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Heart rate variability may be risk factor for depression, not a consequence
While some investigations have suggested that depression may lead to later unfavorable effects on heart rate variability, authors of a newly published study say they have found stronger evidence that the opposite is true.
Lower heart rate variability was independently associated with later increases in depressive symptoms, according to results of the longitudinal, twin difference study.
When researchers looked at the opposite direction, they found earlier depressive symptoms were associated with lower heart rate variability at follow-up in the study; however, investigators said those associations were not as robust and were largely explainable by antidepressant use.
That meant reduced heart rate variability is more likely a risk factor for depression, rather than a consequence, according to Minxuan Huang, ScM, of the department of epidemiology at Emory University Rollins School of Public Health, Atlanta, and his coinvestigators.
“These findings point to a central role of the autonomic nervous system in the regulation of mood and depression vulnerability,” they wrote in a report on the study appearing in JAMA Psychiatry.
The published analysis included 146 male twins, or 73 pairs, who participated in the national Vietnam Era Twin Registry.
Previous studies have linked depression to heart rate variability, a noninvasive index of cardiac autonomic nervous system regulation. However, these studies are not consistent on whether depression affects heart rate variability or vice versa, and the studies have been limited in their ability to assess the relationship between those two variables over time, the investigators said.
By contrast, the current study evaluated depression and heart rate variability at two time points: a baseline assessment conducted during 2002-2006 and a at a 7-year follow-up visit.
Investigators found consistent associations between heart rate variability on 24-hour electrocardiogram monitoring at baseline and scores on the Beck Depression Inventory-II at the 7-year follow-up, with beta coefficients ranging from –0.14 to –0.29, the report showed.
By contrast, the associations were less consistent between BDI-II score at the baseline visit and heart rate variability at follow-up, the investigators said. “These associations were largely explained by antidepressant use, which when added to the model, weakened the associations.”
These findings may help guide future research aimed at identifying individuals at a higher risk of later depression, the authors said, noting that treatment studies also are warranted. “Future interventions modulating autonomic nervous system regulation may be useful for the prevention and treatment of depression.” The study was supported by the National Institutes of Health. The Department of Veterans Affairs has supported the Vietnam Era Twin Registry. The researchers had no conflicts of interest.
SOURCE: Huang M et al. JAMA Psychiatry. 2018 May 16. doi: 10.1001/jamapsychiatry.2018.0747.
While some investigations have suggested that depression may lead to later unfavorable effects on heart rate variability, authors of a newly published study say they have found stronger evidence that the opposite is true.
Lower heart rate variability was independently associated with later increases in depressive symptoms, according to results of the longitudinal, twin difference study.
When researchers looked at the opposite direction, they found earlier depressive symptoms were associated with lower heart rate variability at follow-up in the study; however, investigators said those associations were not as robust and were largely explainable by antidepressant use.
That meant reduced heart rate variability is more likely a risk factor for depression, rather than a consequence, according to Minxuan Huang, ScM, of the department of epidemiology at Emory University Rollins School of Public Health, Atlanta, and his coinvestigators.
“These findings point to a central role of the autonomic nervous system in the regulation of mood and depression vulnerability,” they wrote in a report on the study appearing in JAMA Psychiatry.
The published analysis included 146 male twins, or 73 pairs, who participated in the national Vietnam Era Twin Registry.
Previous studies have linked depression to heart rate variability, a noninvasive index of cardiac autonomic nervous system regulation. However, these studies are not consistent on whether depression affects heart rate variability or vice versa, and the studies have been limited in their ability to assess the relationship between those two variables over time, the investigators said.
By contrast, the current study evaluated depression and heart rate variability at two time points: a baseline assessment conducted during 2002-2006 and a at a 7-year follow-up visit.
Investigators found consistent associations between heart rate variability on 24-hour electrocardiogram monitoring at baseline and scores on the Beck Depression Inventory-II at the 7-year follow-up, with beta coefficients ranging from –0.14 to –0.29, the report showed.
By contrast, the associations were less consistent between BDI-II score at the baseline visit and heart rate variability at follow-up, the investigators said. “These associations were largely explained by antidepressant use, which when added to the model, weakened the associations.”
These findings may help guide future research aimed at identifying individuals at a higher risk of later depression, the authors said, noting that treatment studies also are warranted. “Future interventions modulating autonomic nervous system regulation may be useful for the prevention and treatment of depression.” The study was supported by the National Institutes of Health. The Department of Veterans Affairs has supported the Vietnam Era Twin Registry. The researchers had no conflicts of interest.
SOURCE: Huang M et al. JAMA Psychiatry. 2018 May 16. doi: 10.1001/jamapsychiatry.2018.0747.
While some investigations have suggested that depression may lead to later unfavorable effects on heart rate variability, authors of a newly published study say they have found stronger evidence that the opposite is true.
Lower heart rate variability was independently associated with later increases in depressive symptoms, according to results of the longitudinal, twin difference study.
When researchers looked at the opposite direction, they found earlier depressive symptoms were associated with lower heart rate variability at follow-up in the study; however, investigators said those associations were not as robust and were largely explainable by antidepressant use.
That meant reduced heart rate variability is more likely a risk factor for depression, rather than a consequence, according to Minxuan Huang, ScM, of the department of epidemiology at Emory University Rollins School of Public Health, Atlanta, and his coinvestigators.
“These findings point to a central role of the autonomic nervous system in the regulation of mood and depression vulnerability,” they wrote in a report on the study appearing in JAMA Psychiatry.
The published analysis included 146 male twins, or 73 pairs, who participated in the national Vietnam Era Twin Registry.
Previous studies have linked depression to heart rate variability, a noninvasive index of cardiac autonomic nervous system regulation. However, these studies are not consistent on whether depression affects heart rate variability or vice versa, and the studies have been limited in their ability to assess the relationship between those two variables over time, the investigators said.
By contrast, the current study evaluated depression and heart rate variability at two time points: a baseline assessment conducted during 2002-2006 and a at a 7-year follow-up visit.
Investigators found consistent associations between heart rate variability on 24-hour electrocardiogram monitoring at baseline and scores on the Beck Depression Inventory-II at the 7-year follow-up, with beta coefficients ranging from –0.14 to –0.29, the report showed.
By contrast, the associations were less consistent between BDI-II score at the baseline visit and heart rate variability at follow-up, the investigators said. “These associations were largely explained by antidepressant use, which when added to the model, weakened the associations.”
These findings may help guide future research aimed at identifying individuals at a higher risk of later depression, the authors said, noting that treatment studies also are warranted. “Future interventions modulating autonomic nervous system regulation may be useful for the prevention and treatment of depression.” The study was supported by the National Institutes of Health. The Department of Veterans Affairs has supported the Vietnam Era Twin Registry. The researchers had no conflicts of interest.
SOURCE: Huang M et al. JAMA Psychiatry. 2018 May 16. doi: 10.1001/jamapsychiatry.2018.0747.
FROM JAMA PSYCHIATRY
Key clinical point:
Major finding: There were consistent associations between baseline heart rate variability and later depression scores (beta coefficients ranged from –0.14 to –0.29).
Study details: A longitudinal twin difference study including 166 individuals in the Vietnam Era Twin Registry, including baseline assessments conducted during 2002-2006 plus a 7-year follow-up visit.
Disclosures: The study was supported by the National Institutes of Health. The Department of Veterans Affairs has supported the Vietnam Era Twin Registry. Study authors had no conflicts of interest.
Source: Huang M et al. JAMA Psychiatry. 2018 May 16. doi: 10.1001/jamapsychiatry.2018.0747.
Two more and counting: Suicide in medical trainees
Like everyone in the arc of social media impact, I was shocked and terribly saddened by the recent suicides of two New York women in medicine – a final-year medical student on May 1 and a second-year resident on May 5. As a specialist in physician health, a former training director, a long-standing member of our institution’s medical student admissions committee, and the ombudsman for our medical students, I am finding these tragedies harder and harder to reconcile. Something isn’t working. But before I get to that, what follows is a bulleted list of some events of the past couple of weeks that may give a context for my statements and have informed my two recommendations.
- May 3, 2018: I give an invited GI grand rounds on stress, burnout, depression, and suicide in physicians. The residents are quiet and say nothing. Faculty members seem only concerned about preventing and eradicating burnout – and not that interested in anything more severe.
- May 5: A psychiatry resident from Melbourne arrives to spend 10 days with me to do an elective in physician health. As in the United States, there is a significant suicide death rate in medical students and residents Down Under. In the afternoon, I present a paper at the annual meeting of the American Academy of Psychodynamic Psychiatry and Psychoanalysis on the use of psychotherapy in treatment-resistant suicidal depression in physicians. There is increasing hope that this essential modality of care will return to the contemporary psychiatrist’s toolbox.
- May 6: At the annual meeting of the American Psychiatric Association in New York, I’m the discussant for powerful heartfelt papers of five psychiatrists (mostly early career psychiatrists and one resident) that talked about living with a psychiatric illness. The audience is huge, and we hear narratives about internal stigma, self-disclosure, external stigma, shunning, bullying, acceptance, rejection, alienation, connection, and love by peers and family. The authenticity and valor of the speakers create an atmosphere of safety, which enables psychiatrists in attendance from all over the world to share their personal stories – some at the microphone, some privately.
- May 7: Again at the APA, I chair and facilitate a workshop on physician suicide. We hear from four speakers, all women, who have lost a loved one to suicide – a husband, a father, a brother, a son – all doctors. Two of the speakers are psychiatrists. The stories are gripping, detailed, and tender. Yes, the atmosphere is very sad, but there is not a pall. We learn how these doctors lived, not just how they died. They all loved medicine; they were creative; they cared deeply; they suffered silently; and with shame, they lost hope. Again, a big audience of psychiatrists, many of whom share their own stories, that they, too, had lost a physician son, wife, or mother to suicide. Some of their deceased family members fell through the cracks and did not receive the life-saving care they deserved; some, fearing assaults to their medical license, hospital privileges, or insurance, refused to see anyone. They died untreated.
- May 8: Still at the APA, a psychiatrist colleague and I collaborate on a clinical case conference. Each of us describes losing a physician patient to suicide. We walk the attendees through the clinical details of assessment, treatment, and the aftermath of their deaths. We talk openly and frankly about our feelings, grief, outreach to colleagues and the family, and our own personal journeys of learning, growth, and healing. The clinician audience members give constructive feedback, and some share their own stories of losing patients to suicide. Like the day before, some psychiatrists are grieving the loss of a physician son or sibling to suicide. As mental health professionals, they suffer from an additional layer of failure and guilt that a loved one died “under their watch.”
- May 8: I rush across the Javits Center to catch the discussant for a concurrent symposium on physician burnout and depression. She foregoes any prepared remarks to share her previous 48 hours with the audience. She is the training director of the program that lost the second-year resident on May 5. She did not learn of the death until 24 hours later. We are all on the edge of our seats as we listen to this grieving, courageous woman, a seasoned psychiatrist and educator, who has been blindsided by this tragedy. She has not slept. She called all of her residents and broke the news personally as best she could. Aided by “After A Suicide: A Toolkit for Residency/Fellowship Programs” (American Foundation for Suicide Prevention), she and her colleagues instituted a plan of action and worked with administration and faculty. Her strength and commitment to the well-being of her trainees is palpable and magnanimous. When the session ends, many of us stand in line to give her a hug. It is a stark reminder of how many lives are affected when someone you know or care about takes his/her own life – and how, in the house of medicine, medical students and residents really are part of an institutional family.
- May 10: I facilitate a meeting of our 12 second-year residents, many of whom knew of or had met the resident who died. Almost everyone speaks, shares their feelings, poses questions, and calls for answers and change. There is disbelief, sadness, confusion, some guilt, and lots of anger. Also a feeling of disillusionment or paradox about the field of psychiatry: “Of all branches of medicine, shouldn’t residents who are struggling with psychiatric issues feel safe, protected, cared for in psychiatry?” There is also a feeling of lip service being paid to personal treatment, as in quoted statements: “By all means, get treatment for your issues, but don’t let it encroach on your duty hours” or “It’s good you’re getting help, but do you still have to go weekly?”
In the immediate aftermath of suicide, feelings run high, as they should. But rather than wait it out – and fearing a return to “business as usual” – let me make only two suggestions:
2. In psychiatry, we need to redouble our efforts in fighting the stigma attached to psychiatric illness in trainees. It is unconscionable that medical students and residents are dying of treatable disorders (I’ve never heard of a doctor dying of cancer who didn’t go to an oncologist at least once), yet too many are not availing themselves of services we provide – even when they’re free of charge or covered by insurance. And are we certain that, when they knock on our doors, we are providing them with state-of-the-art care? Is it possible that unrecognized internal stigma and shame deep within us might make us hesitant to help our trainees in their hour of need? Or cut corners? Or not get a second opinion? Very few psychiatrists on faculty of our medical schools divulge their personal experiences of depression, posttraumatic stress disorders, substance use disorders, and more (with the exception of being in therapy during residency, which is normative and isn’t stigmatized). Coming out is leveling, humane, and respectful – and it shrinks the power differential in the teaching dyad. It might even save a life.
Dr. Myers is a professor of clinical psychiatry at State University of New York, Brooklyn, and the author of “Why Physicians Die by Suicide: Lessons Learned From Their Families and Others Who Cared.”
Like everyone in the arc of social media impact, I was shocked and terribly saddened by the recent suicides of two New York women in medicine – a final-year medical student on May 1 and a second-year resident on May 5. As a specialist in physician health, a former training director, a long-standing member of our institution’s medical student admissions committee, and the ombudsman for our medical students, I am finding these tragedies harder and harder to reconcile. Something isn’t working. But before I get to that, what follows is a bulleted list of some events of the past couple of weeks that may give a context for my statements and have informed my two recommendations.
- May 3, 2018: I give an invited GI grand rounds on stress, burnout, depression, and suicide in physicians. The residents are quiet and say nothing. Faculty members seem only concerned about preventing and eradicating burnout – and not that interested in anything more severe.
- May 5: A psychiatry resident from Melbourne arrives to spend 10 days with me to do an elective in physician health. As in the United States, there is a significant suicide death rate in medical students and residents Down Under. In the afternoon, I present a paper at the annual meeting of the American Academy of Psychodynamic Psychiatry and Psychoanalysis on the use of psychotherapy in treatment-resistant suicidal depression in physicians. There is increasing hope that this essential modality of care will return to the contemporary psychiatrist’s toolbox.
- May 6: At the annual meeting of the American Psychiatric Association in New York, I’m the discussant for powerful heartfelt papers of five psychiatrists (mostly early career psychiatrists and one resident) that talked about living with a psychiatric illness. The audience is huge, and we hear narratives about internal stigma, self-disclosure, external stigma, shunning, bullying, acceptance, rejection, alienation, connection, and love by peers and family. The authenticity and valor of the speakers create an atmosphere of safety, which enables psychiatrists in attendance from all over the world to share their personal stories – some at the microphone, some privately.
- May 7: Again at the APA, I chair and facilitate a workshop on physician suicide. We hear from four speakers, all women, who have lost a loved one to suicide – a husband, a father, a brother, a son – all doctors. Two of the speakers are psychiatrists. The stories are gripping, detailed, and tender. Yes, the atmosphere is very sad, but there is not a pall. We learn how these doctors lived, not just how they died. They all loved medicine; they were creative; they cared deeply; they suffered silently; and with shame, they lost hope. Again, a big audience of psychiatrists, many of whom share their own stories, that they, too, had lost a physician son, wife, or mother to suicide. Some of their deceased family members fell through the cracks and did not receive the life-saving care they deserved; some, fearing assaults to their medical license, hospital privileges, or insurance, refused to see anyone. They died untreated.
- May 8: Still at the APA, a psychiatrist colleague and I collaborate on a clinical case conference. Each of us describes losing a physician patient to suicide. We walk the attendees through the clinical details of assessment, treatment, and the aftermath of their deaths. We talk openly and frankly about our feelings, grief, outreach to colleagues and the family, and our own personal journeys of learning, growth, and healing. The clinician audience members give constructive feedback, and some share their own stories of losing patients to suicide. Like the day before, some psychiatrists are grieving the loss of a physician son or sibling to suicide. As mental health professionals, they suffer from an additional layer of failure and guilt that a loved one died “under their watch.”
- May 8: I rush across the Javits Center to catch the discussant for a concurrent symposium on physician burnout and depression. She foregoes any prepared remarks to share her previous 48 hours with the audience. She is the training director of the program that lost the second-year resident on May 5. She did not learn of the death until 24 hours later. We are all on the edge of our seats as we listen to this grieving, courageous woman, a seasoned psychiatrist and educator, who has been blindsided by this tragedy. She has not slept. She called all of her residents and broke the news personally as best she could. Aided by “After A Suicide: A Toolkit for Residency/Fellowship Programs” (American Foundation for Suicide Prevention), she and her colleagues instituted a plan of action and worked with administration and faculty. Her strength and commitment to the well-being of her trainees is palpable and magnanimous. When the session ends, many of us stand in line to give her a hug. It is a stark reminder of how many lives are affected when someone you know or care about takes his/her own life – and how, in the house of medicine, medical students and residents really are part of an institutional family.
- May 10: I facilitate a meeting of our 12 second-year residents, many of whom knew of or had met the resident who died. Almost everyone speaks, shares their feelings, poses questions, and calls for answers and change. There is disbelief, sadness, confusion, some guilt, and lots of anger. Also a feeling of disillusionment or paradox about the field of psychiatry: “Of all branches of medicine, shouldn’t residents who are struggling with psychiatric issues feel safe, protected, cared for in psychiatry?” There is also a feeling of lip service being paid to personal treatment, as in quoted statements: “By all means, get treatment for your issues, but don’t let it encroach on your duty hours” or “It’s good you’re getting help, but do you still have to go weekly?”
In the immediate aftermath of suicide, feelings run high, as they should. But rather than wait it out – and fearing a return to “business as usual” – let me make only two suggestions:
2. In psychiatry, we need to redouble our efforts in fighting the stigma attached to psychiatric illness in trainees. It is unconscionable that medical students and residents are dying of treatable disorders (I’ve never heard of a doctor dying of cancer who didn’t go to an oncologist at least once), yet too many are not availing themselves of services we provide – even when they’re free of charge or covered by insurance. And are we certain that, when they knock on our doors, we are providing them with state-of-the-art care? Is it possible that unrecognized internal stigma and shame deep within us might make us hesitant to help our trainees in their hour of need? Or cut corners? Or not get a second opinion? Very few psychiatrists on faculty of our medical schools divulge their personal experiences of depression, posttraumatic stress disorders, substance use disorders, and more (with the exception of being in therapy during residency, which is normative and isn’t stigmatized). Coming out is leveling, humane, and respectful – and it shrinks the power differential in the teaching dyad. It might even save a life.
Dr. Myers is a professor of clinical psychiatry at State University of New York, Brooklyn, and the author of “Why Physicians Die by Suicide: Lessons Learned From Their Families and Others Who Cared.”
Like everyone in the arc of social media impact, I was shocked and terribly saddened by the recent suicides of two New York women in medicine – a final-year medical student on May 1 and a second-year resident on May 5. As a specialist in physician health, a former training director, a long-standing member of our institution’s medical student admissions committee, and the ombudsman for our medical students, I am finding these tragedies harder and harder to reconcile. Something isn’t working. But before I get to that, what follows is a bulleted list of some events of the past couple of weeks that may give a context for my statements and have informed my two recommendations.
- May 3, 2018: I give an invited GI grand rounds on stress, burnout, depression, and suicide in physicians. The residents are quiet and say nothing. Faculty members seem only concerned about preventing and eradicating burnout – and not that interested in anything more severe.
- May 5: A psychiatry resident from Melbourne arrives to spend 10 days with me to do an elective in physician health. As in the United States, there is a significant suicide death rate in medical students and residents Down Under. In the afternoon, I present a paper at the annual meeting of the American Academy of Psychodynamic Psychiatry and Psychoanalysis on the use of psychotherapy in treatment-resistant suicidal depression in physicians. There is increasing hope that this essential modality of care will return to the contemporary psychiatrist’s toolbox.
- May 6: At the annual meeting of the American Psychiatric Association in New York, I’m the discussant for powerful heartfelt papers of five psychiatrists (mostly early career psychiatrists and one resident) that talked about living with a psychiatric illness. The audience is huge, and we hear narratives about internal stigma, self-disclosure, external stigma, shunning, bullying, acceptance, rejection, alienation, connection, and love by peers and family. The authenticity and valor of the speakers create an atmosphere of safety, which enables psychiatrists in attendance from all over the world to share their personal stories – some at the microphone, some privately.
- May 7: Again at the APA, I chair and facilitate a workshop on physician suicide. We hear from four speakers, all women, who have lost a loved one to suicide – a husband, a father, a brother, a son – all doctors. Two of the speakers are psychiatrists. The stories are gripping, detailed, and tender. Yes, the atmosphere is very sad, but there is not a pall. We learn how these doctors lived, not just how they died. They all loved medicine; they were creative; they cared deeply; they suffered silently; and with shame, they lost hope. Again, a big audience of psychiatrists, many of whom share their own stories, that they, too, had lost a physician son, wife, or mother to suicide. Some of their deceased family members fell through the cracks and did not receive the life-saving care they deserved; some, fearing assaults to their medical license, hospital privileges, or insurance, refused to see anyone. They died untreated.
- May 8: Still at the APA, a psychiatrist colleague and I collaborate on a clinical case conference. Each of us describes losing a physician patient to suicide. We walk the attendees through the clinical details of assessment, treatment, and the aftermath of their deaths. We talk openly and frankly about our feelings, grief, outreach to colleagues and the family, and our own personal journeys of learning, growth, and healing. The clinician audience members give constructive feedback, and some share their own stories of losing patients to suicide. Like the day before, some psychiatrists are grieving the loss of a physician son or sibling to suicide. As mental health professionals, they suffer from an additional layer of failure and guilt that a loved one died “under their watch.”
- May 8: I rush across the Javits Center to catch the discussant for a concurrent symposium on physician burnout and depression. She foregoes any prepared remarks to share her previous 48 hours with the audience. She is the training director of the program that lost the second-year resident on May 5. She did not learn of the death until 24 hours later. We are all on the edge of our seats as we listen to this grieving, courageous woman, a seasoned psychiatrist and educator, who has been blindsided by this tragedy. She has not slept. She called all of her residents and broke the news personally as best she could. Aided by “After A Suicide: A Toolkit for Residency/Fellowship Programs” (American Foundation for Suicide Prevention), she and her colleagues instituted a plan of action and worked with administration and faculty. Her strength and commitment to the well-being of her trainees is palpable and magnanimous. When the session ends, many of us stand in line to give her a hug. It is a stark reminder of how many lives are affected when someone you know or care about takes his/her own life – and how, in the house of medicine, medical students and residents really are part of an institutional family.
- May 10: I facilitate a meeting of our 12 second-year residents, many of whom knew of or had met the resident who died. Almost everyone speaks, shares their feelings, poses questions, and calls for answers and change. There is disbelief, sadness, confusion, some guilt, and lots of anger. Also a feeling of disillusionment or paradox about the field of psychiatry: “Of all branches of medicine, shouldn’t residents who are struggling with psychiatric issues feel safe, protected, cared for in psychiatry?” There is also a feeling of lip service being paid to personal treatment, as in quoted statements: “By all means, get treatment for your issues, but don’t let it encroach on your duty hours” or “It’s good you’re getting help, but do you still have to go weekly?”
In the immediate aftermath of suicide, feelings run high, as they should. But rather than wait it out – and fearing a return to “business as usual” – let me make only two suggestions:
2. In psychiatry, we need to redouble our efforts in fighting the stigma attached to psychiatric illness in trainees. It is unconscionable that medical students and residents are dying of treatable disorders (I’ve never heard of a doctor dying of cancer who didn’t go to an oncologist at least once), yet too many are not availing themselves of services we provide – even when they’re free of charge or covered by insurance. And are we certain that, when they knock on our doors, we are providing them with state-of-the-art care? Is it possible that unrecognized internal stigma and shame deep within us might make us hesitant to help our trainees in their hour of need? Or cut corners? Or not get a second opinion? Very few psychiatrists on faculty of our medical schools divulge their personal experiences of depression, posttraumatic stress disorders, substance use disorders, and more (with the exception of being in therapy during residency, which is normative and isn’t stigmatized). Coming out is leveling, humane, and respectful – and it shrinks the power differential in the teaching dyad. It might even save a life.
Dr. Myers is a professor of clinical psychiatry at State University of New York, Brooklyn, and the author of “Why Physicians Die by Suicide: Lessons Learned From Their Families and Others Who Cared.”
Digital Ischemia From Accidental Epinephrine Injection
Patients presenting to the ED with injuries due to accidental self-injection with an epinephrine pen typically receive treatment to alleviate symptoms and reduce the potential of digital ischemia leading to gangrene and loss of tissue and function. Although there is no consensus or set guidelines in the literature regarding the management protocol of such cases, many reports support pharmacological intervention. There are, however, other reports that advocate conservative, nonpharmaceutical management (eg, immersing the affected digit in warm water) or an observation-only approach.
We present the first case report in Saudi Arabia of digital ischemia due to accidental injection of an epinephrine autoinjector, along with a review of the literature and management recommendations.
Case
A 28-year-old woman presented to the ED in significant pain and discomfort 20 minutes after she accidentally injected the entire contents of her aunt’s epinephrine autoinjector (0.3 mg of 1:1000) into her right thumb. The patient, who was in significant pain and discomfort, stated that she was unable to remove the injector needle, which was firmly embedded in the bone of the palmer aspect of the distal phalanx in a manner similar to that of an intraosseous injection (Figure 1).
The patient’s vital signs and oxygen saturation on presentation were within normal limits. The emergency physician successfully removed the embedded needle through moderate countertraction. On examination, the patient’s right thumb was pale and cold, and had poor capillary refill (Figure 2). Due to concerns of the potential for digital tissue ischemia leading to tissue loss and gangrene, warm, moist compresses were applied to the affected thumb, followed by 2% topical nitroglycerin paste, after which the thumb was covered with an occlusive dressing. Since there was no improvement in circulation after 20 minutes, an infiltrate of 5 mg (0.5 mL of 10 mg/mL) of phentolamine (α-agonist) mixed with 2.5 mL of 2% lidocaine was injected at the puncture site and base of the right thumb.1 Hyperemia developed immediately at both injection sites, and the patient’s right thumb returned to a normal color and sensation 1 hour later, with a return to normal capillary refill. She remained in stable condition and was discharged home. Prior to discharge, the patient was educated on the proper handling and administration of an epinephrine autoinjector.
Discussion
Epinephrine is an ὰ- and β-adrenergic agonist that binds to the ὰ-adrenergic receptors of blood vessels, causing an increase in vascular resistance and vasoconstriction. Although the plasma half-life of epinephrine is approximately 2 to 3 minutes, subcutaneous or intramuscular injection resulting in local vasoconstriction may delay absorption; therefore, the effects of epinephrine may last much longer than its half-life.
The incidence of accidental injection from an epinephrine autoinjector is estimated to be 1 per 50,000 units dispensed.2 To date, there are no established treatment guidelines on managing cases of digital injection. An online PubMed and Google Scholar search of the literature found one systematic review,3 four observational studies,4-7 seven case series,8-14 and several case reports1,15-33 on the subject. Most of the patients in the published retrospective studies (71%) were treated conservatively with warming of the affected hand and observation, and the majority of patients in the case reports (87%) were treated pharmacologically, most commonly with topical nitroglycerin and phentolamine.1,3-34 All of the patients in both the retrospective studies and case reports had restoration of perfusion without necrosis, irrespective of treatment modality. However, patients who were managed conservatively or who were treated with topical nitroglycerin required a longer duration of stay in the ED, suffered from severe reperfusion pain, and in some cases, had a longer time to complete recovery (≥10 weeks).8
Pharmaceutical and Nonpharmaceutical Management
Phentolamine. Phentolamine is a nonselective ὰ-adrenergic antagonist that binds to ὰ1 and ὰ2 receptors of blood vessels, resulting in a decrease in peripheral vascular resistance and vasodilation. Phentolamine directly antagonizes the effect of epinephrine by blocking the ὰ-adrenergic receptors, which in our patient resulted in immediate return of digital circulation and full resolution of symptoms.
Topical Nitroglycerin. Nitroglycerin is a nitrate vasodilator that when metabolically converted to nitric oxide, results in smooth muscle relaxation, venodilation, and arteriodilation. Patients suffering from digital ischemia and vasoconstriction may be treated with topical nitroglycerin paste to reverse ischemia by causing smooth muscle relaxation of digital blood vessels. Conservative Management. As previously noted, not all cases of digital epinephrine injection are treated pharmacologically. Some patients are not treated, but kept in observation until the ischemic effects of epinephrine have resolved. Likewise, some patients are treated conservatively with warm water compresses or by fully immersing the affected digit in warm water to facilitate reversal of vasoconstriction and ischemia.3,8
Treatment Efficacy
In 2007, Fitzcharles-Bowe et al8 published a review of 59 cases of digital injection with high-dose epinephrine from 1989 to 2005. In this review, 32 of the 59 patients received no treatment, 25 patients received pharmacological treatment and in two patients, the treatment was unknown. Phentolamine was the most commonly used pharmacological agent (15 of 25 cases or 60%). Although none of the patients experienced digital necrosis, those treated with a local infiltration of phentolamine experienced a faster resolution of symptoms and normalization of perfusion. In 2004, Turner1 reported a case of a 10-year-old boy who was treated with phentolamine following an accidental injection of epinephrine into his left hand. While circulation returned to the affected digit within 5 minutes of receiving the phentolamine injection, the patient continued to experience reduced sensation in the digit 6 weeks later.8
Interestingly, one of the coauthors of the Fitzcharles-Bowe et al8 report intentionally injected three of the digits of his left hand (middle, ring, and small fingers) at the same time with high-dose epinephrine to carefully observe and document the outcomes. All three of the digits became very pale and cool, with decreased sensation. The author treated himself conservatively (observation-only). He experienced spontaneous return of circulation in two of the digits within 6 to 10 hours. Although there was some spontaneous return of circulation to the third digit after 13 hours, the author noted prolonged, intense reperfusion pain 4 hours after return of circulation. He also suffered from neuropraxia in the third digit, which did not fully resolve until 10 weeks after the injury.8
A review of the literature shows phentolamine to be a safe and effective treatment for patients presenting with digital ischemia, with no long-term adverse effects or complications. Moreover, phentolamine appears to be safe and effective for use in both adult and pediatric patients.3,8,35-38
Accidental Injection Prevention
Some of the cases of accidental epinephrine injection are due to user error. For example, a novice user may be holding the incorrect end of the injector in his or her hand when attempting to administer/deploy the device, resulting in premature dislodgement of the needle.39
Although, most of the autoinjector devices available today are user-friendly, we believe the addition of a safety feature such as a trigger or safety-lock may further help to reduce accidents. The European Medicines Agency recommends that all patients and caregivers receive training on the proper handling and administration of epinephrine autoinjectors, citing this as the most important factor to ensure successful use of an epinephrine autoinjector and reduce accidental injury.40 The patient in this case had not received any formal education or training regarding autoinjector use prior to this incident.
Safety of Lidocaine-Containing Epinephrine in Digital Anesthesia
Aside from cases of accidental digital epinephrine injection, clinicians have traditionally been taught to avoid using lidocaine with epinephrine for digital anesthesia. However, since the introduction of commercial lidocaine with epinephrine in 1948, there are no case reports of digital gangrene from commercially available lidocaine-epinephrine formulations.41,42 In a multicenter prospective study by Lalonde et al43 of 3,110 consecutive cases of elective injection of low-dose epinephrine in the hand, the authors concluded the likelihood of finger infarction is remote, particularly with possible phentolamine rescue therapy. Moreover, lidocaine-containing epinephrine (1%-2%) has a much lower concentration of epinephrine per mL of solution (5-10 mcg/mL) and appears to be safe for digital use.
Conclusion
This case describes the presentation and treatment of accidental digital injection of epinephrine, highlighting and supporting the benefits of local infiltration with phentolamine and observation until full recovery of perfusion. Local treatment with phentolamine not only facilitates recovery and return of capillary refill, but also shortens the duration of symptoms and alleviates vasoconstriction. In less severe cases, watchful waiting and observation may be appropriate and effective.
This case also underscores the importance of patient and caregiver education on the proper handling and administration of epinephrine autoinjectors to decrease the incidence of accidental injection.
1. Turner MJ. Accidental Epipen injection into a digit - the value of a Google search. Ann R Coll Surg Engl. 2004;86(3):218-219. doi:10.1308/003588404323043391.
2. McGovern SJ. Treatment of accidental digital injection of adrenaline from an auto-injector device. J Accid Emerg Med. 1997;14(6):379-380.
3. Wright M. Treatment after accidental injection with epinephrine autoinjector: a systematic review. J Allergy & Therapy. 2014;5(3):1000175. doi:10.4172/2155-6121.1000175.
4. Mrvos R, Anderson BD, Krenzelok EP. Accidental injection of epinephrine from an autoinjector: invasive treatment not always required. South Med J. 2002;95(3):318-320.
5. Muck AE, Bebarta VS, Borys DJ, Morgan DL. Six years of epinephrine digital injections: absence of significant local or systemic effects. Ann Emerg Med. 2010;56(3):270-274. doi:10.1016/j.annemergmed.2010.02.019.
6. Simons FE, Edwards ES, Read EJ Jr, Clark S, Liebelt EL. Voluntarily reported unintentional injections from epinephrine auto-injectors. J Allergy Clin Immunol. 2010;125(2):419-423. doi:10.1016/j.jaci.2009.10.056.
7. Blume-Odom CM, Scalzo AJ, Weber JA. EpiPen accidental injection-134 cases over 10 years. Clin Toxicol. 2010;48:651.
8. Fitzcharles-Bowe C, Denkler K, Lalonde D. Finger injection with high-dose (1:1,000) epinephrine: Does it cause finger necrosis and should it be treated? Hand. 2007;2(1):5-11. doi:10.1007/s11552-006-9012-4.
9. Velissariou I, Cottrell S, Berry K, Wilson B. Management of adrenaline (epinephrine) induced digital ischaemia in children after accidental injection from an EpiPen. Emerg Med J. 2004;21(3):387-388.
10. ElMaraghy MW, ElMaraghy AW, Evans HB. Digital adrenaline injection injuries: a case series and review. Can J Plast Surg. 1998;6:196-200.
11. Skorpinski EW, McGeady SJ, Yousef E. Two cases of accidental epinephrine injection into a finger. J Allergy Clin Immunol. 2006;117(2):463-464.
12. Nagaraj J, Reddy S, Murray R, Murphy N. Use of glyceryl trinitrate patches in the treatment of accidental digital injection of epinephrine from an autoinjector. Eur J Emerg Med. 2009;16(4):227-228. doi:10.1097/MEJ.0b013e328306f0ee.
13. Stier PA, Bogner MP, Webster K, Leikin JB, Burda A. Use of subcutaneous terbutaline to reverse peripheral ischemia. Am J Emerg Med. 1999;17(1):91-94.
14. Lee G, Thomas PC. Accidental digital injection of adrenaline from an autoinjector device. J Accid Emerg Med. 1998;15(4):287.
15. Baris S, Saricoban HE, Ak K, Ozdemir C. Papaverine chloride as a topical vasodilator in accidental injection of adrenaline into a digital finger. Allergy. 2011;66(11):1495-1496. doi:10.1111/j.1398-9995.2011.02664.x.
16. Buse K, Hein W, Drager N. Making Sense of Global Health Governance: A Policy Perspective. Basingstoke, England: Palgrave Macmillan UK; 2009.
17. Sherman SC. Digital Epipen® injection: a case of conservative management. J Emerg Med. 2011;41(6):672-674. doi:10.1016/j.jemermed.2009.07.027.
18. Janssen RL, Roeleveld-Versteegh AB, Wessels-Basten SJ, Hendriks T. [Auto-injection with epinephrine in the finger of a 5-year-old child]. Ned Tijdschr Geneeskd. 2008;152(17):1005-1008.
19. Singh T, Randhawa S, Khanna R. The EpiPen and the ischaemic finger. Eur J Emerg Med. 2007;14(4):222-223.
20. Barkhordarian AR, Wakelin SH, Paes TR. Accidental digital injection of adrenaline from an autoinjector device. Br J Dermatol. 2000;143(6):1359.
21. Deshmukh N, Tolland JT. Treatment of accidental epinephrine injection in a finger. J Emerg Med. 1989;7(4):408.
22. Hinterberger JW, Kintzi HE. Phentolamine reversal of epinephrine-induced digital vasospasm. How to save an ischemic finger. Arch Fam Med. 1994;3(2):193-195.
23. Peyko V, Cohen V, Jellinek-Cohen SP, Pearl-Davis M. Evaluation and treatment of accidental autoinjection of epinephrine. Am J Health Syst Pharm. 2013;70(9):778-781. doi:10.2146/ajhp120316.
24. Hardy SJ, Agostini DE. Accidental epinephrine auto-injector-induced digital ischemia reversed by phentolamine digital block. J Am Osteopath Assoc. 1995;95(6):377-378.
25. Kaspersen J, Vedsted P. [Accidental injection of adrenaline in a finger with EpiPen]. Ugeskr Laeger. 1998;160(45):6531-6532.
26. Schintler MV, Arbab E, Aberer W, Spendel S, Scharnagl E. Accidental perforating bone injury using the EpiPen autoinjection device. Allergy. 2005;60(2):259-260.
27. Khairalla E. Epinephrine-induced digital ischemia relieved by phentolamine. Plast Reconstr Surg. 2001;108(6):1831-1832.
28. Murali KS, Nayeem N. Accidental digital injection of adrenaline from an autoinjector device. J Accid Emerg Med. 1998;15(4):287.
29. Sellens C, Morrison L. Accidental injection of epinephrine by a child: a unique approach to treatment. CJEM. 1999;1(1):34-36.
30. Klemawesch P. Hyperbaric oxygen relieves severe digital ischaemia from accidental EpiPen injection. 2009 American Academy of Allergy, Asthma and Immunology Annual Meeting.
31. McCauley WA, Gerace RV, Scilley C. Treatment of accidental digital injection of epinephrine. Ann Emerg Med. 1991;20(6):665-668.
32. Mathez C, Favrat B, Staeger P. Management options for accidental injection of epinephrine from an autoinjector: a case report. J Med Case Rep. 2009;3:7268. doi:10.4076/1752-1947-3-7268.
33. Molony D. Adrenaline-induced digital ischaemia reversed with phentolamine. ANZ J Surg. 2006;76(12):1125-1126.
34. Carrascosa MF, Gallastegui-Menéndez A, Teja-Santamaría C, Caviedes JR. Accidental finger ischaemia induced by epinephrine autoinjector. BMJ Case Rep. 2013;2013. pii:bcr2013200783. doi:10.1136/bcr-2013-200783.
35. Patel R, Kumar H. Epinephrine induced digital ischemia after accidental injection from an auto-injector device. Indian Pediatr. 2013;50(2):247.
36. Xu J, Holt A. Use of Phentolamine in the treatment of Epipen induced digital ischemia. BMJ Case Rep. 2012;2012. doi:10.1136/bcr.12.2011.5450.
37. McNeil C, Copeland J. Accidental digital epinephrine injection: to treat or not to treat? Can Fam Physician. 2014;60(8):726-728.
38. Bodkin RP, Acquisto NM, Gunyan H, Wiegand TJ. Two cases of accidental injection of epinephrine into a digit treated with subcutaneous phentolamine injections. Case Rep Emerg Med. 2013;2013:586207. doi:10.1155/2013/586207.
39. Simons FE, Lieberman PL, Read EJ Jr, Edwards ES. Hazards of unintentional injection of epinephrine from autoinjectors: a systematic review. Ann Allergy Asthma Immunol. 2009;102(4):282-287. doi:10.1016/S1081-1206(10)60332-8.
40. European Medicines Agency. Better training tools recommended to support patients using adrenaline auto-injectors. European Medicines Agency, 2015.
41. Denkler K. A comprehensive review of epinephrine in the finger: to do or not to do.
42. Thomson CJ, Lalonde DH, Denkler KA, Feicht AJ. A critical look at the evidence for and against elective epinephrine use in the finger. Plast Reconstr Surg. 2007;119(1):260-266.
43. Lalonde D, Bell M, Benoit P, Sparkes G, Denkler K, Chang P. A multicenter prospective study of 3,110 consecutive cases of elective epinephrine use in the fingers and hand: the Dalhousie Project clinical phase. J Hand Surg Am. 2005;30(5):1061-1067. doi:10.1016/j.jhsa.2005.05.006.
Patients presenting to the ED with injuries due to accidental self-injection with an epinephrine pen typically receive treatment to alleviate symptoms and reduce the potential of digital ischemia leading to gangrene and loss of tissue and function. Although there is no consensus or set guidelines in the literature regarding the management protocol of such cases, many reports support pharmacological intervention. There are, however, other reports that advocate conservative, nonpharmaceutical management (eg, immersing the affected digit in warm water) or an observation-only approach.
We present the first case report in Saudi Arabia of digital ischemia due to accidental injection of an epinephrine autoinjector, along with a review of the literature and management recommendations.
Case
A 28-year-old woman presented to the ED in significant pain and discomfort 20 minutes after she accidentally injected the entire contents of her aunt’s epinephrine autoinjector (0.3 mg of 1:1000) into her right thumb. The patient, who was in significant pain and discomfort, stated that she was unable to remove the injector needle, which was firmly embedded in the bone of the palmer aspect of the distal phalanx in a manner similar to that of an intraosseous injection (Figure 1).
The patient’s vital signs and oxygen saturation on presentation were within normal limits. The emergency physician successfully removed the embedded needle through moderate countertraction. On examination, the patient’s right thumb was pale and cold, and had poor capillary refill (Figure 2). Due to concerns of the potential for digital tissue ischemia leading to tissue loss and gangrene, warm, moist compresses were applied to the affected thumb, followed by 2% topical nitroglycerin paste, after which the thumb was covered with an occlusive dressing. Since there was no improvement in circulation after 20 minutes, an infiltrate of 5 mg (0.5 mL of 10 mg/mL) of phentolamine (α-agonist) mixed with 2.5 mL of 2% lidocaine was injected at the puncture site and base of the right thumb.1 Hyperemia developed immediately at both injection sites, and the patient’s right thumb returned to a normal color and sensation 1 hour later, with a return to normal capillary refill. She remained in stable condition and was discharged home. Prior to discharge, the patient was educated on the proper handling and administration of an epinephrine autoinjector.
Discussion
Epinephrine is an ὰ- and β-adrenergic agonist that binds to the ὰ-adrenergic receptors of blood vessels, causing an increase in vascular resistance and vasoconstriction. Although the plasma half-life of epinephrine is approximately 2 to 3 minutes, subcutaneous or intramuscular injection resulting in local vasoconstriction may delay absorption; therefore, the effects of epinephrine may last much longer than its half-life.
The incidence of accidental injection from an epinephrine autoinjector is estimated to be 1 per 50,000 units dispensed.2 To date, there are no established treatment guidelines on managing cases of digital injection. An online PubMed and Google Scholar search of the literature found one systematic review,3 four observational studies,4-7 seven case series,8-14 and several case reports1,15-33 on the subject. Most of the patients in the published retrospective studies (71%) were treated conservatively with warming of the affected hand and observation, and the majority of patients in the case reports (87%) were treated pharmacologically, most commonly with topical nitroglycerin and phentolamine.1,3-34 All of the patients in both the retrospective studies and case reports had restoration of perfusion without necrosis, irrespective of treatment modality. However, patients who were managed conservatively or who were treated with topical nitroglycerin required a longer duration of stay in the ED, suffered from severe reperfusion pain, and in some cases, had a longer time to complete recovery (≥10 weeks).8
Pharmaceutical and Nonpharmaceutical Management
Phentolamine. Phentolamine is a nonselective ὰ-adrenergic antagonist that binds to ὰ1 and ὰ2 receptors of blood vessels, resulting in a decrease in peripheral vascular resistance and vasodilation. Phentolamine directly antagonizes the effect of epinephrine by blocking the ὰ-adrenergic receptors, which in our patient resulted in immediate return of digital circulation and full resolution of symptoms.
Topical Nitroglycerin. Nitroglycerin is a nitrate vasodilator that when metabolically converted to nitric oxide, results in smooth muscle relaxation, venodilation, and arteriodilation. Patients suffering from digital ischemia and vasoconstriction may be treated with topical nitroglycerin paste to reverse ischemia by causing smooth muscle relaxation of digital blood vessels. Conservative Management. As previously noted, not all cases of digital epinephrine injection are treated pharmacologically. Some patients are not treated, but kept in observation until the ischemic effects of epinephrine have resolved. Likewise, some patients are treated conservatively with warm water compresses or by fully immersing the affected digit in warm water to facilitate reversal of vasoconstriction and ischemia.3,8
Treatment Efficacy
In 2007, Fitzcharles-Bowe et al8 published a review of 59 cases of digital injection with high-dose epinephrine from 1989 to 2005. In this review, 32 of the 59 patients received no treatment, 25 patients received pharmacological treatment and in two patients, the treatment was unknown. Phentolamine was the most commonly used pharmacological agent (15 of 25 cases or 60%). Although none of the patients experienced digital necrosis, those treated with a local infiltration of phentolamine experienced a faster resolution of symptoms and normalization of perfusion. In 2004, Turner1 reported a case of a 10-year-old boy who was treated with phentolamine following an accidental injection of epinephrine into his left hand. While circulation returned to the affected digit within 5 minutes of receiving the phentolamine injection, the patient continued to experience reduced sensation in the digit 6 weeks later.8
Interestingly, one of the coauthors of the Fitzcharles-Bowe et al8 report intentionally injected three of the digits of his left hand (middle, ring, and small fingers) at the same time with high-dose epinephrine to carefully observe and document the outcomes. All three of the digits became very pale and cool, with decreased sensation. The author treated himself conservatively (observation-only). He experienced spontaneous return of circulation in two of the digits within 6 to 10 hours. Although there was some spontaneous return of circulation to the third digit after 13 hours, the author noted prolonged, intense reperfusion pain 4 hours after return of circulation. He also suffered from neuropraxia in the third digit, which did not fully resolve until 10 weeks after the injury.8
A review of the literature shows phentolamine to be a safe and effective treatment for patients presenting with digital ischemia, with no long-term adverse effects or complications. Moreover, phentolamine appears to be safe and effective for use in both adult and pediatric patients.3,8,35-38
Accidental Injection Prevention
Some of the cases of accidental epinephrine injection are due to user error. For example, a novice user may be holding the incorrect end of the injector in his or her hand when attempting to administer/deploy the device, resulting in premature dislodgement of the needle.39
Although, most of the autoinjector devices available today are user-friendly, we believe the addition of a safety feature such as a trigger or safety-lock may further help to reduce accidents. The European Medicines Agency recommends that all patients and caregivers receive training on the proper handling and administration of epinephrine autoinjectors, citing this as the most important factor to ensure successful use of an epinephrine autoinjector and reduce accidental injury.40 The patient in this case had not received any formal education or training regarding autoinjector use prior to this incident.
Safety of Lidocaine-Containing Epinephrine in Digital Anesthesia
Aside from cases of accidental digital epinephrine injection, clinicians have traditionally been taught to avoid using lidocaine with epinephrine for digital anesthesia. However, since the introduction of commercial lidocaine with epinephrine in 1948, there are no case reports of digital gangrene from commercially available lidocaine-epinephrine formulations.41,42 In a multicenter prospective study by Lalonde et al43 of 3,110 consecutive cases of elective injection of low-dose epinephrine in the hand, the authors concluded the likelihood of finger infarction is remote, particularly with possible phentolamine rescue therapy. Moreover, lidocaine-containing epinephrine (1%-2%) has a much lower concentration of epinephrine per mL of solution (5-10 mcg/mL) and appears to be safe for digital use.
Conclusion
This case describes the presentation and treatment of accidental digital injection of epinephrine, highlighting and supporting the benefits of local infiltration with phentolamine and observation until full recovery of perfusion. Local treatment with phentolamine not only facilitates recovery and return of capillary refill, but also shortens the duration of symptoms and alleviates vasoconstriction. In less severe cases, watchful waiting and observation may be appropriate and effective.
This case also underscores the importance of patient and caregiver education on the proper handling and administration of epinephrine autoinjectors to decrease the incidence of accidental injection.
Patients presenting to the ED with injuries due to accidental self-injection with an epinephrine pen typically receive treatment to alleviate symptoms and reduce the potential of digital ischemia leading to gangrene and loss of tissue and function. Although there is no consensus or set guidelines in the literature regarding the management protocol of such cases, many reports support pharmacological intervention. There are, however, other reports that advocate conservative, nonpharmaceutical management (eg, immersing the affected digit in warm water) or an observation-only approach.
We present the first case report in Saudi Arabia of digital ischemia due to accidental injection of an epinephrine autoinjector, along with a review of the literature and management recommendations.
Case
A 28-year-old woman presented to the ED in significant pain and discomfort 20 minutes after she accidentally injected the entire contents of her aunt’s epinephrine autoinjector (0.3 mg of 1:1000) into her right thumb. The patient, who was in significant pain and discomfort, stated that she was unable to remove the injector needle, which was firmly embedded in the bone of the palmer aspect of the distal phalanx in a manner similar to that of an intraosseous injection (Figure 1).
The patient’s vital signs and oxygen saturation on presentation were within normal limits. The emergency physician successfully removed the embedded needle through moderate countertraction. On examination, the patient’s right thumb was pale and cold, and had poor capillary refill (Figure 2). Due to concerns of the potential for digital tissue ischemia leading to tissue loss and gangrene, warm, moist compresses were applied to the affected thumb, followed by 2% topical nitroglycerin paste, after which the thumb was covered with an occlusive dressing. Since there was no improvement in circulation after 20 minutes, an infiltrate of 5 mg (0.5 mL of 10 mg/mL) of phentolamine (α-agonist) mixed with 2.5 mL of 2% lidocaine was injected at the puncture site and base of the right thumb.1 Hyperemia developed immediately at both injection sites, and the patient’s right thumb returned to a normal color and sensation 1 hour later, with a return to normal capillary refill. She remained in stable condition and was discharged home. Prior to discharge, the patient was educated on the proper handling and administration of an epinephrine autoinjector.
Discussion
Epinephrine is an ὰ- and β-adrenergic agonist that binds to the ὰ-adrenergic receptors of blood vessels, causing an increase in vascular resistance and vasoconstriction. Although the plasma half-life of epinephrine is approximately 2 to 3 minutes, subcutaneous or intramuscular injection resulting in local vasoconstriction may delay absorption; therefore, the effects of epinephrine may last much longer than its half-life.
The incidence of accidental injection from an epinephrine autoinjector is estimated to be 1 per 50,000 units dispensed.2 To date, there are no established treatment guidelines on managing cases of digital injection. An online PubMed and Google Scholar search of the literature found one systematic review,3 four observational studies,4-7 seven case series,8-14 and several case reports1,15-33 on the subject. Most of the patients in the published retrospective studies (71%) were treated conservatively with warming of the affected hand and observation, and the majority of patients in the case reports (87%) were treated pharmacologically, most commonly with topical nitroglycerin and phentolamine.1,3-34 All of the patients in both the retrospective studies and case reports had restoration of perfusion without necrosis, irrespective of treatment modality. However, patients who were managed conservatively or who were treated with topical nitroglycerin required a longer duration of stay in the ED, suffered from severe reperfusion pain, and in some cases, had a longer time to complete recovery (≥10 weeks).8
Pharmaceutical and Nonpharmaceutical Management
Phentolamine. Phentolamine is a nonselective ὰ-adrenergic antagonist that binds to ὰ1 and ὰ2 receptors of blood vessels, resulting in a decrease in peripheral vascular resistance and vasodilation. Phentolamine directly antagonizes the effect of epinephrine by blocking the ὰ-adrenergic receptors, which in our patient resulted in immediate return of digital circulation and full resolution of symptoms.
Topical Nitroglycerin. Nitroglycerin is a nitrate vasodilator that when metabolically converted to nitric oxide, results in smooth muscle relaxation, venodilation, and arteriodilation. Patients suffering from digital ischemia and vasoconstriction may be treated with topical nitroglycerin paste to reverse ischemia by causing smooth muscle relaxation of digital blood vessels. Conservative Management. As previously noted, not all cases of digital epinephrine injection are treated pharmacologically. Some patients are not treated, but kept in observation until the ischemic effects of epinephrine have resolved. Likewise, some patients are treated conservatively with warm water compresses or by fully immersing the affected digit in warm water to facilitate reversal of vasoconstriction and ischemia.3,8
Treatment Efficacy
In 2007, Fitzcharles-Bowe et al8 published a review of 59 cases of digital injection with high-dose epinephrine from 1989 to 2005. In this review, 32 of the 59 patients received no treatment, 25 patients received pharmacological treatment and in two patients, the treatment was unknown. Phentolamine was the most commonly used pharmacological agent (15 of 25 cases or 60%). Although none of the patients experienced digital necrosis, those treated with a local infiltration of phentolamine experienced a faster resolution of symptoms and normalization of perfusion. In 2004, Turner1 reported a case of a 10-year-old boy who was treated with phentolamine following an accidental injection of epinephrine into his left hand. While circulation returned to the affected digit within 5 minutes of receiving the phentolamine injection, the patient continued to experience reduced sensation in the digit 6 weeks later.8
Interestingly, one of the coauthors of the Fitzcharles-Bowe et al8 report intentionally injected three of the digits of his left hand (middle, ring, and small fingers) at the same time with high-dose epinephrine to carefully observe and document the outcomes. All three of the digits became very pale and cool, with decreased sensation. The author treated himself conservatively (observation-only). He experienced spontaneous return of circulation in two of the digits within 6 to 10 hours. Although there was some spontaneous return of circulation to the third digit after 13 hours, the author noted prolonged, intense reperfusion pain 4 hours after return of circulation. He also suffered from neuropraxia in the third digit, which did not fully resolve until 10 weeks after the injury.8
A review of the literature shows phentolamine to be a safe and effective treatment for patients presenting with digital ischemia, with no long-term adverse effects or complications. Moreover, phentolamine appears to be safe and effective for use in both adult and pediatric patients.3,8,35-38
Accidental Injection Prevention
Some of the cases of accidental epinephrine injection are due to user error. For example, a novice user may be holding the incorrect end of the injector in his or her hand when attempting to administer/deploy the device, resulting in premature dislodgement of the needle.39
Although, most of the autoinjector devices available today are user-friendly, we believe the addition of a safety feature such as a trigger or safety-lock may further help to reduce accidents. The European Medicines Agency recommends that all patients and caregivers receive training on the proper handling and administration of epinephrine autoinjectors, citing this as the most important factor to ensure successful use of an epinephrine autoinjector and reduce accidental injury.40 The patient in this case had not received any formal education or training regarding autoinjector use prior to this incident.
Safety of Lidocaine-Containing Epinephrine in Digital Anesthesia
Aside from cases of accidental digital epinephrine injection, clinicians have traditionally been taught to avoid using lidocaine with epinephrine for digital anesthesia. However, since the introduction of commercial lidocaine with epinephrine in 1948, there are no case reports of digital gangrene from commercially available lidocaine-epinephrine formulations.41,42 In a multicenter prospective study by Lalonde et al43 of 3,110 consecutive cases of elective injection of low-dose epinephrine in the hand, the authors concluded the likelihood of finger infarction is remote, particularly with possible phentolamine rescue therapy. Moreover, lidocaine-containing epinephrine (1%-2%) has a much lower concentration of epinephrine per mL of solution (5-10 mcg/mL) and appears to be safe for digital use.
Conclusion
This case describes the presentation and treatment of accidental digital injection of epinephrine, highlighting and supporting the benefits of local infiltration with phentolamine and observation until full recovery of perfusion. Local treatment with phentolamine not only facilitates recovery and return of capillary refill, but also shortens the duration of symptoms and alleviates vasoconstriction. In less severe cases, watchful waiting and observation may be appropriate and effective.
This case also underscores the importance of patient and caregiver education on the proper handling and administration of epinephrine autoinjectors to decrease the incidence of accidental injection.
1. Turner MJ. Accidental Epipen injection into a digit - the value of a Google search. Ann R Coll Surg Engl. 2004;86(3):218-219. doi:10.1308/003588404323043391.
2. McGovern SJ. Treatment of accidental digital injection of adrenaline from an auto-injector device. J Accid Emerg Med. 1997;14(6):379-380.
3. Wright M. Treatment after accidental injection with epinephrine autoinjector: a systematic review. J Allergy & Therapy. 2014;5(3):1000175. doi:10.4172/2155-6121.1000175.
4. Mrvos R, Anderson BD, Krenzelok EP. Accidental injection of epinephrine from an autoinjector: invasive treatment not always required. South Med J. 2002;95(3):318-320.
5. Muck AE, Bebarta VS, Borys DJ, Morgan DL. Six years of epinephrine digital injections: absence of significant local or systemic effects. Ann Emerg Med. 2010;56(3):270-274. doi:10.1016/j.annemergmed.2010.02.019.
6. Simons FE, Edwards ES, Read EJ Jr, Clark S, Liebelt EL. Voluntarily reported unintentional injections from epinephrine auto-injectors. J Allergy Clin Immunol. 2010;125(2):419-423. doi:10.1016/j.jaci.2009.10.056.
7. Blume-Odom CM, Scalzo AJ, Weber JA. EpiPen accidental injection-134 cases over 10 years. Clin Toxicol. 2010;48:651.
8. Fitzcharles-Bowe C, Denkler K, Lalonde D. Finger injection with high-dose (1:1,000) epinephrine: Does it cause finger necrosis and should it be treated? Hand. 2007;2(1):5-11. doi:10.1007/s11552-006-9012-4.
9. Velissariou I, Cottrell S, Berry K, Wilson B. Management of adrenaline (epinephrine) induced digital ischaemia in children after accidental injection from an EpiPen. Emerg Med J. 2004;21(3):387-388.
10. ElMaraghy MW, ElMaraghy AW, Evans HB. Digital adrenaline injection injuries: a case series and review. Can J Plast Surg. 1998;6:196-200.
11. Skorpinski EW, McGeady SJ, Yousef E. Two cases of accidental epinephrine injection into a finger. J Allergy Clin Immunol. 2006;117(2):463-464.
12. Nagaraj J, Reddy S, Murray R, Murphy N. Use of glyceryl trinitrate patches in the treatment of accidental digital injection of epinephrine from an autoinjector. Eur J Emerg Med. 2009;16(4):227-228. doi:10.1097/MEJ.0b013e328306f0ee.
13. Stier PA, Bogner MP, Webster K, Leikin JB, Burda A. Use of subcutaneous terbutaline to reverse peripheral ischemia. Am J Emerg Med. 1999;17(1):91-94.
14. Lee G, Thomas PC. Accidental digital injection of adrenaline from an autoinjector device. J Accid Emerg Med. 1998;15(4):287.
15. Baris S, Saricoban HE, Ak K, Ozdemir C. Papaverine chloride as a topical vasodilator in accidental injection of adrenaline into a digital finger. Allergy. 2011;66(11):1495-1496. doi:10.1111/j.1398-9995.2011.02664.x.
16. Buse K, Hein W, Drager N. Making Sense of Global Health Governance: A Policy Perspective. Basingstoke, England: Palgrave Macmillan UK; 2009.
17. Sherman SC. Digital Epipen® injection: a case of conservative management. J Emerg Med. 2011;41(6):672-674. doi:10.1016/j.jemermed.2009.07.027.
18. Janssen RL, Roeleveld-Versteegh AB, Wessels-Basten SJ, Hendriks T. [Auto-injection with epinephrine in the finger of a 5-year-old child]. Ned Tijdschr Geneeskd. 2008;152(17):1005-1008.
19. Singh T, Randhawa S, Khanna R. The EpiPen and the ischaemic finger. Eur J Emerg Med. 2007;14(4):222-223.
20. Barkhordarian AR, Wakelin SH, Paes TR. Accidental digital injection of adrenaline from an autoinjector device. Br J Dermatol. 2000;143(6):1359.
21. Deshmukh N, Tolland JT. Treatment of accidental epinephrine injection in a finger. J Emerg Med. 1989;7(4):408.
22. Hinterberger JW, Kintzi HE. Phentolamine reversal of epinephrine-induced digital vasospasm. How to save an ischemic finger. Arch Fam Med. 1994;3(2):193-195.
23. Peyko V, Cohen V, Jellinek-Cohen SP, Pearl-Davis M. Evaluation and treatment of accidental autoinjection of epinephrine. Am J Health Syst Pharm. 2013;70(9):778-781. doi:10.2146/ajhp120316.
24. Hardy SJ, Agostini DE. Accidental epinephrine auto-injector-induced digital ischemia reversed by phentolamine digital block. J Am Osteopath Assoc. 1995;95(6):377-378.
25. Kaspersen J, Vedsted P. [Accidental injection of adrenaline in a finger with EpiPen]. Ugeskr Laeger. 1998;160(45):6531-6532.
26. Schintler MV, Arbab E, Aberer W, Spendel S, Scharnagl E. Accidental perforating bone injury using the EpiPen autoinjection device. Allergy. 2005;60(2):259-260.
27. Khairalla E. Epinephrine-induced digital ischemia relieved by phentolamine. Plast Reconstr Surg. 2001;108(6):1831-1832.
28. Murali KS, Nayeem N. Accidental digital injection of adrenaline from an autoinjector device. J Accid Emerg Med. 1998;15(4):287.
29. Sellens C, Morrison L. Accidental injection of epinephrine by a child: a unique approach to treatment. CJEM. 1999;1(1):34-36.
30. Klemawesch P. Hyperbaric oxygen relieves severe digital ischaemia from accidental EpiPen injection. 2009 American Academy of Allergy, Asthma and Immunology Annual Meeting.
31. McCauley WA, Gerace RV, Scilley C. Treatment of accidental digital injection of epinephrine. Ann Emerg Med. 1991;20(6):665-668.
32. Mathez C, Favrat B, Staeger P. Management options for accidental injection of epinephrine from an autoinjector: a case report. J Med Case Rep. 2009;3:7268. doi:10.4076/1752-1947-3-7268.
33. Molony D. Adrenaline-induced digital ischaemia reversed with phentolamine. ANZ J Surg. 2006;76(12):1125-1126.
34. Carrascosa MF, Gallastegui-Menéndez A, Teja-Santamaría C, Caviedes JR. Accidental finger ischaemia induced by epinephrine autoinjector. BMJ Case Rep. 2013;2013. pii:bcr2013200783. doi:10.1136/bcr-2013-200783.
35. Patel R, Kumar H. Epinephrine induced digital ischemia after accidental injection from an auto-injector device. Indian Pediatr. 2013;50(2):247.
36. Xu J, Holt A. Use of Phentolamine in the treatment of Epipen induced digital ischemia. BMJ Case Rep. 2012;2012. doi:10.1136/bcr.12.2011.5450.
37. McNeil C, Copeland J. Accidental digital epinephrine injection: to treat or not to treat? Can Fam Physician. 2014;60(8):726-728.
38. Bodkin RP, Acquisto NM, Gunyan H, Wiegand TJ. Two cases of accidental injection of epinephrine into a digit treated with subcutaneous phentolamine injections. Case Rep Emerg Med. 2013;2013:586207. doi:10.1155/2013/586207.
39. Simons FE, Lieberman PL, Read EJ Jr, Edwards ES. Hazards of unintentional injection of epinephrine from autoinjectors: a systematic review. Ann Allergy Asthma Immunol. 2009;102(4):282-287. doi:10.1016/S1081-1206(10)60332-8.
40. European Medicines Agency. Better training tools recommended to support patients using adrenaline auto-injectors. European Medicines Agency, 2015.
41. Denkler K. A comprehensive review of epinephrine in the finger: to do or not to do.
42. Thomson CJ, Lalonde DH, Denkler KA, Feicht AJ. A critical look at the evidence for and against elective epinephrine use in the finger. Plast Reconstr Surg. 2007;119(1):260-266.
43. Lalonde D, Bell M, Benoit P, Sparkes G, Denkler K, Chang P. A multicenter prospective study of 3,110 consecutive cases of elective epinephrine use in the fingers and hand: the Dalhousie Project clinical phase. J Hand Surg Am. 2005;30(5):1061-1067. doi:10.1016/j.jhsa.2005.05.006.
1. Turner MJ. Accidental Epipen injection into a digit - the value of a Google search. Ann R Coll Surg Engl. 2004;86(3):218-219. doi:10.1308/003588404323043391.
2. McGovern SJ. Treatment of accidental digital injection of adrenaline from an auto-injector device. J Accid Emerg Med. 1997;14(6):379-380.
3. Wright M. Treatment after accidental injection with epinephrine autoinjector: a systematic review. J Allergy & Therapy. 2014;5(3):1000175. doi:10.4172/2155-6121.1000175.
4. Mrvos R, Anderson BD, Krenzelok EP. Accidental injection of epinephrine from an autoinjector: invasive treatment not always required. South Med J. 2002;95(3):318-320.
5. Muck AE, Bebarta VS, Borys DJ, Morgan DL. Six years of epinephrine digital injections: absence of significant local or systemic effects. Ann Emerg Med. 2010;56(3):270-274. doi:10.1016/j.annemergmed.2010.02.019.
6. Simons FE, Edwards ES, Read EJ Jr, Clark S, Liebelt EL. Voluntarily reported unintentional injections from epinephrine auto-injectors. J Allergy Clin Immunol. 2010;125(2):419-423. doi:10.1016/j.jaci.2009.10.056.
7. Blume-Odom CM, Scalzo AJ, Weber JA. EpiPen accidental injection-134 cases over 10 years. Clin Toxicol. 2010;48:651.
8. Fitzcharles-Bowe C, Denkler K, Lalonde D. Finger injection with high-dose (1:1,000) epinephrine: Does it cause finger necrosis and should it be treated? Hand. 2007;2(1):5-11. doi:10.1007/s11552-006-9012-4.
9. Velissariou I, Cottrell S, Berry K, Wilson B. Management of adrenaline (epinephrine) induced digital ischaemia in children after accidental injection from an EpiPen. Emerg Med J. 2004;21(3):387-388.
10. ElMaraghy MW, ElMaraghy AW, Evans HB. Digital adrenaline injection injuries: a case series and review. Can J Plast Surg. 1998;6:196-200.
11. Skorpinski EW, McGeady SJ, Yousef E. Two cases of accidental epinephrine injection into a finger. J Allergy Clin Immunol. 2006;117(2):463-464.
12. Nagaraj J, Reddy S, Murray R, Murphy N. Use of glyceryl trinitrate patches in the treatment of accidental digital injection of epinephrine from an autoinjector. Eur J Emerg Med. 2009;16(4):227-228. doi:10.1097/MEJ.0b013e328306f0ee.
13. Stier PA, Bogner MP, Webster K, Leikin JB, Burda A. Use of subcutaneous terbutaline to reverse peripheral ischemia. Am J Emerg Med. 1999;17(1):91-94.
14. Lee G, Thomas PC. Accidental digital injection of adrenaline from an autoinjector device. J Accid Emerg Med. 1998;15(4):287.
15. Baris S, Saricoban HE, Ak K, Ozdemir C. Papaverine chloride as a topical vasodilator in accidental injection of adrenaline into a digital finger. Allergy. 2011;66(11):1495-1496. doi:10.1111/j.1398-9995.2011.02664.x.
16. Buse K, Hein W, Drager N. Making Sense of Global Health Governance: A Policy Perspective. Basingstoke, England: Palgrave Macmillan UK; 2009.
17. Sherman SC. Digital Epipen® injection: a case of conservative management. J Emerg Med. 2011;41(6):672-674. doi:10.1016/j.jemermed.2009.07.027.
18. Janssen RL, Roeleveld-Versteegh AB, Wessels-Basten SJ, Hendriks T. [Auto-injection with epinephrine in the finger of a 5-year-old child]. Ned Tijdschr Geneeskd. 2008;152(17):1005-1008.
19. Singh T, Randhawa S, Khanna R. The EpiPen and the ischaemic finger. Eur J Emerg Med. 2007;14(4):222-223.
20. Barkhordarian AR, Wakelin SH, Paes TR. Accidental digital injection of adrenaline from an autoinjector device. Br J Dermatol. 2000;143(6):1359.
21. Deshmukh N, Tolland JT. Treatment of accidental epinephrine injection in a finger. J Emerg Med. 1989;7(4):408.
22. Hinterberger JW, Kintzi HE. Phentolamine reversal of epinephrine-induced digital vasospasm. How to save an ischemic finger. Arch Fam Med. 1994;3(2):193-195.
23. Peyko V, Cohen V, Jellinek-Cohen SP, Pearl-Davis M. Evaluation and treatment of accidental autoinjection of epinephrine. Am J Health Syst Pharm. 2013;70(9):778-781. doi:10.2146/ajhp120316.
24. Hardy SJ, Agostini DE. Accidental epinephrine auto-injector-induced digital ischemia reversed by phentolamine digital block. J Am Osteopath Assoc. 1995;95(6):377-378.
25. Kaspersen J, Vedsted P. [Accidental injection of adrenaline in a finger with EpiPen]. Ugeskr Laeger. 1998;160(45):6531-6532.
26. Schintler MV, Arbab E, Aberer W, Spendel S, Scharnagl E. Accidental perforating bone injury using the EpiPen autoinjection device. Allergy. 2005;60(2):259-260.
27. Khairalla E. Epinephrine-induced digital ischemia relieved by phentolamine. Plast Reconstr Surg. 2001;108(6):1831-1832.
28. Murali KS, Nayeem N. Accidental digital injection of adrenaline from an autoinjector device. J Accid Emerg Med. 1998;15(4):287.
29. Sellens C, Morrison L. Accidental injection of epinephrine by a child: a unique approach to treatment. CJEM. 1999;1(1):34-36.
30. Klemawesch P. Hyperbaric oxygen relieves severe digital ischaemia from accidental EpiPen injection. 2009 American Academy of Allergy, Asthma and Immunology Annual Meeting.
31. McCauley WA, Gerace RV, Scilley C. Treatment of accidental digital injection of epinephrine. Ann Emerg Med. 1991;20(6):665-668.
32. Mathez C, Favrat B, Staeger P. Management options for accidental injection of epinephrine from an autoinjector: a case report. J Med Case Rep. 2009;3:7268. doi:10.4076/1752-1947-3-7268.
33. Molony D. Adrenaline-induced digital ischaemia reversed with phentolamine. ANZ J Surg. 2006;76(12):1125-1126.
34. Carrascosa MF, Gallastegui-Menéndez A, Teja-Santamaría C, Caviedes JR. Accidental finger ischaemia induced by epinephrine autoinjector. BMJ Case Rep. 2013;2013. pii:bcr2013200783. doi:10.1136/bcr-2013-200783.
35. Patel R, Kumar H. Epinephrine induced digital ischemia after accidental injection from an auto-injector device. Indian Pediatr. 2013;50(2):247.
36. Xu J, Holt A. Use of Phentolamine in the treatment of Epipen induced digital ischemia. BMJ Case Rep. 2012;2012. doi:10.1136/bcr.12.2011.5450.
37. McNeil C, Copeland J. Accidental digital epinephrine injection: to treat or not to treat? Can Fam Physician. 2014;60(8):726-728.
38. Bodkin RP, Acquisto NM, Gunyan H, Wiegand TJ. Two cases of accidental injection of epinephrine into a digit treated with subcutaneous phentolamine injections. Case Rep Emerg Med. 2013;2013:586207. doi:10.1155/2013/586207.
39. Simons FE, Lieberman PL, Read EJ Jr, Edwards ES. Hazards of unintentional injection of epinephrine from autoinjectors: a systematic review. Ann Allergy Asthma Immunol. 2009;102(4):282-287. doi:10.1016/S1081-1206(10)60332-8.
40. European Medicines Agency. Better training tools recommended to support patients using adrenaline auto-injectors. European Medicines Agency, 2015.
41. Denkler K. A comprehensive review of epinephrine in the finger: to do or not to do.
42. Thomson CJ, Lalonde DH, Denkler KA, Feicht AJ. A critical look at the evidence for and against elective epinephrine use in the finger. Plast Reconstr Surg. 2007;119(1):260-266.
43. Lalonde D, Bell M, Benoit P, Sparkes G, Denkler K, Chang P. A multicenter prospective study of 3,110 consecutive cases of elective epinephrine use in the fingers and hand: the Dalhousie Project clinical phase. J Hand Surg Am. 2005;30(5):1061-1067. doi:10.1016/j.jhsa.2005.05.006.
Cognitive-behavioral therapy modified for maximum efficacy in the elderly
NEW YORK – For elderly individuals with depression exacerbated by physical limitations and personal losses, cognitive-behavioral therapy is a powerful tool for improving quality of life, according to the faculty of a workshop on this topic at the annual meeting of the American Psychiatric Association.
“The focus is on coping skills. It is about how to persevere in the face of adversity,” explained David A. Casey, MD, professor and chair of the department of psychiatry and behavioral sciences at University of Louisville (Ky.).
“It is not always a fair characterization, but CBT is often perceived as a strategy to address negative thoughts that are not real – but many of my elderly patients have losses and difficulties that are very real,” Dr. Casey said.
In the elderly who become increasingly isolated because of the loss of spouses, friends, and siblings while contending with medical problems that cause pain and limit activities, depression can engender withdrawal, a common coping mechanism, he said.
“Withdrawal may be an unexamined response to a sense of helplessness created by the problems of aging, but it can create a vicious cycle when depression contributes to lack of physical activity and further withdrawal,” explained Dr. Casey, who believes that mild cognitive impairment does not preclude the use of CBT.
CBT provides a “here-and-now” approach in which patients are reconnected to daily life by first identifying the activities that once provided pleasure or satisfaction and then developing a plan to reintroduce them into daily life. Except for its value in identifying activities meaningful to the patient, the history that preceded depression or psychological distress is less important than developing an immediate strategy to rebuilding an active life.
“Some patients are essentially immobilized by their withdrawal and convinced that their problems are unsolvable, but most will improve their quality of life through CBT,” he maintained.
There are data to support this contention, according to Jesse H. Wright III, MD, PhD, director of the Depression Center at the University of Louisville. He cited controlled studies demonstrating the efficacy of CBT relative to no CBT in relieving depression in the elderly.
“The evidence suggests that combining CBT with pharmacotherapy is better than either alone for managing depression in this age group,” Dr. Wright said.
In developing a therapeutic plan through CBT, patients are given assignments designed to develop participation in meaningful activities. These must be realistic within physical limitations and within the patient’s readiness to engage. Small steps toward a goal might be needed. At each therapeutic encounter, goals are set, and progress should be evaluated at the subsequent therapeutic encounter.
Dr. Casey cautioned. He said a rehearsal of the actions needed to achieve the assigned goals might be helpful before the patient leaves the treatment session. This allows the clinician to recognize and address potential obstacles, including practical issues, such as mobility, or psychological issues, such as fear of physical activities.
Developing persistence in the face of high levels of negativity can be a challenge not only for the patient but also for the physician. According to Dr. Casey, maintaining a positive attitude can be challenging after treating a series of highly withdrawn and discouraged patients. But he emphasized the need for a professional orientation, recognizing that incremental gains in patient well-being, not cure, should be considered a reasonable goal.
“If I can improve the patient’s quality of life, this is a significant success,” he said. He believes it is sometimes necessary to distract patients from potential problems to focus on expected benefits.
“Patients can have a view of their limitations that is accurate but unhelpful,” Dr. Casey said. The goal of CBT is to move the focus to strategies that can restore lost interest and pleasure in daily life.
Dr. Casey and Dr. Wright reported no potential conflicts of interest related to this topic.
NEW YORK – For elderly individuals with depression exacerbated by physical limitations and personal losses, cognitive-behavioral therapy is a powerful tool for improving quality of life, according to the faculty of a workshop on this topic at the annual meeting of the American Psychiatric Association.
“The focus is on coping skills. It is about how to persevere in the face of adversity,” explained David A. Casey, MD, professor and chair of the department of psychiatry and behavioral sciences at University of Louisville (Ky.).
“It is not always a fair characterization, but CBT is often perceived as a strategy to address negative thoughts that are not real – but many of my elderly patients have losses and difficulties that are very real,” Dr. Casey said.
In the elderly who become increasingly isolated because of the loss of spouses, friends, and siblings while contending with medical problems that cause pain and limit activities, depression can engender withdrawal, a common coping mechanism, he said.
“Withdrawal may be an unexamined response to a sense of helplessness created by the problems of aging, but it can create a vicious cycle when depression contributes to lack of physical activity and further withdrawal,” explained Dr. Casey, who believes that mild cognitive impairment does not preclude the use of CBT.
CBT provides a “here-and-now” approach in which patients are reconnected to daily life by first identifying the activities that once provided pleasure or satisfaction and then developing a plan to reintroduce them into daily life. Except for its value in identifying activities meaningful to the patient, the history that preceded depression or psychological distress is less important than developing an immediate strategy to rebuilding an active life.
“Some patients are essentially immobilized by their withdrawal and convinced that their problems are unsolvable, but most will improve their quality of life through CBT,” he maintained.
There are data to support this contention, according to Jesse H. Wright III, MD, PhD, director of the Depression Center at the University of Louisville. He cited controlled studies demonstrating the efficacy of CBT relative to no CBT in relieving depression in the elderly.
“The evidence suggests that combining CBT with pharmacotherapy is better than either alone for managing depression in this age group,” Dr. Wright said.
In developing a therapeutic plan through CBT, patients are given assignments designed to develop participation in meaningful activities. These must be realistic within physical limitations and within the patient’s readiness to engage. Small steps toward a goal might be needed. At each therapeutic encounter, goals are set, and progress should be evaluated at the subsequent therapeutic encounter.
Dr. Casey cautioned. He said a rehearsal of the actions needed to achieve the assigned goals might be helpful before the patient leaves the treatment session. This allows the clinician to recognize and address potential obstacles, including practical issues, such as mobility, or psychological issues, such as fear of physical activities.
Developing persistence in the face of high levels of negativity can be a challenge not only for the patient but also for the physician. According to Dr. Casey, maintaining a positive attitude can be challenging after treating a series of highly withdrawn and discouraged patients. But he emphasized the need for a professional orientation, recognizing that incremental gains in patient well-being, not cure, should be considered a reasonable goal.
“If I can improve the patient’s quality of life, this is a significant success,” he said. He believes it is sometimes necessary to distract patients from potential problems to focus on expected benefits.
“Patients can have a view of their limitations that is accurate but unhelpful,” Dr. Casey said. The goal of CBT is to move the focus to strategies that can restore lost interest and pleasure in daily life.
Dr. Casey and Dr. Wright reported no potential conflicts of interest related to this topic.
NEW YORK – For elderly individuals with depression exacerbated by physical limitations and personal losses, cognitive-behavioral therapy is a powerful tool for improving quality of life, according to the faculty of a workshop on this topic at the annual meeting of the American Psychiatric Association.
“The focus is on coping skills. It is about how to persevere in the face of adversity,” explained David A. Casey, MD, professor and chair of the department of psychiatry and behavioral sciences at University of Louisville (Ky.).
“It is not always a fair characterization, but CBT is often perceived as a strategy to address negative thoughts that are not real – but many of my elderly patients have losses and difficulties that are very real,” Dr. Casey said.
In the elderly who become increasingly isolated because of the loss of spouses, friends, and siblings while contending with medical problems that cause pain and limit activities, depression can engender withdrawal, a common coping mechanism, he said.
“Withdrawal may be an unexamined response to a sense of helplessness created by the problems of aging, but it can create a vicious cycle when depression contributes to lack of physical activity and further withdrawal,” explained Dr. Casey, who believes that mild cognitive impairment does not preclude the use of CBT.
CBT provides a “here-and-now” approach in which patients are reconnected to daily life by first identifying the activities that once provided pleasure or satisfaction and then developing a plan to reintroduce them into daily life. Except for its value in identifying activities meaningful to the patient, the history that preceded depression or psychological distress is less important than developing an immediate strategy to rebuilding an active life.
“Some patients are essentially immobilized by their withdrawal and convinced that their problems are unsolvable, but most will improve their quality of life through CBT,” he maintained.
There are data to support this contention, according to Jesse H. Wright III, MD, PhD, director of the Depression Center at the University of Louisville. He cited controlled studies demonstrating the efficacy of CBT relative to no CBT in relieving depression in the elderly.
“The evidence suggests that combining CBT with pharmacotherapy is better than either alone for managing depression in this age group,” Dr. Wright said.
In developing a therapeutic plan through CBT, patients are given assignments designed to develop participation in meaningful activities. These must be realistic within physical limitations and within the patient’s readiness to engage. Small steps toward a goal might be needed. At each therapeutic encounter, goals are set, and progress should be evaluated at the subsequent therapeutic encounter.
Dr. Casey cautioned. He said a rehearsal of the actions needed to achieve the assigned goals might be helpful before the patient leaves the treatment session. This allows the clinician to recognize and address potential obstacles, including practical issues, such as mobility, or psychological issues, such as fear of physical activities.
Developing persistence in the face of high levels of negativity can be a challenge not only for the patient but also for the physician. According to Dr. Casey, maintaining a positive attitude can be challenging after treating a series of highly withdrawn and discouraged patients. But he emphasized the need for a professional orientation, recognizing that incremental gains in patient well-being, not cure, should be considered a reasonable goal.
“If I can improve the patient’s quality of life, this is a significant success,” he said. He believes it is sometimes necessary to distract patients from potential problems to focus on expected benefits.
“Patients can have a view of their limitations that is accurate but unhelpful,” Dr. Casey said. The goal of CBT is to move the focus to strategies that can restore lost interest and pleasure in daily life.
Dr. Casey and Dr. Wright reported no potential conflicts of interest related to this topic.
EXPERT ANALYSIS FROM APA
Poor sleep tied to suicidal behaviors in college students
Poor sleep is associated with increased suicidal behaviors in college students – even when controlling for depression, a study of 1,700 students shows.
“Furthermore, findings suggest that some specific sleep components – shorter sleep duration, more frequent bad dreams, feeling too cold while sleeping, and greater sleep medication use – are particularly associated with increased suicidal behaviors in college students,” reported Stephen P. Becker, PhD, of the Cincinnati Children’s Hospital Center, and his associates.
The researchers recruited students from two universities. Most of the students (65%) were female, white (82%), and in their first year of college (63%). The participants’ sleep was assessed using the nine-item Pittsburgh Sleep Quality Index (PSQI), their depressive symptoms were assessed using the Depressive Anxiety Stress Scales-21, and their suicidal behavior was assessed using the Suicidal Behaviors Questionnaire-Revised (SBQ-R), which is a four-item, self-report measure.
About two-thirds of the students (64%) were found to have sleep problems (total PSQI score greater than 5), and 24% were found to have suicide risk (total SBQ-R score of at least 7). Of the students who were found to have suicide risk, 83% also had sleep problems.
Using regression analysis, Dr. Becker and his associates found that the odds of being classified with suicide risk were 6.5 times greater for students with depression and 2.7 times greater for those with sleep problems.
The results add to the literature suggesting that the researchers wrote.
SOURCE: Becker SP et al. J Psychiatr Res. 2018 Apr;99:123-8.
Poor sleep is associated with increased suicidal behaviors in college students – even when controlling for depression, a study of 1,700 students shows.
“Furthermore, findings suggest that some specific sleep components – shorter sleep duration, more frequent bad dreams, feeling too cold while sleeping, and greater sleep medication use – are particularly associated with increased suicidal behaviors in college students,” reported Stephen P. Becker, PhD, of the Cincinnati Children’s Hospital Center, and his associates.
The researchers recruited students from two universities. Most of the students (65%) were female, white (82%), and in their first year of college (63%). The participants’ sleep was assessed using the nine-item Pittsburgh Sleep Quality Index (PSQI), their depressive symptoms were assessed using the Depressive Anxiety Stress Scales-21, and their suicidal behavior was assessed using the Suicidal Behaviors Questionnaire-Revised (SBQ-R), which is a four-item, self-report measure.
About two-thirds of the students (64%) were found to have sleep problems (total PSQI score greater than 5), and 24% were found to have suicide risk (total SBQ-R score of at least 7). Of the students who were found to have suicide risk, 83% also had sleep problems.
Using regression analysis, Dr. Becker and his associates found that the odds of being classified with suicide risk were 6.5 times greater for students with depression and 2.7 times greater for those with sleep problems.
The results add to the literature suggesting that the researchers wrote.
SOURCE: Becker SP et al. J Psychiatr Res. 2018 Apr;99:123-8.
Poor sleep is associated with increased suicidal behaviors in college students – even when controlling for depression, a study of 1,700 students shows.
“Furthermore, findings suggest that some specific sleep components – shorter sleep duration, more frequent bad dreams, feeling too cold while sleeping, and greater sleep medication use – are particularly associated with increased suicidal behaviors in college students,” reported Stephen P. Becker, PhD, of the Cincinnati Children’s Hospital Center, and his associates.
The researchers recruited students from two universities. Most of the students (65%) were female, white (82%), and in their first year of college (63%). The participants’ sleep was assessed using the nine-item Pittsburgh Sleep Quality Index (PSQI), their depressive symptoms were assessed using the Depressive Anxiety Stress Scales-21, and their suicidal behavior was assessed using the Suicidal Behaviors Questionnaire-Revised (SBQ-R), which is a four-item, self-report measure.
About two-thirds of the students (64%) were found to have sleep problems (total PSQI score greater than 5), and 24% were found to have suicide risk (total SBQ-R score of at least 7). Of the students who were found to have suicide risk, 83% also had sleep problems.
Using regression analysis, Dr. Becker and his associates found that the odds of being classified with suicide risk were 6.5 times greater for students with depression and 2.7 times greater for those with sleep problems.
The results add to the literature suggesting that the researchers wrote.
SOURCE: Becker SP et al. J Psychiatr Res. 2018 Apr;99:123-8.
FROM THE JOURNAL OF PSYCHIATRIC RESEARCH
Elagolix shows long-term efficacy
AUSTIN, TEX. – A new treatment for endometriosis-related pain, Elagolix, showed evidence of being effective long term, according to a study presented at the annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists.
Elagolix, an oral nonpeptide gonadotropin-releasing hormone (GnRH) antagonist, manufactured by AbbVie, would be the first treatment of its kind if approved by the Food and Drug Administration, and would fulfill a needed relief for a more tolerable approach to severe endometriosis patients, according to presenter Eric S. Surrey, MD, medical director at the Colorado Center of Reproductive Medicine, Lone Tree.
“There have been no new medications approved for a long time for systematic endometriosis and there is a huge gap because the current options are expensive, and they are often injectable drugs,” said Dr. Surrey in an interview. “This would be an oral agent, which would be fabulous because it allows for a lot of flexibility and for many patients this could be much less concerning than using something long acting.”
To test the long-term effects of Elagolix, investigators studied 570 women with moderate to severe endometriosis-related pain who had gathered to participate in a previous phase 3, randomized, placebo-controlled trial concerning the drug’s effectiveness.
In the two extension studies, all participants were given either a 150- or 200-mg dose of Elagolix.
Average age of each patient group was between 31 and 34 years, and all groups were majority white, with a mean length of time from surgical diagnosis ranging from 45.5 to 56.6 months.
Patient improvements in dysmenorrhea and nonmenstrual pelvic pain continued between the first 6 months and 12 months of treatment, with a decrease of 46%-77% in the overall number of analgesics taken per day.
After 12 months of consecutive treatment, patients given 150 mg of Elagolix saw mean dysmenorrhea scores improve by 49%-53% from baseline, and by 82% for those at 200 mg, with certain expected adverse events, according to Dr. Surrey.
One of the most common adverse events associated with Elagolix was hot flashes, an unsurprising finding for Dr. Surrey and his colleagues considering Elagolix is a drug that lowers estrogen levels. However, any hot flashes patients experienced during the trial were still better than those associated with current medications, according to Dr. Surrey.
“In this extension study nobody dropped out because of hot flashes in the additional 6-month extension time,” Dr. Surrey explained. “If you look at the gold standard drug for endometriosis now, which is a GnRH agonist, which are highly available and are either injectable or implants, [patients taking these drugs] can have very severe hot flashes that require additional medication to alleviate the hot flashes at the same time.”
Patients did also experience some loss in bone density; however, Dr. Surrey argues the frequency and level of these adverse events is still better than current treatment options. One patient was required to discontinue the trial for bone density loss.
Currently, Elagolix is under FDA priority review, and if approved will be the first oral endometriosis treatment approved in over a decade, according to Dr. Surrey.
Dr. Surrey and several coauthors receive financial support from AbbVie as consultants, board members, and/or employees. Dr. Surrey and Dr. Taylor receive additional support from companies including Pfizer, Bayer, and Obseva.
SOURCE: Surrey ES et al. ACOG 2018, Abstract 11OP.
Having had the opportunity to review Dr. Eric Surrey's abstract for this year's annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists, entitled "Long-term Safety and Efficacy of Elagolix Treatment in Women With Endometriosis-associated Pain," I believe use of Elagolix, an oral nonpeptide gonadotropin-releasing hormone (GnRH) antagonist, is a much-needed advancement in the long-term treatment of endometriosis-related pain. The fact that it is an oral medication, thus, not requiring a monthly or 3-month injection as does Lupron Depot (leuprolide acetate), the most popular GnRH agonist in the United States, is advantageous both for the patient and the busy office staff.
While I certainly understand that it is easy to compare data regarding bone loss in the use of an oral antagonist, Elagolix, with historical data with the GnRH agonist and note a lessening of bone loss in the Elagolix patients, it would be interesting to compare bone loss in patients utilizing Elagolix with bone loss in those treated with GnRH-agonist plus add-back therapy. Many practitioners will utilize progesterone supplementation or estrogen/progesterone supplementation when using GnRH-agonist therapy to decrease this risk. Furthermore, it would be interesting, in the future, to evaluate the impact on efficacy and bone loss if progesterone and estrogen/progesterone add-back were utilized in Elagolix therapy.
While I certainly realize and deeply respect Dr. Surrey's vast experience as both a clinical researcher and clinician utilizing a GnRH-agonist regimen, I am curious as to the basis of Dr. Surrey's comments regarding less severe hot flashes in comparison to GnRH-agonist treatment. I am not aware of any head-to-head studies comparing hot flashes between GnRH agonists (in particular, leuprolide acetate) and Elagolix.
Without a side-by-side comparison utilizing a validated scoring system, I find it hard to accept this conclusion.
Nevertheless, after reviewing this study and Dr. Surrey's comments, I look forward to utilizing Elagolix in my practice for long-term treatment of endometriosis-related pain.
Charles Miller, MD, is a minimally invasive gynecologic surgeon in Naperville, Ill., and a past president of the AAGL. He is a consultant and involved in research for AbbVie.
Having had the opportunity to review Dr. Eric Surrey's abstract for this year's annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists, entitled "Long-term Safety and Efficacy of Elagolix Treatment in Women With Endometriosis-associated Pain," I believe use of Elagolix, an oral nonpeptide gonadotropin-releasing hormone (GnRH) antagonist, is a much-needed advancement in the long-term treatment of endometriosis-related pain. The fact that it is an oral medication, thus, not requiring a monthly or 3-month injection as does Lupron Depot (leuprolide acetate), the most popular GnRH agonist in the United States, is advantageous both for the patient and the busy office staff.
While I certainly understand that it is easy to compare data regarding bone loss in the use of an oral antagonist, Elagolix, with historical data with the GnRH agonist and note a lessening of bone loss in the Elagolix patients, it would be interesting to compare bone loss in patients utilizing Elagolix with bone loss in those treated with GnRH-agonist plus add-back therapy. Many practitioners will utilize progesterone supplementation or estrogen/progesterone supplementation when using GnRH-agonist therapy to decrease this risk. Furthermore, it would be interesting, in the future, to evaluate the impact on efficacy and bone loss if progesterone and estrogen/progesterone add-back were utilized in Elagolix therapy.
While I certainly realize and deeply respect Dr. Surrey's vast experience as both a clinical researcher and clinician utilizing a GnRH-agonist regimen, I am curious as to the basis of Dr. Surrey's comments regarding less severe hot flashes in comparison to GnRH-agonist treatment. I am not aware of any head-to-head studies comparing hot flashes between GnRH agonists (in particular, leuprolide acetate) and Elagolix.
Without a side-by-side comparison utilizing a validated scoring system, I find it hard to accept this conclusion.
Nevertheless, after reviewing this study and Dr. Surrey's comments, I look forward to utilizing Elagolix in my practice for long-term treatment of endometriosis-related pain.
Charles Miller, MD, is a minimally invasive gynecologic surgeon in Naperville, Ill., and a past president of the AAGL. He is a consultant and involved in research for AbbVie.
Having had the opportunity to review Dr. Eric Surrey's abstract for this year's annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists, entitled "Long-term Safety and Efficacy of Elagolix Treatment in Women With Endometriosis-associated Pain," I believe use of Elagolix, an oral nonpeptide gonadotropin-releasing hormone (GnRH) antagonist, is a much-needed advancement in the long-term treatment of endometriosis-related pain. The fact that it is an oral medication, thus, not requiring a monthly or 3-month injection as does Lupron Depot (leuprolide acetate), the most popular GnRH agonist in the United States, is advantageous both for the patient and the busy office staff.
While I certainly understand that it is easy to compare data regarding bone loss in the use of an oral antagonist, Elagolix, with historical data with the GnRH agonist and note a lessening of bone loss in the Elagolix patients, it would be interesting to compare bone loss in patients utilizing Elagolix with bone loss in those treated with GnRH-agonist plus add-back therapy. Many practitioners will utilize progesterone supplementation or estrogen/progesterone supplementation when using GnRH-agonist therapy to decrease this risk. Furthermore, it would be interesting, in the future, to evaluate the impact on efficacy and bone loss if progesterone and estrogen/progesterone add-back were utilized in Elagolix therapy.
While I certainly realize and deeply respect Dr. Surrey's vast experience as both a clinical researcher and clinician utilizing a GnRH-agonist regimen, I am curious as to the basis of Dr. Surrey's comments regarding less severe hot flashes in comparison to GnRH-agonist treatment. I am not aware of any head-to-head studies comparing hot flashes between GnRH agonists (in particular, leuprolide acetate) and Elagolix.
Without a side-by-side comparison utilizing a validated scoring system, I find it hard to accept this conclusion.
Nevertheless, after reviewing this study and Dr. Surrey's comments, I look forward to utilizing Elagolix in my practice for long-term treatment of endometriosis-related pain.
Charles Miller, MD, is a minimally invasive gynecologic surgeon in Naperville, Ill., and a past president of the AAGL. He is a consultant and involved in research for AbbVie.
AUSTIN, TEX. – A new treatment for endometriosis-related pain, Elagolix, showed evidence of being effective long term, according to a study presented at the annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists.
Elagolix, an oral nonpeptide gonadotropin-releasing hormone (GnRH) antagonist, manufactured by AbbVie, would be the first treatment of its kind if approved by the Food and Drug Administration, and would fulfill a needed relief for a more tolerable approach to severe endometriosis patients, according to presenter Eric S. Surrey, MD, medical director at the Colorado Center of Reproductive Medicine, Lone Tree.
“There have been no new medications approved for a long time for systematic endometriosis and there is a huge gap because the current options are expensive, and they are often injectable drugs,” said Dr. Surrey in an interview. “This would be an oral agent, which would be fabulous because it allows for a lot of flexibility and for many patients this could be much less concerning than using something long acting.”
To test the long-term effects of Elagolix, investigators studied 570 women with moderate to severe endometriosis-related pain who had gathered to participate in a previous phase 3, randomized, placebo-controlled trial concerning the drug’s effectiveness.
In the two extension studies, all participants were given either a 150- or 200-mg dose of Elagolix.
Average age of each patient group was between 31 and 34 years, and all groups were majority white, with a mean length of time from surgical diagnosis ranging from 45.5 to 56.6 months.
Patient improvements in dysmenorrhea and nonmenstrual pelvic pain continued between the first 6 months and 12 months of treatment, with a decrease of 46%-77% in the overall number of analgesics taken per day.
After 12 months of consecutive treatment, patients given 150 mg of Elagolix saw mean dysmenorrhea scores improve by 49%-53% from baseline, and by 82% for those at 200 mg, with certain expected adverse events, according to Dr. Surrey.
One of the most common adverse events associated with Elagolix was hot flashes, an unsurprising finding for Dr. Surrey and his colleagues considering Elagolix is a drug that lowers estrogen levels. However, any hot flashes patients experienced during the trial were still better than those associated with current medications, according to Dr. Surrey.
“In this extension study nobody dropped out because of hot flashes in the additional 6-month extension time,” Dr. Surrey explained. “If you look at the gold standard drug for endometriosis now, which is a GnRH agonist, which are highly available and are either injectable or implants, [patients taking these drugs] can have very severe hot flashes that require additional medication to alleviate the hot flashes at the same time.”
Patients did also experience some loss in bone density; however, Dr. Surrey argues the frequency and level of these adverse events is still better than current treatment options. One patient was required to discontinue the trial for bone density loss.
Currently, Elagolix is under FDA priority review, and if approved will be the first oral endometriosis treatment approved in over a decade, according to Dr. Surrey.
Dr. Surrey and several coauthors receive financial support from AbbVie as consultants, board members, and/or employees. Dr. Surrey and Dr. Taylor receive additional support from companies including Pfizer, Bayer, and Obseva.
SOURCE: Surrey ES et al. ACOG 2018, Abstract 11OP.
AUSTIN, TEX. – A new treatment for endometriosis-related pain, Elagolix, showed evidence of being effective long term, according to a study presented at the annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists.
Elagolix, an oral nonpeptide gonadotropin-releasing hormone (GnRH) antagonist, manufactured by AbbVie, would be the first treatment of its kind if approved by the Food and Drug Administration, and would fulfill a needed relief for a more tolerable approach to severe endometriosis patients, according to presenter Eric S. Surrey, MD, medical director at the Colorado Center of Reproductive Medicine, Lone Tree.
“There have been no new medications approved for a long time for systematic endometriosis and there is a huge gap because the current options are expensive, and they are often injectable drugs,” said Dr. Surrey in an interview. “This would be an oral agent, which would be fabulous because it allows for a lot of flexibility and for many patients this could be much less concerning than using something long acting.”
To test the long-term effects of Elagolix, investigators studied 570 women with moderate to severe endometriosis-related pain who had gathered to participate in a previous phase 3, randomized, placebo-controlled trial concerning the drug’s effectiveness.
In the two extension studies, all participants were given either a 150- or 200-mg dose of Elagolix.
Average age of each patient group was between 31 and 34 years, and all groups were majority white, with a mean length of time from surgical diagnosis ranging from 45.5 to 56.6 months.
Patient improvements in dysmenorrhea and nonmenstrual pelvic pain continued between the first 6 months and 12 months of treatment, with a decrease of 46%-77% in the overall number of analgesics taken per day.
After 12 months of consecutive treatment, patients given 150 mg of Elagolix saw mean dysmenorrhea scores improve by 49%-53% from baseline, and by 82% for those at 200 mg, with certain expected adverse events, according to Dr. Surrey.
One of the most common adverse events associated with Elagolix was hot flashes, an unsurprising finding for Dr. Surrey and his colleagues considering Elagolix is a drug that lowers estrogen levels. However, any hot flashes patients experienced during the trial were still better than those associated with current medications, according to Dr. Surrey.
“In this extension study nobody dropped out because of hot flashes in the additional 6-month extension time,” Dr. Surrey explained. “If you look at the gold standard drug for endometriosis now, which is a GnRH agonist, which are highly available and are either injectable or implants, [patients taking these drugs] can have very severe hot flashes that require additional medication to alleviate the hot flashes at the same time.”
Patients did also experience some loss in bone density; however, Dr. Surrey argues the frequency and level of these adverse events is still better than current treatment options. One patient was required to discontinue the trial for bone density loss.
Currently, Elagolix is under FDA priority review, and if approved will be the first oral endometriosis treatment approved in over a decade, according to Dr. Surrey.
Dr. Surrey and several coauthors receive financial support from AbbVie as consultants, board members, and/or employees. Dr. Surrey and Dr. Taylor receive additional support from companies including Pfizer, Bayer, and Obseva.
SOURCE: Surrey ES et al. ACOG 2018, Abstract 11OP.
REPORTING FROM ACOG 2018
Key clinical point: New treatment for endometriosis-related pain shows long-term efficacy.
Major finding: Pain significantly decreased in test groups, compared with placebo (P less than .05).
Data source: A phase 3, randomized trial of 570 women with moderate to severe endometriosis.
Disclosures: Dr. Surrey and several coauthors receive financial support from AbbVie as consultants, board members, and/or employees. Dr. Surrey and Dr. Taylor receive additional support from companies including Pfizer, Bayer, and Obseva.
Source: Surrey ES et al. ACOG 2018, Abstract 11OP.
Which infants with invasive bacterial infections are at risk for adverse outcomes?
TORONTO – Among infants up to 60 days old with an invasive bacterial infection, adverse outcomes are associated with prematurity, ill appearance, and bacterial meningitis, a multicenter retrospective analysis found.
“Young infants are susceptible to serious bacterial infections, particularly when they’re less than 60 days of age,” Christopher Pruitt, MD, said at the annual Pediatric Academic Societies meeting. “Among these infants, bacteremia and bacterial meningitis, also referred to as invasive bacterial infections, are associated with higher rates of morbidity and mortality.”
The primary outcome measure was occurrence of an adverse clinical outcome within 30 days following the index ED visit. Adverse outcomes were defined as use of mechanical ventilation, vasoactive medications, any neurologic sequelae, and death. The researchers used a mixed-effects logistic regression model and retained covariates with a P value of less than .10. Covariates analyzed included age less than 28 days, prematurity, presence or absence of a complex chronic condition, presence of fever, ill appearance, bacterial meningitis, and concordant empiric antimicrobial therapy.
Of the 442 infants included in the final analysis, the majority (80%) had bacteremia, 14% had bacterial meningitis plus bacteremia, and 6% had bacterial meningitis only. “For purposes of this study, patients with bacterial meningitis with or without bacteremia were categorized as having bacterial meningitis,” Dr. Pruitt said. He and his associates found that 14.5% of infants had one or more adverse outcomes. Adverse outcomes occurred in 39% of infants with bacterial meningitis, compared with 8.2% of infants with isolated bacteremia. Need for mechanical ventilation, vasoactive medications, and neurologic disability also was more common among infants with bacterial meningitis than it was among children with isolated bacteremia. There were 10 deaths overall, which amounted to about 2% in both groups.
On multivariate analysis, the rate of adverse outcomes was significantly higher for patients with bacterial meningitis than it was for those with isolated bacteremia (adjusted odds ratio, 8.8), for premature versus term infants (AOR, 5.9), for infants who were ill appearing versus non-ill appearing (AOR, 3.9), and for infants with no fever versus those with fever (AOR, 2.4). No significant associations with 30-day adverse outcomes were seen in patients with a complex chronic condition, compared with those without a complex chronic condition (AOR, 2.0), nor in the those aged 29-60 days versus those younger than 29 days (15% vs. 14%, respectively; AOR 0.7).
“When looking at the most common scenario – a full-term infant without an ill appearance, and bacteremia as opposed to bacterial meningitis – 3 of these 219 infants, or 1.4%, had an adverse outcome,” said Dr. Pruitt, who cares for patients in the ED at Children’s of Alabama in Birmingham. “And there were no deaths.” He also reported that 12 infants with invasive bacterial infections were discharged from the index ED visit without antimicrobial treatment. All had bacteremia and none had an adverse outcome.
Dr. Pruitt acknowledged certain limitations of the study, including its retrospective design, that the outcomes were limited to 30 days, and the fact that the findings may not be generalizable to nontertiary settings. “Our findings have important implications for the care of infants with invasive bacterial infections,” he concluded. “In particular, the high rate of adverse outcomes for infants with bacterial meningitis can provide some context for clinicians in assessing the need for diagnostic evaluation for invasive bacterial infection and discussing testing and treatment with parents. Our findings may also help to inform inpatient management for hospitalized infants with invasive bacterial infections, as well as anticipatory guidance for parents, particularly around follow-up. Further prospective studies evaluating the long-term outcomes of infants with invasive bacterial infections are needed.”
The study was supported in part by a grant from the National Institutes of Health. Dr. Pruitt reported having no financial disclosures.
TORONTO – Among infants up to 60 days old with an invasive bacterial infection, adverse outcomes are associated with prematurity, ill appearance, and bacterial meningitis, a multicenter retrospective analysis found.
“Young infants are susceptible to serious bacterial infections, particularly when they’re less than 60 days of age,” Christopher Pruitt, MD, said at the annual Pediatric Academic Societies meeting. “Among these infants, bacteremia and bacterial meningitis, also referred to as invasive bacterial infections, are associated with higher rates of morbidity and mortality.”
The primary outcome measure was occurrence of an adverse clinical outcome within 30 days following the index ED visit. Adverse outcomes were defined as use of mechanical ventilation, vasoactive medications, any neurologic sequelae, and death. The researchers used a mixed-effects logistic regression model and retained covariates with a P value of less than .10. Covariates analyzed included age less than 28 days, prematurity, presence or absence of a complex chronic condition, presence of fever, ill appearance, bacterial meningitis, and concordant empiric antimicrobial therapy.
Of the 442 infants included in the final analysis, the majority (80%) had bacteremia, 14% had bacterial meningitis plus bacteremia, and 6% had bacterial meningitis only. “For purposes of this study, patients with bacterial meningitis with or without bacteremia were categorized as having bacterial meningitis,” Dr. Pruitt said. He and his associates found that 14.5% of infants had one or more adverse outcomes. Adverse outcomes occurred in 39% of infants with bacterial meningitis, compared with 8.2% of infants with isolated bacteremia. Need for mechanical ventilation, vasoactive medications, and neurologic disability also was more common among infants with bacterial meningitis than it was among children with isolated bacteremia. There were 10 deaths overall, which amounted to about 2% in both groups.
On multivariate analysis, the rate of adverse outcomes was significantly higher for patients with bacterial meningitis than it was for those with isolated bacteremia (adjusted odds ratio, 8.8), for premature versus term infants (AOR, 5.9), for infants who were ill appearing versus non-ill appearing (AOR, 3.9), and for infants with no fever versus those with fever (AOR, 2.4). No significant associations with 30-day adverse outcomes were seen in patients with a complex chronic condition, compared with those without a complex chronic condition (AOR, 2.0), nor in the those aged 29-60 days versus those younger than 29 days (15% vs. 14%, respectively; AOR 0.7).
“When looking at the most common scenario – a full-term infant without an ill appearance, and bacteremia as opposed to bacterial meningitis – 3 of these 219 infants, or 1.4%, had an adverse outcome,” said Dr. Pruitt, who cares for patients in the ED at Children’s of Alabama in Birmingham. “And there were no deaths.” He also reported that 12 infants with invasive bacterial infections were discharged from the index ED visit without antimicrobial treatment. All had bacteremia and none had an adverse outcome.
Dr. Pruitt acknowledged certain limitations of the study, including its retrospective design, that the outcomes were limited to 30 days, and the fact that the findings may not be generalizable to nontertiary settings. “Our findings have important implications for the care of infants with invasive bacterial infections,” he concluded. “In particular, the high rate of adverse outcomes for infants with bacterial meningitis can provide some context for clinicians in assessing the need for diagnostic evaluation for invasive bacterial infection and discussing testing and treatment with parents. Our findings may also help to inform inpatient management for hospitalized infants with invasive bacterial infections, as well as anticipatory guidance for parents, particularly around follow-up. Further prospective studies evaluating the long-term outcomes of infants with invasive bacterial infections are needed.”
The study was supported in part by a grant from the National Institutes of Health. Dr. Pruitt reported having no financial disclosures.
TORONTO – Among infants up to 60 days old with an invasive bacterial infection, adverse outcomes are associated with prematurity, ill appearance, and bacterial meningitis, a multicenter retrospective analysis found.
“Young infants are susceptible to serious bacterial infections, particularly when they’re less than 60 days of age,” Christopher Pruitt, MD, said at the annual Pediatric Academic Societies meeting. “Among these infants, bacteremia and bacterial meningitis, also referred to as invasive bacterial infections, are associated with higher rates of morbidity and mortality.”
The primary outcome measure was occurrence of an adverse clinical outcome within 30 days following the index ED visit. Adverse outcomes were defined as use of mechanical ventilation, vasoactive medications, any neurologic sequelae, and death. The researchers used a mixed-effects logistic regression model and retained covariates with a P value of less than .10. Covariates analyzed included age less than 28 days, prematurity, presence or absence of a complex chronic condition, presence of fever, ill appearance, bacterial meningitis, and concordant empiric antimicrobial therapy.
Of the 442 infants included in the final analysis, the majority (80%) had bacteremia, 14% had bacterial meningitis plus bacteremia, and 6% had bacterial meningitis only. “For purposes of this study, patients with bacterial meningitis with or without bacteremia were categorized as having bacterial meningitis,” Dr. Pruitt said. He and his associates found that 14.5% of infants had one or more adverse outcomes. Adverse outcomes occurred in 39% of infants with bacterial meningitis, compared with 8.2% of infants with isolated bacteremia. Need for mechanical ventilation, vasoactive medications, and neurologic disability also was more common among infants with bacterial meningitis than it was among children with isolated bacteremia. There were 10 deaths overall, which amounted to about 2% in both groups.
On multivariate analysis, the rate of adverse outcomes was significantly higher for patients with bacterial meningitis than it was for those with isolated bacteremia (adjusted odds ratio, 8.8), for premature versus term infants (AOR, 5.9), for infants who were ill appearing versus non-ill appearing (AOR, 3.9), and for infants with no fever versus those with fever (AOR, 2.4). No significant associations with 30-day adverse outcomes were seen in patients with a complex chronic condition, compared with those without a complex chronic condition (AOR, 2.0), nor in the those aged 29-60 days versus those younger than 29 days (15% vs. 14%, respectively; AOR 0.7).
“When looking at the most common scenario – a full-term infant without an ill appearance, and bacteremia as opposed to bacterial meningitis – 3 of these 219 infants, or 1.4%, had an adverse outcome,” said Dr. Pruitt, who cares for patients in the ED at Children’s of Alabama in Birmingham. “And there were no deaths.” He also reported that 12 infants with invasive bacterial infections were discharged from the index ED visit without antimicrobial treatment. All had bacteremia and none had an adverse outcome.
Dr. Pruitt acknowledged certain limitations of the study, including its retrospective design, that the outcomes were limited to 30 days, and the fact that the findings may not be generalizable to nontertiary settings. “Our findings have important implications for the care of infants with invasive bacterial infections,” he concluded. “In particular, the high rate of adverse outcomes for infants with bacterial meningitis can provide some context for clinicians in assessing the need for diagnostic evaluation for invasive bacterial infection and discussing testing and treatment with parents. Our findings may also help to inform inpatient management for hospitalized infants with invasive bacterial infections, as well as anticipatory guidance for parents, particularly around follow-up. Further prospective studies evaluating the long-term outcomes of infants with invasive bacterial infections are needed.”
The study was supported in part by a grant from the National Institutes of Health. Dr. Pruitt reported having no financial disclosures.
REPORTING FROM PAS 2018
Key clinical point:
Major finding: The rate of adverse outcomes was significantly higher for patients with bacterial meningitis versus those with isolated bacteremia (adjusted odds ratio, 8.8) and for premature versus term infants (AOR, 5.9).
Study details: A multicenter, retrospective review of 442 infants with invasive bacterial infections who were initially evaluated in the ED.
Disclosures: The study was supported in part by a grant from the National Institutes of Health. Dr. Pruitt reported having no financial disclosures.
Probiotics reduce the risk of Clostridium difficile –associated diarrhea in patients receiving antibiotics
Background: Antibiotic use is associated with an increased risk of C. difficile infection. Multiple studies have investigated the effects of probiotics in reducing the risk of C. difficile infection with varied results. This meta-analysis aims to assess the efficacy and safety of probiotics in reducing the risk of CDAD in patients taking antibiotics.
Study design: Meta-analysis.
Setting: A comprehensive electronic search for randomized, controlled trials investigating probiotics for prevention of CDAD or C. difficile infection were considered for inclusion. There were no language, publication status, or date limits applied.
Synopsis: This meta-analysis included 31 trials (8,672 participants) evaluating the relationship between probiotics and CDAD. The outcomes were pooled using a random effects model to calculate risk ratios and 95% confidence intervals. A complete case analysis suggested that probiotics reduce the risk of CDAD by 60% (1.5% vs. 4.0%; relative risk, 0.40; 95% confidence interval, 0.3-0.52), although a post-hoc subgroup analysis showed a statistically significant benefit only among patients with a high CDAD baseline risk (greater than 5%). Adverse events were assessed in 32 trials (8,305 participants), and the pooled analysis indicated that probiotic use reduced the risk of adverse events by 17% (RR, 0.83; 95% CI, 0.71-0.97).
Limitations to this meta-analysis include missing data from patients lost to follow-up and lack of success in testing all fecal samples. Lastly, that the strongest data for the beneficial effects of probiotics were demonstrated in patients with a high baseline risk of developing CDAD limits the study’s applicability to the general population.
Bottom line: Probiotic use in immunocompetent patients undergoing treatment with antibiotics decreases the incidence of CDAD without an increase in adverse events.
Citation: Goldenberg JZ et al. Probiotics for the prevention of Clostridium difficile–associated diarrhea in adults and children. Cochrane Database Syst Rev. 2017. doi: 10.1002/14651858.CD006095.pub4.
Dr. Skinner is a hospitalist at Denver Health Medical Center and an assistant professor of medicine at the University of Colorado at Denver, Aurora.
Background: Antibiotic use is associated with an increased risk of C. difficile infection. Multiple studies have investigated the effects of probiotics in reducing the risk of C. difficile infection with varied results. This meta-analysis aims to assess the efficacy and safety of probiotics in reducing the risk of CDAD in patients taking antibiotics.
Study design: Meta-analysis.
Setting: A comprehensive electronic search for randomized, controlled trials investigating probiotics for prevention of CDAD or C. difficile infection were considered for inclusion. There were no language, publication status, or date limits applied.
Synopsis: This meta-analysis included 31 trials (8,672 participants) evaluating the relationship between probiotics and CDAD. The outcomes were pooled using a random effects model to calculate risk ratios and 95% confidence intervals. A complete case analysis suggested that probiotics reduce the risk of CDAD by 60% (1.5% vs. 4.0%; relative risk, 0.40; 95% confidence interval, 0.3-0.52), although a post-hoc subgroup analysis showed a statistically significant benefit only among patients with a high CDAD baseline risk (greater than 5%). Adverse events were assessed in 32 trials (8,305 participants), and the pooled analysis indicated that probiotic use reduced the risk of adverse events by 17% (RR, 0.83; 95% CI, 0.71-0.97).
Limitations to this meta-analysis include missing data from patients lost to follow-up and lack of success in testing all fecal samples. Lastly, that the strongest data for the beneficial effects of probiotics were demonstrated in patients with a high baseline risk of developing CDAD limits the study’s applicability to the general population.
Bottom line: Probiotic use in immunocompetent patients undergoing treatment with antibiotics decreases the incidence of CDAD without an increase in adverse events.
Citation: Goldenberg JZ et al. Probiotics for the prevention of Clostridium difficile–associated diarrhea in adults and children. Cochrane Database Syst Rev. 2017. doi: 10.1002/14651858.CD006095.pub4.
Dr. Skinner is a hospitalist at Denver Health Medical Center and an assistant professor of medicine at the University of Colorado at Denver, Aurora.
Background: Antibiotic use is associated with an increased risk of C. difficile infection. Multiple studies have investigated the effects of probiotics in reducing the risk of C. difficile infection with varied results. This meta-analysis aims to assess the efficacy and safety of probiotics in reducing the risk of CDAD in patients taking antibiotics.
Study design: Meta-analysis.
Setting: A comprehensive electronic search for randomized, controlled trials investigating probiotics for prevention of CDAD or C. difficile infection were considered for inclusion. There were no language, publication status, or date limits applied.
Synopsis: This meta-analysis included 31 trials (8,672 participants) evaluating the relationship between probiotics and CDAD. The outcomes were pooled using a random effects model to calculate risk ratios and 95% confidence intervals. A complete case analysis suggested that probiotics reduce the risk of CDAD by 60% (1.5% vs. 4.0%; relative risk, 0.40; 95% confidence interval, 0.3-0.52), although a post-hoc subgroup analysis showed a statistically significant benefit only among patients with a high CDAD baseline risk (greater than 5%). Adverse events were assessed in 32 trials (8,305 participants), and the pooled analysis indicated that probiotic use reduced the risk of adverse events by 17% (RR, 0.83; 95% CI, 0.71-0.97).
Limitations to this meta-analysis include missing data from patients lost to follow-up and lack of success in testing all fecal samples. Lastly, that the strongest data for the beneficial effects of probiotics were demonstrated in patients with a high baseline risk of developing CDAD limits the study’s applicability to the general population.
Bottom line: Probiotic use in immunocompetent patients undergoing treatment with antibiotics decreases the incidence of CDAD without an increase in adverse events.
Citation: Goldenberg JZ et al. Probiotics for the prevention of Clostridium difficile–associated diarrhea in adults and children. Cochrane Database Syst Rev. 2017. doi: 10.1002/14651858.CD006095.pub4.
Dr. Skinner is a hospitalist at Denver Health Medical Center and an assistant professor of medicine at the University of Colorado at Denver, Aurora.
Boston and beyond: Stay connected at #AACE2018
Come on. Everyone knows the best part of any conference is meeting up with colleagues, mentors, and friends. So here’s how to do it at (or away from) the annual meeting of the American Association of Clinical Endocrinologists in Boston on May 16-20.
No one is immune from the pull of colleagues past, present, and even future, not even the program chair Vin Tangpricha, MD, who gave the lowdown in an interview on the best venues for getting in touch.
- Thursday Night Chapter Receptions: After the first full day of the meeting, start in the room for your home chapter, then jump to your home state’s chapter, then your training chapter, and so on. This is the easiest and most exciting way at the meeting to connect with your web of colleagues, Dr. Tangpricha suggested enthusiastically. And don’t forget about AACE members from across the globe in the International Chapter Reception, in the biggest (and most fun, by some reports) party room by far. The receptions for all 22 domestic chapters and international members representing 102 countries will be held in the Sheraton Boston Hotel at 6 p.m.
- Wine and Cheese Reception: A Friday night tradition at AACE, from 4:30 p.m. to 6:30 p.m. in the exhibit hall, this offers a needed break at the end of the second full day of sessions to chat with colleagues, see exhibits, and check out posters.
- Women’s Luncheon: Thursday from 12 p.m. to 2:00 p.m. on Level C. In its fifth year, this luncheon has practically outgrown the meeting, with women entering endocrinology outpacing men. Good luck getting tickets; it’s always popular, Dr. Tangpricha said. SeanPavonePhot/Thinkstock
- College Breakfast With the Masters: This first-time-ever event welcomes and celebrates all past Masters of the American College of Endocrinology (MACEs). In this free, ticketed event on Saturday morning from 6:30 a.m. to 8 a.m., the largest assembly of MACEs ever gathered in the same room will be introduced to newer AACE fellows, who will then have the opportunity to meet with Masters and gather their insights on how to further their own careers in endocrinology, Dr. Tangpricha said.
- President’s Gala: This ticketed event open to members and family is always a great finale to the meeting, held Saturday night after the convocation, is one Dr. Tangpricha always looks forward to. This family-friendly event features food, libations, and live music.
- Social networking: Stay in touch with attendees and endocrinologists following the events and news from the meeting at #AACE2018, and with a Boston Strong–inspired hashtag of #ClinicalEndoStrong.
Come on. Everyone knows the best part of any conference is meeting up with colleagues, mentors, and friends. So here’s how to do it at (or away from) the annual meeting of the American Association of Clinical Endocrinologists in Boston on May 16-20.
No one is immune from the pull of colleagues past, present, and even future, not even the program chair Vin Tangpricha, MD, who gave the lowdown in an interview on the best venues for getting in touch.
- Thursday Night Chapter Receptions: After the first full day of the meeting, start in the room for your home chapter, then jump to your home state’s chapter, then your training chapter, and so on. This is the easiest and most exciting way at the meeting to connect with your web of colleagues, Dr. Tangpricha suggested enthusiastically. And don’t forget about AACE members from across the globe in the International Chapter Reception, in the biggest (and most fun, by some reports) party room by far. The receptions for all 22 domestic chapters and international members representing 102 countries will be held in the Sheraton Boston Hotel at 6 p.m.
- Wine and Cheese Reception: A Friday night tradition at AACE, from 4:30 p.m. to 6:30 p.m. in the exhibit hall, this offers a needed break at the end of the second full day of sessions to chat with colleagues, see exhibits, and check out posters.
- Women’s Luncheon: Thursday from 12 p.m. to 2:00 p.m. on Level C. In its fifth year, this luncheon has practically outgrown the meeting, with women entering endocrinology outpacing men. Good luck getting tickets; it’s always popular, Dr. Tangpricha said. SeanPavonePhot/Thinkstock
- College Breakfast With the Masters: This first-time-ever event welcomes and celebrates all past Masters of the American College of Endocrinology (MACEs). In this free, ticketed event on Saturday morning from 6:30 a.m. to 8 a.m., the largest assembly of MACEs ever gathered in the same room will be introduced to newer AACE fellows, who will then have the opportunity to meet with Masters and gather their insights on how to further their own careers in endocrinology, Dr. Tangpricha said.
- President’s Gala: This ticketed event open to members and family is always a great finale to the meeting, held Saturday night after the convocation, is one Dr. Tangpricha always looks forward to. This family-friendly event features food, libations, and live music.
- Social networking: Stay in touch with attendees and endocrinologists following the events and news from the meeting at #AACE2018, and with a Boston Strong–inspired hashtag of #ClinicalEndoStrong.
Come on. Everyone knows the best part of any conference is meeting up with colleagues, mentors, and friends. So here’s how to do it at (or away from) the annual meeting of the American Association of Clinical Endocrinologists in Boston on May 16-20.
No one is immune from the pull of colleagues past, present, and even future, not even the program chair Vin Tangpricha, MD, who gave the lowdown in an interview on the best venues for getting in touch.
- Thursday Night Chapter Receptions: After the first full day of the meeting, start in the room for your home chapter, then jump to your home state’s chapter, then your training chapter, and so on. This is the easiest and most exciting way at the meeting to connect with your web of colleagues, Dr. Tangpricha suggested enthusiastically. And don’t forget about AACE members from across the globe in the International Chapter Reception, in the biggest (and most fun, by some reports) party room by far. The receptions for all 22 domestic chapters and international members representing 102 countries will be held in the Sheraton Boston Hotel at 6 p.m.
- Wine and Cheese Reception: A Friday night tradition at AACE, from 4:30 p.m. to 6:30 p.m. in the exhibit hall, this offers a needed break at the end of the second full day of sessions to chat with colleagues, see exhibits, and check out posters.
- Women’s Luncheon: Thursday from 12 p.m. to 2:00 p.m. on Level C. In its fifth year, this luncheon has practically outgrown the meeting, with women entering endocrinology outpacing men. Good luck getting tickets; it’s always popular, Dr. Tangpricha said. SeanPavonePhot/Thinkstock
- College Breakfast With the Masters: This first-time-ever event welcomes and celebrates all past Masters of the American College of Endocrinology (MACEs). In this free, ticketed event on Saturday morning from 6:30 a.m. to 8 a.m., the largest assembly of MACEs ever gathered in the same room will be introduced to newer AACE fellows, who will then have the opportunity to meet with Masters and gather their insights on how to further their own careers in endocrinology, Dr. Tangpricha said.
- President’s Gala: This ticketed event open to members and family is always a great finale to the meeting, held Saturday night after the convocation, is one Dr. Tangpricha always looks forward to. This family-friendly event features food, libations, and live music.
- Social networking: Stay in touch with attendees and endocrinologists following the events and news from the meeting at #AACE2018, and with a Boston Strong–inspired hashtag of #ClinicalEndoStrong.
FROM AACE 2018
MDedge Daily News: Suicide prevention gets ‘standard care’ recommendations
effective episodic migraine treatment, e-cigarette usage has changed, and there is evidence that marketing perks increased opioid prescriptions. Listen to the MDedge Daily News Also in today’s edition of the Daily News Podcast, fremanezumab may be an Podcast for all the details ons today’s top news.
effective episodic migraine treatment, e-cigarette usage has changed, and there is evidence that marketing perks increased opioid prescriptions. Listen to the MDedge Daily News Also in today’s edition of the Daily News Podcast, fremanezumab may be an Podcast for all the details ons today’s top news.
effective episodic migraine treatment, e-cigarette usage has changed, and there is evidence that marketing perks increased opioid prescriptions. Listen to the MDedge Daily News Also in today’s edition of the Daily News Podcast, fremanezumab may be an Podcast for all the details ons today’s top news.