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Postpartum depression often tricky to diagnose
LAS VEGAS – Diagnosing postpartum depression can be tricky because of the wide range of body changes that occur during the postpartum period, but vigilance is warranted with mothers who express a lack of sleep and a lack of social support.
at an annual psychopharmacology update held by the Nevada Psychiatric Association. “This gives you information about depression and insomnia. Make sure to ask about anxiety symptoms. Also ask about any thoughts of suicide or harming the infant, and support from family and friends when she’s under stress and taking care of the baby.”
According to Dr. Friedman, a perinatal and forensic psychiatrist at Case Western Reserve University, Cleveland, social risk factors for postpartum depression (PPD) include being a victim of intimate partner violence and/or abuse, negative life events, decreased social support, relationship issues, and socioeconomic status. Psychological risk factors include anxiety/depression in pregnancy, personal or family history of PPD, and substance misuse. Biological risk factors include medical illness, multiple births, and having an infant with low birth weight/prematurity.
PPD affects 10%-20% of new mothers and peaks at 12 weeks. Postpartum psychosis, meanwhile, occurs in about 1-2 of every 1,000 deliveries. Anxiety comorbidity is common.
In the neonatal intensive care unit (NICU), PPD rates might increase from 28% to 70% depending on the study. Risk factors include personal or family history, disturbed relationships, unfavorable socioeconomic factors, and stressful life events. Obstetrical risk factors might include conception by assisted reproductive technologies and having a stillbirth in the year before conception. NICU-specific risk factors include less-effective coping strategies, greater perception of maternal role disruption, and decreased perception of nursing support. “A lot of mothers [in the NICU] talk to me about being on a roller roaster every day about what’s going to happen with their baby,” Dr. Friedman said.
The most widely used measure to screen for PPD is the 10-item self-rating Edinburgh Postnatal Depression Scale . A total score of 10 or more is considered a flag for the need to follow up for possible depressive symptoms. She advises clinicians to pay particular attention to how patients respond to item No. 10 on the scale, which reads, “The thought of harming myself has occurred to me.” (Optional answers range from “Yes, quite often” to “Never.”) She also recommends administering the screen at both pediatric and obstetrical office visits, “because mothers are more likely to attend a pediatrics appointment than her own [postpartum] follow-up.”
The differential diagnosis of PPD includes the baby blues, postpartum psychosis, postpartum anxiety/PTSD, medical causes, substance use disorder, and PPD in bipolar disorder. Baby blues is not synonymous with PPD. It affects the majority (50%-80%) of new mothers and is characterized by emotional sensitivity, mood lability, and irritability. It usually occurs within 5 days and resolves by the second week post partum.
Postpartum psychosis (PPP) occurs in about 1-2 of every 1,000 deliveries, typically in the first 2 weeks after delivery. The onset occurs rapidly, and PPP is most frequently correlated with bipolar disorder over time. PPP itself is characterized by grandiose bizarre delusions, mood lability, hallucinations, confusion, and disorganized behavior. “This can occur as a new onset of mental illness as well, so getting collateral information about her behaviors is important,” she said.
Dr. Friedman explained that those events occur post partum largely because of sleep deprivation and increasing stress as the woman adjusts to a mothering role. Hormonal shifts also occur, with a drop in estrogen levels. Obstetrical complications also might factor in.
Postpartum obsessive-compulsive disorder (OCD) is commonly comorbid with PPD and is distinguished by ego-dystonic intrusive thoughts. The mother might have intense distress that she is going to harm the infant and might start to avoid holding the baby out of concern. “Common things I’ve heard from women with postpartum OCD are: ‘I’m afraid I’m going to put the baby in the microwave or in the oven instead of dinner’ or ‘I’m afraid I’m going to leave the baby in the car overnight and she’ll freeze to death,’ ” she said.
Postpartum PTSD can be triggered by a traumatic event experience in the birthing process, such as an emergency C-section. Affected mothers avoid the infant and hospital, “reexperience” the trauma, are easily startled, irritable, and disconnected. Dr. Friedman also noted that early parental PTSD symptoms predict sleep and eating problems in childhood and less sensitive/more controlling maternal behaviors.
Medical conditions that mimic PPD include anemia, thyroid disease, hypoactive delirium, infections, and alcohol/substance use disorder.
The best available data show that mothers with PPD are more withdrawn, disengaged, display more hostility, and are more likely to have disrupted attachment with their babies, Dr. Friedman said. They also are less likely to employ healthy child development practices and to breastfeed. Untreated depression might lead to psychotic symptoms, suicide, or homicide. Paternal PPD also occurs in an estimated 10% of fathers and is moderately correlated with maternal PPD.
Potential risks of PPD include impaired bonding, attachment disturbance, language development, cognitive skills, and behavior problems.
Potential risks of untreated PPD include child neglect or abuse because of active symptoms, suicide, and psychotic or maltreatment-related infanticide. “If the mother is taking about harming herself, I often ask: ‘Have you thought of what would happen to your baby if you were to take your own life?’ ” Dr. Friedman offered. Peripartum suicide risk is lower than in the general female population, but it represents about 20% of peripartum deaths. Overdose is the most common method. “However, uncommon and dramatic methods are more common in this population,” she said. “Teens and stigmatized single mothers are at greater risk.”
Dr. Friedman noted that clinicians face risk of a malpractice lawsuit if they fail to treat, abandon the patient, fail to provide informed consent, and if there are bad outcomes. The best approach is to proactively communicate with the patient, partner, pediatrics, and obstetrics. “Conduct an individual risk-benefit assessment with the individual patient’s history,” she advised. “Don’t do anything knee jerk. Consult when needed, document, and consider lactation and future pregnancy possibility in women of reproductive age.”
Nonpharmacologic therapy might be the first line of treatment for mild to moderate symptoms. Options include cognitive-behavioral therapy, interpersonal psychotherapy, family therapy, psychodynamic psychotherapy, and supportive psychotherapy. She recommends close follow-up and conducting a careful medication history. Electroconvulsive therapy remains a possibility.
If medication use is warranted, “weigh the benefits of breastfeeding with the usually low drug exposure of the infant,” Dr. Friedman advised. “We want to use the least number of medications at an effective dose to optimize treatment. Newer medications have less perinatal data. Sertraline and paroxetine are usually the preferred selective serotonin reuptake inhibitors in lactation. However, fluoxetine or citalopram might be used depending on the patient’s response history/use in pregnancy.”
Dr. Friedman reported no disclosures.
LAS VEGAS – Diagnosing postpartum depression can be tricky because of the wide range of body changes that occur during the postpartum period, but vigilance is warranted with mothers who express a lack of sleep and a lack of social support.
at an annual psychopharmacology update held by the Nevada Psychiatric Association. “This gives you information about depression and insomnia. Make sure to ask about anxiety symptoms. Also ask about any thoughts of suicide or harming the infant, and support from family and friends when she’s under stress and taking care of the baby.”
According to Dr. Friedman, a perinatal and forensic psychiatrist at Case Western Reserve University, Cleveland, social risk factors for postpartum depression (PPD) include being a victim of intimate partner violence and/or abuse, negative life events, decreased social support, relationship issues, and socioeconomic status. Psychological risk factors include anxiety/depression in pregnancy, personal or family history of PPD, and substance misuse. Biological risk factors include medical illness, multiple births, and having an infant with low birth weight/prematurity.
PPD affects 10%-20% of new mothers and peaks at 12 weeks. Postpartum psychosis, meanwhile, occurs in about 1-2 of every 1,000 deliveries. Anxiety comorbidity is common.
In the neonatal intensive care unit (NICU), PPD rates might increase from 28% to 70% depending on the study. Risk factors include personal or family history, disturbed relationships, unfavorable socioeconomic factors, and stressful life events. Obstetrical risk factors might include conception by assisted reproductive technologies and having a stillbirth in the year before conception. NICU-specific risk factors include less-effective coping strategies, greater perception of maternal role disruption, and decreased perception of nursing support. “A lot of mothers [in the NICU] talk to me about being on a roller roaster every day about what’s going to happen with their baby,” Dr. Friedman said.
The most widely used measure to screen for PPD is the 10-item self-rating Edinburgh Postnatal Depression Scale . A total score of 10 or more is considered a flag for the need to follow up for possible depressive symptoms. She advises clinicians to pay particular attention to how patients respond to item No. 10 on the scale, which reads, “The thought of harming myself has occurred to me.” (Optional answers range from “Yes, quite often” to “Never.”) She also recommends administering the screen at both pediatric and obstetrical office visits, “because mothers are more likely to attend a pediatrics appointment than her own [postpartum] follow-up.”
The differential diagnosis of PPD includes the baby blues, postpartum psychosis, postpartum anxiety/PTSD, medical causes, substance use disorder, and PPD in bipolar disorder. Baby blues is not synonymous with PPD. It affects the majority (50%-80%) of new mothers and is characterized by emotional sensitivity, mood lability, and irritability. It usually occurs within 5 days and resolves by the second week post partum.
Postpartum psychosis (PPP) occurs in about 1-2 of every 1,000 deliveries, typically in the first 2 weeks after delivery. The onset occurs rapidly, and PPP is most frequently correlated with bipolar disorder over time. PPP itself is characterized by grandiose bizarre delusions, mood lability, hallucinations, confusion, and disorganized behavior. “This can occur as a new onset of mental illness as well, so getting collateral information about her behaviors is important,” she said.
Dr. Friedman explained that those events occur post partum largely because of sleep deprivation and increasing stress as the woman adjusts to a mothering role. Hormonal shifts also occur, with a drop in estrogen levels. Obstetrical complications also might factor in.
Postpartum obsessive-compulsive disorder (OCD) is commonly comorbid with PPD and is distinguished by ego-dystonic intrusive thoughts. The mother might have intense distress that she is going to harm the infant and might start to avoid holding the baby out of concern. “Common things I’ve heard from women with postpartum OCD are: ‘I’m afraid I’m going to put the baby in the microwave or in the oven instead of dinner’ or ‘I’m afraid I’m going to leave the baby in the car overnight and she’ll freeze to death,’ ” she said.
Postpartum PTSD can be triggered by a traumatic event experience in the birthing process, such as an emergency C-section. Affected mothers avoid the infant and hospital, “reexperience” the trauma, are easily startled, irritable, and disconnected. Dr. Friedman also noted that early parental PTSD symptoms predict sleep and eating problems in childhood and less sensitive/more controlling maternal behaviors.
Medical conditions that mimic PPD include anemia, thyroid disease, hypoactive delirium, infections, and alcohol/substance use disorder.
The best available data show that mothers with PPD are more withdrawn, disengaged, display more hostility, and are more likely to have disrupted attachment with their babies, Dr. Friedman said. They also are less likely to employ healthy child development practices and to breastfeed. Untreated depression might lead to psychotic symptoms, suicide, or homicide. Paternal PPD also occurs in an estimated 10% of fathers and is moderately correlated with maternal PPD.
Potential risks of PPD include impaired bonding, attachment disturbance, language development, cognitive skills, and behavior problems.
Potential risks of untreated PPD include child neglect or abuse because of active symptoms, suicide, and psychotic or maltreatment-related infanticide. “If the mother is taking about harming herself, I often ask: ‘Have you thought of what would happen to your baby if you were to take your own life?’ ” Dr. Friedman offered. Peripartum suicide risk is lower than in the general female population, but it represents about 20% of peripartum deaths. Overdose is the most common method. “However, uncommon and dramatic methods are more common in this population,” she said. “Teens and stigmatized single mothers are at greater risk.”
Dr. Friedman noted that clinicians face risk of a malpractice lawsuit if they fail to treat, abandon the patient, fail to provide informed consent, and if there are bad outcomes. The best approach is to proactively communicate with the patient, partner, pediatrics, and obstetrics. “Conduct an individual risk-benefit assessment with the individual patient’s history,” she advised. “Don’t do anything knee jerk. Consult when needed, document, and consider lactation and future pregnancy possibility in women of reproductive age.”
Nonpharmacologic therapy might be the first line of treatment for mild to moderate symptoms. Options include cognitive-behavioral therapy, interpersonal psychotherapy, family therapy, psychodynamic psychotherapy, and supportive psychotherapy. She recommends close follow-up and conducting a careful medication history. Electroconvulsive therapy remains a possibility.
If medication use is warranted, “weigh the benefits of breastfeeding with the usually low drug exposure of the infant,” Dr. Friedman advised. “We want to use the least number of medications at an effective dose to optimize treatment. Newer medications have less perinatal data. Sertraline and paroxetine are usually the preferred selective serotonin reuptake inhibitors in lactation. However, fluoxetine or citalopram might be used depending on the patient’s response history/use in pregnancy.”
Dr. Friedman reported no disclosures.
LAS VEGAS – Diagnosing postpartum depression can be tricky because of the wide range of body changes that occur during the postpartum period, but vigilance is warranted with mothers who express a lack of sleep and a lack of social support.
at an annual psychopharmacology update held by the Nevada Psychiatric Association. “This gives you information about depression and insomnia. Make sure to ask about anxiety symptoms. Also ask about any thoughts of suicide or harming the infant, and support from family and friends when she’s under stress and taking care of the baby.”
According to Dr. Friedman, a perinatal and forensic psychiatrist at Case Western Reserve University, Cleveland, social risk factors for postpartum depression (PPD) include being a victim of intimate partner violence and/or abuse, negative life events, decreased social support, relationship issues, and socioeconomic status. Psychological risk factors include anxiety/depression in pregnancy, personal or family history of PPD, and substance misuse. Biological risk factors include medical illness, multiple births, and having an infant with low birth weight/prematurity.
PPD affects 10%-20% of new mothers and peaks at 12 weeks. Postpartum psychosis, meanwhile, occurs in about 1-2 of every 1,000 deliveries. Anxiety comorbidity is common.
In the neonatal intensive care unit (NICU), PPD rates might increase from 28% to 70% depending on the study. Risk factors include personal or family history, disturbed relationships, unfavorable socioeconomic factors, and stressful life events. Obstetrical risk factors might include conception by assisted reproductive technologies and having a stillbirth in the year before conception. NICU-specific risk factors include less-effective coping strategies, greater perception of maternal role disruption, and decreased perception of nursing support. “A lot of mothers [in the NICU] talk to me about being on a roller roaster every day about what’s going to happen with their baby,” Dr. Friedman said.
The most widely used measure to screen for PPD is the 10-item self-rating Edinburgh Postnatal Depression Scale . A total score of 10 or more is considered a flag for the need to follow up for possible depressive symptoms. She advises clinicians to pay particular attention to how patients respond to item No. 10 on the scale, which reads, “The thought of harming myself has occurred to me.” (Optional answers range from “Yes, quite often” to “Never.”) She also recommends administering the screen at both pediatric and obstetrical office visits, “because mothers are more likely to attend a pediatrics appointment than her own [postpartum] follow-up.”
The differential diagnosis of PPD includes the baby blues, postpartum psychosis, postpartum anxiety/PTSD, medical causes, substance use disorder, and PPD in bipolar disorder. Baby blues is not synonymous with PPD. It affects the majority (50%-80%) of new mothers and is characterized by emotional sensitivity, mood lability, and irritability. It usually occurs within 5 days and resolves by the second week post partum.
Postpartum psychosis (PPP) occurs in about 1-2 of every 1,000 deliveries, typically in the first 2 weeks after delivery. The onset occurs rapidly, and PPP is most frequently correlated with bipolar disorder over time. PPP itself is characterized by grandiose bizarre delusions, mood lability, hallucinations, confusion, and disorganized behavior. “This can occur as a new onset of mental illness as well, so getting collateral information about her behaviors is important,” she said.
Dr. Friedman explained that those events occur post partum largely because of sleep deprivation and increasing stress as the woman adjusts to a mothering role. Hormonal shifts also occur, with a drop in estrogen levels. Obstetrical complications also might factor in.
Postpartum obsessive-compulsive disorder (OCD) is commonly comorbid with PPD and is distinguished by ego-dystonic intrusive thoughts. The mother might have intense distress that she is going to harm the infant and might start to avoid holding the baby out of concern. “Common things I’ve heard from women with postpartum OCD are: ‘I’m afraid I’m going to put the baby in the microwave or in the oven instead of dinner’ or ‘I’m afraid I’m going to leave the baby in the car overnight and she’ll freeze to death,’ ” she said.
Postpartum PTSD can be triggered by a traumatic event experience in the birthing process, such as an emergency C-section. Affected mothers avoid the infant and hospital, “reexperience” the trauma, are easily startled, irritable, and disconnected. Dr. Friedman also noted that early parental PTSD symptoms predict sleep and eating problems in childhood and less sensitive/more controlling maternal behaviors.
Medical conditions that mimic PPD include anemia, thyroid disease, hypoactive delirium, infections, and alcohol/substance use disorder.
The best available data show that mothers with PPD are more withdrawn, disengaged, display more hostility, and are more likely to have disrupted attachment with their babies, Dr. Friedman said. They also are less likely to employ healthy child development practices and to breastfeed. Untreated depression might lead to psychotic symptoms, suicide, or homicide. Paternal PPD also occurs in an estimated 10% of fathers and is moderately correlated with maternal PPD.
Potential risks of PPD include impaired bonding, attachment disturbance, language development, cognitive skills, and behavior problems.
Potential risks of untreated PPD include child neglect or abuse because of active symptoms, suicide, and psychotic or maltreatment-related infanticide. “If the mother is taking about harming herself, I often ask: ‘Have you thought of what would happen to your baby if you were to take your own life?’ ” Dr. Friedman offered. Peripartum suicide risk is lower than in the general female population, but it represents about 20% of peripartum deaths. Overdose is the most common method. “However, uncommon and dramatic methods are more common in this population,” she said. “Teens and stigmatized single mothers are at greater risk.”
Dr. Friedman noted that clinicians face risk of a malpractice lawsuit if they fail to treat, abandon the patient, fail to provide informed consent, and if there are bad outcomes. The best approach is to proactively communicate with the patient, partner, pediatrics, and obstetrics. “Conduct an individual risk-benefit assessment with the individual patient’s history,” she advised. “Don’t do anything knee jerk. Consult when needed, document, and consider lactation and future pregnancy possibility in women of reproductive age.”
Nonpharmacologic therapy might be the first line of treatment for mild to moderate symptoms. Options include cognitive-behavioral therapy, interpersonal psychotherapy, family therapy, psychodynamic psychotherapy, and supportive psychotherapy. She recommends close follow-up and conducting a careful medication history. Electroconvulsive therapy remains a possibility.
If medication use is warranted, “weigh the benefits of breastfeeding with the usually low drug exposure of the infant,” Dr. Friedman advised. “We want to use the least number of medications at an effective dose to optimize treatment. Newer medications have less perinatal data. Sertraline and paroxetine are usually the preferred selective serotonin reuptake inhibitors in lactation. However, fluoxetine or citalopram might be used depending on the patient’s response history/use in pregnancy.”
Dr. Friedman reported no disclosures.
EXPERT ANALYSIS FROM NPA 2019
When to suspect a severe skin reaction to an AED
NEW ORLEANS – Most skin eruptions in patients taking antiepileptic drugs (AEDs) are relatively benign. With close supervision, some patients with epilepsy may continue treatment despite having a benign drug rash, according to a lecture at the annual meeting of the American Epilepsy Society.
“When do you know that you’re not dealing with that kind of eruption?” said Jeanne M. Young, MD, assistant professor of dermatology at the University of Virginia in Charlottesville.
Signs and symptoms that raise concerns about severe cutaneous reactions include swelling of the face; lesions that are fluid-filled, dusky, or painful; mucus membrane involvement; and signs of systemic involvement.
Associations with anticonvulsants
Diffuse swelling of the face is a hallmark symptom of DRESS. Fluid-filled lesions such as pustules, vesicles, and bullae indicate a condition other than a benign drug eruption. Signs of systemic involvement may include fever, marked eosinophilia, transaminitis, and evidence of lymphocyte activation. “In general, I want to see systemic involvement that can’t be explained by the patient’s other systemic diseases,” Dr. Young said.
A 2018 study found that AEDs are associated with SJS and TEN, and the labels for lamotrigine and carbamazepine include black box warnings about the risk of severe cutaneous adverse events. Carbamazepine’s warning, which was added in 2007, notes that SJS and TEN are significantly more common in patients of Asian ancestry with the human leukocyte antigen allele HLA-B*1502 and that physicians should screen at-risk patients before starting treatment.
Benign drug rashes
Morbilliform drug eruptions, sometimes called benign exanthems, are “by far the most common drug rash that we see” and typically are “the rashes that people refer to as drug rashes,” Dr. Young said. The mechanisms appear to be primarily immune complex mediated and cell mediated. “When the drug is stopped, these rashes tend to go away quite predictably in 2-3 weeks.”
For any class of drug, about 1% of people taking that medication may have this type of reaction, Dr. Young said. “We expect to see erythematous papules and plaques that oftentimes become confluent on the skin.” These reactions generally occur 7-10 days after the first exposure to the medication, and most patients do not have other symptoms, although the rash may itch. In addition, patients may have erythroderma with desquamation. “I think it’s important to point out the difference between desquamation, which is loss of the stratum corneum, and epidermal sloughing, which is what you see in something like [SJS] or TEN, where you’re actually losing the entire epidermis,” Dr. Young said. Recovering from desquamation is “sort of like recovering from a sun burn, and it’s not particularly dangerous.” Management of morbilliform drug eruptions is largely symptomatic.
Treat through, taper, or rechallenge
In the case a benign drug rash, “if you feel like you … need to keep a patient on a drug, you do have that option with close supervision,” Dr. Young said. “Communicate that with the dermatologist. Say, ‘I have really struggled getting this patient stabilized. Can we keep them on this drug?’ ”
The dermatologist may not fully realize the implications of stopping an effective AED in a patient with seizures that have been difficult to control. If the drug rash is benign, treating through may be an option. Patients often resolve the rash while continuing the medication, which may be because of desensitization, Dr. Young said. If a patient’s symptoms are too great to continue the drug, neurologists have the option of slowly tapering the drug and reinitiating with a new drug, Dr. Young said. Neurologists also may choose to rechallenge.
If a patient is on several medications, making it difficult to elucidate a causative agent, after stopping those drugs and allowing the rash to resolve, “there is little danger in restarting a medication,” she said.
Benign rash or DRESS?
“When I see a morbilliform eruption, usually what’s on my mind is, ‘Is this just a drug rash or is this DRESS?’ ” Dr. Young said. DRESS often starts with a morbilliform eruption that is indistinguishable from a benign drug eruption.
“Timing is a major difference,” she said. “If a patient develops a morbilliform drug eruption much later than I would expect, then my suspicion [for DRESS] goes up.” Patients with DRESS often have fever and systemic symptoms. Proposed DRESS diagnostic criteria can be useful, but clinical judgment still plays a key role. If a patient does not satisfy diagnostic criteria but has some signs and is taking a drug that is associated with DRESS, “it is going to make me more suspicious and maybe make me recommend stopping that drug sooner,” she said. Anticonvulsants such as carbamazepine, lamotrigine, and phenobarbital are among the drugs most commonly associated with DRESS.
Toxic erythemas
Patients may present with toxic erythemas, such as fixed drug reactions, erythema multiforme, SJS, and TEN. These drug reactions appear similar on biopsy but have different courses.
A patient with a fixed drug reaction often has a single lesion, and the lesion will occur in the same location every time the patient is exposed to the drug. Patients may develop additional lesions with subsequent exposures. These lesions typically are large, erythematous, well-demarcated plaques with central duskiness. “They can be bullous in the center, and they typically will heal with pigmentation, which is unique to this particular drug reaction,” said Dr. Young. “When it gets more concerning and most important to differentiate is when you get generalized bullous fixed drug eruption.” Generalized bullous fixed drug eruptions mimic and are difficult to clinically distinguish from TEN, which has a much has a much poorer prognosis.
Patients with a fixed drug eruption are not as ill as patients with TEN and tend not to slough their skin to the extent seen with TEN. Interferon gamma, perforin, and Fas ligand have been implicated as mechanisms involved in fixed drug reactions. Unlike in TEN, regulatory T cells are abundant, which may explain why TEN and fixed drug reactions progress differently even though they appear to share pathologic mechanisms, Dr. Young said.
Erythema multiforme generally presents with classic target lesions and little mucosal involvement. Infections, most commonly herpes simplex virus (HSV) 1 and 2, may trigger erythema multiforme. Dr. Young recommends evaluating patients for HSV and checking serologies, even if patients have never had a herpes outbreak. “If you have no evidence for infection, you do have to consider discontinuing a medication,” she said.
Stevens–Johnson syndrome and TEN
SJS and TEN are “the rarest of the severe cutaneous adverse drug reactions” and have “the highest morbidity and mortality,” Dr. Young said. They appear to exist on a continuum where SJS may represent early TEN.
“This is a situation where you expect to see blistering of the skin [and] always mucosal involvement. You need to stop the drug immediately when you suspect this drug reaction,” Dr. Young said.
One reason to distinguish SJS or early TEN from later TEN is that high-dose steroids may play a role in the treatment of SJS or early TEN. “Once you get past about 10% total body surface area, there is good evidence that steroids actually increase morbidity and mortality,” she said.
If the eruption has occurred before, that factor suggests that a diagnosis of erythema multiforme or fixed drug reaction may be more likely than TEN.
An apparent lack of regulatory T cells in TEN could explain why patients with HIV infection are at much higher risk of developing SJS and TEN. Understanding the role that regulatory T cells play in severe drug eruptions may lead to new therapeutic options in the future, Dr. Young said.
Dr. Young had no disclosures.
NEW ORLEANS – Most skin eruptions in patients taking antiepileptic drugs (AEDs) are relatively benign. With close supervision, some patients with epilepsy may continue treatment despite having a benign drug rash, according to a lecture at the annual meeting of the American Epilepsy Society.
“When do you know that you’re not dealing with that kind of eruption?” said Jeanne M. Young, MD, assistant professor of dermatology at the University of Virginia in Charlottesville.
Signs and symptoms that raise concerns about severe cutaneous reactions include swelling of the face; lesions that are fluid-filled, dusky, or painful; mucus membrane involvement; and signs of systemic involvement.
Associations with anticonvulsants
Diffuse swelling of the face is a hallmark symptom of DRESS. Fluid-filled lesions such as pustules, vesicles, and bullae indicate a condition other than a benign drug eruption. Signs of systemic involvement may include fever, marked eosinophilia, transaminitis, and evidence of lymphocyte activation. “In general, I want to see systemic involvement that can’t be explained by the patient’s other systemic diseases,” Dr. Young said.
A 2018 study found that AEDs are associated with SJS and TEN, and the labels for lamotrigine and carbamazepine include black box warnings about the risk of severe cutaneous adverse events. Carbamazepine’s warning, which was added in 2007, notes that SJS and TEN are significantly more common in patients of Asian ancestry with the human leukocyte antigen allele HLA-B*1502 and that physicians should screen at-risk patients before starting treatment.
Benign drug rashes
Morbilliform drug eruptions, sometimes called benign exanthems, are “by far the most common drug rash that we see” and typically are “the rashes that people refer to as drug rashes,” Dr. Young said. The mechanisms appear to be primarily immune complex mediated and cell mediated. “When the drug is stopped, these rashes tend to go away quite predictably in 2-3 weeks.”
For any class of drug, about 1% of people taking that medication may have this type of reaction, Dr. Young said. “We expect to see erythematous papules and plaques that oftentimes become confluent on the skin.” These reactions generally occur 7-10 days after the first exposure to the medication, and most patients do not have other symptoms, although the rash may itch. In addition, patients may have erythroderma with desquamation. “I think it’s important to point out the difference between desquamation, which is loss of the stratum corneum, and epidermal sloughing, which is what you see in something like [SJS] or TEN, where you’re actually losing the entire epidermis,” Dr. Young said. Recovering from desquamation is “sort of like recovering from a sun burn, and it’s not particularly dangerous.” Management of morbilliform drug eruptions is largely symptomatic.
Treat through, taper, or rechallenge
In the case a benign drug rash, “if you feel like you … need to keep a patient on a drug, you do have that option with close supervision,” Dr. Young said. “Communicate that with the dermatologist. Say, ‘I have really struggled getting this patient stabilized. Can we keep them on this drug?’ ”
The dermatologist may not fully realize the implications of stopping an effective AED in a patient with seizures that have been difficult to control. If the drug rash is benign, treating through may be an option. Patients often resolve the rash while continuing the medication, which may be because of desensitization, Dr. Young said. If a patient’s symptoms are too great to continue the drug, neurologists have the option of slowly tapering the drug and reinitiating with a new drug, Dr. Young said. Neurologists also may choose to rechallenge.
If a patient is on several medications, making it difficult to elucidate a causative agent, after stopping those drugs and allowing the rash to resolve, “there is little danger in restarting a medication,” she said.
Benign rash or DRESS?
“When I see a morbilliform eruption, usually what’s on my mind is, ‘Is this just a drug rash or is this DRESS?’ ” Dr. Young said. DRESS often starts with a morbilliform eruption that is indistinguishable from a benign drug eruption.
“Timing is a major difference,” she said. “If a patient develops a morbilliform drug eruption much later than I would expect, then my suspicion [for DRESS] goes up.” Patients with DRESS often have fever and systemic symptoms. Proposed DRESS diagnostic criteria can be useful, but clinical judgment still plays a key role. If a patient does not satisfy diagnostic criteria but has some signs and is taking a drug that is associated with DRESS, “it is going to make me more suspicious and maybe make me recommend stopping that drug sooner,” she said. Anticonvulsants such as carbamazepine, lamotrigine, and phenobarbital are among the drugs most commonly associated with DRESS.
Toxic erythemas
Patients may present with toxic erythemas, such as fixed drug reactions, erythema multiforme, SJS, and TEN. These drug reactions appear similar on biopsy but have different courses.
A patient with a fixed drug reaction often has a single lesion, and the lesion will occur in the same location every time the patient is exposed to the drug. Patients may develop additional lesions with subsequent exposures. These lesions typically are large, erythematous, well-demarcated plaques with central duskiness. “They can be bullous in the center, and they typically will heal with pigmentation, which is unique to this particular drug reaction,” said Dr. Young. “When it gets more concerning and most important to differentiate is when you get generalized bullous fixed drug eruption.” Generalized bullous fixed drug eruptions mimic and are difficult to clinically distinguish from TEN, which has a much has a much poorer prognosis.
Patients with a fixed drug eruption are not as ill as patients with TEN and tend not to slough their skin to the extent seen with TEN. Interferon gamma, perforin, and Fas ligand have been implicated as mechanisms involved in fixed drug reactions. Unlike in TEN, regulatory T cells are abundant, which may explain why TEN and fixed drug reactions progress differently even though they appear to share pathologic mechanisms, Dr. Young said.
Erythema multiforme generally presents with classic target lesions and little mucosal involvement. Infections, most commonly herpes simplex virus (HSV) 1 and 2, may trigger erythema multiforme. Dr. Young recommends evaluating patients for HSV and checking serologies, even if patients have never had a herpes outbreak. “If you have no evidence for infection, you do have to consider discontinuing a medication,” she said.
Stevens–Johnson syndrome and TEN
SJS and TEN are “the rarest of the severe cutaneous adverse drug reactions” and have “the highest morbidity and mortality,” Dr. Young said. They appear to exist on a continuum where SJS may represent early TEN.
“This is a situation where you expect to see blistering of the skin [and] always mucosal involvement. You need to stop the drug immediately when you suspect this drug reaction,” Dr. Young said.
One reason to distinguish SJS or early TEN from later TEN is that high-dose steroids may play a role in the treatment of SJS or early TEN. “Once you get past about 10% total body surface area, there is good evidence that steroids actually increase morbidity and mortality,” she said.
If the eruption has occurred before, that factor suggests that a diagnosis of erythema multiforme or fixed drug reaction may be more likely than TEN.
An apparent lack of regulatory T cells in TEN could explain why patients with HIV infection are at much higher risk of developing SJS and TEN. Understanding the role that regulatory T cells play in severe drug eruptions may lead to new therapeutic options in the future, Dr. Young said.
Dr. Young had no disclosures.
NEW ORLEANS – Most skin eruptions in patients taking antiepileptic drugs (AEDs) are relatively benign. With close supervision, some patients with epilepsy may continue treatment despite having a benign drug rash, according to a lecture at the annual meeting of the American Epilepsy Society.
“When do you know that you’re not dealing with that kind of eruption?” said Jeanne M. Young, MD, assistant professor of dermatology at the University of Virginia in Charlottesville.
Signs and symptoms that raise concerns about severe cutaneous reactions include swelling of the face; lesions that are fluid-filled, dusky, or painful; mucus membrane involvement; and signs of systemic involvement.
Associations with anticonvulsants
Diffuse swelling of the face is a hallmark symptom of DRESS. Fluid-filled lesions such as pustules, vesicles, and bullae indicate a condition other than a benign drug eruption. Signs of systemic involvement may include fever, marked eosinophilia, transaminitis, and evidence of lymphocyte activation. “In general, I want to see systemic involvement that can’t be explained by the patient’s other systemic diseases,” Dr. Young said.
A 2018 study found that AEDs are associated with SJS and TEN, and the labels for lamotrigine and carbamazepine include black box warnings about the risk of severe cutaneous adverse events. Carbamazepine’s warning, which was added in 2007, notes that SJS and TEN are significantly more common in patients of Asian ancestry with the human leukocyte antigen allele HLA-B*1502 and that physicians should screen at-risk patients before starting treatment.
Benign drug rashes
Morbilliform drug eruptions, sometimes called benign exanthems, are “by far the most common drug rash that we see” and typically are “the rashes that people refer to as drug rashes,” Dr. Young said. The mechanisms appear to be primarily immune complex mediated and cell mediated. “When the drug is stopped, these rashes tend to go away quite predictably in 2-3 weeks.”
For any class of drug, about 1% of people taking that medication may have this type of reaction, Dr. Young said. “We expect to see erythematous papules and plaques that oftentimes become confluent on the skin.” These reactions generally occur 7-10 days after the first exposure to the medication, and most patients do not have other symptoms, although the rash may itch. In addition, patients may have erythroderma with desquamation. “I think it’s important to point out the difference between desquamation, which is loss of the stratum corneum, and epidermal sloughing, which is what you see in something like [SJS] or TEN, where you’re actually losing the entire epidermis,” Dr. Young said. Recovering from desquamation is “sort of like recovering from a sun burn, and it’s not particularly dangerous.” Management of morbilliform drug eruptions is largely symptomatic.
Treat through, taper, or rechallenge
In the case a benign drug rash, “if you feel like you … need to keep a patient on a drug, you do have that option with close supervision,” Dr. Young said. “Communicate that with the dermatologist. Say, ‘I have really struggled getting this patient stabilized. Can we keep them on this drug?’ ”
The dermatologist may not fully realize the implications of stopping an effective AED in a patient with seizures that have been difficult to control. If the drug rash is benign, treating through may be an option. Patients often resolve the rash while continuing the medication, which may be because of desensitization, Dr. Young said. If a patient’s symptoms are too great to continue the drug, neurologists have the option of slowly tapering the drug and reinitiating with a new drug, Dr. Young said. Neurologists also may choose to rechallenge.
If a patient is on several medications, making it difficult to elucidate a causative agent, after stopping those drugs and allowing the rash to resolve, “there is little danger in restarting a medication,” she said.
Benign rash or DRESS?
“When I see a morbilliform eruption, usually what’s on my mind is, ‘Is this just a drug rash or is this DRESS?’ ” Dr. Young said. DRESS often starts with a morbilliform eruption that is indistinguishable from a benign drug eruption.
“Timing is a major difference,” she said. “If a patient develops a morbilliform drug eruption much later than I would expect, then my suspicion [for DRESS] goes up.” Patients with DRESS often have fever and systemic symptoms. Proposed DRESS diagnostic criteria can be useful, but clinical judgment still plays a key role. If a patient does not satisfy diagnostic criteria but has some signs and is taking a drug that is associated with DRESS, “it is going to make me more suspicious and maybe make me recommend stopping that drug sooner,” she said. Anticonvulsants such as carbamazepine, lamotrigine, and phenobarbital are among the drugs most commonly associated with DRESS.
Toxic erythemas
Patients may present with toxic erythemas, such as fixed drug reactions, erythema multiforme, SJS, and TEN. These drug reactions appear similar on biopsy but have different courses.
A patient with a fixed drug reaction often has a single lesion, and the lesion will occur in the same location every time the patient is exposed to the drug. Patients may develop additional lesions with subsequent exposures. These lesions typically are large, erythematous, well-demarcated plaques with central duskiness. “They can be bullous in the center, and they typically will heal with pigmentation, which is unique to this particular drug reaction,” said Dr. Young. “When it gets more concerning and most important to differentiate is when you get generalized bullous fixed drug eruption.” Generalized bullous fixed drug eruptions mimic and are difficult to clinically distinguish from TEN, which has a much has a much poorer prognosis.
Patients with a fixed drug eruption are not as ill as patients with TEN and tend not to slough their skin to the extent seen with TEN. Interferon gamma, perforin, and Fas ligand have been implicated as mechanisms involved in fixed drug reactions. Unlike in TEN, regulatory T cells are abundant, which may explain why TEN and fixed drug reactions progress differently even though they appear to share pathologic mechanisms, Dr. Young said.
Erythema multiforme generally presents with classic target lesions and little mucosal involvement. Infections, most commonly herpes simplex virus (HSV) 1 and 2, may trigger erythema multiforme. Dr. Young recommends evaluating patients for HSV and checking serologies, even if patients have never had a herpes outbreak. “If you have no evidence for infection, you do have to consider discontinuing a medication,” she said.
Stevens–Johnson syndrome and TEN
SJS and TEN are “the rarest of the severe cutaneous adverse drug reactions” and have “the highest morbidity and mortality,” Dr. Young said. They appear to exist on a continuum where SJS may represent early TEN.
“This is a situation where you expect to see blistering of the skin [and] always mucosal involvement. You need to stop the drug immediately when you suspect this drug reaction,” Dr. Young said.
One reason to distinguish SJS or early TEN from later TEN is that high-dose steroids may play a role in the treatment of SJS or early TEN. “Once you get past about 10% total body surface area, there is good evidence that steroids actually increase morbidity and mortality,” she said.
If the eruption has occurred before, that factor suggests that a diagnosis of erythema multiforme or fixed drug reaction may be more likely than TEN.
An apparent lack of regulatory T cells in TEN could explain why patients with HIV infection are at much higher risk of developing SJS and TEN. Understanding the role that regulatory T cells play in severe drug eruptions may lead to new therapeutic options in the future, Dr. Young said.
Dr. Young had no disclosures.
EXPERT ANALYSIS FROM AES 2018
Study Design, Population, and Key Outcomes of DECLARE-TIMI 58 Compared With Other Cardiovascular Outcomes Trials for Sodium-Glucose Cotransporter-2 Inhibitors
Click here to read the supplement
- The cardiovascular (CV) safety and efficacy of the sodium-glucose cotransporter-2 inhibitor (SGLT-2i) dapagliflozin was evaluated in the DECLARE-TIMI 58 study.
- The study design and patient population of DECLARE-TIMI 58 differed from those of other CV outcomes trials of SGLT-2is (EMPA-REG OUTCOME and CANVAS)
- Key outcome results between the 3 CV outcomes trials of SGLT-2is may have been affected by variations in the study designs and patient populations, given that DECLARE-TIMI 58 evaluated a larger population of patients with type 2 diabetes (T2D) without prior CV events than the EMPA-REG OUTCOME or CANVAS studies, potentially allowing for a broader generalizability of the study results to patients with T2D in real-world clinical practice.
Click here to read the supplement
About the Author:
Bulent S. Atac, MD
Albert Einstein College of
Medicine and Montefiore Medical Center,
Bronx, New York
Click here to read the supplement
- The cardiovascular (CV) safety and efficacy of the sodium-glucose cotransporter-2 inhibitor (SGLT-2i) dapagliflozin was evaluated in the DECLARE-TIMI 58 study.
- The study design and patient population of DECLARE-TIMI 58 differed from those of other CV outcomes trials of SGLT-2is (EMPA-REG OUTCOME and CANVAS)
- Key outcome results between the 3 CV outcomes trials of SGLT-2is may have been affected by variations in the study designs and patient populations, given that DECLARE-TIMI 58 evaluated a larger population of patients with type 2 diabetes (T2D) without prior CV events than the EMPA-REG OUTCOME or CANVAS studies, potentially allowing for a broader generalizability of the study results to patients with T2D in real-world clinical practice.
Click here to read the supplement
About the Author:
Bulent S. Atac, MD
Albert Einstein College of
Medicine and Montefiore Medical Center,
Bronx, New York
Click here to read the supplement
- The cardiovascular (CV) safety and efficacy of the sodium-glucose cotransporter-2 inhibitor (SGLT-2i) dapagliflozin was evaluated in the DECLARE-TIMI 58 study.
- The study design and patient population of DECLARE-TIMI 58 differed from those of other CV outcomes trials of SGLT-2is (EMPA-REG OUTCOME and CANVAS)
- Key outcome results between the 3 CV outcomes trials of SGLT-2is may have been affected by variations in the study designs and patient populations, given that DECLARE-TIMI 58 evaluated a larger population of patients with type 2 diabetes (T2D) without prior CV events than the EMPA-REG OUTCOME or CANVAS studies, potentially allowing for a broader generalizability of the study results to patients with T2D in real-world clinical practice.
Click here to read the supplement
About the Author:
Bulent S. Atac, MD
Albert Einstein College of
Medicine and Montefiore Medical Center,
Bronx, New York
The amazing work we get to do
Serving people, connecting, and improving care
Stories are told of the first meeting, 20 years ago, where a hat was passed to collect donations to develop a fledgling organization of inpatient physicians. Today, 90% of hospitals with 200+ beds operate with a hospitalist model. Today, we are the Society of Hospital Medicine.
In the early 1900s, health care in many ways was simple. It was a doctor with a shingle hung. It was house calls. Remedies were limited. In the 1940s, companies developed insurance benefits to lure workers during World War II; this third party, the payer, added complexity. Meanwhile, treatment options began to diversify. Then, in the 1960s, Medicare was passed, and the government came into the mix, further increasing this complexity. Diagnostic and treatment options continued to diversify, seemingly exponentially. Some would say it took 30 years for our country to recognize that it had created the most advanced and expensive, as well as one of the least quality-controlled, health systems in the world. Thus, as hospital medicine was conceived in the 1990s, our national health system was awakening to the need – the creative niche – that hospitalists would fill.
When I began my career, I was unaware that I was a hospitalist. The title didn’t exist. Yes, I was working solely in the hospital. I was developing programs to improve care delivery. I was rounding, teaching, collaborating, connecting – everything that we now call hospital medicine. That first job has evolved into my career, one that I find both honorable and enjoyable.
As health care changes with the passing years, being a hospitalist continues to be about serving people, connecting, and improving care. Being a hospitalist is being innovative, willing, and even daring. Dare to try, dare to fail, dare to redesign and try again. Hospital medicine is thinking outside of the box while knowing how to color between the lines. In the coming decades, health care will continue to evolve, and hospital medicine will too. We now encompass surgical comanagement and perioperative care, palliative care, postacute care, and transitions of care services. In corners, hospital medicine is already experimenting with telecare, virtual health, and hospital at home. Our hospital medicine workforce is innovative, diverse, tech savvy and poised for leading.
We are ready and willing to face the pressures affecting health care in the United States today: the recognition of an overwhelming expense to society, the relative underperformance with regard to quality, the increasing complexity of illness and treatment options, the worsening health of the average American citizen, the aging population, the role of medical error in patient harm, the increasing engagement of people in their own care, and the desire to make care better. What our country is facing is actually a phenomenal opportunity, no matter what side of the political aisle you live on. Being in hospital medicine today is being at the center front of this evolutionary stage.
Since joining the SHM board of directors, I continue to find examples of the stellar work of our staff and our members across the country. Having the privilege as a board member to join several Chapter meetings, I have witnessed firsthand the camaraderie, the compassion, the team that makes our Society work. From Houston to San Francisco and from St. Louis to Seattle, I have been honored to work with SHM members that create and nurture local and regional networks with the support of SHM’s Chapters program – a program that now houses more than 50 chapters and has launched regional districts to further support networking and growth. SHM’s chapter venues allow our larger hospital medicine team – yes, the national one – to connect and collaborate.
Take the Pacific Northwest Chapter. In its early years hospitalists from various and competing health systems would convene at a restaurant and just talk. They spoke of how to staff, how to pay, and how to negotiate with hospital leadership. As I have joined chapter meetings in recent years, meetings continue to be the place to share ideas – how to develop new programs; what is the most recent approach to glycemic control, sepsis care, or antibiotic stewardship; how best to approach diagnosis without “anchoring”; and even how to care for each other in the time of loss of a colleague to suicide. It is here in our community that we share experiences, knowledge, new ideas – and this sharing makes us all stronger.
Our hospital medicine community also comes together through areas of shared interest. There are 18 Special Interest Groups (SIGs), focused on specific topic areas. I have been privileged as a board member to work with our Perioperative/Comanagement SIG as it launched in 2017 and has grown rapidly. Currently, the community hosts a “case of the month” hospital medicine discussion as well as a regular journal club webinar that allows participants to review recent literature and interact directly with the authors. As this SIG has grown, shared resources and ideas have allowed for diffusion of knowledge, providing our nation with infrastructure for improving perioperative care. It is networks like this that support our national hospital medicine team to build strength through sharing.
It is our society, our people, that have taken us from the passing of a hat to developing our national community and network. This March, we get to celebrate our field in a new way – Thursday, March 7, 2019, marks the inaugural National Hospitalist Day. Then, March 24-27, our annual conference, Hospital Medicine 2019, will bring thousands of our national team to National Harbor, Maryland. Join your colleagues. Find your niche and your community. Be a part of the change you want to see. While you are there, come introduce yourself to me and let me thank you for the amazing work you are doing.
We are all a part of this movement transforming patient care both on a local and national level. As we move to the future, our innovative, diverse, and connected network of hospital medicine will continue to create and guide health care advances in our country.
Dr. Thompson is professor and chief of the section of hospital medicine at University of Nebraska Medical Center, and medical director of clinical care transitions at Nebraska Medicine, Omaha.
Serving people, connecting, and improving care
Serving people, connecting, and improving care
Stories are told of the first meeting, 20 years ago, where a hat was passed to collect donations to develop a fledgling organization of inpatient physicians. Today, 90% of hospitals with 200+ beds operate with a hospitalist model. Today, we are the Society of Hospital Medicine.
In the early 1900s, health care in many ways was simple. It was a doctor with a shingle hung. It was house calls. Remedies were limited. In the 1940s, companies developed insurance benefits to lure workers during World War II; this third party, the payer, added complexity. Meanwhile, treatment options began to diversify. Then, in the 1960s, Medicare was passed, and the government came into the mix, further increasing this complexity. Diagnostic and treatment options continued to diversify, seemingly exponentially. Some would say it took 30 years for our country to recognize that it had created the most advanced and expensive, as well as one of the least quality-controlled, health systems in the world. Thus, as hospital medicine was conceived in the 1990s, our national health system was awakening to the need – the creative niche – that hospitalists would fill.
When I began my career, I was unaware that I was a hospitalist. The title didn’t exist. Yes, I was working solely in the hospital. I was developing programs to improve care delivery. I was rounding, teaching, collaborating, connecting – everything that we now call hospital medicine. That first job has evolved into my career, one that I find both honorable and enjoyable.
As health care changes with the passing years, being a hospitalist continues to be about serving people, connecting, and improving care. Being a hospitalist is being innovative, willing, and even daring. Dare to try, dare to fail, dare to redesign and try again. Hospital medicine is thinking outside of the box while knowing how to color between the lines. In the coming decades, health care will continue to evolve, and hospital medicine will too. We now encompass surgical comanagement and perioperative care, palliative care, postacute care, and transitions of care services. In corners, hospital medicine is already experimenting with telecare, virtual health, and hospital at home. Our hospital medicine workforce is innovative, diverse, tech savvy and poised for leading.
We are ready and willing to face the pressures affecting health care in the United States today: the recognition of an overwhelming expense to society, the relative underperformance with regard to quality, the increasing complexity of illness and treatment options, the worsening health of the average American citizen, the aging population, the role of medical error in patient harm, the increasing engagement of people in their own care, and the desire to make care better. What our country is facing is actually a phenomenal opportunity, no matter what side of the political aisle you live on. Being in hospital medicine today is being at the center front of this evolutionary stage.
Since joining the SHM board of directors, I continue to find examples of the stellar work of our staff and our members across the country. Having the privilege as a board member to join several Chapter meetings, I have witnessed firsthand the camaraderie, the compassion, the team that makes our Society work. From Houston to San Francisco and from St. Louis to Seattle, I have been honored to work with SHM members that create and nurture local and regional networks with the support of SHM’s Chapters program – a program that now houses more than 50 chapters and has launched regional districts to further support networking and growth. SHM’s chapter venues allow our larger hospital medicine team – yes, the national one – to connect and collaborate.
Take the Pacific Northwest Chapter. In its early years hospitalists from various and competing health systems would convene at a restaurant and just talk. They spoke of how to staff, how to pay, and how to negotiate with hospital leadership. As I have joined chapter meetings in recent years, meetings continue to be the place to share ideas – how to develop new programs; what is the most recent approach to glycemic control, sepsis care, or antibiotic stewardship; how best to approach diagnosis without “anchoring”; and even how to care for each other in the time of loss of a colleague to suicide. It is here in our community that we share experiences, knowledge, new ideas – and this sharing makes us all stronger.
Our hospital medicine community also comes together through areas of shared interest. There are 18 Special Interest Groups (SIGs), focused on specific topic areas. I have been privileged as a board member to work with our Perioperative/Comanagement SIG as it launched in 2017 and has grown rapidly. Currently, the community hosts a “case of the month” hospital medicine discussion as well as a regular journal club webinar that allows participants to review recent literature and interact directly with the authors. As this SIG has grown, shared resources and ideas have allowed for diffusion of knowledge, providing our nation with infrastructure for improving perioperative care. It is networks like this that support our national hospital medicine team to build strength through sharing.
It is our society, our people, that have taken us from the passing of a hat to developing our national community and network. This March, we get to celebrate our field in a new way – Thursday, March 7, 2019, marks the inaugural National Hospitalist Day. Then, March 24-27, our annual conference, Hospital Medicine 2019, will bring thousands of our national team to National Harbor, Maryland. Join your colleagues. Find your niche and your community. Be a part of the change you want to see. While you are there, come introduce yourself to me and let me thank you for the amazing work you are doing.
We are all a part of this movement transforming patient care both on a local and national level. As we move to the future, our innovative, diverse, and connected network of hospital medicine will continue to create and guide health care advances in our country.
Dr. Thompson is professor and chief of the section of hospital medicine at University of Nebraska Medical Center, and medical director of clinical care transitions at Nebraska Medicine, Omaha.
Stories are told of the first meeting, 20 years ago, where a hat was passed to collect donations to develop a fledgling organization of inpatient physicians. Today, 90% of hospitals with 200+ beds operate with a hospitalist model. Today, we are the Society of Hospital Medicine.
In the early 1900s, health care in many ways was simple. It was a doctor with a shingle hung. It was house calls. Remedies were limited. In the 1940s, companies developed insurance benefits to lure workers during World War II; this third party, the payer, added complexity. Meanwhile, treatment options began to diversify. Then, in the 1960s, Medicare was passed, and the government came into the mix, further increasing this complexity. Diagnostic and treatment options continued to diversify, seemingly exponentially. Some would say it took 30 years for our country to recognize that it had created the most advanced and expensive, as well as one of the least quality-controlled, health systems in the world. Thus, as hospital medicine was conceived in the 1990s, our national health system was awakening to the need – the creative niche – that hospitalists would fill.
When I began my career, I was unaware that I was a hospitalist. The title didn’t exist. Yes, I was working solely in the hospital. I was developing programs to improve care delivery. I was rounding, teaching, collaborating, connecting – everything that we now call hospital medicine. That first job has evolved into my career, one that I find both honorable and enjoyable.
As health care changes with the passing years, being a hospitalist continues to be about serving people, connecting, and improving care. Being a hospitalist is being innovative, willing, and even daring. Dare to try, dare to fail, dare to redesign and try again. Hospital medicine is thinking outside of the box while knowing how to color between the lines. In the coming decades, health care will continue to evolve, and hospital medicine will too. We now encompass surgical comanagement and perioperative care, palliative care, postacute care, and transitions of care services. In corners, hospital medicine is already experimenting with telecare, virtual health, and hospital at home. Our hospital medicine workforce is innovative, diverse, tech savvy and poised for leading.
We are ready and willing to face the pressures affecting health care in the United States today: the recognition of an overwhelming expense to society, the relative underperformance with regard to quality, the increasing complexity of illness and treatment options, the worsening health of the average American citizen, the aging population, the role of medical error in patient harm, the increasing engagement of people in their own care, and the desire to make care better. What our country is facing is actually a phenomenal opportunity, no matter what side of the political aisle you live on. Being in hospital medicine today is being at the center front of this evolutionary stage.
Since joining the SHM board of directors, I continue to find examples of the stellar work of our staff and our members across the country. Having the privilege as a board member to join several Chapter meetings, I have witnessed firsthand the camaraderie, the compassion, the team that makes our Society work. From Houston to San Francisco and from St. Louis to Seattle, I have been honored to work with SHM members that create and nurture local and regional networks with the support of SHM’s Chapters program – a program that now houses more than 50 chapters and has launched regional districts to further support networking and growth. SHM’s chapter venues allow our larger hospital medicine team – yes, the national one – to connect and collaborate.
Take the Pacific Northwest Chapter. In its early years hospitalists from various and competing health systems would convene at a restaurant and just talk. They spoke of how to staff, how to pay, and how to negotiate with hospital leadership. As I have joined chapter meetings in recent years, meetings continue to be the place to share ideas – how to develop new programs; what is the most recent approach to glycemic control, sepsis care, or antibiotic stewardship; how best to approach diagnosis without “anchoring”; and even how to care for each other in the time of loss of a colleague to suicide. It is here in our community that we share experiences, knowledge, new ideas – and this sharing makes us all stronger.
Our hospital medicine community also comes together through areas of shared interest. There are 18 Special Interest Groups (SIGs), focused on specific topic areas. I have been privileged as a board member to work with our Perioperative/Comanagement SIG as it launched in 2017 and has grown rapidly. Currently, the community hosts a “case of the month” hospital medicine discussion as well as a regular journal club webinar that allows participants to review recent literature and interact directly with the authors. As this SIG has grown, shared resources and ideas have allowed for diffusion of knowledge, providing our nation with infrastructure for improving perioperative care. It is networks like this that support our national hospital medicine team to build strength through sharing.
It is our society, our people, that have taken us from the passing of a hat to developing our national community and network. This March, we get to celebrate our field in a new way – Thursday, March 7, 2019, marks the inaugural National Hospitalist Day. Then, March 24-27, our annual conference, Hospital Medicine 2019, will bring thousands of our national team to National Harbor, Maryland. Join your colleagues. Find your niche and your community. Be a part of the change you want to see. While you are there, come introduce yourself to me and let me thank you for the amazing work you are doing.
We are all a part of this movement transforming patient care both on a local and national level. As we move to the future, our innovative, diverse, and connected network of hospital medicine will continue to create and guide health care advances in our country.
Dr. Thompson is professor and chief of the section of hospital medicine at University of Nebraska Medical Center, and medical director of clinical care transitions at Nebraska Medicine, Omaha.
Racial disparities uncovered in IBD-related myelosuppressive hospitalizations
LAS VEGAS – Immunosuppressant thiopurine drugs are a common and often successful treatment for patients with inflammatory bowel disease (IBD), but they can cause serious side effects via myelosuppression. Now, a new study suggests that a racial gap may prevent minority patients from being promptly diagnosed with myelosuppressive side effects.
“We found that minority IBD patients – black, Hispanic, Asian/Pacific Islander – had significantly higher hospitalization rates that were due to myelosuppressive events compared to white IBD patients,” lead author Ryan Suk, MS, said in an interview. “Among those IBD patients who were hospitalized due to myelosuppression, black and Hispanic IBD patients had a significantly higher chance of getting admitted as urgent compared to white IBD patients.”
Ms. Suk, a health economics graduate student at the University of Texas, Houston, spoke in an interview prior to the presentation of her study’s findings at the Crohn’s & Colitis Congress - a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.
According to Ms. Suk, multiple studies have previously revealed racial and ethnic disparities in health care access and use by minority patients with IBD.
She pointed to a 2010 study that found black patients with IBD were much less likely than whites were to see a gastroenterologist or IBD specialist at least once a year. She also cited a 2009 study that found black patients with IBD were significantly less adherent than were white patients; researchers linked older age and higher trust in physicians to higher levels of adherence (Am J Gastroenterol. 2010 Oct;105[10]:2202-8; Inflamm Bowel Dis. 2009 Aug;15[8]:1233-9).
In light of these findings, she said, “we questioned what the possible results of thiopurine use could be in minority patients without proper and consistent routine IBD care.”
While thiopurine is considered a standard form of care for IBD patients, Ms. Suk said an estimated one-third of patients must stop the treatment because of side effects such as anemia, leukopenia/neutropenia, and thrombocytopenia.
For the new study, Ms. Suk and her colleagues tracked patients who were hospitalized with a primary diagnosis of IBD or IBD-related complications from 2003-2014 via the Nationwide Inpatient Sample. There were 249,253 white patients, 192,864 black patients, 28,956 Hispanic patients, 17,073 Asian/Pacific Islander patients, and 2,849 patients in the “other” category.
The researchers found higher odds of hospitalization for myelosuppression in minorities compared with non-Hispanic whites: Non-Hispanic blacks (adjusted odds ratio = 1.3; 95% confidence interval [1.2-1.4], vs. whites), Hispanics (aOR = 1.6; 95% CI [1.4-1.7], vs. whites), and Asian/Pacific Islanders (aOR = 2.3; 95% CI [1.9-2.8], vs. whites).
The researchers found that among patients diagnosed with myelosuppression, two groups – non-Hispanic blacks and Hispanics – had higher odds of being admitted urgently, compared with non-Hispanic whites (aOR = 1.7; 95% CI [1.2-2.3] and aOR = 1.6; 95% CI [1.1-2.2] vs. whites, respectively).
“Unlike Asian/Pacific Islander patients, black and Hispanic patients had a higher likelihood of getting hospitalized from myelosuppression and also higher likelihood to get admitted urgently compared to the white cohort,” Ms. Suk said. “It is possible that they have less access to thiopurine management and monitoring, leading to developing more severe adverse events and therefore having urgent myelosuppressive hospitalizations.”
As for Asian/Pacific Islander patients, she noted that they had the highest likelihood of myelosuppression hospitalization but did not have the highest chance of getting admitted as urgent. “We think that Asians have a higher risk of myelosuppression due to genetic factors, not from less access to care, and thus they had more elective hospitalizations,” she said.
The researchers also linked Medicaid, self-pay, and no-charge patients to higher levels of myelosuppression hospitalizations. “This shows that patients who have less access to care [need more] urgent admission from myelosuppressive events,” Ms. Suk said.
No funding was reported, and the study authors had no relevant disclosures.
SOURCE: Suk R et al. Crohn’s & Colitis Congress, Abstract P059.
LAS VEGAS – Immunosuppressant thiopurine drugs are a common and often successful treatment for patients with inflammatory bowel disease (IBD), but they can cause serious side effects via myelosuppression. Now, a new study suggests that a racial gap may prevent minority patients from being promptly diagnosed with myelosuppressive side effects.
“We found that minority IBD patients – black, Hispanic, Asian/Pacific Islander – had significantly higher hospitalization rates that were due to myelosuppressive events compared to white IBD patients,” lead author Ryan Suk, MS, said in an interview. “Among those IBD patients who were hospitalized due to myelosuppression, black and Hispanic IBD patients had a significantly higher chance of getting admitted as urgent compared to white IBD patients.”
Ms. Suk, a health economics graduate student at the University of Texas, Houston, spoke in an interview prior to the presentation of her study’s findings at the Crohn’s & Colitis Congress - a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.
According to Ms. Suk, multiple studies have previously revealed racial and ethnic disparities in health care access and use by minority patients with IBD.
She pointed to a 2010 study that found black patients with IBD were much less likely than whites were to see a gastroenterologist or IBD specialist at least once a year. She also cited a 2009 study that found black patients with IBD were significantly less adherent than were white patients; researchers linked older age and higher trust in physicians to higher levels of adherence (Am J Gastroenterol. 2010 Oct;105[10]:2202-8; Inflamm Bowel Dis. 2009 Aug;15[8]:1233-9).
In light of these findings, she said, “we questioned what the possible results of thiopurine use could be in minority patients without proper and consistent routine IBD care.”
While thiopurine is considered a standard form of care for IBD patients, Ms. Suk said an estimated one-third of patients must stop the treatment because of side effects such as anemia, leukopenia/neutropenia, and thrombocytopenia.
For the new study, Ms. Suk and her colleagues tracked patients who were hospitalized with a primary diagnosis of IBD or IBD-related complications from 2003-2014 via the Nationwide Inpatient Sample. There were 249,253 white patients, 192,864 black patients, 28,956 Hispanic patients, 17,073 Asian/Pacific Islander patients, and 2,849 patients in the “other” category.
The researchers found higher odds of hospitalization for myelosuppression in minorities compared with non-Hispanic whites: Non-Hispanic blacks (adjusted odds ratio = 1.3; 95% confidence interval [1.2-1.4], vs. whites), Hispanics (aOR = 1.6; 95% CI [1.4-1.7], vs. whites), and Asian/Pacific Islanders (aOR = 2.3; 95% CI [1.9-2.8], vs. whites).
The researchers found that among patients diagnosed with myelosuppression, two groups – non-Hispanic blacks and Hispanics – had higher odds of being admitted urgently, compared with non-Hispanic whites (aOR = 1.7; 95% CI [1.2-2.3] and aOR = 1.6; 95% CI [1.1-2.2] vs. whites, respectively).
“Unlike Asian/Pacific Islander patients, black and Hispanic patients had a higher likelihood of getting hospitalized from myelosuppression and also higher likelihood to get admitted urgently compared to the white cohort,” Ms. Suk said. “It is possible that they have less access to thiopurine management and monitoring, leading to developing more severe adverse events and therefore having urgent myelosuppressive hospitalizations.”
As for Asian/Pacific Islander patients, she noted that they had the highest likelihood of myelosuppression hospitalization but did not have the highest chance of getting admitted as urgent. “We think that Asians have a higher risk of myelosuppression due to genetic factors, not from less access to care, and thus they had more elective hospitalizations,” she said.
The researchers also linked Medicaid, self-pay, and no-charge patients to higher levels of myelosuppression hospitalizations. “This shows that patients who have less access to care [need more] urgent admission from myelosuppressive events,” Ms. Suk said.
No funding was reported, and the study authors had no relevant disclosures.
SOURCE: Suk R et al. Crohn’s & Colitis Congress, Abstract P059.
LAS VEGAS – Immunosuppressant thiopurine drugs are a common and often successful treatment for patients with inflammatory bowel disease (IBD), but they can cause serious side effects via myelosuppression. Now, a new study suggests that a racial gap may prevent minority patients from being promptly diagnosed with myelosuppressive side effects.
“We found that minority IBD patients – black, Hispanic, Asian/Pacific Islander – had significantly higher hospitalization rates that were due to myelosuppressive events compared to white IBD patients,” lead author Ryan Suk, MS, said in an interview. “Among those IBD patients who were hospitalized due to myelosuppression, black and Hispanic IBD patients had a significantly higher chance of getting admitted as urgent compared to white IBD patients.”
Ms. Suk, a health economics graduate student at the University of Texas, Houston, spoke in an interview prior to the presentation of her study’s findings at the Crohn’s & Colitis Congress - a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association.
According to Ms. Suk, multiple studies have previously revealed racial and ethnic disparities in health care access and use by minority patients with IBD.
She pointed to a 2010 study that found black patients with IBD were much less likely than whites were to see a gastroenterologist or IBD specialist at least once a year. She also cited a 2009 study that found black patients with IBD were significantly less adherent than were white patients; researchers linked older age and higher trust in physicians to higher levels of adherence (Am J Gastroenterol. 2010 Oct;105[10]:2202-8; Inflamm Bowel Dis. 2009 Aug;15[8]:1233-9).
In light of these findings, she said, “we questioned what the possible results of thiopurine use could be in minority patients without proper and consistent routine IBD care.”
While thiopurine is considered a standard form of care for IBD patients, Ms. Suk said an estimated one-third of patients must stop the treatment because of side effects such as anemia, leukopenia/neutropenia, and thrombocytopenia.
For the new study, Ms. Suk and her colleagues tracked patients who were hospitalized with a primary diagnosis of IBD or IBD-related complications from 2003-2014 via the Nationwide Inpatient Sample. There were 249,253 white patients, 192,864 black patients, 28,956 Hispanic patients, 17,073 Asian/Pacific Islander patients, and 2,849 patients in the “other” category.
The researchers found higher odds of hospitalization for myelosuppression in minorities compared with non-Hispanic whites: Non-Hispanic blacks (adjusted odds ratio = 1.3; 95% confidence interval [1.2-1.4], vs. whites), Hispanics (aOR = 1.6; 95% CI [1.4-1.7], vs. whites), and Asian/Pacific Islanders (aOR = 2.3; 95% CI [1.9-2.8], vs. whites).
The researchers found that among patients diagnosed with myelosuppression, two groups – non-Hispanic blacks and Hispanics – had higher odds of being admitted urgently, compared with non-Hispanic whites (aOR = 1.7; 95% CI [1.2-2.3] and aOR = 1.6; 95% CI [1.1-2.2] vs. whites, respectively).
“Unlike Asian/Pacific Islander patients, black and Hispanic patients had a higher likelihood of getting hospitalized from myelosuppression and also higher likelihood to get admitted urgently compared to the white cohort,” Ms. Suk said. “It is possible that they have less access to thiopurine management and monitoring, leading to developing more severe adverse events and therefore having urgent myelosuppressive hospitalizations.”
As for Asian/Pacific Islander patients, she noted that they had the highest likelihood of myelosuppression hospitalization but did not have the highest chance of getting admitted as urgent. “We think that Asians have a higher risk of myelosuppression due to genetic factors, not from less access to care, and thus they had more elective hospitalizations,” she said.
The researchers also linked Medicaid, self-pay, and no-charge patients to higher levels of myelosuppression hospitalizations. “This shows that patients who have less access to care [need more] urgent admission from myelosuppressive events,” Ms. Suk said.
No funding was reported, and the study authors had no relevant disclosures.
SOURCE: Suk R et al. Crohn’s & Colitis Congress, Abstract P059.
REPORTING FROM THE CROHN’S & COLITIS CONGRESS
VA Forges a Historic Partnership with the National Shooting Sports Foundation and the American Foundation for Suicide Prevention to Prevent Veteran Suicide
As new standards for access dominated recent media coverage of veterans’ health care headlines, the launch of a historically unprecedented collaboration to prevent veterans’ suicide went completely unnoticed.
On January 31, the Department of Veterans Affairs (VA) announced a partnership with the National Shooting Sports Foundation (NSSF), a firearms industry association that works to promote, protect and preserve hunting and shooting sports, and the American Foundation for Suicide Prevention (AFSP), the nation’s largest suicide prevention organization. Together, they are developing a program that empowers communities to engage in safe firearm-storage practices. The program includes information on creating community coalitions that promote and sustain firearm safety, with an emphasis on reaching service members, veterans and their families.
This partnership represents the nation’s biggest advance in forging common ground on an issue where polarization has interfered with lifesaving initiatives. It’s a game changer.
In 2016, about 69% of veteran suicides in the US (71% among male and 41% among female veterans) resulted from a firearm injury. In comparison, the proportion of suicides resulting from a firearm injury among nonveteran adults was 48%.1 The majority of veteran suicides occur with those who do not seek care within the VA healthcare system, which has led the VA to broaden its focus to reach all veterans.
Given the frequency of firearm use as a method of suicide, VA recognizes that suicide prevention efforts must address how veterans store their firearms. The decision to take an action to kill oneself is at times made impulsively—in just a matter of minutes. Securely storing firearms creates precious time and physical space between an individual’s period of risk and the means to act. Studies have demonstrated that delaying access to deadly means can save a life.
VA is striving to be a national leader in suicide prevention, and lethal means safety is an important component of the department’s approach. VA’s lethal means safety initiatives encourage veterans to voluntarily store their firearms safely. Key to this approach is to train mental health and peer providers in veteran-centric counseling methods while promoting resources, including a national consultation call line for both VA and community providers seeking guidance for treatment practices or engaging a veteran in care.
Because many veterans believe that firearms must remain in their homes under all circumstances, in 2018 the VA held the first of its kind open-innovation challenge for safe firearm storage. This challenge led to the creation of numerous lifesaving product designs, which are now under development in the private sector.
The latest partnership further advances VA’s effort to ensure that lethal means safety counseling is culturally relevant, comes from a trusted source and contains no anti-firearm bias. VA respects the important role firearms play in many veterans’ lives and is committed to educating veterans and their families about safe storage of firearms in a way that is consistent with each veteran’s values and priorities.
Nothing will be more effective in diminishing suicide than correcting the false belief among many veterans that the VA wants to take away veterans’ guns. When that misperception is corrected, not only would more at-risk veterans seek out VA mental health care, but it also could become commonplace for veterans, families and friends to speak up because, “Buddies talk to buddies in crisis about safely storing guns.” This is especially important for veterans in rural areas, where the rates of firearm ownership and suicide are the highest. Joining forces with NSSF could spearhead such a shift.
The VA, NSSF and AFSP should be lauded for bridging the divide and driving this far-reaching breakthrough in firearm safety conversations and community alliances. The effort will not only save countless veterans’ lives, but also forge a path to mitigate our national tragedy of suicide.
1. US Department of Veterans Affairs. VA national suicide data report 2005-2016. https://www.mentalhealth.va.gov/docs/data-sheets/OMHSP_National_Suicide_Data_Report_2005-2016_508.pdf. Updated September 2018. Accessed February 15, 2019.
As new standards for access dominated recent media coverage of veterans’ health care headlines, the launch of a historically unprecedented collaboration to prevent veterans’ suicide went completely unnoticed.
On January 31, the Department of Veterans Affairs (VA) announced a partnership with the National Shooting Sports Foundation (NSSF), a firearms industry association that works to promote, protect and preserve hunting and shooting sports, and the American Foundation for Suicide Prevention (AFSP), the nation’s largest suicide prevention organization. Together, they are developing a program that empowers communities to engage in safe firearm-storage practices. The program includes information on creating community coalitions that promote and sustain firearm safety, with an emphasis on reaching service members, veterans and their families.
This partnership represents the nation’s biggest advance in forging common ground on an issue where polarization has interfered with lifesaving initiatives. It’s a game changer.
In 2016, about 69% of veteran suicides in the US (71% among male and 41% among female veterans) resulted from a firearm injury. In comparison, the proportion of suicides resulting from a firearm injury among nonveteran adults was 48%.1 The majority of veteran suicides occur with those who do not seek care within the VA healthcare system, which has led the VA to broaden its focus to reach all veterans.
Given the frequency of firearm use as a method of suicide, VA recognizes that suicide prevention efforts must address how veterans store their firearms. The decision to take an action to kill oneself is at times made impulsively—in just a matter of minutes. Securely storing firearms creates precious time and physical space between an individual’s period of risk and the means to act. Studies have demonstrated that delaying access to deadly means can save a life.
VA is striving to be a national leader in suicide prevention, and lethal means safety is an important component of the department’s approach. VA’s lethal means safety initiatives encourage veterans to voluntarily store their firearms safely. Key to this approach is to train mental health and peer providers in veteran-centric counseling methods while promoting resources, including a national consultation call line for both VA and community providers seeking guidance for treatment practices or engaging a veteran in care.
Because many veterans believe that firearms must remain in their homes under all circumstances, in 2018 the VA held the first of its kind open-innovation challenge for safe firearm storage. This challenge led to the creation of numerous lifesaving product designs, which are now under development in the private sector.
The latest partnership further advances VA’s effort to ensure that lethal means safety counseling is culturally relevant, comes from a trusted source and contains no anti-firearm bias. VA respects the important role firearms play in many veterans’ lives and is committed to educating veterans and their families about safe storage of firearms in a way that is consistent with each veteran’s values and priorities.
Nothing will be more effective in diminishing suicide than correcting the false belief among many veterans that the VA wants to take away veterans’ guns. When that misperception is corrected, not only would more at-risk veterans seek out VA mental health care, but it also could become commonplace for veterans, families and friends to speak up because, “Buddies talk to buddies in crisis about safely storing guns.” This is especially important for veterans in rural areas, where the rates of firearm ownership and suicide are the highest. Joining forces with NSSF could spearhead such a shift.
The VA, NSSF and AFSP should be lauded for bridging the divide and driving this far-reaching breakthrough in firearm safety conversations and community alliances. The effort will not only save countless veterans’ lives, but also forge a path to mitigate our national tragedy of suicide.
As new standards for access dominated recent media coverage of veterans’ health care headlines, the launch of a historically unprecedented collaboration to prevent veterans’ suicide went completely unnoticed.
On January 31, the Department of Veterans Affairs (VA) announced a partnership with the National Shooting Sports Foundation (NSSF), a firearms industry association that works to promote, protect and preserve hunting and shooting sports, and the American Foundation for Suicide Prevention (AFSP), the nation’s largest suicide prevention organization. Together, they are developing a program that empowers communities to engage in safe firearm-storage practices. The program includes information on creating community coalitions that promote and sustain firearm safety, with an emphasis on reaching service members, veterans and their families.
This partnership represents the nation’s biggest advance in forging common ground on an issue where polarization has interfered with lifesaving initiatives. It’s a game changer.
In 2016, about 69% of veteran suicides in the US (71% among male and 41% among female veterans) resulted from a firearm injury. In comparison, the proportion of suicides resulting from a firearm injury among nonveteran adults was 48%.1 The majority of veteran suicides occur with those who do not seek care within the VA healthcare system, which has led the VA to broaden its focus to reach all veterans.
Given the frequency of firearm use as a method of suicide, VA recognizes that suicide prevention efforts must address how veterans store their firearms. The decision to take an action to kill oneself is at times made impulsively—in just a matter of minutes. Securely storing firearms creates precious time and physical space between an individual’s period of risk and the means to act. Studies have demonstrated that delaying access to deadly means can save a life.
VA is striving to be a national leader in suicide prevention, and lethal means safety is an important component of the department’s approach. VA’s lethal means safety initiatives encourage veterans to voluntarily store their firearms safely. Key to this approach is to train mental health and peer providers in veteran-centric counseling methods while promoting resources, including a national consultation call line for both VA and community providers seeking guidance for treatment practices or engaging a veteran in care.
Because many veterans believe that firearms must remain in their homes under all circumstances, in 2018 the VA held the first of its kind open-innovation challenge for safe firearm storage. This challenge led to the creation of numerous lifesaving product designs, which are now under development in the private sector.
The latest partnership further advances VA’s effort to ensure that lethal means safety counseling is culturally relevant, comes from a trusted source and contains no anti-firearm bias. VA respects the important role firearms play in many veterans’ lives and is committed to educating veterans and their families about safe storage of firearms in a way that is consistent with each veteran’s values and priorities.
Nothing will be more effective in diminishing suicide than correcting the false belief among many veterans that the VA wants to take away veterans’ guns. When that misperception is corrected, not only would more at-risk veterans seek out VA mental health care, but it also could become commonplace for veterans, families and friends to speak up because, “Buddies talk to buddies in crisis about safely storing guns.” This is especially important for veterans in rural areas, where the rates of firearm ownership and suicide are the highest. Joining forces with NSSF could spearhead such a shift.
The VA, NSSF and AFSP should be lauded for bridging the divide and driving this far-reaching breakthrough in firearm safety conversations and community alliances. The effort will not only save countless veterans’ lives, but also forge a path to mitigate our national tragedy of suicide.
1. US Department of Veterans Affairs. VA national suicide data report 2005-2016. https://www.mentalhealth.va.gov/docs/data-sheets/OMHSP_National_Suicide_Data_Report_2005-2016_508.pdf. Updated September 2018. Accessed February 15, 2019.
1. US Department of Veterans Affairs. VA national suicide data report 2005-2016. https://www.mentalhealth.va.gov/docs/data-sheets/OMHSP_National_Suicide_Data_Report_2005-2016_508.pdf. Updated September 2018. Accessed February 15, 2019.
Depression, Fatigue, and Cognitive Functioning in MS
In the presence of mild levels of depression or significant fatigue in persons with multiple sclerosis (MS), subjective cognitive measures are unlikely to provide accurate estimates of objective cognitive functioning. This according to a recent study that aimed to examine the degree to which depressive symptoms and fatigue in individuals with MS are associated with discrepancies between subjective and objective cognitive impairment. 99 adults with MS completed the Patient Health Questionnaire–8 (PHQ-8), Fatigue Severity Scale (FSS), MS Neuropsychological Screening Questionnaire (MSNQ), and Brief International Cognitive Assessment for MS (BICAMS). Participants were classified as “Accurates,” “Underestimators,” or “Overestimators” based on discrepancies between their MSNQ (subjective) and BICAMS (objective) scores. Researchers found:
- The PHQ-8 (r=.58) and FSS (r=.48) significantly correlated with the MSNQ, but not with the
BICAMS (rs<.07). - Underestimators (ie, participants who underestimated their objective cognitive functioning) exhibited higher PHQ-8 and FSS scores compared to Accurates and Overestimators.
- Optimal cut-scores of ≥6 on the PHQ-8 and ≥36 on the FSS provided fair accuracy (78% and 74%) for identifying Underestimators.
- Identification of Underestimators based on PHQ-8 and FSS scores was not moderated by any demographic or MS clinical variables.
Hughes AJ. Depressive symptoms and fatigue as predictors of objective-subjective discrepancies in cognitive function in multiple sclerosis. [Published online ahead of print January 31, 2019]. Mult Scler Relat Disord. doi:10.1016/j.msard.2019.01.055.
In the presence of mild levels of depression or significant fatigue in persons with multiple sclerosis (MS), subjective cognitive measures are unlikely to provide accurate estimates of objective cognitive functioning. This according to a recent study that aimed to examine the degree to which depressive symptoms and fatigue in individuals with MS are associated with discrepancies between subjective and objective cognitive impairment. 99 adults with MS completed the Patient Health Questionnaire–8 (PHQ-8), Fatigue Severity Scale (FSS), MS Neuropsychological Screening Questionnaire (MSNQ), and Brief International Cognitive Assessment for MS (BICAMS). Participants were classified as “Accurates,” “Underestimators,” or “Overestimators” based on discrepancies between their MSNQ (subjective) and BICAMS (objective) scores. Researchers found:
- The PHQ-8 (r=.58) and FSS (r=.48) significantly correlated with the MSNQ, but not with the
BICAMS (rs<.07). - Underestimators (ie, participants who underestimated their objective cognitive functioning) exhibited higher PHQ-8 and FSS scores compared to Accurates and Overestimators.
- Optimal cut-scores of ≥6 on the PHQ-8 and ≥36 on the FSS provided fair accuracy (78% and 74%) for identifying Underestimators.
- Identification of Underestimators based on PHQ-8 and FSS scores was not moderated by any demographic or MS clinical variables.
Hughes AJ. Depressive symptoms and fatigue as predictors of objective-subjective discrepancies in cognitive function in multiple sclerosis. [Published online ahead of print January 31, 2019]. Mult Scler Relat Disord. doi:10.1016/j.msard.2019.01.055.
In the presence of mild levels of depression or significant fatigue in persons with multiple sclerosis (MS), subjective cognitive measures are unlikely to provide accurate estimates of objective cognitive functioning. This according to a recent study that aimed to examine the degree to which depressive symptoms and fatigue in individuals with MS are associated with discrepancies between subjective and objective cognitive impairment. 99 adults with MS completed the Patient Health Questionnaire–8 (PHQ-8), Fatigue Severity Scale (FSS), MS Neuropsychological Screening Questionnaire (MSNQ), and Brief International Cognitive Assessment for MS (BICAMS). Participants were classified as “Accurates,” “Underestimators,” or “Overestimators” based on discrepancies between their MSNQ (subjective) and BICAMS (objective) scores. Researchers found:
- The PHQ-8 (r=.58) and FSS (r=.48) significantly correlated with the MSNQ, but not with the
BICAMS (rs<.07). - Underestimators (ie, participants who underestimated their objective cognitive functioning) exhibited higher PHQ-8 and FSS scores compared to Accurates and Overestimators.
- Optimal cut-scores of ≥6 on the PHQ-8 and ≥36 on the FSS provided fair accuracy (78% and 74%) for identifying Underestimators.
- Identification of Underestimators based on PHQ-8 and FSS scores was not moderated by any demographic or MS clinical variables.
Hughes AJ. Depressive symptoms and fatigue as predictors of objective-subjective discrepancies in cognitive function in multiple sclerosis. [Published online ahead of print January 31, 2019]. Mult Scler Relat Disord. doi:10.1016/j.msard.2019.01.055.
What cardiologists need to know about ARVC
SNOWMASS, COLO. – Electrophysiologist N.A. Mark Estes III, MD, has a piece of advice for his general cardiology colleagues regarding arrhythmogenic right ventricular cardiomyopathy (ARVC), an inherited arrhythmia syndrome that’s one of the most common causes of sudden death in athletes under the age of 40 years.
“When you have a patient with syncope and an ECG abnormality that suggests ARVC, you immediately restrict activity and immediately go on to imaging. And then it’s time to get that patient off to somebody who deals with these patients all the time,” he said at the Annual Cardiovascular Conference at Snowmass sponsored by the American College of Cardiology.
ARVC is thought to affect 1 in 5,000 people. It’s the cause of sudden death in roughly 5% of young athletes in the United States and 25% in Italy, with the disparity believed to be largely caused by underrecognition of the disease.
Dr. Estes was a coauthor of a 2015 international task force consensus statement on the treatment of ARVC (Eur Heart J. 2015 Dec 7;36[46]:3227-37). An updated report that incorporates much new information is due to be released in May 2019.
“The new guidelines are going to put some very clear limits on physical activity: Less than 7 METs [metabolic equivalents], which is about a brisk walk. Exercise is not good with ARVC,” said Dr. Estes, professor of medicine at the University of Pittsburgh.
Patients with ARVC absolutely must be restricted from participation in competitive sports, a step whose importance was demonstrated in the North American Multidisciplinary Study of ARVC, for which Dr. Estes was a coauthor. That study, too recent for inclusion in the 2015 task force consensus statement, showed that competitive sport was associated with a 100% increased risk of ventricular tachyarrhythmias and death, as well as earlier presentation with symptoms, compared with patients with ARVC who engaged in much less intense recreational athletic activity, who in turn didn’t have a risk level any different from inactive patients. That being said, however, the investigators also noted that the absolute risk of ventricular tachyarrhythmias or death remained high even in the inactive and recreational sports participants, at 23% by 2 years post diagnosis (Eur Heart J. 2015 Jul 14;36[27]:1735-43).
ARVC has three phases: An early concealed phase, with an associated high rate of syncope or sudden cardiac death; an intermediate phase marked by frequent arrhythmias; and a late phase involving cardiomyopathy and heart failure. Pathologically, the disease involves progressive loss of myocytes caused by abnormalities of plakoglobin and plakophilin, which Dr. Estes described as “essentially the glue that holds the sarcomeres together.” As myocytes are lost they are replaced by fibrofatty deposits, mostly in the right ventricle, creating a substrate for ventricular arrhythmias.
When to suspect ARVC?
“Anyone who has syncope with exertion automatically has a red flag because there is almost certainly something causing that event that’s potentially malignant,” according to the cardiologist.
An early, sensitive, and reasonably specific hallmark of ARVC on the 12-lead ECG is T wave inversion in right precordial leads V1, V2, and V3 or beyond. An epsilon wave – a small positive deflection at the end of the QRS complex – is present in about one in five patients with ARVC and is diagnostic of the condition.
“It’s an ECG you want to commit to memory. And when you see it, think ARVC,” Dr. Estes advised.
Abnormalities on MRI and 2D echocardiography include right ventricular enlargement and wall motion abnormalities, with left ventricular involvement becoming common in more advanced disease.
The detailed structural, electrographic, functional imaging, histologic, and clinical diagnostic criteria for ARVC, known as the 2010 Task Force Criteria, are readily available (Circulation. 2010 Apr 6;121[13]:1533-41). So are guidelines on genetic testing, which practitioners need to understand is now the standard of care for patients with ARVC and, in the event they are found to have a pathogenic mutation, in first-degree family members as well (Europace. 2011 Aug;13(8):1077-109).
“These days all you need to do is simply Google ‘syncope’ and ‘ARVC’ and you will get to the guidelines,” Dr. Estes advised. “It’s virtually impossible to keep up with all this information, but you should know how to access it and apply it in an individual patient. And learn the role of genetic testing. It’s very much an evolving area, quite mature for the long QT syndromes, but not a robust database for ARVC now. Yet there’s no doubt it’s going to be used more and more for diagnosis, risk stratification, and therapy of ARVC in the future.”
Once the diagnosis of ARVC is made in accordance with the 2010 Task Force Criteria, risk stratification and decision making about definitive therapy become paramount. The international task force consensus statement gives a Class I recommendation to implantable cardioverter defibrillator (ICD) therapy in high-risk ARVC patients, defined as those who’ve had a cardiac arrest, sustained ventricular tachycardia, or have severe right and/or left ventricular dysfunction. ICD therapy gets a Class IIa recommendation in those with at least one of the major risk factors: syncope, nonsustained ventricular tachycardia, and moderate ventricular dysfunction. For ARVC patients with one or more minor risk factors, which include frequent premature ventricular contractions and inducible ventricular tachycardia upon electrophysiological testing, the strength of the recommendation for ICD therapy drops to Class IIb, or “may be considered.” And for low-risk patients, those with confirmed ARVC but no phenotypic expressions of the disorder, the ICD recommendation is Class III, meaning nonindicated.
“There’s a very low threshold for putting in an ICD in patients with ARVC because if you eliminate the arrhythmic mortality, progression to heart failure needing advanced therapies or transplant is extremely rare as long as they’re restricted from athletics,” Dr. Estes said.
He reported serving as a consultant to Boston Scientific, Medtronic, and St. Jude Medical.bjancin@mdedge.com
SNOWMASS, COLO. – Electrophysiologist N.A. Mark Estes III, MD, has a piece of advice for his general cardiology colleagues regarding arrhythmogenic right ventricular cardiomyopathy (ARVC), an inherited arrhythmia syndrome that’s one of the most common causes of sudden death in athletes under the age of 40 years.
“When you have a patient with syncope and an ECG abnormality that suggests ARVC, you immediately restrict activity and immediately go on to imaging. And then it’s time to get that patient off to somebody who deals with these patients all the time,” he said at the Annual Cardiovascular Conference at Snowmass sponsored by the American College of Cardiology.
ARVC is thought to affect 1 in 5,000 people. It’s the cause of sudden death in roughly 5% of young athletes in the United States and 25% in Italy, with the disparity believed to be largely caused by underrecognition of the disease.
Dr. Estes was a coauthor of a 2015 international task force consensus statement on the treatment of ARVC (Eur Heart J. 2015 Dec 7;36[46]:3227-37). An updated report that incorporates much new information is due to be released in May 2019.
“The new guidelines are going to put some very clear limits on physical activity: Less than 7 METs [metabolic equivalents], which is about a brisk walk. Exercise is not good with ARVC,” said Dr. Estes, professor of medicine at the University of Pittsburgh.
Patients with ARVC absolutely must be restricted from participation in competitive sports, a step whose importance was demonstrated in the North American Multidisciplinary Study of ARVC, for which Dr. Estes was a coauthor. That study, too recent for inclusion in the 2015 task force consensus statement, showed that competitive sport was associated with a 100% increased risk of ventricular tachyarrhythmias and death, as well as earlier presentation with symptoms, compared with patients with ARVC who engaged in much less intense recreational athletic activity, who in turn didn’t have a risk level any different from inactive patients. That being said, however, the investigators also noted that the absolute risk of ventricular tachyarrhythmias or death remained high even in the inactive and recreational sports participants, at 23% by 2 years post diagnosis (Eur Heart J. 2015 Jul 14;36[27]:1735-43).
ARVC has three phases: An early concealed phase, with an associated high rate of syncope or sudden cardiac death; an intermediate phase marked by frequent arrhythmias; and a late phase involving cardiomyopathy and heart failure. Pathologically, the disease involves progressive loss of myocytes caused by abnormalities of plakoglobin and plakophilin, which Dr. Estes described as “essentially the glue that holds the sarcomeres together.” As myocytes are lost they are replaced by fibrofatty deposits, mostly in the right ventricle, creating a substrate for ventricular arrhythmias.
When to suspect ARVC?
“Anyone who has syncope with exertion automatically has a red flag because there is almost certainly something causing that event that’s potentially malignant,” according to the cardiologist.
An early, sensitive, and reasonably specific hallmark of ARVC on the 12-lead ECG is T wave inversion in right precordial leads V1, V2, and V3 or beyond. An epsilon wave – a small positive deflection at the end of the QRS complex – is present in about one in five patients with ARVC and is diagnostic of the condition.
“It’s an ECG you want to commit to memory. And when you see it, think ARVC,” Dr. Estes advised.
Abnormalities on MRI and 2D echocardiography include right ventricular enlargement and wall motion abnormalities, with left ventricular involvement becoming common in more advanced disease.
The detailed structural, electrographic, functional imaging, histologic, and clinical diagnostic criteria for ARVC, known as the 2010 Task Force Criteria, are readily available (Circulation. 2010 Apr 6;121[13]:1533-41). So are guidelines on genetic testing, which practitioners need to understand is now the standard of care for patients with ARVC and, in the event they are found to have a pathogenic mutation, in first-degree family members as well (Europace. 2011 Aug;13(8):1077-109).
“These days all you need to do is simply Google ‘syncope’ and ‘ARVC’ and you will get to the guidelines,” Dr. Estes advised. “It’s virtually impossible to keep up with all this information, but you should know how to access it and apply it in an individual patient. And learn the role of genetic testing. It’s very much an evolving area, quite mature for the long QT syndromes, but not a robust database for ARVC now. Yet there’s no doubt it’s going to be used more and more for diagnosis, risk stratification, and therapy of ARVC in the future.”
Once the diagnosis of ARVC is made in accordance with the 2010 Task Force Criteria, risk stratification and decision making about definitive therapy become paramount. The international task force consensus statement gives a Class I recommendation to implantable cardioverter defibrillator (ICD) therapy in high-risk ARVC patients, defined as those who’ve had a cardiac arrest, sustained ventricular tachycardia, or have severe right and/or left ventricular dysfunction. ICD therapy gets a Class IIa recommendation in those with at least one of the major risk factors: syncope, nonsustained ventricular tachycardia, and moderate ventricular dysfunction. For ARVC patients with one or more minor risk factors, which include frequent premature ventricular contractions and inducible ventricular tachycardia upon electrophysiological testing, the strength of the recommendation for ICD therapy drops to Class IIb, or “may be considered.” And for low-risk patients, those with confirmed ARVC but no phenotypic expressions of the disorder, the ICD recommendation is Class III, meaning nonindicated.
“There’s a very low threshold for putting in an ICD in patients with ARVC because if you eliminate the arrhythmic mortality, progression to heart failure needing advanced therapies or transplant is extremely rare as long as they’re restricted from athletics,” Dr. Estes said.
He reported serving as a consultant to Boston Scientific, Medtronic, and St. Jude Medical.bjancin@mdedge.com
SNOWMASS, COLO. – Electrophysiologist N.A. Mark Estes III, MD, has a piece of advice for his general cardiology colleagues regarding arrhythmogenic right ventricular cardiomyopathy (ARVC), an inherited arrhythmia syndrome that’s one of the most common causes of sudden death in athletes under the age of 40 years.
“When you have a patient with syncope and an ECG abnormality that suggests ARVC, you immediately restrict activity and immediately go on to imaging. And then it’s time to get that patient off to somebody who deals with these patients all the time,” he said at the Annual Cardiovascular Conference at Snowmass sponsored by the American College of Cardiology.
ARVC is thought to affect 1 in 5,000 people. It’s the cause of sudden death in roughly 5% of young athletes in the United States and 25% in Italy, with the disparity believed to be largely caused by underrecognition of the disease.
Dr. Estes was a coauthor of a 2015 international task force consensus statement on the treatment of ARVC (Eur Heart J. 2015 Dec 7;36[46]:3227-37). An updated report that incorporates much new information is due to be released in May 2019.
“The new guidelines are going to put some very clear limits on physical activity: Less than 7 METs [metabolic equivalents], which is about a brisk walk. Exercise is not good with ARVC,” said Dr. Estes, professor of medicine at the University of Pittsburgh.
Patients with ARVC absolutely must be restricted from participation in competitive sports, a step whose importance was demonstrated in the North American Multidisciplinary Study of ARVC, for which Dr. Estes was a coauthor. That study, too recent for inclusion in the 2015 task force consensus statement, showed that competitive sport was associated with a 100% increased risk of ventricular tachyarrhythmias and death, as well as earlier presentation with symptoms, compared with patients with ARVC who engaged in much less intense recreational athletic activity, who in turn didn’t have a risk level any different from inactive patients. That being said, however, the investigators also noted that the absolute risk of ventricular tachyarrhythmias or death remained high even in the inactive and recreational sports participants, at 23% by 2 years post diagnosis (Eur Heart J. 2015 Jul 14;36[27]:1735-43).
ARVC has three phases: An early concealed phase, with an associated high rate of syncope or sudden cardiac death; an intermediate phase marked by frequent arrhythmias; and a late phase involving cardiomyopathy and heart failure. Pathologically, the disease involves progressive loss of myocytes caused by abnormalities of plakoglobin and plakophilin, which Dr. Estes described as “essentially the glue that holds the sarcomeres together.” As myocytes are lost they are replaced by fibrofatty deposits, mostly in the right ventricle, creating a substrate for ventricular arrhythmias.
When to suspect ARVC?
“Anyone who has syncope with exertion automatically has a red flag because there is almost certainly something causing that event that’s potentially malignant,” according to the cardiologist.
An early, sensitive, and reasonably specific hallmark of ARVC on the 12-lead ECG is T wave inversion in right precordial leads V1, V2, and V3 or beyond. An epsilon wave – a small positive deflection at the end of the QRS complex – is present in about one in five patients with ARVC and is diagnostic of the condition.
“It’s an ECG you want to commit to memory. And when you see it, think ARVC,” Dr. Estes advised.
Abnormalities on MRI and 2D echocardiography include right ventricular enlargement and wall motion abnormalities, with left ventricular involvement becoming common in more advanced disease.
The detailed structural, electrographic, functional imaging, histologic, and clinical diagnostic criteria for ARVC, known as the 2010 Task Force Criteria, are readily available (Circulation. 2010 Apr 6;121[13]:1533-41). So are guidelines on genetic testing, which practitioners need to understand is now the standard of care for patients with ARVC and, in the event they are found to have a pathogenic mutation, in first-degree family members as well (Europace. 2011 Aug;13(8):1077-109).
“These days all you need to do is simply Google ‘syncope’ and ‘ARVC’ and you will get to the guidelines,” Dr. Estes advised. “It’s virtually impossible to keep up with all this information, but you should know how to access it and apply it in an individual patient. And learn the role of genetic testing. It’s very much an evolving area, quite mature for the long QT syndromes, but not a robust database for ARVC now. Yet there’s no doubt it’s going to be used more and more for diagnosis, risk stratification, and therapy of ARVC in the future.”
Once the diagnosis of ARVC is made in accordance with the 2010 Task Force Criteria, risk stratification and decision making about definitive therapy become paramount. The international task force consensus statement gives a Class I recommendation to implantable cardioverter defibrillator (ICD) therapy in high-risk ARVC patients, defined as those who’ve had a cardiac arrest, sustained ventricular tachycardia, or have severe right and/or left ventricular dysfunction. ICD therapy gets a Class IIa recommendation in those with at least one of the major risk factors: syncope, nonsustained ventricular tachycardia, and moderate ventricular dysfunction. For ARVC patients with one or more minor risk factors, which include frequent premature ventricular contractions and inducible ventricular tachycardia upon electrophysiological testing, the strength of the recommendation for ICD therapy drops to Class IIb, or “may be considered.” And for low-risk patients, those with confirmed ARVC but no phenotypic expressions of the disorder, the ICD recommendation is Class III, meaning nonindicated.
“There’s a very low threshold for putting in an ICD in patients with ARVC because if you eliminate the arrhythmic mortality, progression to heart failure needing advanced therapies or transplant is extremely rare as long as they’re restricted from athletics,” Dr. Estes said.
He reported serving as a consultant to Boston Scientific, Medtronic, and St. Jude Medical.bjancin@mdedge.com
REPORTING FROM ACC SNOWMASS 2019
Trait Conscientiousness and SDMT Decline in MS
Higher baseline trait conscientiousness predicts slower rates of longitudinal cognitive decline in multiple sclerosis (MS), according to a recent study. Researchers conducted a retrospective analysis of 531 patients with MS whose data were gleaned from a multi-study database, aggregated over 16 years. Linear mixed effects modeling was applied to estimate the average rate of decline on Symbol Digit Modalities Test (SDMT) performance and to predict rates of decline using baseline clinical variables. They found:
- Participants exhibited an average estimated decline of 0.22 SDMT raw-score points/year.
- There was a significant main effect of time from baseline (t = −2.78), test form (t = 2.13), disease course (t = 2.91), age (t = −2.76), sex (t = −2.71), subjective cognitive impairment (t = −2.00), premorbid verbal intelligence (t = 5.14), and trait Conscientiousness (t = 2.69).
- A significant interaction emerged for Conscientiousness and time from baseline (t = 2.57).
Fuchs TA, Wojcik C, Wilding GE, et al. Trait Conscientiousness predicts rate of longitudinal SDMT decline in multiple sclerosis. [Published online ahead of print January 7, 2019]. Mult Scler. doi:10.1177%2F1352458518820272.
Higher baseline trait conscientiousness predicts slower rates of longitudinal cognitive decline in multiple sclerosis (MS), according to a recent study. Researchers conducted a retrospective analysis of 531 patients with MS whose data were gleaned from a multi-study database, aggregated over 16 years. Linear mixed effects modeling was applied to estimate the average rate of decline on Symbol Digit Modalities Test (SDMT) performance and to predict rates of decline using baseline clinical variables. They found:
- Participants exhibited an average estimated decline of 0.22 SDMT raw-score points/year.
- There was a significant main effect of time from baseline (t = −2.78), test form (t = 2.13), disease course (t = 2.91), age (t = −2.76), sex (t = −2.71), subjective cognitive impairment (t = −2.00), premorbid verbal intelligence (t = 5.14), and trait Conscientiousness (t = 2.69).
- A significant interaction emerged for Conscientiousness and time from baseline (t = 2.57).
Fuchs TA, Wojcik C, Wilding GE, et al. Trait Conscientiousness predicts rate of longitudinal SDMT decline in multiple sclerosis. [Published online ahead of print January 7, 2019]. Mult Scler. doi:10.1177%2F1352458518820272.
Higher baseline trait conscientiousness predicts slower rates of longitudinal cognitive decline in multiple sclerosis (MS), according to a recent study. Researchers conducted a retrospective analysis of 531 patients with MS whose data were gleaned from a multi-study database, aggregated over 16 years. Linear mixed effects modeling was applied to estimate the average rate of decline on Symbol Digit Modalities Test (SDMT) performance and to predict rates of decline using baseline clinical variables. They found:
- Participants exhibited an average estimated decline of 0.22 SDMT raw-score points/year.
- There was a significant main effect of time from baseline (t = −2.78), test form (t = 2.13), disease course (t = 2.91), age (t = −2.76), sex (t = −2.71), subjective cognitive impairment (t = −2.00), premorbid verbal intelligence (t = 5.14), and trait Conscientiousness (t = 2.69).
- A significant interaction emerged for Conscientiousness and time from baseline (t = 2.57).
Fuchs TA, Wojcik C, Wilding GE, et al. Trait Conscientiousness predicts rate of longitudinal SDMT decline in multiple sclerosis. [Published online ahead of print January 7, 2019]. Mult Scler. doi:10.1177%2F1352458518820272.
Minimally invasive ICH lysis safely helps when clot adequately shrinks
HONOLULU – A minimally invasive approach to lysing an intracerebral hemorrhage clot was safe but failed to produce a statistically significant improvement in long-term functional outcome when compared with usual medical management in a phase 3 randomized trial of 499 patients. However, the results also showed that when the procedure met its acute goal of cutting residual clot to a volume of 15 mL or less, it significantly boosted the percentage of patients with a modified Rankin Scale score of 0-3 when assessed a year after treatment, Daniel F. Hanley Jr., MD, said at the International Stroke Conference, sponsored by the American Heart Association.
“Improved function and increased survival was produced by surgical [clot] reduction to 15 mL or less,” said Dr. Hanley, professor of neurology at Johns Hopkins University, Baltimore, and one of the organizers of the MISTIE III trial.
When assessed by another measure, treated patients showed significant, long-term functional improvement compared with controls when their clot burden dropped by at least 70% following the lytic procedure.
“This is the first description of specific thresholds of hematoma evacuation that impact functional outcomes in intracerebral hemorrhage surgery trials,” said Issam A. Awad, MD, professor of surgery and director of neurovascular surgery at the University of Chicago and coprincipal investigator of the trial.
The problem in the trial was that the surgeons who performed the interventions did not treat many patients aggressively enough to reach these thresholds. They achieved the prespecified goal of residual clot of 15 mL or less in 59% of patients, Dr. Hanley reported, even though the study protocol called for serial infusions of 1 mg of tissue plasminogen activator (Alteplase) into the clot via a placed catheter as many as nine times, administered at 8 hour intervals, with treatment to continue until patients reached the goal residual volume or until they had received all nine doses. In actual practice during the study, operators administered a median of four lytic doses.
“We showed that this goal was important, but not all sites embraced the goal,” Dr. Hanley said. Even though the participating clinicians had a specific interest in intracerebral hemorrhage patients and in this procedure, several nonetheless “had a poor understanding of the goal,” he said in an interview. He attributed the less-than-aggressive approach many operators took to the safety concern that further doses of the lytic drug could trigger recurrent hemorrhage.
“We showed that the goal was important. I think they will embrace the [hematoma evacuation] goal when they see these data,” Dr. Hanley predicted.
An as-treated analysis of the data that focused on the 145 of 246 patients who were treated with minimally invasive lysis and reached the target residual volume and who were then functionally assessed a year later, showed that the rate of patients with a modified Rankin Scale score of 0-3 was 53%, compared with 42% among the controls, an 11% difference.
This shows “a large treatment effect. This is a big, transformative treatment,” Dr. Hanley said. “Our data clearly show that more than half the patients had a positive outcome when their surgeons were more aggressive about clot removal.” He cautioned that the trial was not just about the volume of clot removed but was also about doing it in a gentle way, with a minimum of tissue trauma. Other approaches to reducing hematoma volume may be faster or more complete but they cannot now match the record of safety and efficacy documented in MISTIE III for minimally invasive clot lysis, Dr. Hanley noted.
MISTIE III (Minimally Invasive Surgery Plus Rt-PA for ICH Evacuation Phase III) enrolled patients at 78 centers in the United States and several other countries during 2013-2017. Patients had to enroll 12-72 hours after onset and present with a hematoma volume of at least 30 mL. Participating neurosurgeons used image-guided neuronavigation to place a 4- to 6-mm cannula through the clot, ideally straight through the hematoma’s long axis and with the tip placed within the largest clot segment. Among the 110 surgeons who performed this procedure during the study, 88% had never done it before, and operator and site experience linked with better performance. No surgeon who had already performed four minimally invasive lytic cases, and no center that had already performed seven cases, had a subsequent patient with a residual volume that exceeded 30 mL, Dr. Awad said. The surgical experience during the trial showed that catheter repositioning and using a second catheter were both safe ways to maximize evacuation of the hematoma, he added.
The trial’s primary endpoint, the rate of patients with a modified Rankin Scale score of 0-3 at 1 year after treatment in a modified intention-to-treat analysis that included all patients regardless of the amount of hematoma evacuation they received, showed a 45% rate among the patients who underwent minimally invasive lysis and a 41% rate among those in the control arm, a difference that was not statistically significant. Safety assessments showed that patients treated with the investigational approach had significantly lower mortality 7 days after treatment: 0.8% compared with 4.0%. By 1 year after treatment, mortality was cut by one-third in the minimally invasive patients, compared with the control patients, also a statistically significant difference. The rates of symptomatic bleeds and brain infections were similar in the two treatment groups, Dr. Hanley reported. Concurrently with his talk at the conference, a paper with the primary study results appeared online (Lancet. 2019 Feb 7. doi: 10.1016/S0140-6736[19]30195-3).
MISTIE III was supported by the National Institute of Neurological Disorders and Stroke. The trial received no commercial support aside from free tissue plasminogen activator (Alteplase) supplied by Genentech. Dr. Hanley has been a consultant to BrainScope, Neurotrope, Portola, and Op2Lysis, and he has served as an expert witness on behalf of Medtronic. Dr. Awad had no disclosures.
SOURCE: Hanley DF et al. ISC 2019, Abstract LB4; Awad IS et al. ISC 2019, Abstract LB5.
The MISTIE III results showed that this approach to clot lysis is safe and feasible for surgeons to perform even if they have had limited experience with the procedure. I think that based on these findings, minimally-invasive clot lysis will become widely adopted. It’s pretty simple to perform in most patients. At my center in Houston, we already use it on a routine basis in patients like those enrolled in MISTIE III.
Some people may focus on the neutral primary endpoint result from the MISTIE III trial, but the study made two very important findings. First, the results showed that we have improved medical management of patients who have an intracerebral hemorrhage. The 1-year functional outcomes of patients in the control group of the study who had a 41% rate of scoring 0-3 on the modified Rankin Scale after 1 year was much better than we have seen in these patients in the past. Second, the results gave a clear signal that the more clot an operator can lyse to get the residual clot to 15 mL or less, the better patients do. Faster clot lysis might also be important.
It’s hard to call the minimally-invasive approach used in MISTIE III the new standard-of-care approach for these patients given the neutral primary endpoint of the study. On the other hand, if you have a treatment that poses little risk to patients and that you know could benefit them if it succeeds in minimizing residual clot volume, then it makes sense to try it. It’s a low-risk treatment with reasonable potential for benefit. Its demonstrated safety is very important.
Louise D. McCullough, MD, PhD , is a professor of neurology and chair of neurology at the University of Texas, Houston. She had no disclosures. She made these comments in an interview.
The MISTIE III results showed that this approach to clot lysis is safe and feasible for surgeons to perform even if they have had limited experience with the procedure. I think that based on these findings, minimally-invasive clot lysis will become widely adopted. It’s pretty simple to perform in most patients. At my center in Houston, we already use it on a routine basis in patients like those enrolled in MISTIE III.
Some people may focus on the neutral primary endpoint result from the MISTIE III trial, but the study made two very important findings. First, the results showed that we have improved medical management of patients who have an intracerebral hemorrhage. The 1-year functional outcomes of patients in the control group of the study who had a 41% rate of scoring 0-3 on the modified Rankin Scale after 1 year was much better than we have seen in these patients in the past. Second, the results gave a clear signal that the more clot an operator can lyse to get the residual clot to 15 mL or less, the better patients do. Faster clot lysis might also be important.
It’s hard to call the minimally-invasive approach used in MISTIE III the new standard-of-care approach for these patients given the neutral primary endpoint of the study. On the other hand, if you have a treatment that poses little risk to patients and that you know could benefit them if it succeeds in minimizing residual clot volume, then it makes sense to try it. It’s a low-risk treatment with reasonable potential for benefit. Its demonstrated safety is very important.
Louise D. McCullough, MD, PhD , is a professor of neurology and chair of neurology at the University of Texas, Houston. She had no disclosures. She made these comments in an interview.
The MISTIE III results showed that this approach to clot lysis is safe and feasible for surgeons to perform even if they have had limited experience with the procedure. I think that based on these findings, minimally-invasive clot lysis will become widely adopted. It’s pretty simple to perform in most patients. At my center in Houston, we already use it on a routine basis in patients like those enrolled in MISTIE III.
Some people may focus on the neutral primary endpoint result from the MISTIE III trial, but the study made two very important findings. First, the results showed that we have improved medical management of patients who have an intracerebral hemorrhage. The 1-year functional outcomes of patients in the control group of the study who had a 41% rate of scoring 0-3 on the modified Rankin Scale after 1 year was much better than we have seen in these patients in the past. Second, the results gave a clear signal that the more clot an operator can lyse to get the residual clot to 15 mL or less, the better patients do. Faster clot lysis might also be important.
It’s hard to call the minimally-invasive approach used in MISTIE III the new standard-of-care approach for these patients given the neutral primary endpoint of the study. On the other hand, if you have a treatment that poses little risk to patients and that you know could benefit them if it succeeds in minimizing residual clot volume, then it makes sense to try it. It’s a low-risk treatment with reasonable potential for benefit. Its demonstrated safety is very important.
Louise D. McCullough, MD, PhD , is a professor of neurology and chair of neurology at the University of Texas, Houston. She had no disclosures. She made these comments in an interview.
HONOLULU – A minimally invasive approach to lysing an intracerebral hemorrhage clot was safe but failed to produce a statistically significant improvement in long-term functional outcome when compared with usual medical management in a phase 3 randomized trial of 499 patients. However, the results also showed that when the procedure met its acute goal of cutting residual clot to a volume of 15 mL or less, it significantly boosted the percentage of patients with a modified Rankin Scale score of 0-3 when assessed a year after treatment, Daniel F. Hanley Jr., MD, said at the International Stroke Conference, sponsored by the American Heart Association.
“Improved function and increased survival was produced by surgical [clot] reduction to 15 mL or less,” said Dr. Hanley, professor of neurology at Johns Hopkins University, Baltimore, and one of the organizers of the MISTIE III trial.
When assessed by another measure, treated patients showed significant, long-term functional improvement compared with controls when their clot burden dropped by at least 70% following the lytic procedure.
“This is the first description of specific thresholds of hematoma evacuation that impact functional outcomes in intracerebral hemorrhage surgery trials,” said Issam A. Awad, MD, professor of surgery and director of neurovascular surgery at the University of Chicago and coprincipal investigator of the trial.
The problem in the trial was that the surgeons who performed the interventions did not treat many patients aggressively enough to reach these thresholds. They achieved the prespecified goal of residual clot of 15 mL or less in 59% of patients, Dr. Hanley reported, even though the study protocol called for serial infusions of 1 mg of tissue plasminogen activator (Alteplase) into the clot via a placed catheter as many as nine times, administered at 8 hour intervals, with treatment to continue until patients reached the goal residual volume or until they had received all nine doses. In actual practice during the study, operators administered a median of four lytic doses.
“We showed that this goal was important, but not all sites embraced the goal,” Dr. Hanley said. Even though the participating clinicians had a specific interest in intracerebral hemorrhage patients and in this procedure, several nonetheless “had a poor understanding of the goal,” he said in an interview. He attributed the less-than-aggressive approach many operators took to the safety concern that further doses of the lytic drug could trigger recurrent hemorrhage.
“We showed that the goal was important. I think they will embrace the [hematoma evacuation] goal when they see these data,” Dr. Hanley predicted.
An as-treated analysis of the data that focused on the 145 of 246 patients who were treated with minimally invasive lysis and reached the target residual volume and who were then functionally assessed a year later, showed that the rate of patients with a modified Rankin Scale score of 0-3 was 53%, compared with 42% among the controls, an 11% difference.
This shows “a large treatment effect. This is a big, transformative treatment,” Dr. Hanley said. “Our data clearly show that more than half the patients had a positive outcome when their surgeons were more aggressive about clot removal.” He cautioned that the trial was not just about the volume of clot removed but was also about doing it in a gentle way, with a minimum of tissue trauma. Other approaches to reducing hematoma volume may be faster or more complete but they cannot now match the record of safety and efficacy documented in MISTIE III for minimally invasive clot lysis, Dr. Hanley noted.
MISTIE III (Minimally Invasive Surgery Plus Rt-PA for ICH Evacuation Phase III) enrolled patients at 78 centers in the United States and several other countries during 2013-2017. Patients had to enroll 12-72 hours after onset and present with a hematoma volume of at least 30 mL. Participating neurosurgeons used image-guided neuronavigation to place a 4- to 6-mm cannula through the clot, ideally straight through the hematoma’s long axis and with the tip placed within the largest clot segment. Among the 110 surgeons who performed this procedure during the study, 88% had never done it before, and operator and site experience linked with better performance. No surgeon who had already performed four minimally invasive lytic cases, and no center that had already performed seven cases, had a subsequent patient with a residual volume that exceeded 30 mL, Dr. Awad said. The surgical experience during the trial showed that catheter repositioning and using a second catheter were both safe ways to maximize evacuation of the hematoma, he added.
The trial’s primary endpoint, the rate of patients with a modified Rankin Scale score of 0-3 at 1 year after treatment in a modified intention-to-treat analysis that included all patients regardless of the amount of hematoma evacuation they received, showed a 45% rate among the patients who underwent minimally invasive lysis and a 41% rate among those in the control arm, a difference that was not statistically significant. Safety assessments showed that patients treated with the investigational approach had significantly lower mortality 7 days after treatment: 0.8% compared with 4.0%. By 1 year after treatment, mortality was cut by one-third in the minimally invasive patients, compared with the control patients, also a statistically significant difference. The rates of symptomatic bleeds and brain infections were similar in the two treatment groups, Dr. Hanley reported. Concurrently with his talk at the conference, a paper with the primary study results appeared online (Lancet. 2019 Feb 7. doi: 10.1016/S0140-6736[19]30195-3).
MISTIE III was supported by the National Institute of Neurological Disorders and Stroke. The trial received no commercial support aside from free tissue plasminogen activator (Alteplase) supplied by Genentech. Dr. Hanley has been a consultant to BrainScope, Neurotrope, Portola, and Op2Lysis, and he has served as an expert witness on behalf of Medtronic. Dr. Awad had no disclosures.
SOURCE: Hanley DF et al. ISC 2019, Abstract LB4; Awad IS et al. ISC 2019, Abstract LB5.
HONOLULU – A minimally invasive approach to lysing an intracerebral hemorrhage clot was safe but failed to produce a statistically significant improvement in long-term functional outcome when compared with usual medical management in a phase 3 randomized trial of 499 patients. However, the results also showed that when the procedure met its acute goal of cutting residual clot to a volume of 15 mL or less, it significantly boosted the percentage of patients with a modified Rankin Scale score of 0-3 when assessed a year after treatment, Daniel F. Hanley Jr., MD, said at the International Stroke Conference, sponsored by the American Heart Association.
“Improved function and increased survival was produced by surgical [clot] reduction to 15 mL or less,” said Dr. Hanley, professor of neurology at Johns Hopkins University, Baltimore, and one of the organizers of the MISTIE III trial.
When assessed by another measure, treated patients showed significant, long-term functional improvement compared with controls when their clot burden dropped by at least 70% following the lytic procedure.
“This is the first description of specific thresholds of hematoma evacuation that impact functional outcomes in intracerebral hemorrhage surgery trials,” said Issam A. Awad, MD, professor of surgery and director of neurovascular surgery at the University of Chicago and coprincipal investigator of the trial.
The problem in the trial was that the surgeons who performed the interventions did not treat many patients aggressively enough to reach these thresholds. They achieved the prespecified goal of residual clot of 15 mL or less in 59% of patients, Dr. Hanley reported, even though the study protocol called for serial infusions of 1 mg of tissue plasminogen activator (Alteplase) into the clot via a placed catheter as many as nine times, administered at 8 hour intervals, with treatment to continue until patients reached the goal residual volume or until they had received all nine doses. In actual practice during the study, operators administered a median of four lytic doses.
“We showed that this goal was important, but not all sites embraced the goal,” Dr. Hanley said. Even though the participating clinicians had a specific interest in intracerebral hemorrhage patients and in this procedure, several nonetheless “had a poor understanding of the goal,” he said in an interview. He attributed the less-than-aggressive approach many operators took to the safety concern that further doses of the lytic drug could trigger recurrent hemorrhage.
“We showed that the goal was important. I think they will embrace the [hematoma evacuation] goal when they see these data,” Dr. Hanley predicted.
An as-treated analysis of the data that focused on the 145 of 246 patients who were treated with minimally invasive lysis and reached the target residual volume and who were then functionally assessed a year later, showed that the rate of patients with a modified Rankin Scale score of 0-3 was 53%, compared with 42% among the controls, an 11% difference.
This shows “a large treatment effect. This is a big, transformative treatment,” Dr. Hanley said. “Our data clearly show that more than half the patients had a positive outcome when their surgeons were more aggressive about clot removal.” He cautioned that the trial was not just about the volume of clot removed but was also about doing it in a gentle way, with a minimum of tissue trauma. Other approaches to reducing hematoma volume may be faster or more complete but they cannot now match the record of safety and efficacy documented in MISTIE III for minimally invasive clot lysis, Dr. Hanley noted.
MISTIE III (Minimally Invasive Surgery Plus Rt-PA for ICH Evacuation Phase III) enrolled patients at 78 centers in the United States and several other countries during 2013-2017. Patients had to enroll 12-72 hours after onset and present with a hematoma volume of at least 30 mL. Participating neurosurgeons used image-guided neuronavigation to place a 4- to 6-mm cannula through the clot, ideally straight through the hematoma’s long axis and with the tip placed within the largest clot segment. Among the 110 surgeons who performed this procedure during the study, 88% had never done it before, and operator and site experience linked with better performance. No surgeon who had already performed four minimally invasive lytic cases, and no center that had already performed seven cases, had a subsequent patient with a residual volume that exceeded 30 mL, Dr. Awad said. The surgical experience during the trial showed that catheter repositioning and using a second catheter were both safe ways to maximize evacuation of the hematoma, he added.
The trial’s primary endpoint, the rate of patients with a modified Rankin Scale score of 0-3 at 1 year after treatment in a modified intention-to-treat analysis that included all patients regardless of the amount of hematoma evacuation they received, showed a 45% rate among the patients who underwent minimally invasive lysis and a 41% rate among those in the control arm, a difference that was not statistically significant. Safety assessments showed that patients treated with the investigational approach had significantly lower mortality 7 days after treatment: 0.8% compared with 4.0%. By 1 year after treatment, mortality was cut by one-third in the minimally invasive patients, compared with the control patients, also a statistically significant difference. The rates of symptomatic bleeds and brain infections were similar in the two treatment groups, Dr. Hanley reported. Concurrently with his talk at the conference, a paper with the primary study results appeared online (Lancet. 2019 Feb 7. doi: 10.1016/S0140-6736[19]30195-3).
MISTIE III was supported by the National Institute of Neurological Disorders and Stroke. The trial received no commercial support aside from free tissue plasminogen activator (Alteplase) supplied by Genentech. Dr. Hanley has been a consultant to BrainScope, Neurotrope, Portola, and Op2Lysis, and he has served as an expert witness on behalf of Medtronic. Dr. Awad had no disclosures.
SOURCE: Hanley DF et al. ISC 2019, Abstract LB4; Awad IS et al. ISC 2019, Abstract LB5.
REPORTING FROM ISC 2019
Key clinical point: Minimally-invasive intracerebral clot lysis was safe and often effective when the residual clot shrank to 15 mL or less.
Major finding: One year after entry, 45% of MISTIE-treated patients and 41% of controls had a modified Rankin Scale score of 0-3.
Study details: MISTIE III, a multicenter, international, randomized trial of 499 patients.
Disclosures: MISTIE III was supported by the National Institute of Neurological Disorders and Stroke. The trial received no commercial support aside from free tissue plasminogen activator (Alteplase) supplied by Genentech. Dr. Hanley has been a consultant to BrainScope, Neurotrope, Portola, and Op2Lysis, and he has served as an expert witness on behalf of Medtronic. Dr. Awad had no disclosures.
Source: Hanley DF et al. ISC 2019, Abstract LB4; Awad IS et al. ISC 2019, Abstract LB5.
