebri, which is an increase in intracranial pressure from the use of medication, or other disease states such as anemia, kidney disease, or Down syndrome. Minocycline use is the most common medication cause and usually presents 1-2 months after normal use.⁴ Discontinuing the drug does lead to resolution. Retinoids, vitamin A products, growth hormone, and steroids also have been implicated. Given that acne is a common complaint amongst teens, knowledge of these side effects is important.⁴

In 2013, the criteria for diagnosis of pseudotumor cerebri was revised. Currently, the presence of papilledema, normal neurologic exam except for abnormal sixth cranial nerve, normal cerebral spinal fluid, elevated lumbar opening pressure, and normal imaging are needed for a definitive diagnosis. A probable diagnosis can be made if papilledema is not present but there abducens nerve palsy.²

In a routine physical exam, when I questioned a patient on any medication that was used daily, she replied she took ibuprofen daily for headaches and that she had been doing this for several months. Headaches were not in her chief complaints as she had learned to live with and ignore this symptom. Upon further evaluation, she was slightly overweight and has a questionable fundoscopic exam. After further evaluation by an ophthalmologist and a neurologist, pseudotumor cerebri was diagnosed.

Index of suspicion is key in correctly diagnosing patients, and understanding the changing landscape of medicine will lead to more thoughtful questioning during routine health exams and better outcomes for your patients.
 

Dr. Pearce is a pediatrician in Frankfort, Ill. She said she had no relevant financial disclosures. Email her at [email protected].

References

1. Am J Ophthalmol. 2015 Feb;159(2):344-52.e1.

2. Horm Res Paediatr. 2014;81(4):217-25.

3. Clin Imaging. 2018 May 24. doi: 10.1016/j.clinimag.2018.05.020.

4. Am J Ophthalmol. 1998 Jul;126(1):116-21.

5. Glob Pediatr Health. 2018. doi:10.1177/2333794X18785550.

Pseudotumor cerebri, benign intracranial hypertension, and idiopathic intracranial hypertension are all terms to describe a syndrome of increased intracranial pressure, headaches, vision loss, or changes without an associated mass lesion.¹ The condition was considered relatively rare, presenting most commonly in obese women in childbearing years. Surprisingly, with the obesity rates increasing among children and adolescents, rates of pseudotumor cerebri also are rising sharply in these populations.²

Obesity is the fastest growing morbidity among adolescents. The Centers for Disease Control and Prevention reported 32% of children 2-19 years were obese.¹ This reality is impacting many areas of an adolescent’s health, but it also is changing the landscape of diseases that present in this age group. Although pediatric and adult pseudotumor cerebri always have had slightly varied features, many features were similar such as the papilledema, vision loss, headaches, and sixth nerve palsy. Obesity and female predominance tended to present more in the adult population, as many pediatric patients were not obese,² and had fewer associated symptoms at the time of diagnosis, and the cause was thought to idiopathic.

Now, with the increase in obesity, more adolescents and more male patients are presenting with pseudotumor cerebri as a cause for their headache, and 57%-100% are obese, making it a compounding factor.³

Pediatric populations also are at risk of secondary pseudotumor cerebri, which is an increase in intracranial pressure from the use of medication, or other disease states such as anemia, kidney disease, or Down syndrome. Minocycline use is the most common medication cause and usually presents 1-2 months after normal use.⁴ Discontinuing the drug does lead to resolution. Retinoids, vitamin A products, growth hormone, and steroids also have been implicated. Given that acne is a common complaint amongst teens, knowledge of these side effects is important.⁴

In 2013, the criteria for diagnosis of pseudotumor cerebri was revised. Currently, the presence of papilledema, normal neurologic exam except for abnormal sixth cranial nerve, normal cerebral spinal fluid, elevated lumbar opening pressure, and normal imaging are needed for a definitive diagnosis. A probable diagnosis can be made if papilledema is not present but there abducens nerve palsy.²

In a routine physical exam, when I questioned a patient on any medication that was used daily, she replied she took ibuprofen daily for headaches and that she had been doing this for several months. Headaches were not in her chief complaints as she had learned to live with and ignore this symptom. Upon further evaluation, she was slightly overweight and has a questionable fundoscopic exam. After further evaluation by an ophthalmologist and a neurologist, pseudotumor cerebri was diagnosed.

Index of suspicion is key in correctly diagnosing patients, and understanding the changing landscape of medicine will lead to more thoughtful questioning during routine health exams and better outcomes for your patients.
 

Dr. Pearce is a pediatrician in Frankfort, Ill. She said she had no relevant financial disclosures. Email her at [email protected].

References

1. Am J Ophthalmol. 2015 Feb;159(2):344-52.e1.

2. Horm Res Paediatr. 2014;81(4):217-25.

3. Clin Imaging. 2018 May 24. doi: 10.1016/j.clinimag.2018.05.020.

4. Am J Ophthalmol. 1998 Jul;126(1):116-21.

5. Glob Pediatr Health. 2018. doi:10.1177/2333794X18785550.

There is consensus within both the medical and public health communities that an integrated model of health care, in which behavioral health is integrated into primary care settings, is the optimal way to improve the health of a population (not just treat disease) while managing costs and improving the patient’s experience of care. Such a model is especially compelling for pediatric care.

There are 74 million children under 18 years in the United States and the prevalence of psychiatric disorders in youth is 20%, or 15 million; after vaccinations and following development, managing psychiatric symptoms is the most common issue in pediatric primary care.

While some psychiatric illnesses can be well managed by primary care clinicians alone, some illnesses require specialized therapy or more complex pharmacologic treatment. Untreated or inadequately treated childhood mental illness can lead to a longer and worse course of illness, academic difficulties, emergence of associated illnesses (such as substance use disorders), and legal problems. For those children with chronic medical conditions, emotional disorders cause distress, and affect adherence and family functioning. We will discuss some practical strategies to begin to bring behavioral health care into the pediatric primary care setting. The dream of tomorrow’s integrated behavioral health care should not preclude the possibility of coordinated or better colocated behavioral health care today.

Start by implementing behavioral health screening into annual and sick visits. Broad instruments, such as the Pediatric Symptom Checklist (PSC, 35 items) or the Child Behavior Check List (CBCL, 113 items) can be filled out by caregivers in the waiting room or online before a visit, and can suggest specific disorders or simply the need for a full psychiatric assessment. Electronic medical records may have publicly available questionnaires such as PSC built into their software, facilitating use of a tablet or home computer, and may ease scoring and downloading of results. Depending on the structure of your practice, you could have one clinician in charge of managing screening. You may become comfortable diagnosing certain disorders, such as ADHD, a major depressive episode, or an anxiety disorder, and you may begin medication treatment when appropriate. You can use instruments developed for specific disease entities (such as ADHD, obsessive compulsive disorder [OCD], anxiety, or depression) to monitor your patient’s treatment response, and they may be done virtually to minimize unnecessary visits.

Treatment algorithms for most psychiatric illnesses are available through the American Academy of Pediatrics and the American Academy of Child and Adolescent Psychiatry, and can guide you through the early stages of treatment. Psychotherapy is the first-line treatment for mild to moderate anxiety and mood disorders, and it is critical to the treatment of more severe disorders. Difficulty in finding a therapist who is skilled in a specific treatment, is a good fit, and accepts insurance can be a significant barrier to care. Establishing a coordinated relationship with a team of therapists can facilitate referrals. Some states have programs in which primary care physicians can have telephone consultations with mental health clinicians or to access referral services for therapy, such as the Massachusetts Child Psychiatry Access Project.

If you have a busy enough practice, consider bringing a social worker or psychologist to work with you. Such a clinician could perform diagnostic assessments, ongoing therapy, parent guidance, family work, or care coordination. Consider how to make it cost-effective for this clinician and your group, whether by inviting that person to sublet one of your offices, or having that person directly employed by you and benefiting from your office staff and patient flow. Many states now reimburse for screening and these funds could contribute to the expense of a social worker. This approach would bring you from coordination to true colocation, which greatly improves the likelihood of compliance with therapy, enhances coordination of a patient’s care, creates opportunities for ongoing education between disciplines, and diminishes stigma of acknowledging a mental illness. Anxiety disorders are the most common illnesses of youth, with mood disorders emerging in adolescence, and substance use disorders in later adolescence. Consider this in seeking a clinician with a specific interest or skill set (such as cognitive behavioral therapy for anxiety or mood problems, dialectical behavior therapy for chronic suicidality, or motivational interviewing for substance abuse).

KatarzynaBialasiewicz/Thinkstock

There may be funds available to support your investment in integrated care. Under the Affordable Care Act, Medicaid enhanced funding for Health Homes for enrolled children. There have been federal grants for primary care offices to engage in different levels of integration and measure outcomes (Project LAUNCH – Linking Actions for Unmet Needs in Children’s Health). There may be funding at the state level or from private foundations dedicated to public health research and initiatives. Even if you do not invest in procuring outside funding, you should consider how to measure patient outcomes once you are making any efforts at integrating behavioral health care into your practice. Outcome measures include questionnaire scores, treatment adherence, number of school absences, number of office or ED visits, or global measurements, such as the Child Global Assessment Scale (CGAS). Such data can inform you about how to adjust your approach, and could contribute to the larger effort to understand what strategies are most effective and feasible. Addressing the behavioral health needs of your patients could meaningfully contribute to the efforts to make the vision of integrated care – that which truly promotes health in our young people – a reality.

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton Wellesley Hospital, also in Boston. Dr. Jellinek is professor emeritus of psychiatry and pediatrics at Harvard Medical School, Boston. Email them at [email protected].

There is consensus within both the medical and public health communities that an integrated model of health care, in which behavioral health is integrated into primary care settings, is the optimal way to improve the health of a population (not just treat disease) while managing costs and improving the patient’s experience of care. Such a model is especially compelling for pediatric care.

There are 74 million children under 18 years in the United States and the prevalence of psychiatric disorders in youth is 20%, or 15 million; after vaccinations and following development, managing psychiatric symptoms is the most common issue in pediatric primary care.

While some psychiatric illnesses can be well managed by primary care clinicians alone, some illnesses require specialized therapy or more complex pharmacologic treatment. Untreated or inadequately treated childhood mental illness can lead to a longer and worse course of illness, academic difficulties, emergence of associated illnesses (such as substance use disorders), and legal problems. For those children with chronic medical conditions, emotional disorders cause distress, and affect adherence and family functioning. We will discuss some practical strategies to begin to bring behavioral health care into the pediatric primary care setting. The dream of tomorrow’s integrated behavioral health care should not preclude the possibility of coordinated or better colocated behavioral health care today.

Start by implementing behavioral health screening into annual and sick visits. Broad instruments, such as the Pediatric Symptom Checklist (PSC, 35 items) or the Child Behavior Check List (CBCL, 113 items) can be filled out by caregivers in the waiting room or online before a visit, and can suggest specific disorders or simply the need for a full psychiatric assessment. Electronic medical records may have publicly available questionnaires such as PSC built into their software, facilitating use of a tablet or home computer, and may ease scoring and downloading of results. Depending on the structure of your practice, you could have one clinician in charge of managing screening. You may become comfortable diagnosing certain disorders, such as ADHD, a major depressive episode, or an anxiety disorder, and you may begin medication treatment when appropriate. You can use instruments developed for specific disease entities (such as ADHD, obsessive compulsive disorder [OCD], anxiety, or depression) to monitor your patient’s treatment response, and they may be done virtually to minimize unnecessary visits.

Treatment algorithms for most psychiatric illnesses are available through the American Academy of Pediatrics and the American Academy of Child and Adolescent Psychiatry, and can guide you through the early stages of treatment. Psychotherapy is the first-line treatment for mild to moderate anxiety and mood disorders, and it is critical to the treatment of more severe disorders. Difficulty in finding a therapist who is skilled in a specific treatment, is a good fit, and accepts insurance can be a significant barrier to care. Establishing a coordinated relationship with a team of therapists can facilitate referrals. Some states have programs in which primary care physicians can have telephone consultations with mental health clinicians or to access referral services for therapy, such as the Massachusetts Child Psychiatry Access Project.

If you have a busy enough practice, consider bringing a social worker or psychologist to work with you. Such a clinician could perform diagnostic assessments, ongoing therapy, parent guidance, family work, or care coordination. Consider how to make it cost-effective for this clinician and your group, whether by inviting that person to sublet one of your offices, or having that person directly employed by you and benefiting from your office staff and patient flow. Many states now reimburse for screening and these funds could contribute to the expense of a social worker. This approach would bring you from coordination to true colocation, which greatly improves the likelihood of compliance with therapy, enhances coordination of a patient’s care, creates opportunities for ongoing education between disciplines, and diminishes stigma of acknowledging a mental illness. Anxiety disorders are the most common illnesses of youth, with mood disorders emerging in adolescence, and substance use disorders in later adolescence. Consider this in seeking a clinician with a specific interest or skill set (such as cognitive behavioral therapy for anxiety or mood problems, dialectical behavior therapy for chronic suicidality, or motivational interviewing for substance abuse).

KatarzynaBialasiewicz/Thinkstock

There may be funds available to support your investment in integrated care. Under the Affordable Care Act, Medicaid enhanced funding for Health Homes for enrolled children. There have been federal grants for primary care offices to engage in different levels of integration and measure outcomes (Project LAUNCH – Linking Actions for Unmet Needs in Children’s Health). There may be funding at the state level or from private foundations dedicated to public health research and initiatives. Even if you do not invest in procuring outside funding, you should consider how to measure patient outcomes once you are making any efforts at integrating behavioral health care into your practice. Outcome measures include questionnaire scores, treatment adherence, number of school absences, number of office or ED visits, or global measurements, such as the Child Global Assessment Scale (CGAS). Such data can inform you about how to adjust your approach, and could contribute to the larger effort to understand what strategies are most effective and feasible. Addressing the behavioral health needs of your patients could meaningfully contribute to the efforts to make the vision of integrated care – that which truly promotes health in our young people – a reality.

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton Wellesley Hospital, also in Boston. Dr. Jellinek is professor emeritus of psychiatry and pediatrics at Harvard Medical School, Boston. Email them at [email protected].

There is consensus within both the medical and public health communities that an integrated model of health care, in which behavioral health is integrated into primary care settings, is the optimal way to improve the health of a population (not just treat disease) while managing costs and improving the patient’s experience of care. Such a model is especially compelling for pediatric care.

There are 74 million children under 18 years in the United States and the prevalence of psychiatric disorders in youth is 20%, or 15 million; after vaccinations and following development, managing psychiatric symptoms is the most common issue in pediatric primary care.

While some psychiatric illnesses can be well managed by primary care clinicians alone, some illnesses require specialized therapy or more complex pharmacologic treatment. Untreated or inadequately treated childhood mental illness can lead to a longer and worse course of illness, academic difficulties, emergence of associated illnesses (such as substance use disorders), and legal problems. For those children with chronic medical conditions, emotional disorders cause distress, and affect adherence and family functioning. We will discuss some practical strategies to begin to bring behavioral health care into the pediatric primary care setting. The dream of tomorrow’s integrated behavioral health care should not preclude the possibility of coordinated or better colocated behavioral health care today.

Start by implementing behavioral health screening into annual and sick visits. Broad instruments, such as the Pediatric Symptom Checklist (PSC, 35 items) or the Child Behavior Check List (CBCL, 113 items) can be filled out by caregivers in the waiting room or online before a visit, and can suggest specific disorders or simply the need for a full psychiatric assessment. Electronic medical records may have publicly available questionnaires such as PSC built into their software, facilitating use of a tablet or home computer, and may ease scoring and downloading of results. Depending on the structure of your practice, you could have one clinician in charge of managing screening. You may become comfortable diagnosing certain disorders, such as ADHD, a major depressive episode, or an anxiety disorder, and you may begin medication treatment when appropriate. You can use instruments developed for specific disease entities (such as ADHD, obsessive compulsive disorder [OCD], anxiety, or depression) to monitor your patient’s treatment response, and they may be done virtually to minimize unnecessary visits.

Treatment algorithms for most psychiatric illnesses are available through the American Academy of Pediatrics and the American Academy of Child and Adolescent Psychiatry, and can guide you through the early stages of treatment. Psychotherapy is the first-line treatment for mild to moderate anxiety and mood disorders, and it is critical to the treatment of more severe disorders. Difficulty in finding a therapist who is skilled in a specific treatment, is a good fit, and accepts insurance can be a significant barrier to care. Establishing a coordinated relationship with a team of therapists can facilitate referrals. Some states have programs in which primary care physicians can have telephone consultations with mental health clinicians or to access referral services for therapy, such as the Massachusetts Child Psychiatry Access Project.

If you have a busy enough practice, consider bringing a social worker or psychologist to work with you. Such a clinician could perform diagnostic assessments, ongoing therapy, parent guidance, family work, or care coordination. Consider how to make it cost-effective for this clinician and your group, whether by inviting that person to sublet one of your offices, or having that person directly employed by you and benefiting from your office staff and patient flow. Many states now reimburse for screening and these funds could contribute to the expense of a social worker. This approach would bring you from coordination to true colocation, which greatly improves the likelihood of compliance with therapy, enhances coordination of a patient’s care, creates opportunities for ongoing education between disciplines, and diminishes stigma of acknowledging a mental illness. Anxiety disorders are the most common illnesses of youth, with mood disorders emerging in adolescence, and substance use disorders in later adolescence. Consider this in seeking a clinician with a specific interest or skill set (such as cognitive behavioral therapy for anxiety or mood problems, dialectical behavior therapy for chronic suicidality, or motivational interviewing for substance abuse).

KatarzynaBialasiewicz/Thinkstock

There may be funds available to support your investment in integrated care. Under the Affordable Care Act, Medicaid enhanced funding for Health Homes for enrolled children. There have been federal grants for primary care offices to engage in different levels of integration and measure outcomes (Project LAUNCH – Linking Actions for Unmet Needs in Children’s Health). There may be funding at the state level or from private foundations dedicated to public health research and initiatives. Even if you do not invest in procuring outside funding, you should consider how to measure patient outcomes once you are making any efforts at integrating behavioral health care into your practice. Outcome measures include questionnaire scores, treatment adherence, number of school absences, number of office or ED visits, or global measurements, such as the Child Global Assessment Scale (CGAS). Such data can inform you about how to adjust your approach, and could contribute to the larger effort to understand what strategies are most effective and feasible. Addressing the behavioral health needs of your patients could meaningfully contribute to the efforts to make the vision of integrated care – that which truly promotes health in our young people – a reality.

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton Wellesley Hospital, also in Boston. Dr. Jellinek is professor emeritus of psychiatry and pediatrics at Harvard Medical School, Boston. Email them at [email protected].

Vesicovaginal fistulas (VVFs) are the most common type of urogenital fistulas – approximately three times more common than ureterovaginal fistulas – and can be a debilitating problem for women.

Most of the research published in recent years on VVFs and other urogenital fistulas comes from developing countries where these abnormal communications are a common complication of obstructed labor. In the United States, despite a relative paucity of data, VVFs are known to occur most often as a sequelae of gynecologic surgery, usually hysterectomy. Estimates of the incidence of VVF and other urogenital fistula formation are debated but have ranged from 0.5% or less after simple hysterectomy to as high as 2% after radical hysterectomy. Most VVFs are believed to occur after hysterectomy performed for benign disease, and many – but not all – are caused by inadvertent bladder injury that was not recognized intraoperatively.

Women who have had one or more cesarean deliveries and those who have had prior pelvic or vaginal surgery are at increased risk. In addition, both radiation therapy and inflammation that occur with diseases such as pelvic inflammatory disease or inflammatory bowel disease can negatively affect tissue quality and healing from surgical procedures – and can lead ultimately to the development of urogenital fistulas – although even less is known about incidence in these cases.
 

Prevention

Intraoperatively, VVFs may best be prevented through careful mobilization of the bladder off the vaginal wall, the use of delayed absorbable sutures (preferably Vicryl sutures), and the use of cystoscopy to assess the bladder for injury. If cystoscopy is not available, retrograde filling with a Foley catheter will still be helpful.

An overly aggressive approach to creating the bladder flap during hysterectomy and other surgeries can increase the risk of devascularization and the subsequent formation of fistulas. When the blood supply is found to have been compromised, affected tissue can be strengthened by oversewing with imbrication. When an inadvertent cystotomy is identified, repair is often best achieved with omental tissue interposed between the bladder and vagina. If there is any doubt about bladder integrity, an interposition graft between the bladder flap and the vaginal cuff will help reduce the incidence of fistula formation. Whenever overlapping suture lines occur (the vaginal cuff and the cystotomy repair), the risk of VVF formation will increase. Other than that using omentum, peritoneal grafts will also work well.

VVF formation may still occur, however, despite recognition and repair of an injury – and despite normal findings on cystoscopy. In patients who have had prior cesarean deliveries or other prior pelvic surgery, for example, tissue devascularization may cause a delayed injury, with the process of tissue necrosis and VVF formation occurring up to a month after surgery. It is important to appreciate the factors that predispose patients to VVF and to anticipate an increased risk, but in many cases of delayed VVF, it’s quite possible that nothing could have been done to prevent the problem.
 

Work-up

Courtesy of John Miklos, MD

Vesicovaginal fistulas typically present as painless, continuous urine leakage from the vagina. The medical history should include standard questions about pelvic health history and symptom characteristics (in order to exclude hematuria or leakage of fluid other than urine), as well as questions aimed at differentiating symptoms of VVF from other causes of urinary incontinence, such as stress incontinence. In my experience, urine leakage is often incorrectly dismissed as stress incontinence when it is actually VVF. A high index of suspicion will help make an earlier diagnosis. This does not usually change the management, but helps manage the anxiety, expectations, and needs of the patient.

I recommend beginning the work-up for a suspected VVF with a thorough cystoscopic evaluation of the bladder for injury. An irregular appearance of the bladder, signs of inflammation, and poor or absent ureteral efflux are often indicative of VVF in the presence of vaginal leakage. Following cystoscopy, I perform a split speculum examination of the vagina. Most injuries will be on the anterior wall or the apex (cuff). A recently formed fistula may appear as a hole or as a small, red area of granulation tissue with no visible opening.

Courtesy of John Miklos, MD

It can be difficult to visualize the vaginal fistula opening of more mature fistulas; similarly, very small fistulas may be difficult to find because of their size and the anatomy of the vagina. When a prior hysterectomy has led to a fistula, the vaginal fistula opening is typically located in the upper third of the vagina or at the vaginal cuff. If cuff sutures are still intact, this may also make localization of the fistula more difficult.

Leakage in the vagina can sometimes be detected with a retrograde filling of the bladder; other times, it is possible to detect leakage without filling the bladder. In all cases, it’s important to remember that more than one fistula – and more than one fistula type – may be present. A VVF and ureterovaginal fistula will sometimes occur together, which means that abnormal cystoscopy findings in a patient who experiences leakage does not necessarily rule out the presence of a concurrent ureterovaginal fistula.

Phenazopyridine (Pyridium) administered orally will turn the urine orange and can help visualize the leakage of urine into the vagina. When used in combination with the use of blue dye (methylene blue) infused into the bladder, a VVF may be distinguished from a ureterovaginal fistula. To completely evaluate the number and location of fistulas, however, imaging studies are necessary. In my experience, a CT urogram with IV contrast can also help localize ureteral injuries.
 

Surgical treatment

VVFs can almost always be repaired vaginally. If the fistula is too high in location or too complex, then an abdominal approach, either robotic, laparoscopic, or open, may be necessary. I prefer a vaginal approach to VVF repair whenever feasible because of its straightforward nature, lower morbidity, and high rate of success on the first attempt. Failure rates are between 5% and 20% for each attempt, so more than one surgery may be required. It is not unreasonable to attempt two or three vaginal approach repairs if each successive attempt results in a smaller fistula. A decision to go abdominal must be made based on the chances of a successful vaginal approach and on the patient’s wishes.

Courtesy of Dionysios Veronikis, MD

Successful fistula repair requires tension-free suture lines, no overlapping suture lines, and good vascular supply to the tissue. The timing of repair has long been controversial, but barring the presence of active pelvic infection, which may require an immediate surgical approach, the timing of fistula repair depends almost solely on the quality of the surrounding tissue. This relates to the need for a good vascular supply.

Early repair can be done if the tissue is pliable and healthy. But in general, if surgery is performed too close to the time of injury, the surrounding tissue will be erythematous and likely to break down with closure. The goal is to wait until the granulation tissue has dissipated and the area is no longer inflamed; after gynecologic surgery, this generally occurs within 6-12 weeks.

Regular vaginal exams about every 2 weeks can be used to monitor progress. During the waiting period, catheterization of the bladder can improve comfort for the patient and may even allow for spontaneous closure of the fistula. In fact, I usually tell patients who are diagnosed with a VVF within the first few weeks after surgery that spontaneous closure is a possible outcome given continuous urinary drainage for up to 30 days, provided that the VVF is small enough. This may be optimistic thinking on the part of the surgeon and the patient, but there is little downside to this approach.

The Latzko technique described in 1992 is still widely used for vaginal repair of VVFs. With this approach, the vaginal epithelium is incised around the fistula, and vaginal epithelial flaps are raised and removed around the fistula tract (in a circle of about 2-3 cm in diameter) for a multilayer approximation of healthy tissues. Several layers are sometimes needed, but in most cases, two layers are sufficient.

In my experience, a modified approach to the traditional Latzko procedure is more successful. Prior to closure, either anterior or posterior to the VVF, a small rim of vaginal epithelium is removed and, on the other side, the epithelium is mobilized at least 1 cm lateral to the fistula on both sides, and about 2 cm distal. This allows for the creation of a small, modified, thumbnail flap that completely patches the fistula closure without tension and without the need for any overlapping suture lines. The key is to secure flap tissue from the side where there appears to be more vaginal tissue. The tissue should be loose; if there appears to be any strain, the repair is likely to fail.

There are not enough data from the United States or other developed countries to demonstrate the superiority of this modified approach, but data from the obstetric population in Africa – and my own experience – suggest that it yields better outcomes.

A VVF that is larger may require the use of additional sources of tissue. A graft called the Martius graft, or labial fibrofatty tissue graft, is sometimes used to reinforce repairs of larger fistulas, even those that are high in the vaginal vault. The procedure involves a vertical incision on the inner side of the labium majus and detachment of fibroadipose tissue from its underlying bulbocavernosus muscle. This fat-pad flap is vascularized and thus serves as a pedicled graft. It can be tunneled under the vaginal epithelium to reach the site of closure. The procedure has limited use with the vaginal approach to VVF, but is important to be aware of.

Other sources of grafts or flaps that can sometimes be used with the vaginal approach include the gracilis muscle, the gluteal muscle and peritoneum, and fasciocutaneous tissue from the inner thigh.

The avoidance of overlapping suture lines and multiple layers of closure will help ensure a water-tight closure. If there is any leakage upon testing the integrity of the repair, particularly one that is vaginally approached, such leakage will continue and the repair will have been unsuccessful. In an abdominal surgery for VVF, a small amount of remaining leakage will probably resolve on its own after 10-14 days of catheter placement.

Placement of a Jackson-Pratt (JP) drain is controversial. It has been suggested that a JP drain placed on continuous suction will pull urine out of the bladder and increase the risk of a fistula. I don’t place a JP drain in my repairs as I find them to not be helpful. A cystogram can be done 1 week after repair to confirm healing, but there is some debate about whether or not the procedure is useful at that point. In my experience, if the patient does not have a cystogram and gets postrepair leakage, I have the same information as I would have obtained through a positive finding on a cystogram.
 

Dr. Garely is chair of obstetrics and gynecology and director of urogynecology and pelvic reconstructive surgery at the South Nassau Communities Hospital, Oceanside, N.Y., and a clinical professor of obstetrics, gynecology, and reproductive science at the Icahn School of Medicine at Mount Sinai, New York. He has no disclosures related to this column.

Vesicovaginal fistulas (VVFs) are the most common type of urogenital fistulas – approximately three times more common than ureterovaginal fistulas – and can be a debilitating problem for women.

Most of the research published in recent years on VVFs and other urogenital fistulas comes from developing countries where these abnormal communications are a common complication of obstructed labor. In the United States, despite a relative paucity of data, VVFs are known to occur most often as a sequelae of gynecologic surgery, usually hysterectomy. Estimates of the incidence of VVF and other urogenital fistula formation are debated but have ranged from 0.5% or less after simple hysterectomy to as high as 2% after radical hysterectomy. Most VVFs are believed to occur after hysterectomy performed for benign disease, and many – but not all – are caused by inadvertent bladder injury that was not recognized intraoperatively.

Women who have had one or more cesarean deliveries and those who have had prior pelvic or vaginal surgery are at increased risk. In addition, both radiation therapy and inflammation that occur with diseases such as pelvic inflammatory disease or inflammatory bowel disease can negatively affect tissue quality and healing from surgical procedures – and can lead ultimately to the development of urogenital fistulas – although even less is known about incidence in these cases.
 

Prevention

Intraoperatively, VVFs may best be prevented through careful mobilization of the bladder off the vaginal wall, the use of delayed absorbable sutures (preferably Vicryl sutures), and the use of cystoscopy to assess the bladder for injury. If cystoscopy is not available, retrograde filling with a Foley catheter will still be helpful.

An overly aggressive approach to creating the bladder flap during hysterectomy and other surgeries can increase the risk of devascularization and the subsequent formation of fistulas. When the blood supply is found to have been compromised, affected tissue can be strengthened by oversewing with imbrication. When an inadvertent cystotomy is identified, repair is often best achieved with omental tissue interposed between the bladder and vagina. If there is any doubt about bladder integrity, an interposition graft between the bladder flap and the vaginal cuff will help reduce the incidence of fistula formation. Whenever overlapping suture lines occur (the vaginal cuff and the cystotomy repair), the risk of VVF formation will increase. Other than that using omentum, peritoneal grafts will also work well.

VVF formation may still occur, however, despite recognition and repair of an injury – and despite normal findings on cystoscopy. In patients who have had prior cesarean deliveries or other prior pelvic surgery, for example, tissue devascularization may cause a delayed injury, with the process of tissue necrosis and VVF formation occurring up to a month after surgery. It is important to appreciate the factors that predispose patients to VVF and to anticipate an increased risk, but in many cases of delayed VVF, it’s quite possible that nothing could have been done to prevent the problem.
 

Work-up

Courtesy of John Miklos, MD

Vesicovaginal fistulas typically present as painless, continuous urine leakage from the vagina. The medical history should include standard questions about pelvic health history and symptom characteristics (in order to exclude hematuria or leakage of fluid other than urine), as well as questions aimed at differentiating symptoms of VVF from other causes of urinary incontinence, such as stress incontinence. In my experience, urine leakage is often incorrectly dismissed as stress incontinence when it is actually VVF. A high index of suspicion will help make an earlier diagnosis. This does not usually change the management, but helps manage the anxiety, expectations, and needs of the patient.

I recommend beginning the work-up for a suspected VVF with a thorough cystoscopic evaluation of the bladder for injury. An irregular appearance of the bladder, signs of inflammation, and poor or absent ureteral efflux are often indicative of VVF in the presence of vaginal leakage. Following cystoscopy, I perform a split speculum examination of the vagina. Most injuries will be on the anterior wall or the apex (cuff). A recently formed fistula may appear as a hole or as a small, red area of granulation tissue with no visible opening.

Courtesy of John Miklos, MD

It can be difficult to visualize the vaginal fistula opening of more mature fistulas; similarly, very small fistulas may be difficult to find because of their size and the anatomy of the vagina. When a prior hysterectomy has led to a fistula, the vaginal fistula opening is typically located in the upper third of the vagina or at the vaginal cuff. If cuff sutures are still intact, this may also make localization of the fistula more difficult.

Leakage in the vagina can sometimes be detected with a retrograde filling of the bladder; other times, it is possible to detect leakage without filling the bladder. In all cases, it’s important to remember that more than one fistula – and more than one fistula type – may be present. A VVF and ureterovaginal fistula will sometimes occur together, which means that abnormal cystoscopy findings in a patient who experiences leakage does not necessarily rule out the presence of a concurrent ureterovaginal fistula.

Phenazopyridine (Pyridium) administered orally will turn the urine orange and can help visualize the leakage of urine into the vagina. When used in combination with the use of blue dye (methylene blue) infused into the bladder, a VVF may be distinguished from a ureterovaginal fistula. To completely evaluate the number and location of fistulas, however, imaging studies are necessary. In my experience, a CT urogram with IV contrast can also help localize ureteral injuries.
 

Surgical treatment

VVFs can almost always be repaired vaginally. If the fistula is too high in location or too complex, then an abdominal approach, either robotic, laparoscopic, or open, may be necessary. I prefer a vaginal approach to VVF repair whenever feasible because of its straightforward nature, lower morbidity, and high rate of success on the first attempt. Failure rates are between 5% and 20% for each attempt, so more than one surgery may be required. It is not unreasonable to attempt two or three vaginal approach repairs if each successive attempt results in a smaller fistula. A decision to go abdominal must be made based on the chances of a successful vaginal approach and on the patient’s wishes.

Courtesy of Dionysios Veronikis, MD

Successful fistula repair requires tension-free suture lines, no overlapping suture lines, and good vascular supply to the tissue. The timing of repair has long been controversial, but barring the presence of active pelvic infection, which may require an immediate surgical approach, the timing of fistula repair depends almost solely on the quality of the surrounding tissue. This relates to the need for a good vascular supply.

Early repair can be done if the tissue is pliable and healthy. But in general, if surgery is performed too close to the time of injury, the surrounding tissue will be erythematous and likely to break down with closure. The goal is to wait until the granulation tissue has dissipated and the area is no longer inflamed; after gynecologic surgery, this generally occurs within 6-12 weeks.

Regular vaginal exams about every 2 weeks can be used to monitor progress. During the waiting period, catheterization of the bladder can improve comfort for the patient and may even allow for spontaneous closure of the fistula. In fact, I usually tell patients who are diagnosed with a VVF within the first few weeks after surgery that spontaneous closure is a possible outcome given continuous urinary drainage for up to 30 days, provided that the VVF is small enough. This may be optimistic thinking on the part of the surgeon and the patient, but there is little downside to this approach.

The Latzko technique described in 1992 is still widely used for vaginal repair of VVFs. With this approach, the vaginal epithelium is incised around the fistula, and vaginal epithelial flaps are raised and removed around the fistula tract (in a circle of about 2-3 cm in diameter) for a multilayer approximation of healthy tissues. Several layers are sometimes needed, but in most cases, two layers are sufficient.

In my experience, a modified approach to the traditional Latzko procedure is more successful. Prior to closure, either anterior or posterior to the VVF, a small rim of vaginal epithelium is removed and, on the other side, the epithelium is mobilized at least 1 cm lateral to the fistula on both sides, and about 2 cm distal. This allows for the creation of a small, modified, thumbnail flap that completely patches the fistula closure without tension and without the need for any overlapping suture lines. The key is to secure flap tissue from the side where there appears to be more vaginal tissue. The tissue should be loose; if there appears to be any strain, the repair is likely to fail.

There are not enough data from the United States or other developed countries to demonstrate the superiority of this modified approach, but data from the obstetric population in Africa – and my own experience – suggest that it yields better outcomes.

A VVF that is larger may require the use of additional sources of tissue. A graft called the Martius graft, or labial fibrofatty tissue graft, is sometimes used to reinforce repairs of larger fistulas, even those that are high in the vaginal vault. The procedure involves a vertical incision on the inner side of the labium majus and detachment of fibroadipose tissue from its underlying bulbocavernosus muscle. This fat-pad flap is vascularized and thus serves as a pedicled graft. It can be tunneled under the vaginal epithelium to reach the site of closure. The procedure has limited use with the vaginal approach to VVF, but is important to be aware of.

Other sources of grafts or flaps that can sometimes be used with the vaginal approach include the gracilis muscle, the gluteal muscle and peritoneum, and fasciocutaneous tissue from the inner thigh.

The avoidance of overlapping suture lines and multiple layers of closure will help ensure a water-tight closure. If there is any leakage upon testing the integrity of the repair, particularly one that is vaginally approached, such leakage will continue and the repair will have been unsuccessful. In an abdominal surgery for VVF, a small amount of remaining leakage will probably resolve on its own after 10-14 days of catheter placement.

Placement of a Jackson-Pratt (JP) drain is controversial. It has been suggested that a JP drain placed on continuous suction will pull urine out of the bladder and increase the risk of a fistula. I don’t place a JP drain in my repairs as I find them to not be helpful. A cystogram can be done 1 week after repair to confirm healing, but there is some debate about whether or not the procedure is useful at that point. In my experience, if the patient does not have a cystogram and gets postrepair leakage, I have the same information as I would have obtained through a positive finding on a cystogram.
 

Dr. Garely is chair of obstetrics and gynecology and director of urogynecology and pelvic reconstructive surgery at the South Nassau Communities Hospital, Oceanside, N.Y., and a clinical professor of obstetrics, gynecology, and reproductive science at the Icahn School of Medicine at Mount Sinai, New York. He has no disclosures related to this column.

Vesicovaginal fistulas (VVFs) are the most common type of urogenital fistulas – approximately three times more common than ureterovaginal fistulas – and can be a debilitating problem for women.

Most of the research published in recent years on VVFs and other urogenital fistulas comes from developing countries where these abnormal communications are a common complication of obstructed labor. In the United States, despite a relative paucity of data, VVFs are known to occur most often as a sequelae of gynecologic surgery, usually hysterectomy. Estimates of the incidence of VVF and other urogenital fistula formation are debated but have ranged from 0.5% or less after simple hysterectomy to as high as 2% after radical hysterectomy. Most VVFs are believed to occur after hysterectomy performed for benign disease, and many – but not all – are caused by inadvertent bladder injury that was not recognized intraoperatively.

Women who have had one or more cesarean deliveries and those who have had prior pelvic or vaginal surgery are at increased risk. In addition, both radiation therapy and inflammation that occur with diseases such as pelvic inflammatory disease or inflammatory bowel disease can negatively affect tissue quality and healing from surgical procedures – and can lead ultimately to the development of urogenital fistulas – although even less is known about incidence in these cases.
 

Prevention

Intraoperatively, VVFs may best be prevented through careful mobilization of the bladder off the vaginal wall, the use of delayed absorbable sutures (preferably Vicryl sutures), and the use of cystoscopy to assess the bladder for injury. If cystoscopy is not available, retrograde filling with a Foley catheter will still be helpful.

An overly aggressive approach to creating the bladder flap during hysterectomy and other surgeries can increase the risk of devascularization and the subsequent formation of fistulas. When the blood supply is found to have been compromised, affected tissue can be strengthened by oversewing with imbrication. When an inadvertent cystotomy is identified, repair is often best achieved with omental tissue interposed between the bladder and vagina. If there is any doubt about bladder integrity, an interposition graft between the bladder flap and the vaginal cuff will help reduce the incidence of fistula formation. Whenever overlapping suture lines occur (the vaginal cuff and the cystotomy repair), the risk of VVF formation will increase. Other than that using omentum, peritoneal grafts will also work well.

VVF formation may still occur, however, despite recognition and repair of an injury – and despite normal findings on cystoscopy. In patients who have had prior cesarean deliveries or other prior pelvic surgery, for example, tissue devascularization may cause a delayed injury, with the process of tissue necrosis and VVF formation occurring up to a month after surgery. It is important to appreciate the factors that predispose patients to VVF and to anticipate an increased risk, but in many cases of delayed VVF, it’s quite possible that nothing could have been done to prevent the problem.
 

Work-up

Courtesy of John Miklos, MD

Vesicovaginal fistulas typically present as painless, continuous urine leakage from the vagina. The medical history should include standard questions about pelvic health history and symptom characteristics (in order to exclude hematuria or leakage of fluid other than urine), as well as questions aimed at differentiating symptoms of VVF from other causes of urinary incontinence, such as stress incontinence. In my experience, urine leakage is often incorrectly dismissed as stress incontinence when it is actually VVF. A high index of suspicion will help make an earlier diagnosis. This does not usually change the management, but helps manage the anxiety, expectations, and needs of the patient.

I recommend beginning the work-up for a suspected VVF with a thorough cystoscopic evaluation of the bladder for injury. An irregular appearance of the bladder, signs of inflammation, and poor or absent ureteral efflux are often indicative of VVF in the presence of vaginal leakage. Following cystoscopy, I perform a split speculum examination of the vagina. Most injuries will be on the anterior wall or the apex (cuff). A recently formed fistula may appear as a hole or as a small, red area of granulation tissue with no visible opening.

Courtesy of John Miklos, MD

It can be difficult to visualize the vaginal fistula opening of more mature fistulas; similarly, very small fistulas may be difficult to find because of their size and the anatomy of the vagina. When a prior hysterectomy has led to a fistula, the vaginal fistula opening is typically located in the upper third of the vagina or at the vaginal cuff. If cuff sutures are still intact, this may also make localization of the fistula more difficult.

Leakage in the vagina can sometimes be detected with a retrograde filling of the bladder; other times, it is possible to detect leakage without filling the bladder. In all cases, it’s important to remember that more than one fistula – and more than one fistula type – may be present. A VVF and ureterovaginal fistula will sometimes occur together, which means that abnormal cystoscopy findings in a patient who experiences leakage does not necessarily rule out the presence of a concurrent ureterovaginal fistula.

Phenazopyridine (Pyridium) administered orally will turn the urine orange and can help visualize the leakage of urine into the vagina. When used in combination with the use of blue dye (methylene blue) infused into the bladder, a VVF may be distinguished from a ureterovaginal fistula. To completely evaluate the number and location of fistulas, however, imaging studies are necessary. In my experience, a CT urogram with IV contrast can also help localize ureteral injuries.
 

Surgical treatment

VVFs can almost always be repaired vaginally. If the fistula is too high in location or too complex, then an abdominal approach, either robotic, laparoscopic, or open, may be necessary. I prefer a vaginal approach to VVF repair whenever feasible because of its straightforward nature, lower morbidity, and high rate of success on the first attempt. Failure rates are between 5% and 20% for each attempt, so more than one surgery may be required. It is not unreasonable to attempt two or three vaginal approach repairs if each successive attempt results in a smaller fistula. A decision to go abdominal must be made based on the chances of a successful vaginal approach and on the patient’s wishes.

Courtesy of Dionysios Veronikis, MD

Successful fistula repair requires tension-free suture lines, no overlapping suture lines, and good vascular supply to the tissue. The timing of repair has long been controversial, but barring the presence of active pelvic infection, which may require an immediate surgical approach, the timing of fistula repair depends almost solely on the quality of the surrounding tissue. This relates to the need for a good vascular supply.

Early repair can be done if the tissue is pliable and healthy. But in general, if surgery is performed too close to the time of injury, the surrounding tissue will be erythematous and likely to break down with closure. The goal is to wait until the granulation tissue has dissipated and the area is no longer inflamed; after gynecologic surgery, this generally occurs within 6-12 weeks.

Regular vaginal exams about every 2 weeks can be used to monitor progress. During the waiting period, catheterization of the bladder can improve comfort for the patient and may even allow for spontaneous closure of the fistula. In fact, I usually tell patients who are diagnosed with a VVF within the first few weeks after surgery that spontaneous closure is a possible outcome given continuous urinary drainage for up to 30 days, provided that the VVF is small enough. This may be optimistic thinking on the part of the surgeon and the patient, but there is little downside to this approach.

The Latzko technique described in 1992 is still widely used for vaginal repair of VVFs. With this approach, the vaginal epithelium is incised around the fistula, and vaginal epithelial flaps are raised and removed around the fistula tract (in a circle of about 2-3 cm in diameter) for a multilayer approximation of healthy tissues. Several layers are sometimes needed, but in most cases, two layers are sufficient.

In my experience, a modified approach to the traditional Latzko procedure is more successful. Prior to closure, either anterior or posterior to the VVF, a small rim of vaginal epithelium is removed and, on the other side, the epithelium is mobilized at least 1 cm lateral to the fistula on both sides, and about 2 cm distal. This allows for the creation of a small, modified, thumbnail flap that completely patches the fistula closure without tension and without the need for any overlapping suture lines. The key is to secure flap tissue from the side where there appears to be more vaginal tissue. The tissue should be loose; if there appears to be any strain, the repair is likely to fail.

There are not enough data from the United States or other developed countries to demonstrate the superiority of this modified approach, but data from the obstetric population in Africa – and my own experience – suggest that it yields better outcomes.

A VVF that is larger may require the use of additional sources of tissue. A graft called the Martius graft, or labial fibrofatty tissue graft, is sometimes used to reinforce repairs of larger fistulas, even those that are high in the vaginal vault. The procedure involves a vertical incision on the inner side of the labium majus and detachment of fibroadipose tissue from its underlying bulbocavernosus muscle. This fat-pad flap is vascularized and thus serves as a pedicled graft. It can be tunneled under the vaginal epithelium to reach the site of closure. The procedure has limited use with the vaginal approach to VVF, but is important to be aware of.

Other sources of grafts or flaps that can sometimes be used with the vaginal approach include the gracilis muscle, the gluteal muscle and peritoneum, and fasciocutaneous tissue from the inner thigh.

The avoidance of overlapping suture lines and multiple layers of closure will help ensure a water-tight closure. If there is any leakage upon testing the integrity of the repair, particularly one that is vaginally approached, such leakage will continue and the repair will have been unsuccessful. In an abdominal surgery for VVF, a small amount of remaining leakage will probably resolve on its own after 10-14 days of catheter placement.

Placement of a Jackson-Pratt (JP) drain is controversial. It has been suggested that a JP drain placed on continuous suction will pull urine out of the bladder and increase the risk of a fistula. I don’t place a JP drain in my repairs as I find them to not be helpful. A cystogram can be done 1 week after repair to confirm healing, but there is some debate about whether or not the procedure is useful at that point. In my experience, if the patient does not have a cystogram and gets postrepair leakage, I have the same information as I would have obtained through a positive finding on a cystogram.
 

Dr. Garely is chair of obstetrics and gynecology and director of urogynecology and pelvic reconstructive surgery at the South Nassau Communities Hospital, Oceanside, N.Y., and a clinical professor of obstetrics, gynecology, and reproductive science at the Icahn School of Medicine at Mount Sinai, New York. He has no disclosures related to this column.

Vesicovaginal fistula continues to be the most common form of genitourinary fistula, with resultant diminishment in quality of life secondary to physical and psychosocial distress. While it has been reported that 1 million women in Sub-Saharan Africa have untreated vesicovaginal fistula secondary to obstetric trauma, vesicovaginal fistulas are relatively rare in the United States. Per the United States National Hospital Discharge Survey, in 2007, fewer than 5,000 vesicovaginal fistula repairs were performed out of over 2.3 million procedures involving the female urinary and genital system.

The rarity of the diagnosis is also reflected in data collected from the English National Health Service, where vesicovaginal fistula occurred in 1 in 788 hysterectomies (although more common in radical hysterectomy, at 1 in 87).

In a recent systematic review and meta-analysis on the management of vesicovaginal fistulas in women following benign gynecologic surgery, Bodner-Adler et al. evaluated 282 full-text articles to identify 124 studies for inclusion (PLoS One. 2017 Feb 22;12[2]:e0171554). Only ten studies involved solely conservative management with prolonged bladder drainage. Dismal success was noted: 8%. Surgery was performed in 96.4% of cases (1379/1430); transvaginal in 39%, transabdominal/transvesical in 36%, laparoscopic/robotic approach in 15%, and transabdominal/transvaginal in 3%. Overall success rate in these surgical cases was 97.98% (95% confidence interval, 96.13%-99.29%); with similar procedural success: transvaginal, 89.96%-97.49%; transabdominal/transvesical, 94.55%-99.18%; and laparoscopic/robotic, 96.85%-99.99%. Studies are very limited comparing the various surgical techniques, with only one study comparing transvaginal, transabdominal, and laparoscopic approaches. Interestingly, in this study, the laparoscopic approach was noted to have the least morbidity (Ou CS et al. J Lapraoendosc Adv Surg Tech A. 2004 Feb;14(1):17-21).

For this edition of the Master Class in Gynecologic Surgery, I have enlisted the assistance of Alan D. Garely, MD, FACOG, FACS, of the Icahn School of Medicine at Mount Sinai, New York. Dr. Garely has served on the board of directors for the American Urogynecologic Society, serves as chair of the gynecology and obstetrics advisory board for the American College of Surgeons, and has published numerous papers and book chapters.

It is a pleasure to welcome Dr. Garely to this edition of the Master Class in Gynecologic Surgery.

Dr. Miller is a minimally invasive gynecologic surgeon in Naperville, Ill., and a past president of the AAGL. He has no disclosures related to this column.

Vesicovaginal fistula continues to be the most common form of genitourinary fistula, with resultant diminishment in quality of life secondary to physical and psychosocial distress. While it has been reported that 1 million women in Sub-Saharan Africa have untreated vesicovaginal fistula secondary to obstetric trauma, vesicovaginal fistulas are relatively rare in the United States. Per the United States National Hospital Discharge Survey, in 2007, fewer than 5,000 vesicovaginal fistula repairs were performed out of over 2.3 million procedures involving the female urinary and genital system.

The rarity of the diagnosis is also reflected in data collected from the English National Health Service, where vesicovaginal fistula occurred in 1 in 788 hysterectomies (although more common in radical hysterectomy, at 1 in 87).

In a recent systematic review and meta-analysis on the management of vesicovaginal fistulas in women following benign gynecologic surgery, Bodner-Adler et al. evaluated 282 full-text articles to identify 124 studies for inclusion (PLoS One. 2017 Feb 22;12[2]:e0171554). Only ten studies involved solely conservative management with prolonged bladder drainage. Dismal success was noted: 8%. Surgery was performed in 96.4% of cases (1379/1430); transvaginal in 39%, transabdominal/transvesical in 36%, laparoscopic/robotic approach in 15%, and transabdominal/transvaginal in 3%. Overall success rate in these surgical cases was 97.98% (95% confidence interval, 96.13%-99.29%); with similar procedural success: transvaginal, 89.96%-97.49%; transabdominal/transvesical, 94.55%-99.18%; and laparoscopic/robotic, 96.85%-99.99%. Studies are very limited comparing the various surgical techniques, with only one study comparing transvaginal, transabdominal, and laparoscopic approaches. Interestingly, in this study, the laparoscopic approach was noted to have the least morbidity (Ou CS et al. J Lapraoendosc Adv Surg Tech A. 2004 Feb;14(1):17-21).

For this edition of the Master Class in Gynecologic Surgery, I have enlisted the assistance of Alan D. Garely, MD, FACOG, FACS, of the Icahn School of Medicine at Mount Sinai, New York. Dr. Garely has served on the board of directors for the American Urogynecologic Society, serves as chair of the gynecology and obstetrics advisory board for the American College of Surgeons, and has published numerous papers and book chapters.

It is a pleasure to welcome Dr. Garely to this edition of the Master Class in Gynecologic Surgery.

Dr. Miller is a minimally invasive gynecologic surgeon in Naperville, Ill., and a past president of the AAGL. He has no disclosures related to this column.

Vesicovaginal fistula continues to be the most common form of genitourinary fistula, with resultant diminishment in quality of life secondary to physical and psychosocial distress. While it has been reported that 1 million women in Sub-Saharan Africa have untreated vesicovaginal fistula secondary to obstetric trauma, vesicovaginal fistulas are relatively rare in the United States. Per the United States National Hospital Discharge Survey, in 2007, fewer than 5,000 vesicovaginal fistula repairs were performed out of over 2.3 million procedures involving the female urinary and genital system.

The rarity of the diagnosis is also reflected in data collected from the English National Health Service, where vesicovaginal fistula occurred in 1 in 788 hysterectomies (although more common in radical hysterectomy, at 1 in 87).

In a recent systematic review and meta-analysis on the management of vesicovaginal fistulas in women following benign gynecologic surgery, Bodner-Adler et al. evaluated 282 full-text articles to identify 124 studies for inclusion (PLoS One. 2017 Feb 22;12[2]:e0171554). Only ten studies involved solely conservative management with prolonged bladder drainage. Dismal success was noted: 8%. Surgery was performed in 96.4% of cases (1379/1430); transvaginal in 39%, transabdominal/transvesical in 36%, laparoscopic/robotic approach in 15%, and transabdominal/transvaginal in 3%. Overall success rate in these surgical cases was 97.98% (95% confidence interval, 96.13%-99.29%); with similar procedural success: transvaginal, 89.96%-97.49%; transabdominal/transvesical, 94.55%-99.18%; and laparoscopic/robotic, 96.85%-99.99%. Studies are very limited comparing the various surgical techniques, with only one study comparing transvaginal, transabdominal, and laparoscopic approaches. Interestingly, in this study, the laparoscopic approach was noted to have the least morbidity (Ou CS et al. J Lapraoendosc Adv Surg Tech A. 2004 Feb;14(1):17-21).

For this edition of the Master Class in Gynecologic Surgery, I have enlisted the assistance of Alan D. Garely, MD, FACOG, FACS, of the Icahn School of Medicine at Mount Sinai, New York. Dr. Garely has served on the board of directors for the American Urogynecologic Society, serves as chair of the gynecology and obstetrics advisory board for the American College of Surgeons, and has published numerous papers and book chapters.

It is a pleasure to welcome Dr. Garely to this edition of the Master Class in Gynecologic Surgery.

Dr. Miller is a minimally invasive gynecologic surgeon in Naperville, Ill., and a past president of the AAGL. He has no disclosures related to this column.

Cervical dysplasia is commonly diagnosed in women who have completed childbearing and don’t desire future fertility. While diagnostic and/or definitive therapy for cervical dysplasia can include hysterectomy, there are important considerations to make when offering this procedure to patients.

Pitfalls

Hysterectomy is commonly requested by patients upon learning of cervical dysplasia, particularly if they have chronic human papillomavirus (HPV) infection and have experienced years of frequent surveillance and interventions. They may see hysterectomy as an option to avoid this close surveillance and to be free of their dysplasia. There are two main concerns with offering hysterectomy as the primary surgical option for the management of dysplasia. Firstly, it may not be curative, and secondly, it may be an inadequate excisional procedure, particularly if the patient has occult invasive disease that has not been adequately diagnosed with a loop electrosurgical excision procedure (LEEP) or a cone biopsy procedure.

It is important to counsel these patients that surgery is not a treatment for high-risk HPV infection, which is the underlying etiology of their disease. With that etiology, HPV infection is likely to persist after hysterectomy and they may develop vaginal or vulvar dysplasia. Therefore, the American Society for Colposcopy and Cervical Pathology recommends that cytology and/or high-risk HPV surveillance continue following hysterectomy if that surgery was performed for dysplasia.¹ Hysterectomy is not a means to avoid years of surveillance testing. Approximately 10% of women who have hysterectomy for cervical dysplasia develop vaginal dysplasia or cancer after surgery.^2,3 This is similar to the likelihood of recurrent dysplasia after an alternative excisional procedure. In my experience, this diagnosis is often met with enormous frustration for the patient who thought that her hysterectomy would be the cure of her HPV-related disease. Thorough colposcopic evaluation of the vagina can be technically challenging after hysterectomy because of difficulty adequately visualizing lesions within the vaginal rugations, particularly within the puckered lateral vaginal fornices, the most common location for dysplasia.³ We will explore the diagnosis and treatment options for vaginal dysplasia further in a future column.

It is critical that, if patients are offered hysterectomy for treatment of cervical dysplasia, they are counseled that it may not be curative, that they will require long-term vaginal surveillance, and that they are at continued risk for vaginal and vulvar cancer.

An additional concern with performing hysterectomy for definitive management of cervical dysplasia is the concern that occult cancer may be missed preoperatively, and that the hysterectomy is inadequate surgical clearance of the disease. Approximately 2%-5% of patients with a high-grade squamous intraepithelial lesion or equivocal Pap test have occult cervical cancer.⁴ A similar proportion of patients with cervical intraepithelial neoplasia stage III or adenocarcinoma in situ on colposcopy biopsy have invasive carcinoma on evaluation of an excisional specimen.⁵ The traditional surgical approach has dictated that a modified (type II) or extended (type III) radical hysterectomy be performed in the setting of FIGO stage IA2 or greater cervical cancer. Radical hysterectomies remove parametrial tissue, effectively achieving a wider margin around the primary lesion. This is important because cervical cancer primarily spreads via direct extension.

The appropriate radicality of surgery for microscopic lesions is debated. It has been proposed that for very small, low-risk lesions, a traditional extrafascial hysterectomy or trachelectomy, or possibly even a large conization, may be adequate.⁶ However, this is controversial, and National Comprehensive Cancer Network guidelines still advocate for radical procedures for these lesions.⁷ Certainly an excisional procedure (LEEP or cone) should first be performed to define the size and histologic features of the lesion, and ideally, evaluation and counseling with a gynecologic oncologist should be performed prior to offering patients with a stage IA2 or greater lesion an extrafascial hysterectomy. Additionally, a separate decision would need to be made regarding the need for lymphadenectomy, as this is typically recommended for patients with stage IA2 or greater lesions.

Patients should be counseled that, if extrafascial (simple) hysterectomy is chosen as the primary excisional procedure, they may require additional therapy (additional surgery, or radiation and possibly chemotherapy) if cancer is found in the specimen and the parametrial margin is inadequate. Additionally, and of more concern, if the lesion is a bulky lesion extending into the parametrium and not recognized preoperatively, a “cut-through” hysterectomy will be inadvertently performed (in which margins are grossly positive). These situations typically feature heavy blood loss with patients at increased risk for immediate surgical complications. Postoperatively, prognosis is substantially worse for patients who have had a cut-through hysterectomy, compared stage for stage with patients who primarily received a radical procedure with negative margins or primary chemotherapy and radiation.⁸ Otherwise said, their risk for death is higher if this error is made. Therefore a thorough examination is essential prior to performing hysterectomy for dysplasia. Any suspicion of bulky cancer should be considered a contraindication for proceeding.
 

Preoperative evaluation

As a rule, no patient should transition directly from cytologic evaluation with Pap screening to hysterectomy. A colposcopic evaluation of the cervix and vagina accompanied with a thorough bimanual rectovaginal examination should always be performed first. Biopsies of the ectocervix and ideally the endocervix should be obtained because the accuracy of histology is greater than that of cytology. For patients with cervical intraepithelial neoplasia stage I lesions, hysterectomy is not appropriate, as these patients have an extremely low risk for the development of cervical cancer, and the risks and costs of hysterectomy are not justified in such a population.

Surgeons should wait at least 6 weeks following conization or LEEP before performing hysterectomy in order to minimize the likelihood of perioperative complications.⁹

Substituting LEEP or cone with hysterectomy

In general, it is the most prudent approach to first perform a diagnostic excision with LEEP or cone biopsy before proceeding with hysterectomy for definitive surgery. However, there may be some situations in which this is not feasible. In patients whose cervix is very small and flush with the vagina, an excisional procedure may not be technically possible without concern for damage to adjacent structures. In these patients, after a thorough exam has evaluated for gross disease, a hysterectomy may be the only way to adequately diagnose and treat high-grade dysplasia through excision. For patients with limited access to resources, transportation, or a concern for noncompliance with follow-up, surgeons may wish to offer patients primary hysterectomy rather than a staged procedure.

Hysterectomy remains a potential option for treatment of cervical dysplasia. However, patients should be made aware of the risks of undertreatment of occult cancers, the need for long-term surveillance testing, and the risk for future vaginal dysplasia or cancer. Ideally a comprehensive, stepwise assessment from cytology to colposcopy and examination to diagnostic excisional procedure will first take place to proceed safely with this approach.

References

1. Saslow D et al. American Cancer Society, American Society for Colposcopy and Cervical Pathology, and American Society for Clinical Pathology screening guidelines for the prevention and early detection of cervical cancer. CA Cancer J Clin. 2012 May-Jun;62(3):147-72.

2. Schockaert S et al. Incidence of vaginal intraepithelial neoplasia after hysterectomy for cervical intraepithelial neoplasia: a retrospective study. Am J Obstet Gynecol. 2008 Aug;199(2):113.e1-5.

3. Kalogirou D et al. Vaginal intraepithelial neoplasia (VAIN) following hysterectomy in patients treated for carcinoma in situ of the cervix. Eur J Gynaecol Oncol. 1997;18(3):188-91.

4. Landy R et al. Evaluating cytology for the detection of invasive cervical cancer. Cytopathology. 2016 Jun;27(3):201-9.

5. Latif NA et al. Management of adenocarcinoma in situ of the uterine cervix: a comparison of loop electrosurgical excision procedure and cold knife conization. J Low Genit Tract Dis. 2015 Apr;19(2):97-102.

6. Bai H et al. The potential for less radical surgery in women with stage IA2-IB1 cervical cancer. Int J Gynaecol Obstet. 2015 Sep;130(3):235-40.

7. National Comprehensive Cancer Network Clinical Practice Guidelines in Oncology. Version 2.2018. 2018 Jun 26.

8. Barber HR et al. Operative management of patients previously operated upon for a benign lesion with cervical cancer as a surprise finding. Am J Obstet Gynecol. 1968 Aug 1;101(7):959-65.

9. Sullivan SA et al. Association between timing of cervical excision procedure to minimally invasive hysterectomy and surgical complications. Gynecol Oncol. 2017 Feb;144(2):294-298.

Cervical dysplasia is commonly diagnosed in women who have completed childbearing and don’t desire future fertility. While diagnostic and/or definitive therapy for cervical dysplasia can include hysterectomy, there are important considerations to make when offering this procedure to patients.

Pitfalls

Hysterectomy is commonly requested by patients upon learning of cervical dysplasia, particularly if they have chronic human papillomavirus (HPV) infection and have experienced years of frequent surveillance and interventions. They may see hysterectomy as an option to avoid this close surveillance and to be free of their dysplasia. There are two main concerns with offering hysterectomy as the primary surgical option for the management of dysplasia. Firstly, it may not be curative, and secondly, it may be an inadequate excisional procedure, particularly if the patient has occult invasive disease that has not been adequately diagnosed with a loop electrosurgical excision procedure (LEEP) or a cone biopsy procedure.

It is important to counsel these patients that surgery is not a treatment for high-risk HPV infection, which is the underlying etiology of their disease. With that etiology, HPV infection is likely to persist after hysterectomy and they may develop vaginal or vulvar dysplasia. Therefore, the American Society for Colposcopy and Cervical Pathology recommends that cytology and/or high-risk HPV surveillance continue following hysterectomy if that surgery was performed for dysplasia.¹ Hysterectomy is not a means to avoid years of surveillance testing. Approximately 10% of women who have hysterectomy for cervical dysplasia develop vaginal dysplasia or cancer after surgery.^2,3 This is similar to the likelihood of recurrent dysplasia after an alternative excisional procedure. In my experience, this diagnosis is often met with enormous frustration for the patient who thought that her hysterectomy would be the cure of her HPV-related disease. Thorough colposcopic evaluation of the vagina can be technically challenging after hysterectomy because of difficulty adequately visualizing lesions within the vaginal rugations, particularly within the puckered lateral vaginal fornices, the most common location for dysplasia.³ We will explore the diagnosis and treatment options for vaginal dysplasia further in a future column.

It is critical that, if patients are offered hysterectomy for treatment of cervical dysplasia, they are counseled that it may not be curative, that they will require long-term vaginal surveillance, and that they are at continued risk for vaginal and vulvar cancer.

An additional concern with performing hysterectomy for definitive management of cervical dysplasia is the concern that occult cancer may be missed preoperatively, and that the hysterectomy is inadequate surgical clearance of the disease. Approximately 2%-5% of patients with a high-grade squamous intraepithelial lesion or equivocal Pap test have occult cervical cancer.⁴ A similar proportion of patients with cervical intraepithelial neoplasia stage III or adenocarcinoma in situ on colposcopy biopsy have invasive carcinoma on evaluation of an excisional specimen.⁵ The traditional surgical approach has dictated that a modified (type II) or extended (type III) radical hysterectomy be performed in the setting of FIGO stage IA2 or greater cervical cancer. Radical hysterectomies remove parametrial tissue, effectively achieving a wider margin around the primary lesion. This is important because cervical cancer primarily spreads via direct extension.

The appropriate radicality of surgery for microscopic lesions is debated. It has been proposed that for very small, low-risk lesions, a traditional extrafascial hysterectomy or trachelectomy, or possibly even a large conization, may be adequate.⁶ However, this is controversial, and National Comprehensive Cancer Network guidelines still advocate for radical procedures for these lesions.⁷ Certainly an excisional procedure (LEEP or cone) should first be performed to define the size and histologic features of the lesion, and ideally, evaluation and counseling with a gynecologic oncologist should be performed prior to offering patients with a stage IA2 or greater lesion an extrafascial hysterectomy. Additionally, a separate decision would need to be made regarding the need for lymphadenectomy, as this is typically recommended for patients with stage IA2 or greater lesions.

Patients should be counseled that, if extrafascial (simple) hysterectomy is chosen as the primary excisional procedure, they may require additional therapy (additional surgery, or radiation and possibly chemotherapy) if cancer is found in the specimen and the parametrial margin is inadequate. Additionally, and of more concern, if the lesion is a bulky lesion extending into the parametrium and not recognized preoperatively, a “cut-through” hysterectomy will be inadvertently performed (in which margins are grossly positive). These situations typically feature heavy blood loss with patients at increased risk for immediate surgical complications. Postoperatively, prognosis is substantially worse for patients who have had a cut-through hysterectomy, compared stage for stage with patients who primarily received a radical procedure with negative margins or primary chemotherapy and radiation.⁸ Otherwise said, their risk for death is higher if this error is made. Therefore a thorough examination is essential prior to performing hysterectomy for dysplasia. Any suspicion of bulky cancer should be considered a contraindication for proceeding.
 

Preoperative evaluation

As a rule, no patient should transition directly from cytologic evaluation with Pap screening to hysterectomy. A colposcopic evaluation of the cervix and vagina accompanied with a thorough bimanual rectovaginal examination should always be performed first. Biopsies of the ectocervix and ideally the endocervix should be obtained because the accuracy of histology is greater than that of cytology. For patients with cervical intraepithelial neoplasia stage I lesions, hysterectomy is not appropriate, as these patients have an extremely low risk for the development of cervical cancer, and the risks and costs of hysterectomy are not justified in such a population.

Surgeons should wait at least 6 weeks following conization or LEEP before performing hysterectomy in order to minimize the likelihood of perioperative complications.⁹

Substituting LEEP or cone with hysterectomy

In general, it is the most prudent approach to first perform a diagnostic excision with LEEP or cone biopsy before proceeding with hysterectomy for definitive surgery. However, there may be some situations in which this is not feasible. In patients whose cervix is very small and flush with the vagina, an excisional procedure may not be technically possible without concern for damage to adjacent structures. In these patients, after a thorough exam has evaluated for gross disease, a hysterectomy may be the only way to adequately diagnose and treat high-grade dysplasia through excision. For patients with limited access to resources, transportation, or a concern for noncompliance with follow-up, surgeons may wish to offer patients primary hysterectomy rather than a staged procedure.

Hysterectomy remains a potential option for treatment of cervical dysplasia. However, patients should be made aware of the risks of undertreatment of occult cancers, the need for long-term surveillance testing, and the risk for future vaginal dysplasia or cancer. Ideally a comprehensive, stepwise assessment from cytology to colposcopy and examination to diagnostic excisional procedure will first take place to proceed safely with this approach.

References

1. Saslow D et al. American Cancer Society, American Society for Colposcopy and Cervical Pathology, and American Society for Clinical Pathology screening guidelines for the prevention and early detection of cervical cancer. CA Cancer J Clin. 2012 May-Jun;62(3):147-72.

2. Schockaert S et al. Incidence of vaginal intraepithelial neoplasia after hysterectomy for cervical intraepithelial neoplasia: a retrospective study. Am J Obstet Gynecol. 2008 Aug;199(2):113.e1-5.

3. Kalogirou D et al. Vaginal intraepithelial neoplasia (VAIN) following hysterectomy in patients treated for carcinoma in situ of the cervix. Eur J Gynaecol Oncol. 1997;18(3):188-91.

4. Landy R et al. Evaluating cytology for the detection of invasive cervical cancer. Cytopathology. 2016 Jun;27(3):201-9.

5. Latif NA et al. Management of adenocarcinoma in situ of the uterine cervix: a comparison of loop electrosurgical excision procedure and cold knife conization. J Low Genit Tract Dis. 2015 Apr;19(2):97-102.

6. Bai H et al. The potential for less radical surgery in women with stage IA2-IB1 cervical cancer. Int J Gynaecol Obstet. 2015 Sep;130(3):235-40.

7. National Comprehensive Cancer Network Clinical Practice Guidelines in Oncology. Version 2.2018. 2018 Jun 26.

8. Barber HR et al. Operative management of patients previously operated upon for a benign lesion with cervical cancer as a surprise finding. Am J Obstet Gynecol. 1968 Aug 1;101(7):959-65.

9. Sullivan SA et al. Association between timing of cervical excision procedure to minimally invasive hysterectomy and surgical complications. Gynecol Oncol. 2017 Feb;144(2):294-298.

Cervical dysplasia is commonly diagnosed in women who have completed childbearing and don’t desire future fertility. While diagnostic and/or definitive therapy for cervical dysplasia can include hysterectomy, there are important considerations to make when offering this procedure to patients.

Pitfalls

Hysterectomy is commonly requested by patients upon learning of cervical dysplasia, particularly if they have chronic human papillomavirus (HPV) infection and have experienced years of frequent surveillance and interventions. They may see hysterectomy as an option to avoid this close surveillance and to be free of their dysplasia. There are two main concerns with offering hysterectomy as the primary surgical option for the management of dysplasia. Firstly, it may not be curative, and secondly, it may be an inadequate excisional procedure, particularly if the patient has occult invasive disease that has not been adequately diagnosed with a loop electrosurgical excision procedure (LEEP) or a cone biopsy procedure.

It is important to counsel these patients that surgery is not a treatment for high-risk HPV infection, which is the underlying etiology of their disease. With that etiology, HPV infection is likely to persist after hysterectomy and they may develop vaginal or vulvar dysplasia. Therefore, the American Society for Colposcopy and Cervical Pathology recommends that cytology and/or high-risk HPV surveillance continue following hysterectomy if that surgery was performed for dysplasia.¹ Hysterectomy is not a means to avoid years of surveillance testing. Approximately 10% of women who have hysterectomy for cervical dysplasia develop vaginal dysplasia or cancer after surgery.^2,3 This is similar to the likelihood of recurrent dysplasia after an alternative excisional procedure. In my experience, this diagnosis is often met with enormous frustration for the patient who thought that her hysterectomy would be the cure of her HPV-related disease. Thorough colposcopic evaluation of the vagina can be technically challenging after hysterectomy because of difficulty adequately visualizing lesions within the vaginal rugations, particularly within the puckered lateral vaginal fornices, the most common location for dysplasia.³ We will explore the diagnosis and treatment options for vaginal dysplasia further in a future column.

It is critical that, if patients are offered hysterectomy for treatment of cervical dysplasia, they are counseled that it may not be curative, that they will require long-term vaginal surveillance, and that they are at continued risk for vaginal and vulvar cancer.

An additional concern with performing hysterectomy for definitive management of cervical dysplasia is the concern that occult cancer may be missed preoperatively, and that the hysterectomy is inadequate surgical clearance of the disease. Approximately 2%-5% of patients with a high-grade squamous intraepithelial lesion or equivocal Pap test have occult cervical cancer.⁴ A similar proportion of patients with cervical intraepithelial neoplasia stage III or adenocarcinoma in situ on colposcopy biopsy have invasive carcinoma on evaluation of an excisional specimen.⁵ The traditional surgical approach has dictated that a modified (type II) or extended (type III) radical hysterectomy be performed in the setting of FIGO stage IA2 or greater cervical cancer. Radical hysterectomies remove parametrial tissue, effectively achieving a wider margin around the primary lesion. This is important because cervical cancer primarily spreads via direct extension.

The appropriate radicality of surgery for microscopic lesions is debated. It has been proposed that for very small, low-risk lesions, a traditional extrafascial hysterectomy or trachelectomy, or possibly even a large conization, may be adequate.⁶ However, this is controversial, and National Comprehensive Cancer Network guidelines still advocate for radical procedures for these lesions.⁷ Certainly an excisional procedure (LEEP or cone) should first be performed to define the size and histologic features of the lesion, and ideally, evaluation and counseling with a gynecologic oncologist should be performed prior to offering patients with a stage IA2 or greater lesion an extrafascial hysterectomy. Additionally, a separate decision would need to be made regarding the need for lymphadenectomy, as this is typically recommended for patients with stage IA2 or greater lesions.

Patients should be counseled that, if extrafascial (simple) hysterectomy is chosen as the primary excisional procedure, they may require additional therapy (additional surgery, or radiation and possibly chemotherapy) if cancer is found in the specimen and the parametrial margin is inadequate. Additionally, and of more concern, if the lesion is a bulky lesion extending into the parametrium and not recognized preoperatively, a “cut-through” hysterectomy will be inadvertently performed (in which margins are grossly positive). These situations typically feature heavy blood loss with patients at increased risk for immediate surgical complications. Postoperatively, prognosis is substantially worse for patients who have had a cut-through hysterectomy, compared stage for stage with patients who primarily received a radical procedure with negative margins or primary chemotherapy and radiation.⁸ Otherwise said, their risk for death is higher if this error is made. Therefore a thorough examination is essential prior to performing hysterectomy for dysplasia. Any suspicion of bulky cancer should be considered a contraindication for proceeding.
 

Preoperative evaluation

As a rule, no patient should transition directly from cytologic evaluation with Pap screening to hysterectomy. A colposcopic evaluation of the cervix and vagina accompanied with a thorough bimanual rectovaginal examination should always be performed first. Biopsies of the ectocervix and ideally the endocervix should be obtained because the accuracy of histology is greater than that of cytology. For patients with cervical intraepithelial neoplasia stage I lesions, hysterectomy is not appropriate, as these patients have an extremely low risk for the development of cervical cancer, and the risks and costs of hysterectomy are not justified in such a population.

Surgeons should wait at least 6 weeks following conization or LEEP before performing hysterectomy in order to minimize the likelihood of perioperative complications.⁹

Substituting LEEP or cone with hysterectomy

In general, it is the most prudent approach to first perform a diagnostic excision with LEEP or cone biopsy before proceeding with hysterectomy for definitive surgery. However, there may be some situations in which this is not feasible. In patients whose cervix is very small and flush with the vagina, an excisional procedure may not be technically possible without concern for damage to adjacent structures. In these patients, after a thorough exam has evaluated for gross disease, a hysterectomy may be the only way to adequately diagnose and treat high-grade dysplasia through excision. For patients with limited access to resources, transportation, or a concern for noncompliance with follow-up, surgeons may wish to offer patients primary hysterectomy rather than a staged procedure.

Hysterectomy remains a potential option for treatment of cervical dysplasia. However, patients should be made aware of the risks of undertreatment of occult cancers, the need for long-term surveillance testing, and the risk for future vaginal dysplasia or cancer. Ideally a comprehensive, stepwise assessment from cytology to colposcopy and examination to diagnostic excisional procedure will first take place to proceed safely with this approach.

References

1. Saslow D et al. American Cancer Society, American Society for Colposcopy and Cervical Pathology, and American Society for Clinical Pathology screening guidelines for the prevention and early detection of cervical cancer. CA Cancer J Clin. 2012 May-Jun;62(3):147-72.

2. Schockaert S et al. Incidence of vaginal intraepithelial neoplasia after hysterectomy for cervical intraepithelial neoplasia: a retrospective study. Am J Obstet Gynecol. 2008 Aug;199(2):113.e1-5.

3. Kalogirou D et al. Vaginal intraepithelial neoplasia (VAIN) following hysterectomy in patients treated for carcinoma in situ of the cervix. Eur J Gynaecol Oncol. 1997;18(3):188-91.

4. Landy R et al. Evaluating cytology for the detection of invasive cervical cancer. Cytopathology. 2016 Jun;27(3):201-9.

5. Latif NA et al. Management of adenocarcinoma in situ of the uterine cervix: a comparison of loop electrosurgical excision procedure and cold knife conization. J Low Genit Tract Dis. 2015 Apr;19(2):97-102.

6. Bai H et al. The potential for less radical surgery in women with stage IA2-IB1 cervical cancer. Int J Gynaecol Obstet. 2015 Sep;130(3):235-40.

7. National Comprehensive Cancer Network Clinical Practice Guidelines in Oncology. Version 2.2018. 2018 Jun 26.

8. Barber HR et al. Operative management of patients previously operated upon for a benign lesion with cervical cancer as a surprise finding. Am J Obstet Gynecol. 1968 Aug 1;101(7):959-65.

9. Sullivan SA et al. Association between timing of cervical excision procedure to minimally invasive hysterectomy and surgical complications. Gynecol Oncol. 2017 Feb;144(2):294-298.