MDedge Psychiatry

For this Psychiatry Leaders’ Perspectives, Awais Aftab, MD, interviewed Alan F. Schatzberg, MD. Dr. Schatzberg is the Kenneth T. Norris, Jr., Professor of Psychiatry and Behavioral Sciences at Stanford University. He served as the Chair of the Department at Stanford until 2010 and currently directs the Stanford Mood Disorders Center. He was the 136th president of the American Psychiatric Association (APA) (2009-2010). He has been an active investigator in the biology and psycho­pharmacology of depressive disorders, and has authored more than 700 publications and abstracts, including Schatzberg’s Manual of Clinical Psychopharmacology. Dr. Schatzberg is also the coeditor of the Textbook of Psychopharmacology with Charles B. Nemeroff, MD, PhD. He is a Past President of the American College of Neuropsychopharmacology (ACNP) and the Society of Biological Psychiatry, and was also the Secretary-General of the International Society of Psychoneuroendocrinology (ISPNE). In 2003, he was elected to the Institute of Medicine of the National Academy of Sciences (National Academy of Medicine). He has received numerous prestigious awards, including the 2005 Distinguished Service in Psychiatry Award from the American College of Psychiatrists, the 2005 Falcone Award from the National Alliance for Research in Schizophrenia and Affective Disorders, the 2014 Kraepelin Gold Medal from the Max Planck Institute of Psychiatry, the 2015 Gold Medal from the Society of Biological Psychiatry, the 2015 Lifetime Achievement Award of the ISPNE, the 2017 Julius Axelrod Mentorship Award from the ACNP, the 2018 Donald Klein, MD, Lifetime Achievement Award from the American Society of Clinical Psychopharmacology, and the 2018 Jules Marmor, MD, Award for Biopsychosocial Research from the APA.

Dr. Aftab: You have devoted much of your career to the development of psychopharmacology. What is your perspective on where the field of psychopharmacology stands at present, especially amid the widespread recognition of “treatment resistance” as a pervasive phenomenon and the scarcity of validated neurobiologic etiological models for psychiatric disorders?

Dr. Schatzberg: We have made considerable progress in the development of new classes of agents for major depression, but as we develop new agents, we still see a large percentage of patients who do not seem to demonstrate adequate responses, particularly in major depressive disorder. This has driven us to look for agents that work differently than previous ones. Although we have some new agents with seeming efficacy and newer mechanisms of action, eg, esketamine, these have largely been derived from clinical, often serendipitous, observations of antidepressant effects rather than from prospective development based on a known pharmacological effect or a biological construct of the disorder. Another intriguing and possibly effective anxiolytic and antidepressive agent is psilocybin, whose potential use is largely derived from clinicians who found it helpful in their practices in combination with psychotherapy. These 2 demonstrate how as we branch out into new territory, we find ourselves moving more and more toward drugs of known clinical risk; eg, mind-altering agents or drugs of abuse. These agents may offer risk-benefit ratios that can ultimately prove to be less attractive than what we might have wanted when we ventured on the journey. Unfortunately, there has been little dialogue about the limitations of several of these agents.

In the case of esketamine, the notion has been that the drug is a blocker of the N-methyl-d-aspartate (NMDA) glutamate receptor, suggesting it is relatively safe. However, we and others have now clearly demonstrated that the antidepressant effect in humans and the antidepressant behavioral effects in rodents are mediated via the mu opioid receptor.^1-3 This implies an abuse and dependence risk, and it is concerning that there has been much emphasis on ketamine’s effect on the NMDA glutamate receptor and not enough on this opioid effect, even though the very active enantiomer esketamine demonstrates relatively equal micromolar binding to both mu and NMDA receptors. Understanding the biology of major depression better and elucidating the key mechanisms of action of agents are both needed if we are to develop more effective and still safe agents.

One approach that has been applied recently is target validation that purports to use functional MRI to assess behavioral and cognitive effects of drugs to allow inferences regarding efficacy in specific disorders. As we have discussed in a recent paper published in the American Journal of Psychiatry,⁴ this can be quite misleading and may provide both false positive and negative information. From my perspective, these tests do not appear sensitive enough to screen for patients having a disorder, nor for assessing possible drug effects in those patients. Thus, it is unclear if they can provide answers today that we can be confident in.

Continue to: Dr. Aftab...

For this Psychiatry Leaders’ Perspectives, Awais Aftab, MD, interviewed Alan F. Schatzberg, MD. Dr. Schatzberg is the Kenneth T. Norris, Jr., Professor of Psychiatry and Behavioral Sciences at Stanford University. He served as the Chair of the Department at Stanford until 2010 and currently directs the Stanford Mood Disorders Center. He was the 136th president of the American Psychiatric Association (APA) (2009-2010). He has been an active investigator in the biology and psycho­pharmacology of depressive disorders, and has authored more than 700 publications and abstracts, including Schatzberg’s Manual of Clinical Psychopharmacology. Dr. Schatzberg is also the coeditor of the Textbook of Psychopharmacology with Charles B. Nemeroff, MD, PhD. He is a Past President of the American College of Neuropsychopharmacology (ACNP) and the Society of Biological Psychiatry, and was also the Secretary-General of the International Society of Psychoneuroendocrinology (ISPNE). In 2003, he was elected to the Institute of Medicine of the National Academy of Sciences (National Academy of Medicine). He has received numerous prestigious awards, including the 2005 Distinguished Service in Psychiatry Award from the American College of Psychiatrists, the 2005 Falcone Award from the National Alliance for Research in Schizophrenia and Affective Disorders, the 2014 Kraepelin Gold Medal from the Max Planck Institute of Psychiatry, the 2015 Gold Medal from the Society of Biological Psychiatry, the 2015 Lifetime Achievement Award of the ISPNE, the 2017 Julius Axelrod Mentorship Award from the ACNP, the 2018 Donald Klein, MD, Lifetime Achievement Award from the American Society of Clinical Psychopharmacology, and the 2018 Jules Marmor, MD, Award for Biopsychosocial Research from the APA.

Dr. Aftab: You have devoted much of your career to the development of psychopharmacology. What is your perspective on where the field of psychopharmacology stands at present, especially amid the widespread recognition of “treatment resistance” as a pervasive phenomenon and the scarcity of validated neurobiologic etiological models for psychiatric disorders?

Dr. Schatzberg: We have made considerable progress in the development of new classes of agents for major depression, but as we develop new agents, we still see a large percentage of patients who do not seem to demonstrate adequate responses, particularly in major depressive disorder. This has driven us to look for agents that work differently than previous ones. Although we have some new agents with seeming efficacy and newer mechanisms of action, eg, esketamine, these have largely been derived from clinical, often serendipitous, observations of antidepressant effects rather than from prospective development based on a known pharmacological effect or a biological construct of the disorder. Another intriguing and possibly effective anxiolytic and antidepressive agent is psilocybin, whose potential use is largely derived from clinicians who found it helpful in their practices in combination with psychotherapy. These 2 demonstrate how as we branch out into new territory, we find ourselves moving more and more toward drugs of known clinical risk; eg, mind-altering agents or drugs of abuse. These agents may offer risk-benefit ratios that can ultimately prove to be less attractive than what we might have wanted when we ventured on the journey. Unfortunately, there has been little dialogue about the limitations of several of these agents.

In the case of esketamine, the notion has been that the drug is a blocker of the N-methyl-d-aspartate (NMDA) glutamate receptor, suggesting it is relatively safe. However, we and others have now clearly demonstrated that the antidepressant effect in humans and the antidepressant behavioral effects in rodents are mediated via the mu opioid receptor.^1-3 This implies an abuse and dependence risk, and it is concerning that there has been much emphasis on ketamine’s effect on the NMDA glutamate receptor and not enough on this opioid effect, even though the very active enantiomer esketamine demonstrates relatively equal micromolar binding to both mu and NMDA receptors. Understanding the biology of major depression better and elucidating the key mechanisms of action of agents are both needed if we are to develop more effective and still safe agents.

One approach that has been applied recently is target validation that purports to use functional MRI to assess behavioral and cognitive effects of drugs to allow inferences regarding efficacy in specific disorders. As we have discussed in a recent paper published in the American Journal of Psychiatry,⁴ this can be quite misleading and may provide both false positive and negative information. From my perspective, these tests do not appear sensitive enough to screen for patients having a disorder, nor for assessing possible drug effects in those patients. Thus, it is unclear if they can provide answers today that we can be confident in.

Continue to: Dr. Aftab...

For this Psychiatry Leaders’ Perspectives, Awais Aftab, MD, interviewed Alan F. Schatzberg, MD. Dr. Schatzberg is the Kenneth T. Norris, Jr., Professor of Psychiatry and Behavioral Sciences at Stanford University. He served as the Chair of the Department at Stanford until 2010 and currently directs the Stanford Mood Disorders Center. He was the 136th president of the American Psychiatric Association (APA) (2009-2010). He has been an active investigator in the biology and psycho­pharmacology of depressive disorders, and has authored more than 700 publications and abstracts, including Schatzberg’s Manual of Clinical Psychopharmacology. Dr. Schatzberg is also the coeditor of the Textbook of Psychopharmacology with Charles B. Nemeroff, MD, PhD. He is a Past President of the American College of Neuropsychopharmacology (ACNP) and the Society of Biological Psychiatry, and was also the Secretary-General of the International Society of Psychoneuroendocrinology (ISPNE). In 2003, he was elected to the Institute of Medicine of the National Academy of Sciences (National Academy of Medicine). He has received numerous prestigious awards, including the 2005 Distinguished Service in Psychiatry Award from the American College of Psychiatrists, the 2005 Falcone Award from the National Alliance for Research in Schizophrenia and Affective Disorders, the 2014 Kraepelin Gold Medal from the Max Planck Institute of Psychiatry, the 2015 Gold Medal from the Society of Biological Psychiatry, the 2015 Lifetime Achievement Award of the ISPNE, the 2017 Julius Axelrod Mentorship Award from the ACNP, the 2018 Donald Klein, MD, Lifetime Achievement Award from the American Society of Clinical Psychopharmacology, and the 2018 Jules Marmor, MD, Award for Biopsychosocial Research from the APA.

Dr. Aftab: You have devoted much of your career to the development of psychopharmacology. What is your perspective on where the field of psychopharmacology stands at present, especially amid the widespread recognition of “treatment resistance” as a pervasive phenomenon and the scarcity of validated neurobiologic etiological models for psychiatric disorders?

Dr. Schatzberg: We have made considerable progress in the development of new classes of agents for major depression, but as we develop new agents, we still see a large percentage of patients who do not seem to demonstrate adequate responses, particularly in major depressive disorder. This has driven us to look for agents that work differently than previous ones. Although we have some new agents with seeming efficacy and newer mechanisms of action, eg, esketamine, these have largely been derived from clinical, often serendipitous, observations of antidepressant effects rather than from prospective development based on a known pharmacological effect or a biological construct of the disorder. Another intriguing and possibly effective anxiolytic and antidepressive agent is psilocybin, whose potential use is largely derived from clinicians who found it helpful in their practices in combination with psychotherapy. These 2 demonstrate how as we branch out into new territory, we find ourselves moving more and more toward drugs of known clinical risk; eg, mind-altering agents or drugs of abuse. These agents may offer risk-benefit ratios that can ultimately prove to be less attractive than what we might have wanted when we ventured on the journey. Unfortunately, there has been little dialogue about the limitations of several of these agents.

In the case of esketamine, the notion has been that the drug is a blocker of the N-methyl-d-aspartate (NMDA) glutamate receptor, suggesting it is relatively safe. However, we and others have now clearly demonstrated that the antidepressant effect in humans and the antidepressant behavioral effects in rodents are mediated via the mu opioid receptor.^1-3 This implies an abuse and dependence risk, and it is concerning that there has been much emphasis on ketamine’s effect on the NMDA glutamate receptor and not enough on this opioid effect, even though the very active enantiomer esketamine demonstrates relatively equal micromolar binding to both mu and NMDA receptors. Understanding the biology of major depression better and elucidating the key mechanisms of action of agents are both needed if we are to develop more effective and still safe agents.

One approach that has been applied recently is target validation that purports to use functional MRI to assess behavioral and cognitive effects of drugs to allow inferences regarding efficacy in specific disorders. As we have discussed in a recent paper published in the American Journal of Psychiatry,⁴ this can be quite misleading and may provide both false positive and negative information. From my perspective, these tests do not appear sensitive enough to screen for patients having a disorder, nor for assessing possible drug effects in those patients. Thus, it is unclear if they can provide answers today that we can be confident in.

Continue to: Dr. Aftab...

Inpatient violence is a significant problem for psychiatric facilities because it can have serious physical and psychological consequences for both staff and patients.¹ Victimized staff can experience decreased productivity and emotional distress, while victimized patients can experience disrupted treatment and delayed discharge.¹ Twenty-five to 35% of psychiatric inpatients display violent behavior during their hospitalization.¹ A subset are extreme offenders.^1,2 This small group of violent patients accounts for the majority of inpatient violence and the most serious injuries.^1,2

Reducing inpatient violence starts with conducting a targeted violence risk assessment to identify patients who are at elevated risk of being violent. Although conducting a targeted violence risk assessment is beyond the scope of this article, here I outline practical steps that clinicians can take to reduce the risk of inpatient violence. These steps complement and overlap with those I described in “Workplace violence: Enhance your safety in outpatient settings” (Pearls, Current Psychiatry, August 2021, p. 37-38). These approaches should be customized for your setting with the possible assistance and input of legal counsel, risk management, and law enforcement.³

Identify underlying motives. Inpatient violence is often a result of 3 primary psychiatric etiologies: difficulty with impulse control, symptoms of psychosis, or predatory traits.¹ Impulsivity drives most of the violence on inpatient units, followed by predatory violence and symptoms of psychosis.¹ Once you identify the psychiatric motive, you can develop an individualized, tailored treatment plan to reduce the risk of violence. The treatment plan can include using de-escalation techniques, administering scheduled and as-needed medications to target underlying symptoms, having patients assume responsibility for their behaviors, holding patients accountable for their behaviors, and other psychosocial interventions.¹ Use seclusion and restraint only when it is the least restrictive means of providing safety.^1,4

Develop plans and policies. As you would do in an outpatient setting, assess for hazards within the inpatient unit. Plan for the possible types of violence that may occur on the unit (eg, physical violence against hospital personnel and/or other patients, verbal harassment, etc).³ Develop policies and procedures to identify, communicate, track, and document patients’ concerning behaviors (eg, posting a safety board where staff can record aggressive behaviors and other safety issues).^3,4 When developing these plans and policies, include patients by creating patient/staff workgroups to develop expectations for civil behavior that apply to both patients and staff, as well as training patients to co-lead groups dealing with accepting responsibility for their own recovery.⁵ These plans and policies should include informing patients that threats and violence will not be tolerated. Frequently review these plans and policies with patients and staff.

Provide communication and education. Maintain strong psychiatric leadership on the unit that encourages open lines of communication. Encourage staff to promptly report incidents. Frequently ask staff if they have any safety concerns, and solicit their opinions on how to reduce risks.⁴ Include discussions about safety during staff and community meetings. Communicate patients’ behaviors that are distressing or undesired (eg, threats, harassment, etc) to all unit personnel.³ Notify staff when you plan to interact with a patient who is at risk for violence or is acutely agitated.⁴ Teach staff how to recognize the nonverbal warning signs of behavior escalation and provide training on proper de-escalation and response.^3,4 Also train staff on how to develop strong therapeutic alliances with patients.¹ After a violent incident, use the postincident debriefing session to gather information that can be used to develop additional interventions and reduce the risk of subsequent violence.¹

Implement common-sense strategies. Ensure that there are adequate numbers of nursing staff during each shift.¹ Avoid overcrowded units, hallways, and common areas. Consider additional monitoring during unit transition times, such as during shift changes, meals, and medication administration.¹ Avoid excessive noise.¹ Employ one-to-one staff observation as clinically indicated.¹ Avoid taking an authoritarian stance when explaining to patients why their requests have been denied⁴; if possible, when you are unable to meet a patient’s demands, offer them choices.^1,4 If feasible, accompany patients to a calmer space where they can de-escalate.¹ Install video surveillance cameras at entrances, exits, and other strategic locations and post signs signaling their presence.³ Install panic buttons at the nursing station and other areas (eg, restrooms).³

Ensure your personal safety. As mentioned previously, do not interact with a patient who has recently been aggressive or has voiced threats without adequate staff support.⁴ During the patient encounter, leave space between you and the patient.¹ Avoid having your back to the exit of the room,^3,4 and make sure the patient is not blocking the exit and that you can leave the room quickly if needed. Don’t wear anything that could be used as a weapon against you (eg, ties or necklaces) or could impede your escape.⁴ Avoid wearing valuables that might be damaged during a “take down.”⁴ If feasible, wear an audible alarm.³

Inpatient violence is a significant problem for psychiatric facilities because it can have serious physical and psychological consequences for both staff and patients.¹ Victimized staff can experience decreased productivity and emotional distress, while victimized patients can experience disrupted treatment and delayed discharge.¹ Twenty-five to 35% of psychiatric inpatients display violent behavior during their hospitalization.¹ A subset are extreme offenders.^1,2 This small group of violent patients accounts for the majority of inpatient violence and the most serious injuries.^1,2

Reducing inpatient violence starts with conducting a targeted violence risk assessment to identify patients who are at elevated risk of being violent. Although conducting a targeted violence risk assessment is beyond the scope of this article, here I outline practical steps that clinicians can take to reduce the risk of inpatient violence. These steps complement and overlap with those I described in “Workplace violence: Enhance your safety in outpatient settings” (Pearls, Current Psychiatry, August 2021, p. 37-38). These approaches should be customized for your setting with the possible assistance and input of legal counsel, risk management, and law enforcement.³

Identify underlying motives. Inpatient violence is often a result of 3 primary psychiatric etiologies: difficulty with impulse control, symptoms of psychosis, or predatory traits.¹ Impulsivity drives most of the violence on inpatient units, followed by predatory violence and symptoms of psychosis.¹ Once you identify the psychiatric motive, you can develop an individualized, tailored treatment plan to reduce the risk of violence. The treatment plan can include using de-escalation techniques, administering scheduled and as-needed medications to target underlying symptoms, having patients assume responsibility for their behaviors, holding patients accountable for their behaviors, and other psychosocial interventions.¹ Use seclusion and restraint only when it is the least restrictive means of providing safety.^1,4

Develop plans and policies. As you would do in an outpatient setting, assess for hazards within the inpatient unit. Plan for the possible types of violence that may occur on the unit (eg, physical violence against hospital personnel and/or other patients, verbal harassment, etc).³ Develop policies and procedures to identify, communicate, track, and document patients’ concerning behaviors (eg, posting a safety board where staff can record aggressive behaviors and other safety issues).^3,4 When developing these plans and policies, include patients by creating patient/staff workgroups to develop expectations for civil behavior that apply to both patients and staff, as well as training patients to co-lead groups dealing with accepting responsibility for their own recovery.⁵ These plans and policies should include informing patients that threats and violence will not be tolerated. Frequently review these plans and policies with patients and staff.

Provide communication and education. Maintain strong psychiatric leadership on the unit that encourages open lines of communication. Encourage staff to promptly report incidents. Frequently ask staff if they have any safety concerns, and solicit their opinions on how to reduce risks.⁴ Include discussions about safety during staff and community meetings. Communicate patients’ behaviors that are distressing or undesired (eg, threats, harassment, etc) to all unit personnel.³ Notify staff when you plan to interact with a patient who is at risk for violence or is acutely agitated.⁴ Teach staff how to recognize the nonverbal warning signs of behavior escalation and provide training on proper de-escalation and response.^3,4 Also train staff on how to develop strong therapeutic alliances with patients.¹ After a violent incident, use the postincident debriefing session to gather information that can be used to develop additional interventions and reduce the risk of subsequent violence.¹

Implement common-sense strategies. Ensure that there are adequate numbers of nursing staff during each shift.¹ Avoid overcrowded units, hallways, and common areas. Consider additional monitoring during unit transition times, such as during shift changes, meals, and medication administration.¹ Avoid excessive noise.¹ Employ one-to-one staff observation as clinically indicated.¹ Avoid taking an authoritarian stance when explaining to patients why their requests have been denied⁴; if possible, when you are unable to meet a patient’s demands, offer them choices.^1,4 If feasible, accompany patients to a calmer space where they can de-escalate.¹ Install video surveillance cameras at entrances, exits, and other strategic locations and post signs signaling their presence.³ Install panic buttons at the nursing station and other areas (eg, restrooms).³

Ensure your personal safety. As mentioned previously, do not interact with a patient who has recently been aggressive or has voiced threats without adequate staff support.⁴ During the patient encounter, leave space between you and the patient.¹ Avoid having your back to the exit of the room,^3,4 and make sure the patient is not blocking the exit and that you can leave the room quickly if needed. Don’t wear anything that could be used as a weapon against you (eg, ties or necklaces) or could impede your escape.⁴ Avoid wearing valuables that might be damaged during a “take down.”⁴ If feasible, wear an audible alarm.³

Inpatient violence is a significant problem for psychiatric facilities because it can have serious physical and psychological consequences for both staff and patients.¹ Victimized staff can experience decreased productivity and emotional distress, while victimized patients can experience disrupted treatment and delayed discharge.¹ Twenty-five to 35% of psychiatric inpatients display violent behavior during their hospitalization.¹ A subset are extreme offenders.^1,2 This small group of violent patients accounts for the majority of inpatient violence and the most serious injuries.^1,2

Reducing inpatient violence starts with conducting a targeted violence risk assessment to identify patients who are at elevated risk of being violent. Although conducting a targeted violence risk assessment is beyond the scope of this article, here I outline practical steps that clinicians can take to reduce the risk of inpatient violence. These steps complement and overlap with those I described in “Workplace violence: Enhance your safety in outpatient settings” (Pearls, Current Psychiatry, August 2021, p. 37-38). These approaches should be customized for your setting with the possible assistance and input of legal counsel, risk management, and law enforcement.³

Identify underlying motives. Inpatient violence is often a result of 3 primary psychiatric etiologies: difficulty with impulse control, symptoms of psychosis, or predatory traits.¹ Impulsivity drives most of the violence on inpatient units, followed by predatory violence and symptoms of psychosis.¹ Once you identify the psychiatric motive, you can develop an individualized, tailored treatment plan to reduce the risk of violence. The treatment plan can include using de-escalation techniques, administering scheduled and as-needed medications to target underlying symptoms, having patients assume responsibility for their behaviors, holding patients accountable for their behaviors, and other psychosocial interventions.¹ Use seclusion and restraint only when it is the least restrictive means of providing safety.^1,4

Develop plans and policies. As you would do in an outpatient setting, assess for hazards within the inpatient unit. Plan for the possible types of violence that may occur on the unit (eg, physical violence against hospital personnel and/or other patients, verbal harassment, etc).³ Develop policies and procedures to identify, communicate, track, and document patients’ concerning behaviors (eg, posting a safety board where staff can record aggressive behaviors and other safety issues).^3,4 When developing these plans and policies, include patients by creating patient/staff workgroups to develop expectations for civil behavior that apply to both patients and staff, as well as training patients to co-lead groups dealing with accepting responsibility for their own recovery.⁵ These plans and policies should include informing patients that threats and violence will not be tolerated. Frequently review these plans and policies with patients and staff.

Provide communication and education. Maintain strong psychiatric leadership on the unit that encourages open lines of communication. Encourage staff to promptly report incidents. Frequently ask staff if they have any safety concerns, and solicit their opinions on how to reduce risks.⁴ Include discussions about safety during staff and community meetings. Communicate patients’ behaviors that are distressing or undesired (eg, threats, harassment, etc) to all unit personnel.³ Notify staff when you plan to interact with a patient who is at risk for violence or is acutely agitated.⁴ Teach staff how to recognize the nonverbal warning signs of behavior escalation and provide training on proper de-escalation and response.^3,4 Also train staff on how to develop strong therapeutic alliances with patients.¹ After a violent incident, use the postincident debriefing session to gather information that can be used to develop additional interventions and reduce the risk of subsequent violence.¹

Implement common-sense strategies. Ensure that there are adequate numbers of nursing staff during each shift.¹ Avoid overcrowded units, hallways, and common areas. Consider additional monitoring during unit transition times, such as during shift changes, meals, and medication administration.¹ Avoid excessive noise.¹ Employ one-to-one staff observation as clinically indicated.¹ Avoid taking an authoritarian stance when explaining to patients why their requests have been denied⁴; if possible, when you are unable to meet a patient’s demands, offer them choices.^1,4 If feasible, accompany patients to a calmer space where they can de-escalate.¹ Install video surveillance cameras at entrances, exits, and other strategic locations and post signs signaling their presence.³ Install panic buttons at the nursing station and other areas (eg, restrooms).³

Ensure your personal safety. As mentioned previously, do not interact with a patient who has recently been aggressive or has voiced threats without adequate staff support.⁴ During the patient encounter, leave space between you and the patient.¹ Avoid having your back to the exit of the room,^3,4 and make sure the patient is not blocking the exit and that you can leave the room quickly if needed. Don’t wear anything that could be used as a weapon against you (eg, ties or necklaces) or could impede your escape.⁴ Avoid wearing valuables that might be damaged during a “take down.”⁴ If feasible, wear an audible alarm.³

Perinatal mental health disorders such as perinatal depression are common complications of pregnancy¹ and cause significant disability in mothers and children.² Yet despite facing higher 12-month rates of depression than White women,³ Black and Hispanic women are less likely than White women to be diagnosed with and receive treatment for postpartum depression.⁴

In addition to leading to >800,000 deaths in the United States alone (as of mid-December 2021),⁵ COVID-19 has disrupted health care delivery, including perinatal mental health services.⁶ Emerging data also describe neuropsychiatric effects of COVID-19 on both infected and uninfected individuals.⁷ Because Black and Hispanic individuals bear a disproportionate burden of COVID-19,⁸ compared to White women, women of color stand to be more adversely impacted by the direct effects of the disease as well as by related disruptions in perinatal psychiatry services.

Reasons for perinatal health disparities are multifactorial, complex, and interrelated. Disparities, which can be seen as proportionate differences in access by members of minority groups compared with groups in the majority, are related to differences in mental health screening, health care accessibility, and decisions to initiate treatment. In this commentary, we define “women of color” as non-White women, and focus on how traditional barriers to perinatal mental health treatment in women of color are exacerbated in the era of COVID-19. We focus primarily on postpartum depression because it is the peripartum mental health disorder with the highest likelihood of uptake in screening and treatment practices; however, disparities may be present in other mental health disorders during this period.

Gaps in screening and identification

Postpartum depression is a source of mitigatable risk for mother and neonate in the peripartum period, and the topic of screening for its presence arises in educational and best practices materials for primary care, OB-GYN, and pediatric care clinicians. Despite considerable evidence demonstrating better outcomes (for mother and child) with early detection and treatment of perinatal mental health disorders, racial and ethnic disparities persist in the screening process. At baseline, Black, Asian, and American Indian and Alaska Native women are less likely than White women to be screened for depression.⁹ Research shows that screening practices differ based on type of clinic, with one study noting that patients of family physicians were more likely to be screened for perinatal depression than were patients of OB-GYNs or nursing midwives.⁹ Even after adjusting for clinic type, racial differences in screening persist, with fewer women of color screened than their White counterparts.⁹ The literature consistently shows that within the same care settings, physicians deliver less information, less supportive talk, and less evidence-based treatment to Black and Hispanic patients and patients of lower economic status.^10-12 Patient-clinician ethnic concordance is shown to positively impact the therapeutic relationship; at present, depressive symptoms are underrecognized in people of color, for whom referral to psychiatric care may be further compounded by inadequate knowledge of psychiatric resources.^10-13

Data from Medicaid programs reveal that compared to White women, Black women are less likely to attend postpartum visits, which leads to a downstream effect on the ability to identify Black women with mental health disorders during the postpartum period.¹⁴ In addition to experiencing fewer opportunities for detection, women of color are more likely to report somatic symptoms of depression, which may not be detected in routinely employed perinatal depression screening tools.¹⁵

Continue to: Disparities in accessibility and treatment...

Disparities in accessibility and treatment

Black women are more likely to present in crisis and, hence, to acute care settings, which is likely related to disparities in screening and early detection.^16,17 In a recent study investigating racial and ethnic differences in postpartum depression care, Chan et al¹⁶ found that Black women experience higher rates of hospital-based care compared with other racial groups. This study highlights the unavailability or inaccessibility of primary preventive measures to women in racial minority groups, which supports earlier studies that reported a correlation between access to care and severity of illness.¹⁶ Women in crisis may experience magnified disparities in access to high-quality care as they encounter institutional racism, potential loss of parental rights, and barriers due to insurance status.^17,18 Furthermore, access to care for patients who are members of racial minority groups is limited in settings where culturally competent practices are absent or diminished, or discriminatory procedures are implicitly accepted and prevalent.^12,19-22 The adverse impact of language constraints on accessibility of care is also well-documented, with recommendations such as ready access to interpreters to mitigate against miscommunications.²³

Black and Hispanic women also experience significant delays between the time of delivery and treatment initiation.⁴ Studies of postpartum depression detection and treatment in specialty and primary care clinics show that, even when they desire treatment, women of color are less likely than White women to be offered treatment for postpartum depression.²⁴ In terms of treatment options, research suggests women of color prefer psychotherapy over medication management.^25,26 However, studies show that White women are more likely to be referred to psychotherapy.²⁷ Research also reveals that Black and Hispanic women who are receptive to psychotropic medications have reduced rates of medication refills,⁴ which suggests that in these patients, counseling and monitoring adverse effects is suboptimal. In terms of treatment for substance use disorders (SUDs), after adjusting for maternal characteristics, Black and Hispanic women are significantly less likely to receive medication-assisted treatment (MAT) in pregnancy,²⁸ and MAT is significantly less likely to be available in neighborhoods more densely populated by individuals of color.^29,30

Several studies have explored possible explanations for discrepancies in treatment, including cultural expectations, differences in socioeconomic class, and racism. The stigma associated with psychiatric illness, misinformation about psychiatric treatments, and financial limitations have a substantial bearing on a patient’s willingness or ability to engage in psychiatric care.²⁵ Regarding SUDs, a fear of legal reprisal is likely to deter women of color from seeking care.³¹ Such fears are not unfounded; research has demonstrated that interactions with Child Protective Services are increased among women of color compared to White women in similar situations.³²

Furthermore, there is evidence that women of color receive less practical support, such as childcare, breastfeeding support, and transportation, during the postpartum period. Despite the preponderance of literature demonstrating the psychological benefits of breastfeeding,^33,34 structural and psychosocial barriers appear to disproportionately affect breastfeeding rates in Hispanic, Black, American Indian, and Native women, with Black women experiencing the lowest rates of breastfeeding overall.³⁵ Women in minority groups additionally experience disproportionate uncertainty about employment-based breastfeeding regulations.^35,36 Specifically, many low-income jobs are not covered under the Family and Medical Leave Act, and compared to White women, Black women return to work on average 2 weeks earlier to jobs that are less welcoming to breastfeeding.³⁵ In addition, insufficient education and support from health care settings and counselors play significant roles in disincentivizing women in minority groups from engaging in recommended breastfeeding and childcare practices.^37,38

Continue to: COVID-19’s influence on these disparities...

COVID-19’s influence on these disparities

The COVID-19 pandemic has disproportionately impacted individuals of color. Black communities have experienced a higher rate of COVID-19 infection and a higher rate of death attributed to COVID-19, even after adjusting for age, poverty, medical comorbidities, and epidemic duration.³⁹ The reasons for the disproportionate effects of the pandemic are complex and deeply ingrained in society.³⁹ Emerging data indicate that COVID-19 might also lead to increased levels of psychological distress, anxiety, and depression in pregnant women^33,40,41 and in Black women in particular.⁴² A survey of 913 pregnant women in Philadelphia conducted in May 2020 found significantly higher rates of anxiety and depression among Black women compared with White women, even after controlling for maternal age, gestational age, socioeconomic status, and marital status.⁴² A cross-sectional study of 163 women found that during the perinatal period, women of color were more likely than their White counterparts to experience negative changes in their mental health.⁴³ These differences are concerning because pregnant women who experience high levels of stress during the pandemic are at high risk for preterm delivery and perinatal complications.⁴⁴

Women of color may be disproportionately excluded by models of care that have become commonplace during the pandemic. Remote obstetric care became more common during the COVID-19 pandemic⁴⁵; however, Black and Hispanic patients have been less likely than White patients to use telehealth services.⁴⁶ Whether the differences are related to a lower likelihood of having a usual source of care, less access to digital resources, decreased awareness of the availability of telehealth, or less familiarity with digital technology, the common factor in all of the hypothesized reasons is structural racism.⁴⁶ This is despite the fact that pregnant Black women report higher rates of concern than their White peers regarding the quality of their prenatal care during the pandemic.⁴² In a small study that surveyed 100 women about their preference for obstetric care, a significantly higher proportion of White women preferred virtual visits, with non-White women preferring in-person visits.⁴⁷ Reasons cited for preferring virtual visits included convenience, safety with respect to viral transmission, compatibility with working from home, and less time waiting for the clinician; reasons cited for preferring in-person visits included a feeling of missing out on important parts of care, receiving less clinician attention, and having less of a connection with their clinician during virtual visits.⁴⁷ Women of color have lower rates of perinatal depression screening than their White counterparts,⁹ and less frequent telehealth visits might lead to a further reduction in the detection and treatment of depression and other mental health conditions in this population.

Along with increasing telehealth services during the pandemic, many hospitals implemented stricter visitation policies for patients, including women giving birth, with the potential for greater detrimental impact on women of color. Before the pandemic, a survey of >2,500 women found that up to 10% of Black women reported experiencing racism during hospitalization for obstetrics-related care.⁴⁸ These women also reported barriers to open and supportive communication with their clinicians.⁴⁸ A recent study by Gur et al⁴² found that pregnant Black women reported more worries about the birthing experience during the pandemic than White women. In a setting with restricted visitors, all women are at risk for having a lonelier birth experience, but women of color who are already concerned about barriers to communication and racist care practices also must contend with their lived experience of systemic inequity, barriers to communication, and concerns about frank racism, without the support and potential advocacy they may usually rely upon to get them through medical experiences. Furthermore, pregnant women with mental illness are at greater risk for pregnancy complications. Together, these data suggest that women in minority groups who are pregnant and have mental illness are particularly vulnerable and are at greater risk without social support and advocacy during hospitalization.

The postpartum period is accompanied by unique concerns in terms of breastfeeding and social support for women of color. Women in minority groups had lower breastfeeding rates before the pandemic. Several studies looked at the impact of COVID-19 and associated restrictions on breastfeeding. In the United Kingdom, women in minority groups were more likely to stop breastfeeding due to the challenges of COVID-19–related restrictions.⁴⁹ Compared with White women, these women were also more likely to report less practical support for breastfeeding during the pandemic.⁴⁹ Other factors associated with low breastfeeding rates include lower levels of education and stressful living conditions.⁴⁹ Though these factors were present before COVID-19, the pandemic has exacerbated these differences. Taken together, the evidence points to a role of long-standing structural and systemic inequity and racism in the health and wellbeing of women in minority groups.

A look towards solutions

Although perinatal mental health racial disparities predate the COVID-19 pandemic, differences in access to screening, identification, and treatment for mental health disorders place pregnant women of color and their children at heightened risk for poor health outcomes compared to their White counterparts during and after the pandemic. Despite the advent and progression of telehealth, existing race-based differences appear to have been maintained or exacerbated. The reasons for disparities are multifactorial and interrelated, and some of the outcomes perpetuate certain drivers of racism, which in turn drive continued inequity. Given the symptoms of depression, it is especially worrisome that clinicians may expect vulnerable women with illness-induced amotivation, anhedonia, and apathy to advocate for their own care.

Overall, the evidence confirms an imperative need—before, during, and after the COVID-19 pandemic—to provide education in mental health and cultural competency to clinicians such as obstetricians and pediatricians, who are more likely to have the first contact with women with perinatal depression. Health systems and government agencies also bear a responsibility to provide avenues for perinatal care clinicians to receive training and to increase access to culturally appropriate treatments through policy and structural changes.

Bottom Line

Racial disparities in perinatal mental health care persist despite widespread incorporation of telehealth into psychiatric services. Until causal factors are appropriately addressed through education, implementation, and structural changes, the benefits that have accompanied expanded psychiatric services via telehealth may only serve to exacerbate these differences.

Perinatal mental health disorders such as perinatal depression are common complications of pregnancy¹ and cause significant disability in mothers and children.² Yet despite facing higher 12-month rates of depression than White women,³ Black and Hispanic women are less likely than White women to be diagnosed with and receive treatment for postpartum depression.⁴

In addition to leading to >800,000 deaths in the United States alone (as of mid-December 2021),⁵ COVID-19 has disrupted health care delivery, including perinatal mental health services.⁶ Emerging data also describe neuropsychiatric effects of COVID-19 on both infected and uninfected individuals.⁷ Because Black and Hispanic individuals bear a disproportionate burden of COVID-19,⁸ compared to White women, women of color stand to be more adversely impacted by the direct effects of the disease as well as by related disruptions in perinatal psychiatry services.

Reasons for perinatal health disparities are multifactorial, complex, and interrelated. Disparities, which can be seen as proportionate differences in access by members of minority groups compared with groups in the majority, are related to differences in mental health screening, health care accessibility, and decisions to initiate treatment. In this commentary, we define “women of color” as non-White women, and focus on how traditional barriers to perinatal mental health treatment in women of color are exacerbated in the era of COVID-19. We focus primarily on postpartum depression because it is the peripartum mental health disorder with the highest likelihood of uptake in screening and treatment practices; however, disparities may be present in other mental health disorders during this period.

Gaps in screening and identification

Postpartum depression is a source of mitigatable risk for mother and neonate in the peripartum period, and the topic of screening for its presence arises in educational and best practices materials for primary care, OB-GYN, and pediatric care clinicians. Despite considerable evidence demonstrating better outcomes (for mother and child) with early detection and treatment of perinatal mental health disorders, racial and ethnic disparities persist in the screening process. At baseline, Black, Asian, and American Indian and Alaska Native women are less likely than White women to be screened for depression.⁹ Research shows that screening practices differ based on type of clinic, with one study noting that patients of family physicians were more likely to be screened for perinatal depression than were patients of OB-GYNs or nursing midwives.⁹ Even after adjusting for clinic type, racial differences in screening persist, with fewer women of color screened than their White counterparts.⁹ The literature consistently shows that within the same care settings, physicians deliver less information, less supportive talk, and less evidence-based treatment to Black and Hispanic patients and patients of lower economic status.^10-12 Patient-clinician ethnic concordance is shown to positively impact the therapeutic relationship; at present, depressive symptoms are underrecognized in people of color, for whom referral to psychiatric care may be further compounded by inadequate knowledge of psychiatric resources.^10-13

Data from Medicaid programs reveal that compared to White women, Black women are less likely to attend postpartum visits, which leads to a downstream effect on the ability to identify Black women with mental health disorders during the postpartum period.¹⁴ In addition to experiencing fewer opportunities for detection, women of color are more likely to report somatic symptoms of depression, which may not be detected in routinely employed perinatal depression screening tools.¹⁵

Continue to: Disparities in accessibility and treatment...

Disparities in accessibility and treatment

Black women are more likely to present in crisis and, hence, to acute care settings, which is likely related to disparities in screening and early detection.^16,17 In a recent study investigating racial and ethnic differences in postpartum depression care, Chan et al¹⁶ found that Black women experience higher rates of hospital-based care compared with other racial groups. This study highlights the unavailability or inaccessibility of primary preventive measures to women in racial minority groups, which supports earlier studies that reported a correlation between access to care and severity of illness.¹⁶ Women in crisis may experience magnified disparities in access to high-quality care as they encounter institutional racism, potential loss of parental rights, and barriers due to insurance status.^17,18 Furthermore, access to care for patients who are members of racial minority groups is limited in settings where culturally competent practices are absent or diminished, or discriminatory procedures are implicitly accepted and prevalent.^12,19-22 The adverse impact of language constraints on accessibility of care is also well-documented, with recommendations such as ready access to interpreters to mitigate against miscommunications.²³

Black and Hispanic women also experience significant delays between the time of delivery and treatment initiation.⁴ Studies of postpartum depression detection and treatment in specialty and primary care clinics show that, even when they desire treatment, women of color are less likely than White women to be offered treatment for postpartum depression.²⁴ In terms of treatment options, research suggests women of color prefer psychotherapy over medication management.^25,26 However, studies show that White women are more likely to be referred to psychotherapy.²⁷ Research also reveals that Black and Hispanic women who are receptive to psychotropic medications have reduced rates of medication refills,⁴ which suggests that in these patients, counseling and monitoring adverse effects is suboptimal. In terms of treatment for substance use disorders (SUDs), after adjusting for maternal characteristics, Black and Hispanic women are significantly less likely to receive medication-assisted treatment (MAT) in pregnancy,²⁸ and MAT is significantly less likely to be available in neighborhoods more densely populated by individuals of color.^29,30

Several studies have explored possible explanations for discrepancies in treatment, including cultural expectations, differences in socioeconomic class, and racism. The stigma associated with psychiatric illness, misinformation about psychiatric treatments, and financial limitations have a substantial bearing on a patient’s willingness or ability to engage in psychiatric care.²⁵ Regarding SUDs, a fear of legal reprisal is likely to deter women of color from seeking care.³¹ Such fears are not unfounded; research has demonstrated that interactions with Child Protective Services are increased among women of color compared to White women in similar situations.³²

Furthermore, there is evidence that women of color receive less practical support, such as childcare, breastfeeding support, and transportation, during the postpartum period. Despite the preponderance of literature demonstrating the psychological benefits of breastfeeding,^33,34 structural and psychosocial barriers appear to disproportionately affect breastfeeding rates in Hispanic, Black, American Indian, and Native women, with Black women experiencing the lowest rates of breastfeeding overall.³⁵ Women in minority groups additionally experience disproportionate uncertainty about employment-based breastfeeding regulations.^35,36 Specifically, many low-income jobs are not covered under the Family and Medical Leave Act, and compared to White women, Black women return to work on average 2 weeks earlier to jobs that are less welcoming to breastfeeding.³⁵ In addition, insufficient education and support from health care settings and counselors play significant roles in disincentivizing women in minority groups from engaging in recommended breastfeeding and childcare practices.^37,38

Continue to: COVID-19’s influence on these disparities...

COVID-19’s influence on these disparities

The COVID-19 pandemic has disproportionately impacted individuals of color. Black communities have experienced a higher rate of COVID-19 infection and a higher rate of death attributed to COVID-19, even after adjusting for age, poverty, medical comorbidities, and epidemic duration.³⁹ The reasons for the disproportionate effects of the pandemic are complex and deeply ingrained in society.³⁹ Emerging data indicate that COVID-19 might also lead to increased levels of psychological distress, anxiety, and depression in pregnant women^33,40,41 and in Black women in particular.⁴² A survey of 913 pregnant women in Philadelphia conducted in May 2020 found significantly higher rates of anxiety and depression among Black women compared with White women, even after controlling for maternal age, gestational age, socioeconomic status, and marital status.⁴² A cross-sectional study of 163 women found that during the perinatal period, women of color were more likely than their White counterparts to experience negative changes in their mental health.⁴³ These differences are concerning because pregnant women who experience high levels of stress during the pandemic are at high risk for preterm delivery and perinatal complications.⁴⁴

Women of color may be disproportionately excluded by models of care that have become commonplace during the pandemic. Remote obstetric care became more common during the COVID-19 pandemic⁴⁵; however, Black and Hispanic patients have been less likely than White patients to use telehealth services.⁴⁶ Whether the differences are related to a lower likelihood of having a usual source of care, less access to digital resources, decreased awareness of the availability of telehealth, or less familiarity with digital technology, the common factor in all of the hypothesized reasons is structural racism.⁴⁶ This is despite the fact that pregnant Black women report higher rates of concern than their White peers regarding the quality of their prenatal care during the pandemic.⁴² In a small study that surveyed 100 women about their preference for obstetric care, a significantly higher proportion of White women preferred virtual visits, with non-White women preferring in-person visits.⁴⁷ Reasons cited for preferring virtual visits included convenience, safety with respect to viral transmission, compatibility with working from home, and less time waiting for the clinician; reasons cited for preferring in-person visits included a feeling of missing out on important parts of care, receiving less clinician attention, and having less of a connection with their clinician during virtual visits.⁴⁷ Women of color have lower rates of perinatal depression screening than their White counterparts,⁹ and less frequent telehealth visits might lead to a further reduction in the detection and treatment of depression and other mental health conditions in this population.

Along with increasing telehealth services during the pandemic, many hospitals implemented stricter visitation policies for patients, including women giving birth, with the potential for greater detrimental impact on women of color. Before the pandemic, a survey of >2,500 women found that up to 10% of Black women reported experiencing racism during hospitalization for obstetrics-related care.⁴⁸ These women also reported barriers to open and supportive communication with their clinicians.⁴⁸ A recent study by Gur et al⁴² found that pregnant Black women reported more worries about the birthing experience during the pandemic than White women. In a setting with restricted visitors, all women are at risk for having a lonelier birth experience, but women of color who are already concerned about barriers to communication and racist care practices also must contend with their lived experience of systemic inequity, barriers to communication, and concerns about frank racism, without the support and potential advocacy they may usually rely upon to get them through medical experiences. Furthermore, pregnant women with mental illness are at greater risk for pregnancy complications. Together, these data suggest that women in minority groups who are pregnant and have mental illness are particularly vulnerable and are at greater risk without social support and advocacy during hospitalization.

The postpartum period is accompanied by unique concerns in terms of breastfeeding and social support for women of color. Women in minority groups had lower breastfeeding rates before the pandemic. Several studies looked at the impact of COVID-19 and associated restrictions on breastfeeding. In the United Kingdom, women in minority groups were more likely to stop breastfeeding due to the challenges of COVID-19–related restrictions.⁴⁹ Compared with White women, these women were also more likely to report less practical support for breastfeeding during the pandemic.⁴⁹ Other factors associated with low breastfeeding rates include lower levels of education and stressful living conditions.⁴⁹ Though these factors were present before COVID-19, the pandemic has exacerbated these differences. Taken together, the evidence points to a role of long-standing structural and systemic inequity and racism in the health and wellbeing of women in minority groups.

A look towards solutions

Although perinatal mental health racial disparities predate the COVID-19 pandemic, differences in access to screening, identification, and treatment for mental health disorders place pregnant women of color and their children at heightened risk for poor health outcomes compared to their White counterparts during and after the pandemic. Despite the advent and progression of telehealth, existing race-based differences appear to have been maintained or exacerbated. The reasons for disparities are multifactorial and interrelated, and some of the outcomes perpetuate certain drivers of racism, which in turn drive continued inequity. Given the symptoms of depression, it is especially worrisome that clinicians may expect vulnerable women with illness-induced amotivation, anhedonia, and apathy to advocate for their own care.

Overall, the evidence confirms an imperative need—before, during, and after the COVID-19 pandemic—to provide education in mental health and cultural competency to clinicians such as obstetricians and pediatricians, who are more likely to have the first contact with women with perinatal depression. Health systems and government agencies also bear a responsibility to provide avenues for perinatal care clinicians to receive training and to increase access to culturally appropriate treatments through policy and structural changes.

Bottom Line

Racial disparities in perinatal mental health care persist despite widespread incorporation of telehealth into psychiatric services. Until causal factors are appropriately addressed through education, implementation, and structural changes, the benefits that have accompanied expanded psychiatric services via telehealth may only serve to exacerbate these differences.

Perinatal mental health disorders such as perinatal depression are common complications of pregnancy¹ and cause significant disability in mothers and children.² Yet despite facing higher 12-month rates of depression than White women,³ Black and Hispanic women are less likely than White women to be diagnosed with and receive treatment for postpartum depression.⁴

In addition to leading to >800,000 deaths in the United States alone (as of mid-December 2021),⁵ COVID-19 has disrupted health care delivery, including perinatal mental health services.⁶ Emerging data also describe neuropsychiatric effects of COVID-19 on both infected and uninfected individuals.⁷ Because Black and Hispanic individuals bear a disproportionate burden of COVID-19,⁸ compared to White women, women of color stand to be more adversely impacted by the direct effects of the disease as well as by related disruptions in perinatal psychiatry services.

Reasons for perinatal health disparities are multifactorial, complex, and interrelated. Disparities, which can be seen as proportionate differences in access by members of minority groups compared with groups in the majority, are related to differences in mental health screening, health care accessibility, and decisions to initiate treatment. In this commentary, we define “women of color” as non-White women, and focus on how traditional barriers to perinatal mental health treatment in women of color are exacerbated in the era of COVID-19. We focus primarily on postpartum depression because it is the peripartum mental health disorder with the highest likelihood of uptake in screening and treatment practices; however, disparities may be present in other mental health disorders during this period.

Gaps in screening and identification

Postpartum depression is a source of mitigatable risk for mother and neonate in the peripartum period, and the topic of screening for its presence arises in educational and best practices materials for primary care, OB-GYN, and pediatric care clinicians. Despite considerable evidence demonstrating better outcomes (for mother and child) with early detection and treatment of perinatal mental health disorders, racial and ethnic disparities persist in the screening process. At baseline, Black, Asian, and American Indian and Alaska Native women are less likely than White women to be screened for depression.⁹ Research shows that screening practices differ based on type of clinic, with one study noting that patients of family physicians were more likely to be screened for perinatal depression than were patients of OB-GYNs or nursing midwives.⁹ Even after adjusting for clinic type, racial differences in screening persist, with fewer women of color screened than their White counterparts.⁹ The literature consistently shows that within the same care settings, physicians deliver less information, less supportive talk, and less evidence-based treatment to Black and Hispanic patients and patients of lower economic status.^10-12 Patient-clinician ethnic concordance is shown to positively impact the therapeutic relationship; at present, depressive symptoms are underrecognized in people of color, for whom referral to psychiatric care may be further compounded by inadequate knowledge of psychiatric resources.^10-13

Data from Medicaid programs reveal that compared to White women, Black women are less likely to attend postpartum visits, which leads to a downstream effect on the ability to identify Black women with mental health disorders during the postpartum period.¹⁴ In addition to experiencing fewer opportunities for detection, women of color are more likely to report somatic symptoms of depression, which may not be detected in routinely employed perinatal depression screening tools.¹⁵

Continue to: Disparities in accessibility and treatment...

Disparities in accessibility and treatment

Black women are more likely to present in crisis and, hence, to acute care settings, which is likely related to disparities in screening and early detection.^16,17 In a recent study investigating racial and ethnic differences in postpartum depression care, Chan et al¹⁶ found that Black women experience higher rates of hospital-based care compared with other racial groups. This study highlights the unavailability or inaccessibility of primary preventive measures to women in racial minority groups, which supports earlier studies that reported a correlation between access to care and severity of illness.¹⁶ Women in crisis may experience magnified disparities in access to high-quality care as they encounter institutional racism, potential loss of parental rights, and barriers due to insurance status.^17,18 Furthermore, access to care for patients who are members of racial minority groups is limited in settings where culturally competent practices are absent or diminished, or discriminatory procedures are implicitly accepted and prevalent.^12,19-22 The adverse impact of language constraints on accessibility of care is also well-documented, with recommendations such as ready access to interpreters to mitigate against miscommunications.²³

Black and Hispanic women also experience significant delays between the time of delivery and treatment initiation.⁴ Studies of postpartum depression detection and treatment in specialty and primary care clinics show that, even when they desire treatment, women of color are less likely than White women to be offered treatment for postpartum depression.²⁴ In terms of treatment options, research suggests women of color prefer psychotherapy over medication management.^25,26 However, studies show that White women are more likely to be referred to psychotherapy.²⁷ Research also reveals that Black and Hispanic women who are receptive to psychotropic medications have reduced rates of medication refills,⁴ which suggests that in these patients, counseling and monitoring adverse effects is suboptimal. In terms of treatment for substance use disorders (SUDs), after adjusting for maternal characteristics, Black and Hispanic women are significantly less likely to receive medication-assisted treatment (MAT) in pregnancy,²⁸ and MAT is significantly less likely to be available in neighborhoods more densely populated by individuals of color.^29,30

Several studies have explored possible explanations for discrepancies in treatment, including cultural expectations, differences in socioeconomic class, and racism. The stigma associated with psychiatric illness, misinformation about psychiatric treatments, and financial limitations have a substantial bearing on a patient’s willingness or ability to engage in psychiatric care.²⁵ Regarding SUDs, a fear of legal reprisal is likely to deter women of color from seeking care.³¹ Such fears are not unfounded; research has demonstrated that interactions with Child Protective Services are increased among women of color compared to White women in similar situations.³²

Furthermore, there is evidence that women of color receive less practical support, such as childcare, breastfeeding support, and transportation, during the postpartum period. Despite the preponderance of literature demonstrating the psychological benefits of breastfeeding,^33,34 structural and psychosocial barriers appear to disproportionately affect breastfeeding rates in Hispanic, Black, American Indian, and Native women, with Black women experiencing the lowest rates of breastfeeding overall.³⁵ Women in minority groups additionally experience disproportionate uncertainty about employment-based breastfeeding regulations.^35,36 Specifically, many low-income jobs are not covered under the Family and Medical Leave Act, and compared to White women, Black women return to work on average 2 weeks earlier to jobs that are less welcoming to breastfeeding.³⁵ In addition, insufficient education and support from health care settings and counselors play significant roles in disincentivizing women in minority groups from engaging in recommended breastfeeding and childcare practices.^37,38

Continue to: COVID-19’s influence on these disparities...

COVID-19’s influence on these disparities

The COVID-19 pandemic has disproportionately impacted individuals of color. Black communities have experienced a higher rate of COVID-19 infection and a higher rate of death attributed to COVID-19, even after adjusting for age, poverty, medical comorbidities, and epidemic duration.³⁹ The reasons for the disproportionate effects of the pandemic are complex and deeply ingrained in society.³⁹ Emerging data indicate that COVID-19 might also lead to increased levels of psychological distress, anxiety, and depression in pregnant women^33,40,41 and in Black women in particular.⁴² A survey of 913 pregnant women in Philadelphia conducted in May 2020 found significantly higher rates of anxiety and depression among Black women compared with White women, even after controlling for maternal age, gestational age, socioeconomic status, and marital status.⁴² A cross-sectional study of 163 women found that during the perinatal period, women of color were more likely than their White counterparts to experience negative changes in their mental health.⁴³ These differences are concerning because pregnant women who experience high levels of stress during the pandemic are at high risk for preterm delivery and perinatal complications.⁴⁴

Women of color may be disproportionately excluded by models of care that have become commonplace during the pandemic. Remote obstetric care became more common during the COVID-19 pandemic⁴⁵; however, Black and Hispanic patients have been less likely than White patients to use telehealth services.⁴⁶ Whether the differences are related to a lower likelihood of having a usual source of care, less access to digital resources, decreased awareness of the availability of telehealth, or less familiarity with digital technology, the common factor in all of the hypothesized reasons is structural racism.⁴⁶ This is despite the fact that pregnant Black women report higher rates of concern than their White peers regarding the quality of their prenatal care during the pandemic.⁴² In a small study that surveyed 100 women about their preference for obstetric care, a significantly higher proportion of White women preferred virtual visits, with non-White women preferring in-person visits.⁴⁷ Reasons cited for preferring virtual visits included convenience, safety with respect to viral transmission, compatibility with working from home, and less time waiting for the clinician; reasons cited for preferring in-person visits included a feeling of missing out on important parts of care, receiving less clinician attention, and having less of a connection with their clinician during virtual visits.⁴⁷ Women of color have lower rates of perinatal depression screening than their White counterparts,⁹ and less frequent telehealth visits might lead to a further reduction in the detection and treatment of depression and other mental health conditions in this population.

Along with increasing telehealth services during the pandemic, many hospitals implemented stricter visitation policies for patients, including women giving birth, with the potential for greater detrimental impact on women of color. Before the pandemic, a survey of >2,500 women found that up to 10% of Black women reported experiencing racism during hospitalization for obstetrics-related care.⁴⁸ These women also reported barriers to open and supportive communication with their clinicians.⁴⁸ A recent study by Gur et al⁴² found that pregnant Black women reported more worries about the birthing experience during the pandemic than White women. In a setting with restricted visitors, all women are at risk for having a lonelier birth experience, but women of color who are already concerned about barriers to communication and racist care practices also must contend with their lived experience of systemic inequity, barriers to communication, and concerns about frank racism, without the support and potential advocacy they may usually rely upon to get them through medical experiences. Furthermore, pregnant women with mental illness are at greater risk for pregnancy complications. Together, these data suggest that women in minority groups who are pregnant and have mental illness are particularly vulnerable and are at greater risk without social support and advocacy during hospitalization.

The postpartum period is accompanied by unique concerns in terms of breastfeeding and social support for women of color. Women in minority groups had lower breastfeeding rates before the pandemic. Several studies looked at the impact of COVID-19 and associated restrictions on breastfeeding. In the United Kingdom, women in minority groups were more likely to stop breastfeeding due to the challenges of COVID-19–related restrictions.⁴⁹ Compared with White women, these women were also more likely to report less practical support for breastfeeding during the pandemic.⁴⁹ Other factors associated with low breastfeeding rates include lower levels of education and stressful living conditions.⁴⁹ Though these factors were present before COVID-19, the pandemic has exacerbated these differences. Taken together, the evidence points to a role of long-standing structural and systemic inequity and racism in the health and wellbeing of women in minority groups.

A look towards solutions

Although perinatal mental health racial disparities predate the COVID-19 pandemic, differences in access to screening, identification, and treatment for mental health disorders place pregnant women of color and their children at heightened risk for poor health outcomes compared to their White counterparts during and after the pandemic. Despite the advent and progression of telehealth, existing race-based differences appear to have been maintained or exacerbated. The reasons for disparities are multifactorial and interrelated, and some of the outcomes perpetuate certain drivers of racism, which in turn drive continued inequity. Given the symptoms of depression, it is especially worrisome that clinicians may expect vulnerable women with illness-induced amotivation, anhedonia, and apathy to advocate for their own care.

Overall, the evidence confirms an imperative need—before, during, and after the COVID-19 pandemic—to provide education in mental health and cultural competency to clinicians such as obstetricians and pediatricians, who are more likely to have the first contact with women with perinatal depression. Health systems and government agencies also bear a responsibility to provide avenues for perinatal care clinicians to receive training and to increase access to culturally appropriate treatments through policy and structural changes.

Bottom Line

Racial disparities in perinatal mental health care persist despite widespread incorporation of telehealth into psychiatric services. Until causal factors are appropriately addressed through education, implementation, and structural changes, the benefits that have accompanied expanded psychiatric services via telehealth may only serve to exacerbate these differences.

Are you still wearing a cloth face mask?

Amid the rapidly spreading Omicron variant, experts stress that we all should swap cloth masks for N95 respirators or 3-ply surgical masks.

For background: N95 respirators are tightly fitting masks that cover your mouth and nose and help prevent contact with droplets and tiny particles in the air from people talking, coughing, sneezing, and spreading in other ways. Usually worn by health care workers and first responders, these masks can filter up to 95% of air droplets and particles, according to the CDC.

KN95 and KN94 masks are similar but are designed to meet international standards, unlike N95s that are approved by the Centers for Disease Control and Prevention’s National Institute for Occupational Safety and Health.

Meanwhile, a 3-ply surgical mask is a looser-fitting mask that can help prevent contact with infected droplets in the air.

But recommendations to opt for N95 and 3-ply surgical masks over cloth masks are nothing new, says Leana Wen, MD, an emergency doctor and public health professor at George Washington University, Washington.

In fact, public health experts have been urging stronger mask protection for months.

“It’s not just with Omicron that we need better masks, it was with Delta, it was with Alpha before that,” Dr. Wen said. “We have known for many months that COVID-19 is airborne, and therefore, a simple cloth mask is not going to cut it.”

Here’s what to know about these protective masks.
 

They’re necessary

Omicron is spreading much faster than previous COVID-19 variants. As it’s up to three times as likely to spread as the Delta variant, mask-wearing is paramount right now, says Anita Gupta, DO, an adjunct assistant professor of anesthesiology and critical care medicine and pain medicine at Johns Hopkins University, Baltimore.

The quality of a mask also matters a lot, said Dr. Wen.

“Double masking, including a well-fitting cloth mask on top of a surgical mask, adds additional protection,” she said. “Ideally, though, people should be wearing an N95, KN95, or KF94 when in indoor settings around other people with unknown vaccination status.”

If wearing an N95 mask causes extreme discomfort, wear it in high-risk settings where there are lots of people, like crowded restaurants and busy commuter trains, says Dr. Wen. “If you’re in a grocery store, there’s plenty of space and ventilation. You may not need an N95. I recommend that people obtain different masks and practice with them in low-risk settings before they go out in public in a high-risk setting.”

But people should wear a 3-ply surgical mask at the very least.
 

Three-ply surgical and N95 mask qualities

With 3-ply surgical masks, the fit of the mask is often more of an issue than its comfort, Dr. Wen said. But there are ways to adjust these masks, especially for those who have smaller heads.

“You can put a rubber band around the ear loops and make them a bit tighter,” said Dr. Wen. “Some people have found that using pins in their hair, that’s another way of keeping the loops in place.”

Another important tip on 3-ply surgical masks and N95s: These masks are reusable.

But how many times you should use them varies, Dr. Wen said. “As an example, if you are sweating a lot, and the mask is now really damp. Or putting it in your purse or backpack, and now it’s misshapen, and you cannot get it back to fit on your face, then it’s time to throw it away.”
 

Protection first

For some, cloth masks became somewhat of a statement, with people sporting logos of their favorite NFL team, or maybe even a fun animal print.

But you should always keep in mind the purpose of wearing a mask, Dr. Wen said. “Mask wearing is very functional and is about reducing your likelihood of contracting COVID. People should also use whatever methods inspire them, too, but for me, it’s purely a functional exercise.”

Mask wearing is not always enjoyable, but it remains critical in keeping people safe from COVID-19, especially the elderly and other high-risk people, Gupta says.

“There is lots of research and experts working hard to stop COVID-19,” she says. “It is important for all of us to remember that wearing a mask alone doesn’t make us safe.”

“We all need to keep washing our hands frequently and maintaining a distance from people, as well.”

For more information on where to find 3-ply surgical masks and N95s, check here or here to start.

A version of this article first appeared on WebMD.com.

Are you still wearing a cloth face mask?

Amid the rapidly spreading Omicron variant, experts stress that we all should swap cloth masks for N95 respirators or 3-ply surgical masks.

For background: N95 respirators are tightly fitting masks that cover your mouth and nose and help prevent contact with droplets and tiny particles in the air from people talking, coughing, sneezing, and spreading in other ways. Usually worn by health care workers and first responders, these masks can filter up to 95% of air droplets and particles, according to the CDC.

KN95 and KN94 masks are similar but are designed to meet international standards, unlike N95s that are approved by the Centers for Disease Control and Prevention’s National Institute for Occupational Safety and Health.

Meanwhile, a 3-ply surgical mask is a looser-fitting mask that can help prevent contact with infected droplets in the air.

But recommendations to opt for N95 and 3-ply surgical masks over cloth masks are nothing new, says Leana Wen, MD, an emergency doctor and public health professor at George Washington University, Washington.

In fact, public health experts have been urging stronger mask protection for months.

“It’s not just with Omicron that we need better masks, it was with Delta, it was with Alpha before that,” Dr. Wen said. “We have known for many months that COVID-19 is airborne, and therefore, a simple cloth mask is not going to cut it.”

Here’s what to know about these protective masks.
 

They’re necessary

Omicron is spreading much faster than previous COVID-19 variants. As it’s up to three times as likely to spread as the Delta variant, mask-wearing is paramount right now, says Anita Gupta, DO, an adjunct assistant professor of anesthesiology and critical care medicine and pain medicine at Johns Hopkins University, Baltimore.

The quality of a mask also matters a lot, said Dr. Wen.

“Double masking, including a well-fitting cloth mask on top of a surgical mask, adds additional protection,” she said. “Ideally, though, people should be wearing an N95, KN95, or KF94 when in indoor settings around other people with unknown vaccination status.”

If wearing an N95 mask causes extreme discomfort, wear it in high-risk settings where there are lots of people, like crowded restaurants and busy commuter trains, says Dr. Wen. “If you’re in a grocery store, there’s plenty of space and ventilation. You may not need an N95. I recommend that people obtain different masks and practice with them in low-risk settings before they go out in public in a high-risk setting.”

But people should wear a 3-ply surgical mask at the very least.
 

Three-ply surgical and N95 mask qualities

With 3-ply surgical masks, the fit of the mask is often more of an issue than its comfort, Dr. Wen said. But there are ways to adjust these masks, especially for those who have smaller heads.

“You can put a rubber band around the ear loops and make them a bit tighter,” said Dr. Wen. “Some people have found that using pins in their hair, that’s another way of keeping the loops in place.”

Another important tip on 3-ply surgical masks and N95s: These masks are reusable.

But how many times you should use them varies, Dr. Wen said. “As an example, if you are sweating a lot, and the mask is now really damp. Or putting it in your purse or backpack, and now it’s misshapen, and you cannot get it back to fit on your face, then it’s time to throw it away.”
 

Protection first

For some, cloth masks became somewhat of a statement, with people sporting logos of their favorite NFL team, or maybe even a fun animal print.

But you should always keep in mind the purpose of wearing a mask, Dr. Wen said. “Mask wearing is very functional and is about reducing your likelihood of contracting COVID. People should also use whatever methods inspire them, too, but for me, it’s purely a functional exercise.”

Mask wearing is not always enjoyable, but it remains critical in keeping people safe from COVID-19, especially the elderly and other high-risk people, Gupta says.

“There is lots of research and experts working hard to stop COVID-19,” she says. “It is important for all of us to remember that wearing a mask alone doesn’t make us safe.”

“We all need to keep washing our hands frequently and maintaining a distance from people, as well.”

For more information on where to find 3-ply surgical masks and N95s, check here or here to start.

A version of this article first appeared on WebMD.com.

Are you still wearing a cloth face mask?

Amid the rapidly spreading Omicron variant, experts stress that we all should swap cloth masks for N95 respirators or 3-ply surgical masks.

For background: N95 respirators are tightly fitting masks that cover your mouth and nose and help prevent contact with droplets and tiny particles in the air from people talking, coughing, sneezing, and spreading in other ways. Usually worn by health care workers and first responders, these masks can filter up to 95% of air droplets and particles, according to the CDC.

KN95 and KN94 masks are similar but are designed to meet international standards, unlike N95s that are approved by the Centers for Disease Control and Prevention’s National Institute for Occupational Safety and Health.

Meanwhile, a 3-ply surgical mask is a looser-fitting mask that can help prevent contact with infected droplets in the air.

But recommendations to opt for N95 and 3-ply surgical masks over cloth masks are nothing new, says Leana Wen, MD, an emergency doctor and public health professor at George Washington University, Washington.

In fact, public health experts have been urging stronger mask protection for months.

“It’s not just with Omicron that we need better masks, it was with Delta, it was with Alpha before that,” Dr. Wen said. “We have known for many months that COVID-19 is airborne, and therefore, a simple cloth mask is not going to cut it.”

Here’s what to know about these protective masks.
 

They’re necessary

Omicron is spreading much faster than previous COVID-19 variants. As it’s up to three times as likely to spread as the Delta variant, mask-wearing is paramount right now, says Anita Gupta, DO, an adjunct assistant professor of anesthesiology and critical care medicine and pain medicine at Johns Hopkins University, Baltimore.

The quality of a mask also matters a lot, said Dr. Wen.

“Double masking, including a well-fitting cloth mask on top of a surgical mask, adds additional protection,” she said. “Ideally, though, people should be wearing an N95, KN95, or KF94 when in indoor settings around other people with unknown vaccination status.”

If wearing an N95 mask causes extreme discomfort, wear it in high-risk settings where there are lots of people, like crowded restaurants and busy commuter trains, says Dr. Wen. “If you’re in a grocery store, there’s plenty of space and ventilation. You may not need an N95. I recommend that people obtain different masks and practice with them in low-risk settings before they go out in public in a high-risk setting.”

But people should wear a 3-ply surgical mask at the very least.
 

Three-ply surgical and N95 mask qualities

With 3-ply surgical masks, the fit of the mask is often more of an issue than its comfort, Dr. Wen said. But there are ways to adjust these masks, especially for those who have smaller heads.

“You can put a rubber band around the ear loops and make them a bit tighter,” said Dr. Wen. “Some people have found that using pins in their hair, that’s another way of keeping the loops in place.”

Another important tip on 3-ply surgical masks and N95s: These masks are reusable.

But how many times you should use them varies, Dr. Wen said. “As an example, if you are sweating a lot, and the mask is now really damp. Or putting it in your purse or backpack, and now it’s misshapen, and you cannot get it back to fit on your face, then it’s time to throw it away.”
 

Protection first

For some, cloth masks became somewhat of a statement, with people sporting logos of their favorite NFL team, or maybe even a fun animal print.

But you should always keep in mind the purpose of wearing a mask, Dr. Wen said. “Mask wearing is very functional and is about reducing your likelihood of contracting COVID. People should also use whatever methods inspire them, too, but for me, it’s purely a functional exercise.”

Mask wearing is not always enjoyable, but it remains critical in keeping people safe from COVID-19, especially the elderly and other high-risk people, Gupta says.

“There is lots of research and experts working hard to stop COVID-19,” she says. “It is important for all of us to remember that wearing a mask alone doesn’t make us safe.”

“We all need to keep washing our hands frequently and maintaining a distance from people, as well.”

For more information on where to find 3-ply surgical masks and N95s, check here or here to start.

A version of this article first appeared on WebMD.com.

With new cases of COVID-19 skyrocketing to more than 240,000 a day recently in the U.S., many people are facing the same situation: A family member or friend tests positive or was exposed to someone who did, and the holiday gathering, visit, or return to work is just days or hours away. Now what?

New guidance issued Dec. 27 by the Centers for Disease Control and Prevention shortens the recommended isolation and quarantine period for the general population, coming after the agency shortened the isolation period for health care workers.

This news organization reached out to two infectious disease specialists to get answers to questions that are frequently asked in these situations.
 

If you have tested positive for COVID-19, what do you do next?

“If you have tested positive, you are infected. At the moment, you are [either] symptomatically affected or presymptomatically infected,’’ said Paul A. Offit, MD, director of the Vaccine Education Center and professor of pediatrics at Children’s Hospital of Philadelphia. At that point, you need to isolate for 5 days, according to the new CDC guidance. (That period has been shortened from 10 days.)

Isolation means separating the infected person from others. Quarantine refers to things you should do if you’re exposed to the virus or you have a close contact infected with COVID-19.

Under the new CDC guidelines, after the 5-day isolation, if the infected person then has no symptoms, he or she can leave isolation and then wear a mask for 5  days.

Those who test positive also need to tell their close contacts they are positive, said Amesh Adalja, MD, a senior scholar at the Johns Hopkins Center for Health Security.  

According to the CDC, the change to a shortened quarantine time is motivated by science ‘’demonstrating that the majority of SARS-CoV-2 transmission occurs early in the course of the illness, generally in the 1-2 days prior to onset of symptoms and the 2-3 days after.”
 

If you have been exposed to someone with COVID-19, what do you do next?

“If they are vaccinated and boosted, the guidance says there is no need to quarantine,” Dr. Adalja said. But the CDC guidance does recommend these people wear a well-fitting mask at all times when around others for 10 days after exposure.

For everyone else, including the unvaccinated and those who are more than 6 months out from their second Pfizer or Moderna vaccine dose, or more than 2 months from their J&J dose, the CDC recommends a quarantine for 5 days – and wearing a mask for the 5 days after that.

On a practical level, Dr. Adalja said he thinks those who are vaccinated but not boosted could also skip the quarantine and wear a mask for 10 days. Dr. Offit agrees. Because many people exposed have trouble quarantining, Dr. Offit advises those exposed who can’t follow that guidance to be sure to wear a mask for 10 days when indoors. The CDC guidance also offers that as another strategy – that if a 5-day quarantine is not feasible, the exposed person should wear a mask for 10 days when around others.

But if  someone who was exposed gets symptoms, that person then enters the infected category and follows that guidance, Dr. Offit said.
 

When should the person who has been exposed get tested?

After the exposure, ‘’you should probably wait 2-3 days,” Dr. Offit said. “The virus has to reproduce itself.”

Testing should be done by those exposed at least once, Dr. Adalja said.

“But there’s data to support daily testing to guide their activities, but this is not CDC guidance. Home tests are sufficient for this purpose.”
 

At what point can the infected person mingle safely with others?

“Technically, if asymptomatic, 10 days without a mask, 5 days with a mask,” said Dr. Adalja. “I think this could also be guided with home test negativity being a gauge [as to whether to mingle].”

A version of this article first appeared on WebMD.com.

With new cases of COVID-19 skyrocketing to more than 240,000 a day recently in the U.S., many people are facing the same situation: A family member or friend tests positive or was exposed to someone who did, and the holiday gathering, visit, or return to work is just days or hours away. Now what?

New guidance issued Dec. 27 by the Centers for Disease Control and Prevention shortens the recommended isolation and quarantine period for the general population, coming after the agency shortened the isolation period for health care workers.

This news organization reached out to two infectious disease specialists to get answers to questions that are frequently asked in these situations.
 

If you have tested positive for COVID-19, what do you do next?

“If you have tested positive, you are infected. At the moment, you are [either] symptomatically affected or presymptomatically infected,’’ said Paul A. Offit, MD, director of the Vaccine Education Center and professor of pediatrics at Children’s Hospital of Philadelphia. At that point, you need to isolate for 5 days, according to the new CDC guidance. (That period has been shortened from 10 days.)

Isolation means separating the infected person from others. Quarantine refers to things you should do if you’re exposed to the virus or you have a close contact infected with COVID-19.

Under the new CDC guidelines, after the 5-day isolation, if the infected person then has no symptoms, he or she can leave isolation and then wear a mask for 5  days.

Those who test positive also need to tell their close contacts they are positive, said Amesh Adalja, MD, a senior scholar at the Johns Hopkins Center for Health Security.  

According to the CDC, the change to a shortened quarantine time is motivated by science ‘’demonstrating that the majority of SARS-CoV-2 transmission occurs early in the course of the illness, generally in the 1-2 days prior to onset of symptoms and the 2-3 days after.”
 

If you have been exposed to someone with COVID-19, what do you do next?

“If they are vaccinated and boosted, the guidance says there is no need to quarantine,” Dr. Adalja said. But the CDC guidance does recommend these people wear a well-fitting mask at all times when around others for 10 days after exposure.

For everyone else, including the unvaccinated and those who are more than 6 months out from their second Pfizer or Moderna vaccine dose, or more than 2 months from their J&J dose, the CDC recommends a quarantine for 5 days – and wearing a mask for the 5 days after that.

On a practical level, Dr. Adalja said he thinks those who are vaccinated but not boosted could also skip the quarantine and wear a mask for 10 days. Dr. Offit agrees. Because many people exposed have trouble quarantining, Dr. Offit advises those exposed who can’t follow that guidance to be sure to wear a mask for 10 days when indoors. The CDC guidance also offers that as another strategy – that if a 5-day quarantine is not feasible, the exposed person should wear a mask for 10 days when around others.

But if  someone who was exposed gets symptoms, that person then enters the infected category and follows that guidance, Dr. Offit said.
 

When should the person who has been exposed get tested?

After the exposure, ‘’you should probably wait 2-3 days,” Dr. Offit said. “The virus has to reproduce itself.”

Testing should be done by those exposed at least once, Dr. Adalja said.

“But there’s data to support daily testing to guide their activities, but this is not CDC guidance. Home tests are sufficient for this purpose.”
 

At what point can the infected person mingle safely with others?

“Technically, if asymptomatic, 10 days without a mask, 5 days with a mask,” said Dr. Adalja. “I think this could also be guided with home test negativity being a gauge [as to whether to mingle].”

A version of this article first appeared on WebMD.com.

With new cases of COVID-19 skyrocketing to more than 240,000 a day recently in the U.S., many people are facing the same situation: A family member or friend tests positive or was exposed to someone who did, and the holiday gathering, visit, or return to work is just days or hours away. Now what?

New guidance issued Dec. 27 by the Centers for Disease Control and Prevention shortens the recommended isolation and quarantine period for the general population, coming after the agency shortened the isolation period for health care workers.

This news organization reached out to two infectious disease specialists to get answers to questions that are frequently asked in these situations.
 

If you have tested positive for COVID-19, what do you do next?

“If you have tested positive, you are infected. At the moment, you are [either] symptomatically affected or presymptomatically infected,’’ said Paul A. Offit, MD, director of the Vaccine Education Center and professor of pediatrics at Children’s Hospital of Philadelphia. At that point, you need to isolate for 5 days, according to the new CDC guidance. (That period has been shortened from 10 days.)

Isolation means separating the infected person from others. Quarantine refers to things you should do if you’re exposed to the virus or you have a close contact infected with COVID-19.

Under the new CDC guidelines, after the 5-day isolation, if the infected person then has no symptoms, he or she can leave isolation and then wear a mask for 5  days.

Those who test positive also need to tell their close contacts they are positive, said Amesh Adalja, MD, a senior scholar at the Johns Hopkins Center for Health Security.  

According to the CDC, the change to a shortened quarantine time is motivated by science ‘’demonstrating that the majority of SARS-CoV-2 transmission occurs early in the course of the illness, generally in the 1-2 days prior to onset of symptoms and the 2-3 days after.”
 

If you have been exposed to someone with COVID-19, what do you do next?

“If they are vaccinated and boosted, the guidance says there is no need to quarantine,” Dr. Adalja said. But the CDC guidance does recommend these people wear a well-fitting mask at all times when around others for 10 days after exposure.

For everyone else, including the unvaccinated and those who are more than 6 months out from their second Pfizer or Moderna vaccine dose, or more than 2 months from their J&J dose, the CDC recommends a quarantine for 5 days – and wearing a mask for the 5 days after that.

On a practical level, Dr. Adalja said he thinks those who are vaccinated but not boosted could also skip the quarantine and wear a mask for 10 days. Dr. Offit agrees. Because many people exposed have trouble quarantining, Dr. Offit advises those exposed who can’t follow that guidance to be sure to wear a mask for 10 days when indoors. The CDC guidance also offers that as another strategy – that if a 5-day quarantine is not feasible, the exposed person should wear a mask for 10 days when around others.

But if  someone who was exposed gets symptoms, that person then enters the infected category and follows that guidance, Dr. Offit said.
 

When should the person who has been exposed get tested?

After the exposure, ‘’you should probably wait 2-3 days,” Dr. Offit said. “The virus has to reproduce itself.”

Testing should be done by those exposed at least once, Dr. Adalja said.

“But there’s data to support daily testing to guide their activities, but this is not CDC guidance. Home tests are sufficient for this purpose.”
 

At what point can the infected person mingle safely with others?

“Technically, if asymptomatic, 10 days without a mask, 5 days with a mask,” said Dr. Adalja. “I think this could also be guided with home test negativity being a gauge [as to whether to mingle].”

A version of this article first appeared on WebMD.com.

Rapid antigen tests for COVID-19 might be less effective at detecting the Omicron variant that is spreading rapidly across the United States, according to the Food and Drug Administration.

Early data suggest that COVID-19 antigen tests “do detect the Omicron variant but may have reduced sensitivity,” the FDA said in a statement posted Dec. 28 on its website.

The FDA is working with the National Institutes of Health’s Rapid Acceleration of Diagnostics (RADx) initiative to assess the performance of antigen tests with patient samples that have the Omicron variant.

The potential for antigen tests to be less sensitive for the Omicron variant emerged in tests using patient samples containing live virus, “which represents the best way to evaluate true test performance in the short term,” the FDA said.

Initial laboratory tests using heat-activated (killed) virus samples found that antigen tests were able to detect the Omicron variant.

“It is important to note that these laboratory data are not a replacement for clinical study evaluations using patient samples with live virus, which are ongoing. The FDA and RADx are continuing to further evaluate the performance of antigen tests using patient samples with live virus,” the FDA said.
 

Testing still important

The agency continues to recommend use of antigen tests as directed in the authorized labeling and in accordance with the instructions included with the tests.

They note that antigen tests are generally less sensitive and less likely to pick up very early infections, compared with molecular tests.

The FDA continues to recommend that an individual with a negative antigen test who has symptoms or a high likelihood of infection because of exposure follow-up with a molecular test to determine if they have COVID-19.

An individual with a positive antigen test should self-isolate and seek follow-up care with a health care provider to determine the next steps.

The FDA, with partners and test developers, are continuing to evaluate test sensitivity, as well as the best timing and frequency of antigen testing.

The agency said that it will provide updated information and any needed recommendations when appropriate.

A version of this article first appeared on Medscape.com.

Rapid antigen tests for COVID-19 might be less effective at detecting the Omicron variant that is spreading rapidly across the United States, according to the Food and Drug Administration.

Early data suggest that COVID-19 antigen tests “do detect the Omicron variant but may have reduced sensitivity,” the FDA said in a statement posted Dec. 28 on its website.

The FDA is working with the National Institutes of Health’s Rapid Acceleration of Diagnostics (RADx) initiative to assess the performance of antigen tests with patient samples that have the Omicron variant.

The potential for antigen tests to be less sensitive for the Omicron variant emerged in tests using patient samples containing live virus, “which represents the best way to evaluate true test performance in the short term,” the FDA said.

Initial laboratory tests using heat-activated (killed) virus samples found that antigen tests were able to detect the Omicron variant.

“It is important to note that these laboratory data are not a replacement for clinical study evaluations using patient samples with live virus, which are ongoing. The FDA and RADx are continuing to further evaluate the performance of antigen tests using patient samples with live virus,” the FDA said.
 

Testing still important

The agency continues to recommend use of antigen tests as directed in the authorized labeling and in accordance with the instructions included with the tests.

They note that antigen tests are generally less sensitive and less likely to pick up very early infections, compared with molecular tests.

The FDA continues to recommend that an individual with a negative antigen test who has symptoms or a high likelihood of infection because of exposure follow-up with a molecular test to determine if they have COVID-19.

An individual with a positive antigen test should self-isolate and seek follow-up care with a health care provider to determine the next steps.

The FDA, with partners and test developers, are continuing to evaluate test sensitivity, as well as the best timing and frequency of antigen testing.

The agency said that it will provide updated information and any needed recommendations when appropriate.

A version of this article first appeared on Medscape.com.

Rapid antigen tests for COVID-19 might be less effective at detecting the Omicron variant that is spreading rapidly across the United States, according to the Food and Drug Administration.

Early data suggest that COVID-19 antigen tests “do detect the Omicron variant but may have reduced sensitivity,” the FDA said in a statement posted Dec. 28 on its website.

The FDA is working with the National Institutes of Health’s Rapid Acceleration of Diagnostics (RADx) initiative to assess the performance of antigen tests with patient samples that have the Omicron variant.

The potential for antigen tests to be less sensitive for the Omicron variant emerged in tests using patient samples containing live virus, “which represents the best way to evaluate true test performance in the short term,” the FDA said.

Initial laboratory tests using heat-activated (killed) virus samples found that antigen tests were able to detect the Omicron variant.

“It is important to note that these laboratory data are not a replacement for clinical study evaluations using patient samples with live virus, which are ongoing. The FDA and RADx are continuing to further evaluate the performance of antigen tests using patient samples with live virus,” the FDA said.
 

Testing still important

The agency continues to recommend use of antigen tests as directed in the authorized labeling and in accordance with the instructions included with the tests.

They note that antigen tests are generally less sensitive and less likely to pick up very early infections, compared with molecular tests.

The FDA continues to recommend that an individual with a negative antigen test who has symptoms or a high likelihood of infection because of exposure follow-up with a molecular test to determine if they have COVID-19.

An individual with a positive antigen test should self-isolate and seek follow-up care with a health care provider to determine the next steps.

The FDA, with partners and test developers, are continuing to evaluate test sensitivity, as well as the best timing and frequency of antigen testing.

The agency said that it will provide updated information and any needed recommendations when appropriate.

A version of this article first appeared on Medscape.com.

CASE GI distress while taking clozapine

Mr. F, age 29, has a history of psychiatric hospitalizations for psychotic episodes. It took a herculean effort to get him to agree to try clozapine, to which he has experienced a modest to good response. Unfortunately, recently he has been experiencing significant upper gastrointestinal (GI) distress. He attributes this to clozapine, and asks if he can discontinue this medication.

HISTORY Nausea becomes severe

Mr. F, age 29, resides in a long-term residential setting for patients with serious mental illness who need additional support following acute hospitalization. He has treatment-refractory schizophrenia. He first developed symptoms at age 18, and experienced multiple psychotic episodes requiring psychiatric hospitalizations that lasted for months. He has had numerous antipsychotic trials and a course of electroconvulsive therapy, with limited benefit.

More recently, Mr. F’s symptoms began to stabilize on a medication regimen that includes clozapine, 350 mg/d at bedtime, and haloperidol, 2 mg/d. He has not required psychiatric hospitalization for the past year.

Within months of initiating clozapine, Mr. F starts to complain daily about symptoms of worsening abdominal pain, abdominal bloating, nausea, intermittent episodes of emesis, and heartburn. The symptoms begin when he wakes up, are worse in the morning, and persist throughout the morning. He has experienced occasional mild constipation, but no diarrhea or weight loss. There have been no major changes in his diet, addition of new medications, or significant use of nonsteroidal anti-inflammatory drugs.

Mr. F’s nausea worsens over the next several weeks, to the point he begins to significantly limit how much he eats to cope with it. His GI symptoms are also impacting his mood and daily functioning.

This is not Mr. F’s first experience with significant GI distress. A few months before his first psychotic episode, Mr. F began developing vision problems, joint and abdominal pain, and a general decline in social and academic functioning. At that time, he underwent a significant workup by both GI and integrative medicine, including stool testing, upper endoscopy, and a Cyrex panel (a complementary medicine approach to exploring for specific autoimmune conditions). Results were largely within expected parameters, though a hydrogen breath test was suggestive of possible small intestine bowel overgrowth. More recently, he has been adhering to a gluten-free diet, which his family felt may help prevent some of his physical symptoms as well as mitigate some of his psychotic symptoms. He now asks if he can stop taking clozapine.

[polldaddy:11008393]

EVALUATION Establishing the correct diagnosis

Initially, Mr. F is diagnosed with gastroesophageal reflux disease (GERD) and attempts to manage his symptoms with pharmacologic and diet-based interventions. He significantly cuts down on soda consumption, and undergoes trials of calcium carbonate, antiemetics, and a PPI. Unfortunately, no material improvements are noted, and he continued to experience significant upper GI distress, especially after meals.

The psychiatric treatment team, Mr. F, and his family seek consultation with a GI specialist, who recommends that Mr. F. undergo a nuclear medicine solid gastric emptying scintigraphy study to evaluate for gastroparesis (delayed gastric emptying).¹ Results demonstrate grade 3 gastroparesis, with 56% radiotracer retainment at 4 hours. Mr. F is relieved to finally have an explanation for his persistent GI symptoms, and discusses his treatment options with the GI consultant and psychiatry team.

Continue to: The authors’ observations...

Mr. F and his family are opposed to starting a dopamine antagonist such as metoclopramide or domperidone (the latter is not FDA-approved but is available by special application to the FDA). These are first-line treatments for gastroparesis, but Mr. F and his family do not want them because of the risk of tardive dyskinesia. This is consistent with their previously expressed concerns regarding first-generation antipsychotics, and is why Mr. F has only been treated with a very low dose of haloperidol while the clozapine was titrated. Instead, Mr. F, his family, the psychiatry treatment team, and the GI specialist agree to pursue a combination of a GI hypomotility diet—which includes frequent small meals (4 to 6 per day), ideally with low fiber, low fat, and increased fluid intake—and a trial of the second line agent for gastroparesis, erythromycin, a medication with known hepatic cytochrome P450 (CYP) drug-drug interactions that impacts the clearance of clozapine.

Shared decision making is an evidence-based approach to engaging patients in medical decision making. It allows clinicians to provide education on potential treatment options and includes a discussion of risks and benefits. It also includes an assessment of the patient’s understanding of their condition, explores attitudes towards treatment, and elicits patient values specific to the desired outcome. Even in very ill patients with schizophrenia, shared decision making has been demonstrated to increase patient perception of involvement in their own care and knowledge about their condition.² Using this framework, Mr. F and his family, as well as the GI and psychiatric teams, felt confident that the agreed-upon approach was the best one for Mr. F.

TREATMENT Erythromycin and continued clozapine

Mr. F. is started on erythromycin, 100 mg 3 times a day. Erythromycin is a prokinetic agent that acts as a motilin agonist and increases the rate of gastric emptying. The liquid formulation of the medication is a suspension typically taken in 3- to 4-week courses, with 1 week “off” to prevent tachyphylaxis.³ Compared to the tablet, the liquid suspension has higher bioavailability, allows for easier dose adjustment, and takes less time to reach peak serum concentrations, which make it the preferred formulation for gastroparesis treatment.

Per the GI consultant’s recommendation, Mr. F receives a total of 3 courses of erythromycin, with some improvement in the frequency of his nausea noted only during the third erythromycin course. His clozapine levels are closely monitored during this time, as well as symptoms of clozapine toxicity (ie, sedation, confusion, hypersalivation, seizures, myoclonic jerks), because erythromycin can directly affect clozapine levels.^4,5 Case reports suggest that when these 2 medications are taken concomitantly, erythromycin inhibits the metabolism of hepatic enzyme CYP3A4, causing increased plasma concentrations of clozapine. Before starting erythromycin, Mr. F’s clozapine levels were 809 ng/mL at 350 mg/d. During the erythromycin courses, his levels are 1,043 to 1,074 ng/mL, despite reducing clozapine to 300 mg/d. However, he does not experience any adverse effects of clozapine (including seizures), which were being monitored closely.

The authors’ observations

Clozapine is the most effective medication for treatment-refractory schizophrenia.⁶ Compared to the other second-generation antipsychotics, it is associated with a lower risk of rehospitalization and treatment discontinuation, a significant decrease of positive symptom burden, and a reduction in suicidality.^7,8 Unfortunately, clozapine use is not without significant risk. FDA black box warnings highlight severe neutropenia, myocarditis, seizures, and hypotension as potentially life-threatening adverse effects that require close monitoring.⁹

Recently, clinicians have increasingly focused on the underrecognized but well-established finding that clozapine can cause significant GI adverse effects. While constipation is a known adverse effect of other antipsychotics, a 2016 meta-analysis of 32 studies estimated that the pooled prevalence of clozapine-associated constipation was 31.2%, and showed that patients receiving clozapine were 3 times more likely to be constipated than patients receiving other antipsychotics (odds ratio 3.02, CI 1.91-4.77, P < .001, n = 11 studies).¹⁰ A 2012 review of 16 studies involving potentially lethal adverse effects of clozapine demonstrated that rates of agranulocytosis and GI hypomotility were nearly identical, but that mortality from constipation was 3.6 to 12.5 times higher than mortality from agranulocytosis.¹¹

In 2020, the FDA issued an increased warning regarding severe bowel-related complications in patients receiving clozapine, ranging in severity from mild discomfort to ileus, bowel obstruction, toxic megacolon, and death.⁹

As exemplified by Mr. F’s case, upper GI symptoms associated with clozapine also are distressing and can have a significant impact on quality of life. Dyspepsia is a common complaint in patients with chronic psychiatric illness. A study of 79 psychiatric inpatients hospitalized long-term found that 80% reported at least 1 symptom of dyspepsia.¹² There are few older studies describing the effect of clozapine on the upper GI system. We and others previously reported on significantly increased use of—not only antacids—but also H2 blockers and prokinetic agents after initiating clozapine, but sample sizes are small.^13-15 These older data and newer studies suggest that GERD is a common upper GI disorder diagnosis following clozapine initiation, perhaps reflecting a knowledge gap and infrequent use of the more complex testing required to confirm a diagnosis of GI motility disorders such as gastroparesis.

In a study of 17 patients receiving clozapine, wireless motility capsules were used to measure whole gut motility, including gastric emptying time, small bowel transit time, and colonic transit time. In 82% of patients, there was demonstrated GI hypomotility in at least 1 region, and 41% of participants exhibited delayed gastric emptying, with a cut-off time of >5 hours required for a gastroparesis diagnosis.¹⁶ This is significantly higher than the prevalence of gastroparesis observed in studies of the general community.¹⁷ The Table^18,19 summarizes the differences between GERD and gastroparesis.

OUTCOME Some improvement

Mr. F experiences limited improvement of some of his nausea symptoms during the third erythromycin cycle and returns to the gastroenterologist for a follow-up appointment. The GI specialist decides to discontinue erythromycin in view of potential drug-drug interactions and Mr. F’s elevated clozapine levels and the associated risks that might entail. Mr. F is again offered the D2 dopamine antagonist metoclopramide, but again refuses due to the risk for tardive dyskinesia. He is asked to continue the GI dysmotility diet. Mr. F finds some relief of nausea symptoms from an over-the-counter product for nausea (a nasal inhalant containing essential oils) and is advised to follow up with the GI specialist in 3 months. Shortly thereafter, he is discharged to live in a less restrictive supportive housing environment, and his follow-up psychiatric care is provided by an assertive community treatment team. Over the next several months, the dosage of clozapine is decreased to 250 mg/d. Mr. F initially experiences worsening psychiatric symptoms, but stabilizes thereafter. He then moves out of state to be closer to his family.

Bottom Line

In patients receiving clozapine, frequent nausea along with clustering of heartburn, abdominal pain, bloating, early satiety, and vomiting (especially after meals) may signal gastroparesis rather than gastroesophageal reflux disease. Such patients may require consultation with a gastroenterologist, a scintigraphy-based gastric emptying test, and treatment if gastroparesis is confirmed.
 

CASE GI distress while taking clozapine

Mr. F, age 29, has a history of psychiatric hospitalizations for psychotic episodes. It took a herculean effort to get him to agree to try clozapine, to which he has experienced a modest to good response. Unfortunately, recently he has been experiencing significant upper gastrointestinal (GI) distress. He attributes this to clozapine, and asks if he can discontinue this medication.

HISTORY Nausea becomes severe

Mr. F, age 29, resides in a long-term residential setting for patients with serious mental illness who need additional support following acute hospitalization. He has treatment-refractory schizophrenia. He first developed symptoms at age 18, and experienced multiple psychotic episodes requiring psychiatric hospitalizations that lasted for months. He has had numerous antipsychotic trials and a course of electroconvulsive therapy, with limited benefit.

More recently, Mr. F’s symptoms began to stabilize on a medication regimen that includes clozapine, 350 mg/d at bedtime, and haloperidol, 2 mg/d. He has not required psychiatric hospitalization for the past year.

Within months of initiating clozapine, Mr. F starts to complain daily about symptoms of worsening abdominal pain, abdominal bloating, nausea, intermittent episodes of emesis, and heartburn. The symptoms begin when he wakes up, are worse in the morning, and persist throughout the morning. He has experienced occasional mild constipation, but no diarrhea or weight loss. There have been no major changes in his diet, addition of new medications, or significant use of nonsteroidal anti-inflammatory drugs.

Mr. F’s nausea worsens over the next several weeks, to the point he begins to significantly limit how much he eats to cope with it. His GI symptoms are also impacting his mood and daily functioning.

This is not Mr. F’s first experience with significant GI distress. A few months before his first psychotic episode, Mr. F began developing vision problems, joint and abdominal pain, and a general decline in social and academic functioning. At that time, he underwent a significant workup by both GI and integrative medicine, including stool testing, upper endoscopy, and a Cyrex panel (a complementary medicine approach to exploring for specific autoimmune conditions). Results were largely within expected parameters, though a hydrogen breath test was suggestive of possible small intestine bowel overgrowth. More recently, he has been adhering to a gluten-free diet, which his family felt may help prevent some of his physical symptoms as well as mitigate some of his psychotic symptoms. He now asks if he can stop taking clozapine.

[polldaddy:11008393]

EVALUATION Establishing the correct diagnosis

Initially, Mr. F is diagnosed with gastroesophageal reflux disease (GERD) and attempts to manage his symptoms with pharmacologic and diet-based interventions. He significantly cuts down on soda consumption, and undergoes trials of calcium carbonate, antiemetics, and a PPI. Unfortunately, no material improvements are noted, and he continued to experience significant upper GI distress, especially after meals.

The psychiatric treatment team, Mr. F, and his family seek consultation with a GI specialist, who recommends that Mr. F. undergo a nuclear medicine solid gastric emptying scintigraphy study to evaluate for gastroparesis (delayed gastric emptying).¹ Results demonstrate grade 3 gastroparesis, with 56% radiotracer retainment at 4 hours. Mr. F is relieved to finally have an explanation for his persistent GI symptoms, and discusses his treatment options with the GI consultant and psychiatry team.

Continue to: The authors’ observations...

Mr. F and his family are opposed to starting a dopamine antagonist such as metoclopramide or domperidone (the latter is not FDA-approved but is available by special application to the FDA). These are first-line treatments for gastroparesis, but Mr. F and his family do not want them because of the risk of tardive dyskinesia. This is consistent with their previously expressed concerns regarding first-generation antipsychotics, and is why Mr. F has only been treated with a very low dose of haloperidol while the clozapine was titrated. Instead, Mr. F, his family, the psychiatry treatment team, and the GI specialist agree to pursue a combination of a GI hypomotility diet—which includes frequent small meals (4 to 6 per day), ideally with low fiber, low fat, and increased fluid intake—and a trial of the second line agent for gastroparesis, erythromycin, a medication with known hepatic cytochrome P450 (CYP) drug-drug interactions that impacts the clearance of clozapine.

Shared decision making is an evidence-based approach to engaging patients in medical decision making. It allows clinicians to provide education on potential treatment options and includes a discussion of risks and benefits. It also includes an assessment of the patient’s understanding of their condition, explores attitudes towards treatment, and elicits patient values specific to the desired outcome. Even in very ill patients with schizophrenia, shared decision making has been demonstrated to increase patient perception of involvement in their own care and knowledge about their condition.² Using this framework, Mr. F and his family, as well as the GI and psychiatric teams, felt confident that the agreed-upon approach was the best one for Mr. F.

TREATMENT Erythromycin and continued clozapine

Mr. F. is started on erythromycin, 100 mg 3 times a day. Erythromycin is a prokinetic agent that acts as a motilin agonist and increases the rate of gastric emptying. The liquid formulation of the medication is a suspension typically taken in 3- to 4-week courses, with 1 week “off” to prevent tachyphylaxis.³ Compared to the tablet, the liquid suspension has higher bioavailability, allows for easier dose adjustment, and takes less time to reach peak serum concentrations, which make it the preferred formulation for gastroparesis treatment.

Per the GI consultant’s recommendation, Mr. F receives a total of 3 courses of erythromycin, with some improvement in the frequency of his nausea noted only during the third erythromycin course. His clozapine levels are closely monitored during this time, as well as symptoms of clozapine toxicity (ie, sedation, confusion, hypersalivation, seizures, myoclonic jerks), because erythromycin can directly affect clozapine levels.^4,5 Case reports suggest that when these 2 medications are taken concomitantly, erythromycin inhibits the metabolism of hepatic enzyme CYP3A4, causing increased plasma concentrations of clozapine. Before starting erythromycin, Mr. F’s clozapine levels were 809 ng/mL at 350 mg/d. During the erythromycin courses, his levels are 1,043 to 1,074 ng/mL, despite reducing clozapine to 300 mg/d. However, he does not experience any adverse effects of clozapine (including seizures), which were being monitored closely.

The authors’ observations

Clozapine is the most effective medication for treatment-refractory schizophrenia.⁶ Compared to the other second-generation antipsychotics, it is associated with a lower risk of rehospitalization and treatment discontinuation, a significant decrease of positive symptom burden, and a reduction in suicidality.^7,8 Unfortunately, clozapine use is not without significant risk. FDA black box warnings highlight severe neutropenia, myocarditis, seizures, and hypotension as potentially life-threatening adverse effects that require close monitoring.⁹

Recently, clinicians have increasingly focused on the underrecognized but well-established finding that clozapine can cause significant GI adverse effects. While constipation is a known adverse effect of other antipsychotics, a 2016 meta-analysis of 32 studies estimated that the pooled prevalence of clozapine-associated constipation was 31.2%, and showed that patients receiving clozapine were 3 times more likely to be constipated than patients receiving other antipsychotics (odds ratio 3.02, CI 1.91-4.77, P < .001, n = 11 studies).¹⁰ A 2012 review of 16 studies involving potentially lethal adverse effects of clozapine demonstrated that rates of agranulocytosis and GI hypomotility were nearly identical, but that mortality from constipation was 3.6 to 12.5 times higher than mortality from agranulocytosis.¹¹

In 2020, the FDA issued an increased warning regarding severe bowel-related complications in patients receiving clozapine, ranging in severity from mild discomfort to ileus, bowel obstruction, toxic megacolon, and death.⁹

As exemplified by Mr. F’s case, upper GI symptoms associated with clozapine also are distressing and can have a significant impact on quality of life. Dyspepsia is a common complaint in patients with chronic psychiatric illness. A study of 79 psychiatric inpatients hospitalized long-term found that 80% reported at least 1 symptom of dyspepsia.¹² There are few older studies describing the effect of clozapine on the upper GI system. We and others previously reported on significantly increased use of—not only antacids—but also H2 blockers and prokinetic agents after initiating clozapine, but sample sizes are small.^13-15 These older data and newer studies suggest that GERD is a common upper GI disorder diagnosis following clozapine initiation, perhaps reflecting a knowledge gap and infrequent use of the more complex testing required to confirm a diagnosis of GI motility disorders such as gastroparesis.

In a study of 17 patients receiving clozapine, wireless motility capsules were used to measure whole gut motility, including gastric emptying time, small bowel transit time, and colonic transit time. In 82% of patients, there was demonstrated GI hypomotility in at least 1 region, and 41% of participants exhibited delayed gastric emptying, with a cut-off time of >5 hours required for a gastroparesis diagnosis.¹⁶ This is significantly higher than the prevalence of gastroparesis observed in studies of the general community.¹⁷ The Table^18,19 summarizes the differences between GERD and gastroparesis.

OUTCOME Some improvement

Mr. F experiences limited improvement of some of his nausea symptoms during the third erythromycin cycle and returns to the gastroenterologist for a follow-up appointment. The GI specialist decides to discontinue erythromycin in view of potential drug-drug interactions and Mr. F’s elevated clozapine levels and the associated risks that might entail. Mr. F is again offered the D2 dopamine antagonist metoclopramide, but again refuses due to the risk for tardive dyskinesia. He is asked to continue the GI dysmotility diet. Mr. F finds some relief of nausea symptoms from an over-the-counter product for nausea (a nasal inhalant containing essential oils) and is advised to follow up with the GI specialist in 3 months. Shortly thereafter, he is discharged to live in a less restrictive supportive housing environment, and his follow-up psychiatric care is provided by an assertive community treatment team. Over the next several months, the dosage of clozapine is decreased to 250 mg/d. Mr. F initially experiences worsening psychiatric symptoms, but stabilizes thereafter. He then moves out of state to be closer to his family.

Bottom Line

In patients receiving clozapine, frequent nausea along with clustering of heartburn, abdominal pain, bloating, early satiety, and vomiting (especially after meals) may signal gastroparesis rather than gastroesophageal reflux disease. Such patients may require consultation with a gastroenterologist, a scintigraphy-based gastric emptying test, and treatment if gastroparesis is confirmed.
 

CASE GI distress while taking clozapine

Mr. F, age 29, has a history of psychiatric hospitalizations for psychotic episodes. It took a herculean effort to get him to agree to try clozapine, to which he has experienced a modest to good response. Unfortunately, recently he has been experiencing significant upper gastrointestinal (GI) distress. He attributes this to clozapine, and asks if he can discontinue this medication.

HISTORY Nausea becomes severe

Mr. F, age 29, resides in a long-term residential setting for patients with serious mental illness who need additional support following acute hospitalization. He has treatment-refractory schizophrenia. He first developed symptoms at age 18, and experienced multiple psychotic episodes requiring psychiatric hospitalizations that lasted for months. He has had numerous antipsychotic trials and a course of electroconvulsive therapy, with limited benefit.

More recently, Mr. F’s symptoms began to stabilize on a medication regimen that includes clozapine, 350 mg/d at bedtime, and haloperidol, 2 mg/d. He has not required psychiatric hospitalization for the past year.

Within months of initiating clozapine, Mr. F starts to complain daily about symptoms of worsening abdominal pain, abdominal bloating, nausea, intermittent episodes of emesis, and heartburn. The symptoms begin when he wakes up, are worse in the morning, and persist throughout the morning. He has experienced occasional mild constipation, but no diarrhea or weight loss. There have been no major changes in his diet, addition of new medications, or significant use of nonsteroidal anti-inflammatory drugs.

Mr. F’s nausea worsens over the next several weeks, to the point he begins to significantly limit how much he eats to cope with it. His GI symptoms are also impacting his mood and daily functioning.

This is not Mr. F’s first experience with significant GI distress. A few months before his first psychotic episode, Mr. F began developing vision problems, joint and abdominal pain, and a general decline in social and academic functioning. At that time, he underwent a significant workup by both GI and integrative medicine, including stool testing, upper endoscopy, and a Cyrex panel (a complementary medicine approach to exploring for specific autoimmune conditions). Results were largely within expected parameters, though a hydrogen breath test was suggestive of possible small intestine bowel overgrowth. More recently, he has been adhering to a gluten-free diet, which his family felt may help prevent some of his physical symptoms as well as mitigate some of his psychotic symptoms. He now asks if he can stop taking clozapine.

[polldaddy:11008393]

EVALUATION Establishing the correct diagnosis

Initially, Mr. F is diagnosed with gastroesophageal reflux disease (GERD) and attempts to manage his symptoms with pharmacologic and diet-based interventions. He significantly cuts down on soda consumption, and undergoes trials of calcium carbonate, antiemetics, and a PPI. Unfortunately, no material improvements are noted, and he continued to experience significant upper GI distress, especially after meals.

The psychiatric treatment team, Mr. F, and his family seek consultation with a GI specialist, who recommends that Mr. F. undergo a nuclear medicine solid gastric emptying scintigraphy study to evaluate for gastroparesis (delayed gastric emptying).¹ Results demonstrate grade 3 gastroparesis, with 56% radiotracer retainment at 4 hours. Mr. F is relieved to finally have an explanation for his persistent GI symptoms, and discusses his treatment options with the GI consultant and psychiatry team.

Continue to: The authors’ observations...

Mr. F and his family are opposed to starting a dopamine antagonist such as metoclopramide or domperidone (the latter is not FDA-approved but is available by special application to the FDA). These are first-line treatments for gastroparesis, but Mr. F and his family do not want them because of the risk of tardive dyskinesia. This is consistent with their previously expressed concerns regarding first-generation antipsychotics, and is why Mr. F has only been treated with a very low dose of haloperidol while the clozapine was titrated. Instead, Mr. F, his family, the psychiatry treatment team, and the GI specialist agree to pursue a combination of a GI hypomotility diet—which includes frequent small meals (4 to 6 per day), ideally with low fiber, low fat, and increased fluid intake—and a trial of the second line agent for gastroparesis, erythromycin, a medication with known hepatic cytochrome P450 (CYP) drug-drug interactions that impacts the clearance of clozapine.

Shared decision making is an evidence-based approach to engaging patients in medical decision making. It allows clinicians to provide education on potential treatment options and includes a discussion of risks and benefits. It also includes an assessment of the patient’s understanding of their condition, explores attitudes towards treatment, and elicits patient values specific to the desired outcome. Even in very ill patients with schizophrenia, shared decision making has been demonstrated to increase patient perception of involvement in their own care and knowledge about their condition.² Using this framework, Mr. F and his family, as well as the GI and psychiatric teams, felt confident that the agreed-upon approach was the best one for Mr. F.

TREATMENT Erythromycin and continued clozapine

Mr. F. is started on erythromycin, 100 mg 3 times a day. Erythromycin is a prokinetic agent that acts as a motilin agonist and increases the rate of gastric emptying. The liquid formulation of the medication is a suspension typically taken in 3- to 4-week courses, with 1 week “off” to prevent tachyphylaxis.³ Compared to the tablet, the liquid suspension has higher bioavailability, allows for easier dose adjustment, and takes less time to reach peak serum concentrations, which make it the preferred formulation for gastroparesis treatment.

Per the GI consultant’s recommendation, Mr. F receives a total of 3 courses of erythromycin, with some improvement in the frequency of his nausea noted only during the third erythromycin course. His clozapine levels are closely monitored during this time, as well as symptoms of clozapine toxicity (ie, sedation, confusion, hypersalivation, seizures, myoclonic jerks), because erythromycin can directly affect clozapine levels.^4,5 Case reports suggest that when these 2 medications are taken concomitantly, erythromycin inhibits the metabolism of hepatic enzyme CYP3A4, causing increased plasma concentrations of clozapine. Before starting erythromycin, Mr. F’s clozapine levels were 809 ng/mL at 350 mg/d. During the erythromycin courses, his levels are 1,043 to 1,074 ng/mL, despite reducing clozapine to 300 mg/d. However, he does not experience any adverse effects of clozapine (including seizures), which were being monitored closely.

The authors’ observations

Clozapine is the most effective medication for treatment-refractory schizophrenia.⁶ Compared to the other second-generation antipsychotics, it is associated with a lower risk of rehospitalization and treatment discontinuation, a significant decrease of positive symptom burden, and a reduction in suicidality.^7,8 Unfortunately, clozapine use is not without significant risk. FDA black box warnings highlight severe neutropenia, myocarditis, seizures, and hypotension as potentially life-threatening adverse effects that require close monitoring.⁹

Recently, clinicians have increasingly focused on the underrecognized but well-established finding that clozapine can cause significant GI adverse effects. While constipation is a known adverse effect of other antipsychotics, a 2016 meta-analysis of 32 studies estimated that the pooled prevalence of clozapine-associated constipation was 31.2%, and showed that patients receiving clozapine were 3 times more likely to be constipated than patients receiving other antipsychotics (odds ratio 3.02, CI 1.91-4.77, P < .001, n = 11 studies).¹⁰ A 2012 review of 16 studies involving potentially lethal adverse effects of clozapine demonstrated that rates of agranulocytosis and GI hypomotility were nearly identical, but that mortality from constipation was 3.6 to 12.5 times higher than mortality from agranulocytosis.¹¹

In 2020, the FDA issued an increased warning regarding severe bowel-related complications in patients receiving clozapine, ranging in severity from mild discomfort to ileus, bowel obstruction, toxic megacolon, and death.⁹

As exemplified by Mr. F’s case, upper GI symptoms associated with clozapine also are distressing and can have a significant impact on quality of life. Dyspepsia is a common complaint in patients with chronic psychiatric illness. A study of 79 psychiatric inpatients hospitalized long-term found that 80% reported at least 1 symptom of dyspepsia.¹² There are few older studies describing the effect of clozapine on the upper GI system. We and others previously reported on significantly increased use of—not only antacids—but also H2 blockers and prokinetic agents after initiating clozapine, but sample sizes are small.^13-15 These older data and newer studies suggest that GERD is a common upper GI disorder diagnosis following clozapine initiation, perhaps reflecting a knowledge gap and infrequent use of the more complex testing required to confirm a diagnosis of GI motility disorders such as gastroparesis.

In a study of 17 patients receiving clozapine, wireless motility capsules were used to measure whole gut motility, including gastric emptying time, small bowel transit time, and colonic transit time. In 82% of patients, there was demonstrated GI hypomotility in at least 1 region, and 41% of participants exhibited delayed gastric emptying, with a cut-off time of >5 hours required for a gastroparesis diagnosis.¹⁶ This is significantly higher than the prevalence of gastroparesis observed in studies of the general community.¹⁷ The Table^18,19 summarizes the differences between GERD and gastroparesis.

OUTCOME Some improvement

Mr. F experiences limited improvement of some of his nausea symptoms during the third erythromycin cycle and returns to the gastroenterologist for a follow-up appointment. The GI specialist decides to discontinue erythromycin in view of potential drug-drug interactions and Mr. F’s elevated clozapine levels and the associated risks that might entail. Mr. F is again offered the D2 dopamine antagonist metoclopramide, but again refuses due to the risk for tardive dyskinesia. He is asked to continue the GI dysmotility diet. Mr. F finds some relief of nausea symptoms from an over-the-counter product for nausea (a nasal inhalant containing essential oils) and is advised to follow up with the GI specialist in 3 months. Shortly thereafter, he is discharged to live in a less restrictive supportive housing environment, and his follow-up psychiatric care is provided by an assertive community treatment team. Over the next several months, the dosage of clozapine is decreased to 250 mg/d. Mr. F initially experiences worsening psychiatric symptoms, but stabilizes thereafter. He then moves out of state to be closer to his family.

Bottom Line

In patients receiving clozapine, frequent nausea along with clustering of heartburn, abdominal pain, bloating, early satiety, and vomiting (especially after meals) may signal gastroparesis rather than gastroesophageal reflux disease. Such patients may require consultation with a gastroenterologist, a scintigraphy-based gastric emptying test, and treatment if gastroparesis is confirmed.
 

The coronavirus that causes COVID-19 can spread to the heart and brain within days of infection and can survive for months in organs, according to a new study by the National Institutes of Health.

The virus can spread to almost every organ system in the body, which could contribute to the ongoing symptoms seen in “long COVID” patients, the study authors wrote. The study is considered one of the most comprehensive reviews of how the virus replicates in human cells and persists in the human body. It is under review for publication in the journal Nature.

“This is remarkably important work,” Ziyad Al-Aly, MD, director of the Clinical Epidemiology Center at the Veterans Affairs St. Louis Health Care System, told Bloomberg News. Dr. Al-Aly wasn’t involved with the NIH study but has researched the long-term effects of COVID-19.

“For a long time now, we have been scratching our heads and asking why long COVID seems to affect so many organ systems,” he said. “This paper sheds some light and may help explain why long COVID can occur even in people who had mild or asymptomatic acute disease.”

The NIH researchers sampled and analyzed tissues from autopsies on 44 patients who died after contracting the coronavirus during the first year of the pandemic. They found persistent virus particles in multiple parts of the body, including the heart and brain, for as long as 230 days after symptoms began. This could represent infection with defective virus particles, they said, which has also been seen in persistent infections among measles patients.

“We don’t yet know what burden of chronic illness will result in years to come,” Raina MacIntyre, PhD, a professor of global biosecurity at the University of New South Wales, Sydney, told Bloomberg News.

“Will we see young-onset cardiac failure in survivors or early-onset dementia?” she asked. “These are unanswered questions which call for a precautionary public health approach to mitigation of the spread of this virus.”

Unlike other COVID-19 autopsy research, the NIH team had a more comprehensive postmortem tissue collection process, which typically occurred within a day of the patient’s death, Bloomberg News reported. The researchers also used a variety of ways to preserve tissue to figure out viral levels. They were able to grow the virus collected from several tissues, including the heart, lungs, small intestine, and adrenal glands.

“Our results collectively show that, while the highest burden of SARS-CoV-2 is in the airways and lung, the virus can disseminate early during infection and infect cells throughout the entire body, including widely throughout the brain,” the study authors wrote.

A version of this article first appeared on WebMD.com.

The coronavirus that causes COVID-19 can spread to the heart and brain within days of infection and can survive for months in organs, according to a new study by the National Institutes of Health.

The virus can spread to almost every organ system in the body, which could contribute to the ongoing symptoms seen in “long COVID” patients, the study authors wrote. The study is considered one of the most comprehensive reviews of how the virus replicates in human cells and persists in the human body. It is under review for publication in the journal Nature.

“This is remarkably important work,” Ziyad Al-Aly, MD, director of the Clinical Epidemiology Center at the Veterans Affairs St. Louis Health Care System, told Bloomberg News. Dr. Al-Aly wasn’t involved with the NIH study but has researched the long-term effects of COVID-19.

“For a long time now, we have been scratching our heads and asking why long COVID seems to affect so many organ systems,” he said. “This paper sheds some light and may help explain why long COVID can occur even in people who had mild or asymptomatic acute disease.”

The NIH researchers sampled and analyzed tissues from autopsies on 44 patients who died after contracting the coronavirus during the first year of the pandemic. They found persistent virus particles in multiple parts of the body, including the heart and brain, for as long as 230 days after symptoms began. This could represent infection with defective virus particles, they said, which has also been seen in persistent infections among measles patients.

“We don’t yet know what burden of chronic illness will result in years to come,” Raina MacIntyre, PhD, a professor of global biosecurity at the University of New South Wales, Sydney, told Bloomberg News.

“Will we see young-onset cardiac failure in survivors or early-onset dementia?” she asked. “These are unanswered questions which call for a precautionary public health approach to mitigation of the spread of this virus.”

Unlike other COVID-19 autopsy research, the NIH team had a more comprehensive postmortem tissue collection process, which typically occurred within a day of the patient’s death, Bloomberg News reported. The researchers also used a variety of ways to preserve tissue to figure out viral levels. They were able to grow the virus collected from several tissues, including the heart, lungs, small intestine, and adrenal glands.

“Our results collectively show that, while the highest burden of SARS-CoV-2 is in the airways and lung, the virus can disseminate early during infection and infect cells throughout the entire body, including widely throughout the brain,” the study authors wrote.

A version of this article first appeared on WebMD.com.

The coronavirus that causes COVID-19 can spread to the heart and brain within days of infection and can survive for months in organs, according to a new study by the National Institutes of Health.

The virus can spread to almost every organ system in the body, which could contribute to the ongoing symptoms seen in “long COVID” patients, the study authors wrote. The study is considered one of the most comprehensive reviews of how the virus replicates in human cells and persists in the human body. It is under review for publication in the journal Nature.

“This is remarkably important work,” Ziyad Al-Aly, MD, director of the Clinical Epidemiology Center at the Veterans Affairs St. Louis Health Care System, told Bloomberg News. Dr. Al-Aly wasn’t involved with the NIH study but has researched the long-term effects of COVID-19.

“For a long time now, we have been scratching our heads and asking why long COVID seems to affect so many organ systems,” he said. “This paper sheds some light and may help explain why long COVID can occur even in people who had mild or asymptomatic acute disease.”

The NIH researchers sampled and analyzed tissues from autopsies on 44 patients who died after contracting the coronavirus during the first year of the pandemic. They found persistent virus particles in multiple parts of the body, including the heart and brain, for as long as 230 days after symptoms began. This could represent infection with defective virus particles, they said, which has also been seen in persistent infections among measles patients.

“We don’t yet know what burden of chronic illness will result in years to come,” Raina MacIntyre, PhD, a professor of global biosecurity at the University of New South Wales, Sydney, told Bloomberg News.

“Will we see young-onset cardiac failure in survivors or early-onset dementia?” she asked. “These are unanswered questions which call for a precautionary public health approach to mitigation of the spread of this virus.”

Unlike other COVID-19 autopsy research, the NIH team had a more comprehensive postmortem tissue collection process, which typically occurred within a day of the patient’s death, Bloomberg News reported. The researchers also used a variety of ways to preserve tissue to figure out viral levels. They were able to grow the virus collected from several tissues, including the heart, lungs, small intestine, and adrenal glands.

“Our results collectively show that, while the highest burden of SARS-CoV-2 is in the airways and lung, the virus can disseminate early during infection and infect cells throughout the entire body, including widely throughout the brain,” the study authors wrote.

A version of this article first appeared on WebMD.com.

As a psychiatrist dedicated to working with people who are experiencing homelessness, I was very impressed with the new book edited by Col. (Ret.) Elspeth Cameron Ritchie, MD, MPH, and Maria D. Llorente, MD, about treating and providing services to this vulnerable population.

Courtesy Springer Publishing

The book, “Clinical Management of the Homeless Patient: Social, Psychiatric, and Medical Issues” (Cham, Switzerland: Springer Nature Switzerland, 2021), offers an in-depth review and analysis of the biopsychosocial complexities that affect how medical and behavioral health conditions present in those who are unhoused. Notably, the book recommends with great sensitivity best practices to address these conditions with care, understanding, and love.

This text, invaluable in particular for those of us clinicians who work with people experiencing homelessness (PEH), provides a historical context of homelessness in the United States, an evaluation of the current state, and indispensable guidance for medical and behavioral health practitioners, case managers, housing navigators, and policy makers alike. It also serves as an inspiring source for those who are considering work in the public sector while reminding those of us in the field why we continue to do this challenging and rewarding work.

Tips can provide hope to clinicians

The volume is divided into four clear sections that are easy to navigate depending on your area of expertise and interest. Each chapter consolidates an extensive literature review into an intriguing and thought-provoking analysis. Part I, “The Big Picture – Social and Medical Issues,” focuses on conditions that disproportionately affect those who are unhoused. The authors offer a glimpse into the unique challenges of managing routine health conditions. They also detail the practical knowledge that’s needed to best care for our most vulnerable neighbors; for example, promoting a shared decision-making model; simplifying treatment plans; prescribing, when possible, medications that are dosed daily – instead of multiple times per day; allowing for walk-in appointments; and addressing cultural, linguistic, and educational barriers.

Most chapters highlight informative case examples that bring the text to life. It can be heartbreaking to recognize and witness the inhumane conditions in which PEH live, and these practical tips and suggestions for future policies based on best practices can help prevent burnout and provide hope for those who care for this community.

Part II, “Psychiatric Issues and Treatments,” presents a brief yet comprehensive history on homelessness, beginning with the deep shame that PEH experienced in Colonial times as the result of cultural and religious influences. Sadly, that negative judgment continues to this day.

The authors also explain how deinstitutionalization and transinstitutionalization have shaped the current state of homelessness, including why many PEH receive their care in emergency departments while incarcerated. This section highlights the barriers of care that are created not just by the patient, but also by the clinicians and systems of care – and what’s needed practically to overcome those challenges.

I appreciate the chapter on substance use disorders. It reminds us that the most commonly used substance among PEH is tobacco, which has serious health effects and for which we have treatment; nevertheless, tobacco use is often overlooked because of the intense focus on opioid use disorder. This section also provides examples of the trauma-informed language to use when addressing difficult and sometimes stigmatizing topics, such as survival sex and trauma history.

The evidence-based discussion continues in Part III with a focus on topics that everyone working with PEH should understand, including food insecurity, the criminal justice system, and sex trafficking. Part IV highlights best practices that should be replicated in every community, including Housing First approaches, medical respite care, and multiple Veterans Administration programs.

Throughout the text, major themes reverberate across the chapters, beginning with empathy. All who work with PEH must understand the conditions and challenges PEH face every day that affect their physical and mental health. The authors offer a stark and pointed reminder that being unhoused amounts to a full-time job just to meet basic needs. In addition, the devastating role of trauma and structural racism in creating and promoting the conditions that lead someone to be unhoused cannot be underestimated.

Fortunately, the primary aim of the book is to highlight solutions, and it’s here that the book shines. While some interventions are well-known, such as the importance of working in multidisciplinary teams, building trust and rapport with our patients, and urging clinicians and institutions to examine their own judgments and biases that might interfere with humane treatment, other suggestions will lead some readers into new territory. The authors, for example, maintain that we need more data and evidence-based research that include PEH. They also make a case for more preventive care and enhanced professional education for all health care workers that centers on trauma-informed care, social determinants of health, and the unique needs of especially vulnerable communities, such as the unhoused LBGTQ+ community and policies that promote best practices, such as Housing First. The book is a stirring read. It offers both inspiration and practical guidance for all who are currently working with or interested in caring for people experiencing homelessness.

Dr. Bird is a psychiatrist with Alameda County Health Care for the Homeless and the TRUST Clinic in Oakland, Calif. She also is a cofounder of StreetHealth, a backpack street medicine team that provides psychiatric and substance use disorder treatment to people experiencing homelessness in downtown Oakland.

Dr. Bird has no disclosures.

As a psychiatrist dedicated to working with people who are experiencing homelessness, I was very impressed with the new book edited by Col. (Ret.) Elspeth Cameron Ritchie, MD, MPH, and Maria D. Llorente, MD, about treating and providing services to this vulnerable population.

Courtesy Springer Publishing

The book, “Clinical Management of the Homeless Patient: Social, Psychiatric, and Medical Issues” (Cham, Switzerland: Springer Nature Switzerland, 2021), offers an in-depth review and analysis of the biopsychosocial complexities that affect how medical and behavioral health conditions present in those who are unhoused. Notably, the book recommends with great sensitivity best practices to address these conditions with care, understanding, and love.

This text, invaluable in particular for those of us clinicians who work with people experiencing homelessness (PEH), provides a historical context of homelessness in the United States, an evaluation of the current state, and indispensable guidance for medical and behavioral health practitioners, case managers, housing navigators, and policy makers alike. It also serves as an inspiring source for those who are considering work in the public sector while reminding those of us in the field why we continue to do this challenging and rewarding work.

Tips can provide hope to clinicians

The volume is divided into four clear sections that are easy to navigate depending on your area of expertise and interest. Each chapter consolidates an extensive literature review into an intriguing and thought-provoking analysis. Part I, “The Big Picture – Social and Medical Issues,” focuses on conditions that disproportionately affect those who are unhoused. The authors offer a glimpse into the unique challenges of managing routine health conditions. They also detail the practical knowledge that’s needed to best care for our most vulnerable neighbors; for example, promoting a shared decision-making model; simplifying treatment plans; prescribing, when possible, medications that are dosed daily – instead of multiple times per day; allowing for walk-in appointments; and addressing cultural, linguistic, and educational barriers.

Most chapters highlight informative case examples that bring the text to life. It can be heartbreaking to recognize and witness the inhumane conditions in which PEH live, and these practical tips and suggestions for future policies based on best practices can help prevent burnout and provide hope for those who care for this community.

Part II, “Psychiatric Issues and Treatments,” presents a brief yet comprehensive history on homelessness, beginning with the deep shame that PEH experienced in Colonial times as the result of cultural and religious influences. Sadly, that negative judgment continues to this day.

The authors also explain how deinstitutionalization and transinstitutionalization have shaped the current state of homelessness, including why many PEH receive their care in emergency departments while incarcerated. This section highlights the barriers of care that are created not just by the patient, but also by the clinicians and systems of care – and what’s needed practically to overcome those challenges.

I appreciate the chapter on substance use disorders. It reminds us that the most commonly used substance among PEH is tobacco, which has serious health effects and for which we have treatment; nevertheless, tobacco use is often overlooked because of the intense focus on opioid use disorder. This section also provides examples of the trauma-informed language to use when addressing difficult and sometimes stigmatizing topics, such as survival sex and trauma history.

The evidence-based discussion continues in Part III with a focus on topics that everyone working with PEH should understand, including food insecurity, the criminal justice system, and sex trafficking. Part IV highlights best practices that should be replicated in every community, including Housing First approaches, medical respite care, and multiple Veterans Administration programs.

Throughout the text, major themes reverberate across the chapters, beginning with empathy. All who work with PEH must understand the conditions and challenges PEH face every day that affect their physical and mental health. The authors offer a stark and pointed reminder that being unhoused amounts to a full-time job just to meet basic needs. In addition, the devastating role of trauma and structural racism in creating and promoting the conditions that lead someone to be unhoused cannot be underestimated.

Fortunately, the primary aim of the book is to highlight solutions, and it’s here that the book shines. While some interventions are well-known, such as the importance of working in multidisciplinary teams, building trust and rapport with our patients, and urging clinicians and institutions to examine their own judgments and biases that might interfere with humane treatment, other suggestions will lead some readers into new territory. The authors, for example, maintain that we need more data and evidence-based research that include PEH. They also make a case for more preventive care and enhanced professional education for all health care workers that centers on trauma-informed care, social determinants of health, and the unique needs of especially vulnerable communities, such as the unhoused LBGTQ+ community and policies that promote best practices, such as Housing First. The book is a stirring read. It offers both inspiration and practical guidance for all who are currently working with or interested in caring for people experiencing homelessness.

Dr. Bird is a psychiatrist with Alameda County Health Care for the Homeless and the TRUST Clinic in Oakland, Calif. She also is a cofounder of StreetHealth, a backpack street medicine team that provides psychiatric and substance use disorder treatment to people experiencing homelessness in downtown Oakland.

Dr. Bird has no disclosures.

As a psychiatrist dedicated to working with people who are experiencing homelessness, I was very impressed with the new book edited by Col. (Ret.) Elspeth Cameron Ritchie, MD, MPH, and Maria D. Llorente, MD, about treating and providing services to this vulnerable population.

Courtesy Springer Publishing

The book, “Clinical Management of the Homeless Patient: Social, Psychiatric, and Medical Issues” (Cham, Switzerland: Springer Nature Switzerland, 2021), offers an in-depth review and analysis of the biopsychosocial complexities that affect how medical and behavioral health conditions present in those who are unhoused. Notably, the book recommends with great sensitivity best practices to address these conditions with care, understanding, and love.

This text, invaluable in particular for those of us clinicians who work with people experiencing homelessness (PEH), provides a historical context of homelessness in the United States, an evaluation of the current state, and indispensable guidance for medical and behavioral health practitioners, case managers, housing navigators, and policy makers alike. It also serves as an inspiring source for those who are considering work in the public sector while reminding those of us in the field why we continue to do this challenging and rewarding work.

Tips can provide hope to clinicians

The volume is divided into four clear sections that are easy to navigate depending on your area of expertise and interest. Each chapter consolidates an extensive literature review into an intriguing and thought-provoking analysis. Part I, “The Big Picture – Social and Medical Issues,” focuses on conditions that disproportionately affect those who are unhoused. The authors offer a glimpse into the unique challenges of managing routine health conditions. They also detail the practical knowledge that’s needed to best care for our most vulnerable neighbors; for example, promoting a shared decision-making model; simplifying treatment plans; prescribing, when possible, medications that are dosed daily – instead of multiple times per day; allowing for walk-in appointments; and addressing cultural, linguistic, and educational barriers.

Most chapters highlight informative case examples that bring the text to life. It can be heartbreaking to recognize and witness the inhumane conditions in which PEH live, and these practical tips and suggestions for future policies based on best practices can help prevent burnout and provide hope for those who care for this community.

Part II, “Psychiatric Issues and Treatments,” presents a brief yet comprehensive history on homelessness, beginning with the deep shame that PEH experienced in Colonial times as the result of cultural and religious influences. Sadly, that negative judgment continues to this day.

The authors also explain how deinstitutionalization and transinstitutionalization have shaped the current state of homelessness, including why many PEH receive their care in emergency departments while incarcerated. This section highlights the barriers of care that are created not just by the patient, but also by the clinicians and systems of care – and what’s needed practically to overcome those challenges.

I appreciate the chapter on substance use disorders. It reminds us that the most commonly used substance among PEH is tobacco, which has serious health effects and for which we have treatment; nevertheless, tobacco use is often overlooked because of the intense focus on opioid use disorder. This section also provides examples of the trauma-informed language to use when addressing difficult and sometimes stigmatizing topics, such as survival sex and trauma history.

The evidence-based discussion continues in Part III with a focus on topics that everyone working with PEH should understand, including food insecurity, the criminal justice system, and sex trafficking. Part IV highlights best practices that should be replicated in every community, including Housing First approaches, medical respite care, and multiple Veterans Administration programs.

Throughout the text, major themes reverberate across the chapters, beginning with empathy. All who work with PEH must understand the conditions and challenges PEH face every day that affect their physical and mental health. The authors offer a stark and pointed reminder that being unhoused amounts to a full-time job just to meet basic needs. In addition, the devastating role of trauma and structural racism in creating and promoting the conditions that lead someone to be unhoused cannot be underestimated.

Fortunately, the primary aim of the book is to highlight solutions, and it’s here that the book shines. While some interventions are well-known, such as the importance of working in multidisciplinary teams, building trust and rapport with our patients, and urging clinicians and institutions to examine their own judgments and biases that might interfere with humane treatment, other suggestions will lead some readers into new territory. The authors, for example, maintain that we need more data and evidence-based research that include PEH. They also make a case for more preventive care and enhanced professional education for all health care workers that centers on trauma-informed care, social determinants of health, and the unique needs of especially vulnerable communities, such as the unhoused LBGTQ+ community and policies that promote best practices, such as Housing First. The book is a stirring read. It offers both inspiration and practical guidance for all who are currently working with or interested in caring for people experiencing homelessness.

Dr. Bird is a psychiatrist with Alameda County Health Care for the Homeless and the TRUST Clinic in Oakland, Calif. She also is a cofounder of StreetHealth, a backpack street medicine team that provides psychiatric and substance use disorder treatment to people experiencing homelessness in downtown Oakland.

Dr. Bird has no disclosures.

Booster shot protection against symptomatic COVID-19 caused by the Omicron variant appears to fade in about 10 weeks, according to new data from Britain.

U.K. health officials shared the data just before Christmas and noted that there haven’t been enough severe cases of the Omicron variant to calculate how well boosters protect against severe disease. But they believe the extra shots provide significant protection against hospitalization and death.

“It will be a few weeks before effectiveness against severe disease with Omicron can be estimated,” U.K. Health Security Agency officials wrote in the report. “However, based on experience with previous variants, this is likely to be substantially higher than the estimates against symptomatic disease.”

Since countries began reporting Omicron cases in November, multiple studies have suggested the variant is better at escaping antibodies from vaccination and previous infection, according to the New York Times. The U.K. report adds to that, noting that both the initial vaccine series and booster doses were less effective and faded faster against the Omicron variant than the Delta variant.

Among those who received two doses of the AstraZeneca vaccine, a booster of the Pfizer or Moderna vaccine was 60% effective at preventing symptomatic disease 2 to 4 weeks after the shot. But after 10 weeks, the Pfizer booster was 35% effective, and the Moderna booster was 45% effective. (The AstraZeneca vaccine is not authorized in the United States, but the Johnson & Johnson shot uses a similar technology, the New York Times reported.)

Among those who received three Pfizer doses, vaccine effectiveness was 70% about a week after the booster but dropped to 45% after 10 weeks. At the same time, those who received an initial two-dose series of the Pfizer vaccine and then a Moderna booster seemed to have 75% effectiveness up to 9 weeks.

The report was based on an analysis of 148,000 Delta cases and 68,000 Omicron cases in the United Kingdom through Dec. 20. So far, the U.K. health officials wrote, Omicron infections appear to be less severe and less likely to lead to hospitalization than Delta infections. At that time, 132 people with lab-confirmed Omicron had been admitted to hospitals, and 14 deaths had been reported among ages 52-96.

“This analysis is preliminary because of the small numbers of Omicron cases currently in hospital and the limited spread of Omicron into older age groups as yet,” the report said.

The reinfection rate has also increased for the Omicron variant, the report found. Among the 116,000 people who had an Omicron infection, about 11,000 -- or 9.5% -- were linked to a previously confirmed infection, which is likely an undercount of reinfections. In the data analyzed, 69 Omicron cases were a third episode of COVID-19 infection, and 290 cases occurred 60-89 days after a first infection.

A version of this article first appeared on WebMD.com.

Booster shot protection against symptomatic COVID-19 caused by the Omicron variant appears to fade in about 10 weeks, according to new data from Britain.

U.K. health officials shared the data just before Christmas and noted that there haven’t been enough severe cases of the Omicron variant to calculate how well boosters protect against severe disease. But they believe the extra shots provide significant protection against hospitalization and death.

“It will be a few weeks before effectiveness against severe disease with Omicron can be estimated,” U.K. Health Security Agency officials wrote in the report. “However, based on experience with previous variants, this is likely to be substantially higher than the estimates against symptomatic disease.”

Since countries began reporting Omicron cases in November, multiple studies have suggested the variant is better at escaping antibodies from vaccination and previous infection, according to the New York Times. The U.K. report adds to that, noting that both the initial vaccine series and booster doses were less effective and faded faster against the Omicron variant than the Delta variant.

Among those who received two doses of the AstraZeneca vaccine, a booster of the Pfizer or Moderna vaccine was 60% effective at preventing symptomatic disease 2 to 4 weeks after the shot. But after 10 weeks, the Pfizer booster was 35% effective, and the Moderna booster was 45% effective. (The AstraZeneca vaccine is not authorized in the United States, but the Johnson & Johnson shot uses a similar technology, the New York Times reported.)

Among those who received three Pfizer doses, vaccine effectiveness was 70% about a week after the booster but dropped to 45% after 10 weeks. At the same time, those who received an initial two-dose series of the Pfizer vaccine and then a Moderna booster seemed to have 75% effectiveness up to 9 weeks.

The report was based on an analysis of 148,000 Delta cases and 68,000 Omicron cases in the United Kingdom through Dec. 20. So far, the U.K. health officials wrote, Omicron infections appear to be less severe and less likely to lead to hospitalization than Delta infections. At that time, 132 people with lab-confirmed Omicron had been admitted to hospitals, and 14 deaths had been reported among ages 52-96.

“This analysis is preliminary because of the small numbers of Omicron cases currently in hospital and the limited spread of Omicron into older age groups as yet,” the report said.

The reinfection rate has also increased for the Omicron variant, the report found. Among the 116,000 people who had an Omicron infection, about 11,000 -- or 9.5% -- were linked to a previously confirmed infection, which is likely an undercount of reinfections. In the data analyzed, 69 Omicron cases were a third episode of COVID-19 infection, and 290 cases occurred 60-89 days after a first infection.

A version of this article first appeared on WebMD.com.

Booster shot protection against symptomatic COVID-19 caused by the Omicron variant appears to fade in about 10 weeks, according to new data from Britain.

U.K. health officials shared the data just before Christmas and noted that there haven’t been enough severe cases of the Omicron variant to calculate how well boosters protect against severe disease. But they believe the extra shots provide significant protection against hospitalization and death.

“It will be a few weeks before effectiveness against severe disease with Omicron can be estimated,” U.K. Health Security Agency officials wrote in the report. “However, based on experience with previous variants, this is likely to be substantially higher than the estimates against symptomatic disease.”

Since countries began reporting Omicron cases in November, multiple studies have suggested the variant is better at escaping antibodies from vaccination and previous infection, according to the New York Times. The U.K. report adds to that, noting that both the initial vaccine series and booster doses were less effective and faded faster against the Omicron variant than the Delta variant.

Among those who received two doses of the AstraZeneca vaccine, a booster of the Pfizer or Moderna vaccine was 60% effective at preventing symptomatic disease 2 to 4 weeks after the shot. But after 10 weeks, the Pfizer booster was 35% effective, and the Moderna booster was 45% effective. (The AstraZeneca vaccine is not authorized in the United States, but the Johnson & Johnson shot uses a similar technology, the New York Times reported.)

Among those who received three Pfizer doses, vaccine effectiveness was 70% about a week after the booster but dropped to 45% after 10 weeks. At the same time, those who received an initial two-dose series of the Pfizer vaccine and then a Moderna booster seemed to have 75% effectiveness up to 9 weeks.

The report was based on an analysis of 148,000 Delta cases and 68,000 Omicron cases in the United Kingdom through Dec. 20. So far, the U.K. health officials wrote, Omicron infections appear to be less severe and less likely to lead to hospitalization than Delta infections. At that time, 132 people with lab-confirmed Omicron had been admitted to hospitals, and 14 deaths had been reported among ages 52-96.

“This analysis is preliminary because of the small numbers of Omicron cases currently in hospital and the limited spread of Omicron into older age groups as yet,” the report said.

The reinfection rate has also increased for the Omicron variant, the report found. Among the 116,000 people who had an Omicron infection, about 11,000 -- or 9.5% -- were linked to a previously confirmed infection, which is likely an undercount of reinfections. In the data analyzed, 69 Omicron cases were a third episode of COVID-19 infection, and 290 cases occurred 60-89 days after a first infection.

A version of this article first appeared on WebMD.com.