It’s time to start asking all patients about intimate partner violence

Article Type
Changed
Thu, 06/27/2019 - 15:10
Display Headline
It’s time to start asking all patients about intimate partner violence

Intimate partner violence (IPV) is a serious public health problem with considerable harmful health consequences. Decades of research have been dedicated to improving the identification of women in abusive heterosexual relationships and interventions that support healthier outcomes. A result of this work has been the recommendation of the US Preventive Services Task Force that all women of childbearing age be screened for IPV and provided with intervention or referral.1

The problem extends further, however: Epidemiologic studies and comprehensive reviews show: 1) a high rate of IPV victimization among heterosexual men and lesbian, gay, bisexual, and transsexual (LGBT) men and women2,3; 2) significant harmful effects on health and greater expectations of prejudice and discrimination among these populations4-6; and 3) evidence that screening and referral for IPV are likely to confer similar benefits for these populations.7 We argue that it is reasonable to ask all patients about abuse in their relationships while the research literature progresses.

We intend this article to serve a number of purposes:

  • support national standards for IPV screening of female patients
  • highlight the need for piloting universal IPV screening for all patients (ie, male and female, across the lifespan)
  • offer recommendations for navigating the process from IPV screening to referral, using insights gained from the substance abuse literature.

We also provide supplemental materials that facilitate establishment of screening and referral protocols for physicians across practice settings.

It’s time to start asking all patients about intimate partner violence
© Joe Gorman

What is intimate partner violence? How can you identify it?

Intimate partner violence includes physical and sexual violence and nonphysical forms of abuse, such as psychological aggression and emotional abuse, perpetrated by a current or former intimate partner.8 TABLE 19-14 provides definitions for each of these behavior categories and example behaviors. Nearly 25% of women and 20% of men report having experienced physical violence from a romantic partner and even higher rates of nonphysical IPV.15 Consequences of IPV victimization include acute and chronic medical illness, injury, and psychological problems, including depression, anxiety, and poor self-esteem.16

What is intimate partner violence?

Intimate partner violence is heterogenous, with differences in severity (eg, frequency and intensity of violence) and laterality (ie, is one partner violent? are both partners violent?).

Intimate partner violence is heterogeneous, with differences in severity (eg, frequency and intensity of violence) and laterality (ie, is one partner violent? are both partners violent?). A recent comprehensive review of the literature revealed that, for 49.2%-69.7% of partner-violent couples across diverse samples, IPV is perpetrated by both partners.17 Furthermore, this bidirectionality is not due entirely to aggression perpetrated in self-defense; rather, across diverse patient samples, that is the case for fewer than one-quarter of males and no more than approximately one-third of females.18 In the remaining cases, bidirectionality may be attributed to other motivations, such as a maladaptive emotional expression or a means by which to get a partner’s attention.18

Women are disproportionately susceptible to harmful outcomes as a result of severe violence, including physical injury, psychological distress (eg, depression and anxiety), and substance abuse.16,19 Some patients in unidirectionally violent relationships experience severe physical violence that may be, or become, life-threatening (0.4%-2.4% of couples in community samples)20—victimization that is traditionally known as “battering.”21

Continue to: These tools can facilitate screening for IPV

 

 

These tools can facilitate screening for IPV

Physicians might have reservations asking about IPV because of 1) concern whether there is sufficient time during an office visit to interview, screen, and refer, 2) feelings of powerlessness to stop violence by or toward a patient, and 3) general discomfort with the topic.22 Additionally, mandated reporting laws regarding IPV vary by state, making it crucial to know one’s own state laws on this issue to protect the safety of the patient and those around them.

Screening increases the likelihood of engaging the patient in supportive services, thus decreasing the isolation that is typical of abuse.

Research has shown that some patients prefer that their health care providers ask about relationship violence directly23; others are more willing to acknowledge IPV if asked using a paper-and-pencil measure, rather than face-to-face questions.24 Either way, screening increases the likelihood of engaging the patient in supportive services, thus decreasing the isolation that is typical of abuse.25 Based on this research, screening that utilizes face-valid items embedded within paperwork completed in the waiting room is recommended as an important first step toward identifying and helping patients who are experiencing IPV. Even under these conditions, however, heterosexual men and sexual minorities might be less willing than heterosexual women to admit experiencing IPV.26,27

A brief vignette that depicts how quickly the screening and referral process can be applied is presented in “IPV screening and referral: A real-world vignette." The vignette is a de-identified composite of heterosexual men experiencing IPV whom we have counseled.

SIDEBAR
IPV screening and referral: A real-world vignette

Physician: Before we wrap up: I noticed on your screening that you have been hurt and threatened a fair amount in the past year. Would it be OK if we spoke about that more?

Patient: My wife is emotional. Sometimes she gets really stressed out and just starts screaming and punching me. That’s just how she is.

Physician: Do you ever feel concerned for your safety?

Patient: Not really. She’s smaller than me and I can generally calm her down. I keep the guns locked up, so she can’t grab those any more. Mostly she just screams at me.

Physician: This may or may not fit with your perception but, based on what you are reporting, your relationship is what is called “at risk”—meaning you are at risk for having your physical or mental health negatively impacted. This actually happens to a lot of men, and there’s a brochure I can give you that has a lot more information about the risks and consequences of being hurt or threatened by a partner. Would you be willing to take a look at it?

Patient: I guess so.

Physician: OK. I’ll have the nurse bring you that brochure, and we can talk more about it next time you come in for an appointment. Would it be OK if we get you back in here 6 months from now?

Patient: Yeah, that could work.

Physician: Great. Let’s do that. Don’t hesitate to give me a call if your situation changes in any way in the meantime.

One model that provides a useful framework for IPV assessment is the Screening, Brief Intervention, and Referral to Treatment (SBIRT) model, which was developed to facilitate assessment of, and referral for, substance abuse—another heavily stigmatized health care problem. The SBIRT approach for substance abuse screening is associated with significant reduction in alcohol and drug abuse 6 months postintervention, as well as improvements in well-being, mental health, and functioning across gender, race and ethnicity, and age.28

IPASSPRT. Inspired by the SBIRT model for substance abuse, we created the Intimate Partner Aggression Screening, Safety Planning, and Referral to Treatment, or IPASSPRT (spoken as “i-passport”) project to provide tools that make IPV screening and referral accessible to a range of health care providers. These tools include a script and safety plan that guide providers through screening, safety planning, and referral in a manner that is collaborative and grounded in the spirit of motivational interviewing. We have made these tools available on the Web for ease of distribution (http://bit.ly/ipassprt; open by linking through “IPASSPRT-Script”).

Continue to: The IPASSPRT script appears lengthy...

 

 

The IPASSPRT script appears lengthy, but progress through its sections is directed by patient need; most patients will not require that all parts be completed. For example, a patient whose screen for IPV is negative and who feels safe in their relationship does not need assessment beyond page 2; on the other hand, the physician might need more information from a patient who is at greater risk for IPV. This response-based progression through the script makes the screening process dynamic, data-driven, and tailored to the patient’s needs—an approach that aids rapport and optimizes the physician’s limited time during the appointment.

In the sections that follow, we describe key components of this script.

What aggression, if any, is present? From whom? The Hurt, Insult, Threaten, and Scream inventory (HITS) (TABLE 2)29 is a widely used screen for IPV that has been validated for use in family medicine. A 4-item scale asks patients to report how often their partner physically hurts, insults, threatens, and screams at them using a 5-point scale (1 point, “never,” to 5 points, “frequently”). Although a score > 10 is indicative of IPV, item-level analysis is encouraged. Attending to which items the patient acknowledges and how often these behaviors occur yields a richer assessment than a summary score. In regard to simply asking a patient, “Do you feel safe at home?” (sensitivity of this question, 8.8%; specificity, 91.2%), the HITS better detects IPV with male and female patient populations in family practice and emergency care settings (sensitivity, 30%-100%; specificity, 86%-99%).27,30

HITS: The Hurt, Insult, Threaten, and Scream Inventory

What contextual factors and related concerns are present? It is important to understand proximal factors that might influence IPV risk to determine what kind of referral or treatment is appropriate—particularly for patients experiencing or engaging in infrequent, noninjurious, and bidirectional forms of IPV. Environmental and contextual stressors, such as financial hardship, unemployment, pregnancy, and discussion of divorce, can increase the risk for IPV.31,32 Situational influences, such as alcohol and drug intoxication, can also increase the risk for IPV. Victims of partner violence are at greater risk for mental health problems, including depression, anxiety, trauma- and stressor-related disorders, and substance use disorders. Risk goes both ways, however: Mental illness predicts subsequent IPV perpetration or victimization, and vice versa.31

Does the patient feel safe? Assessing the situation. Patient perception of safety in the relationship provides important information about the necessity of referral. Asking a patient if they feel unsafe because of the behavior of a current or former partner sheds light on the need for further safety assessment and immediate connection with appropriate resources.

Continue to: The Danger Assessment-5...

 

 

The Danger Assessment-5 (DA-5) (TABLE 333) is a useful 5-item tool for quickly assessing the risk for severe IPV.33 Patients respond to whether:

  • the frequency or severity of violence has increased in the past year
  • the partner has ever used, or threatened to use, a weapon
  • the patient believes the partner is capable of killing her (him)
  • the partner has ever tried to choke or strangle her (him)
  • the partner is violently and constantly jealous.

The Danger Assessment-5

Mental illness predicts subsequent IPV perpetration or victimization and vice versa.

Sensitivity and specificity analyses with a high-risk female sample suggested that 3 affirmative responses indicate a high risk for severe IPV and a need for adequate safety planning.

Brief motivational enhancement intervention. There are 3 components to this intervention.

  • Assess interest in making changes or seeking help. IPV is paradoxical: Many factors complicate the decision to leave or stay, and patients across the spectrum of victimization might have some motivation to stay with their partner. It is important to assess the patient’s motivation to make changes in their relationship.4,34
  • Provide feedback on screening. Sharing the results of screening with patients makes the assessment and referral process collaborative and transparent; collaborative engagement helps patients feel in control and invested in the follow-through.35 In the spirit of this endeavor, physicians are encouraged to refrain from providing raw or total scores from the measures; instead, share the interpretation of those scores, based on the participant’s responses to the screening items, in a matter-of-fact manner. At this point, elicit the patient’s response to this information, listen empathically, and answer questions before proceeding.

Consistent with screening for other serious health problems, we recommend that all patients be provided with information about abuse in romantic relationships. The National Center for Injury Prevention and Control Division of Violence Prevention has published a useful, easy-to-understand fact sheet (www.cdc.gov/violenceprevention/pdf/ipv-factsheet.pdf) that provides an overview of IPV-related behavior, how it influences health outcomes, who is at risk for IPV, and sources for support.

Continue to: Our IPASSPRT interview script...

 

 

Our IPASSPRT interview script (http://bit.ly/ipassprt) outlines how this information can be presented to patients as a typical part of the screening process. Providers are encouraged to share and review the information from the fact sheet with all patients and present it as part of the normal screening process to mitigate the potential for defensiveness on the part of the patient. For patients who screen positive for IPV, it might be important to brainstorm ideas for a safe, secure place to store this fact sheet and other resources from the brief intervention and referral process below (eg, a safety plan and specific referral information) so that the patient can access them quickly and easily, if needed.

For patients who screen negative for IPV, their screen and interview conclude at this point.

  • Provide recommendations based on the screen. Evidence suggests that collaborating with the patient on safety planning and referral can increase the likelihood of their engagement.7 Furthermore, failure to tailor the referral to the needs of the patient can be detrimental36—ie, overshooting the level of intervention might decrease the patient’s future treatment-seeking behavior and undermine their internal coping strategies, increasing the likelihood of future victimization. For that reason, we provide the following guidance on navigating the referral process for patients who screen positive for IPV.

Screening-based referral: A delicate and collaborative process

Referral for IPV victimization. Individual counseling, with or without an IPV focus, might be appropriate for patients at lower levels of risk; immediate connection with local IPV resources is strongly encouraged for patients at higher risk. This is a delicate, collaborative process, in which the physician offers recommendations for referral commensurate to the patient’s risk but must, ultimately, respect the patient’s autonomy by identifying referrals that fit the patient’s goals. We encourage providers to provide risk-informed recommendations and to elicit the patient’s thoughts about that information.

Several online resources are available to help physicians locate and connect with IPV-related resources in their community, including the National Health Resource Center on Domestic Violence (http://ipvhealth.org/), which provides a step-by-step guide to making such connections. We encourage physicians to develop these collaborative partnerships early to facilitate warm handoffs and increase the likelihood that a patient will follow through with the referral after screening.37

Referral for related concerns. As we’ve noted, IPV has numerous physical and mental health consequences, including depression, low self-esteem, trauma- and non-trauma-related anxiety, and substance abuse. In general, cognitive behavioral therapies appear most efficacious for treating these IPV-related consequences, but evidence is limited that such interventions diminish the likelihood of re-victimization.38 Intervention programs that foster problem-solving, solution-seeking, and cognitive restructuring for self-critical thoughts and misconceptions seem to produce the best physical and mental health outcomes.39 For patients who have a substance use disorder, treatment programs that target substance use have demonstrated a reduction in the rate of IPV recidivism.40 These findings indicate that establishing multiple treatment targets might reduce the risk for future aggression in relationships.

Continue to: The Substance Abuse and Mental Health Services Administration...

 

 

The Substance Abuse and Mental Health Services Administration of the US Department of Health and Human Services provides a useful online tool (https://findtreatment.samhsa.gov/) for locating local referrals that address behavioral health and substance-related concerns. The agency also provides a hotline (1-800-662-HELP [4357]) as an alternative resource for information and treatment referrals.

Safety planning can improve outcomes

For a patient who screens above low risk, safety planning with the patient is an important part of improving outcomes and can take several forms. Online resources, such as the Path to Safety interactive Web page (www.thehotline.org/help/path-to-safety/) maintained by The National Domestic Violence Hotline ([800]799-SAFE [7233]), provide information regarding important considerations for safety planning when:

  • living with an abusive partner
  • children are in the home
  • the patient is pregnant
  • pets are involved.

The Web site also provides information regarding legal options and resources related to IPV (eg, an order of protection) and steps for improving safety when leaving an abusive relationship. Patients at risk for IPV can explore the online tool and call the hotline.

For physicians who want to engage in provider-assisted safety planning, we’ve provided further guidance in the IPASSPRT screening script and safety plan (http://bit.ly/ipassprt) (TABLE 4).

Components of a safety plan: A patient guide

Goal: Affirm patients’ strengths and reinforce hope

Psychological aggression is the most common form of relationship aggression; repeated denigration might leave a person with little confidence in their ability to change their relationship or seek out identified resources. That’s why it’s useful to inquire—with genuine curiosity—about a time in the past when the patient accomplished something challenging. The physician’s enthusiastic reflection on this achievement can be a means of highlighting the patient’s ability to accomplish a meaningful goal; of reinforcing their hope; and of eliciting important resources within and around the patient that can facilitate action on their safety plan. (See “IPV-related resources for physicians and patients.”)

SIDEBAR
IPV-related resources for physicians and patients

Intimate Partner Aggression Screening, Safety Planning, and Referral to Treatment (IPASSPRT) Project
http://bit.ly/ipassprt
Online resource with tools designed by the authors, including an SBIRT-inspired script and safety plan template for IPV screening, safety planning, and referral

National Center for Injury Prevention and Control Division of Violence Prevention
www.cdc.gov/violenceprevention/pdf/ipv-factsheet.pdf
Overview of IPV-related behavior, influence on health outcomes, people at risk of IPV, and sources of support, all in a format easily understood by patients

National Health Resource Center on Domestic Violence
http://ipvhealth.org/
Includes guidance on connecting with IPV-related community resources; establishing such connections can facilitate warm handoffs and improve the likelihood that patients will follow through

Path to Safety, a service of The National Domestic Violence Hotline
www.thehotline.org/help/path-to-safety/
Extensive primer on safety plans for patients intending to stay in (or leave) an abusive relationship; includes important considerations for children, pets, and pregnancy, as well as emotional safety and legal options

The National Domestic Violence Hotline
› (800) 799-SAFE (7233)

Substance Abuse and Mental Health Services Administration
www.samhsa.gov/sbirt
Learning resources for the SBIRT protocol for substance abuse
https://findtreatment.samhsa.gov/
Search engine and resources for locating local referrals
› (800) 662-HELP (4357)
Hotline for information and assistance with locating local treatment referral

IPV, intimate partner violence; SBIRT, screening, brief intervention, and referral to treatment.
 

Continue to: Closing the screen and making a referral

 

 

Closing the screen and making a referral

The end of the interview should consist of a summary of topics discussed, including:

  • changes that the patient wants to make (if any)
  • their stated reasons for making those changes
  • the patient’s plan for accomplishing changes.

Physicians should also include their own role in next steps—whether providing a warm handoff to a local IPV referral, agreeing to a follow-up schedule with the patient, or making a call as a mandated reporter. To close out the interview, it is important to affirm respect for the patient’s autonomy in executing the plan.

It’s important to screen all patients—here’s why

A major impetus for this article has been to raise awareness about the need for expanded IPV screening across primary care settings. As mentioned, much of the literature on IPV victimization has focused on women; however, the few epidemiological investigations of victimization rates among men and members of LGBT couples show a high rate of victimization and considerable harmful health outcomes. Driven by stigma surrounding IPV, sex, and sexual minority status, patients might have expectations that they will be judged by a provider or “outed.”

Such barriers can lead many to suffer in silence until the problem can no longer be hidden or the danger becomes more emergent. Compassionate, nonjudgmental screening and collaborative safety planning—such as the approach we describe in this article—help ease the concerns of LGBT victims of IPV and improve the likelihood that conversations you have with them will occur earlier, rather than later, in care.*

Underassessment of IPV (ie, underreporting as well as under-inquiry) because of stigma, misconception, and other factors obscures an accurate estimate of the rate of partner violence and its consequences for all couples. As a consequence, we know little about the dynamics of IPV, best practices for screening, and appropriate referral for couples from these populations. Furthermore, few resources are available to these understudied and underserved groups (eg, shelters for men and for transgender people).

Continue to: Although our immediate approach to IPV screening...

 

 

Although our immediate approach to IPV screening, safety planning, and referral with understudied patient populations might be informed by what we have learned from the experiences of heterosexual women in abusive relationships, such a practice is unsustainable. Unless we expand our scope of screening to all patients, it is unlikely that we will develop the evidence base necessary to 1) warrant stronger IPV screening recommendations for patient groups apart from women of childbearing age, let alone 2) demonstrate the need for additional community resources, and 3) provide comprehensive care in family practice of comparable quality.

The benefits of screening go beyond the individual patient

Screening for violence in the relationship does not take long; the value of asking about its presence in a relationship might offer benefits beyond the individual patient by raising awareness and providing the field of study with more data to increase attention and resources for under-researched and underserved populations. Screening might also combat the stigma that perpetuates the silence of many who deserve access to care.

CORRESPONDENCE
Joel G. Sprunger, PhD, Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, 260 Stetson St, Suite 3200, Cincinnati OH 45219; [email protected].

ACKNOWLEDGMENTS
The authors thank Jeffrey M. Girard, PhD, and Daniel C. Williams, PhD, for their input on the design and content, respectively, of the IPASSPRT screening materials; the authors of the DA-5 and the HITS screening tools, particularly Jacquelyn Campbell, PhD, RN, FAAN, and Kevin Sherin, MD, MPH, MBA, respectively, for permission to include these measures in this article and for their support of its goals; and The Journal of Family Practice’s peer reviewers for their thoughtful feedback throughout the prepublication process.

References

1. Campos-Outcalt D. USPSTF: What’s recommended, what’s not. J Fam Pract. 2014;63:265-269.

2. Black MC, Basile KC, Breiding MJ, et al. National Intimate Partner and Sexual Violence Survey: 2010 Summary Report. Atlanta, GA: National Center for Injury Prevention and Control, Centers for Disease Control and Prevention; 2011:113. www.cdc.gov/violenceprevention/pdf/NISVS_Report2010-a.pdf. Accessed February 20, 2019.

3. West CM. Partner abuse in ethnic minority and gay, lesbian, bisexual, and transgender populations. Partner Abuse. 2012;3:336-357.

4. Hines DA, Malley-Morrison K. Psychological effects of partner abuse against men: a neglected research area. Psychology of Men & Masculinities. 2001;2:75-85.

5. Houston E, McKirnan DJ. Intimate partner abuse among gay and bisexual men: risk correlates and health outcomes. J Urban Health. 2007;84:681-690.

6. Carvalho AF, Lewis RJ, Derlega VJ, et al. Internalized sexual minority stressors and same-sex intimate partner violence. J Fam Violence. 2011;26:501-509.

7. Nicholls TL, Pritchard MM, Reeves KA, et al. Risk assessment in intimate partner violence: a systematic review of contemporary approaches. Partner Abuse. 2013;4:76-168.

8. Intimate partner violence: definitions. Atlanta, GA: National Center for Injury Prevention and Control, Division of Violence Prevention, Centers for Disease Control and Prevention, August 22, 2017. www.cdc.gov/violenceprevention/intimatepartnerviolence/definitions.html. Accessed February 20, 2019.

9. Archer J. Sex differences in aggression between heterosexual partners: a meta-analytic review. Psychol Bull. 2000;126:651-680.

10. Baron RA, Richardson DR. Human Aggression. New York, NY: Springer Science+Business Media; 2004.

11. Breiding MJ, Basile KC, Smith SG, et al. Intimate Partner Violence Surveillance: Uniform Definitions and Recommended Data Elements, Version 2.0. Atlanta, GA: National Center for Injury Prevention and Control, Centers for Disease Control and Prevention; 2015.

12. Murphy CM, Eckhardt CI. Treating the Abusive Partner: An Individualized Cognitive-Behavioral Approach. New York, NY: Guilford Press; 2005.

13. Straus MA, Hamby SL, Boney-McCoy S, et al. The revised Conflict Tactics Scales (CTS2): development and preliminary psychometric data. J Fam Issues. 1996;17:283-316.

14. West CM. Partner abuse in ethnic minority and gay, lesbian, bisexual, and transgender populations. Partner Abuse. 2012;3:336-357.

15. Desmarais SL, Reeves KA, Nicholls TL, et al. Prevalence of physical violence in intimate relationships. Part 1: rates of male and female victimization. Partner Abuse. 2012;3:140-169.

16. Lawrence E, Orengo-Aguayo R, Langer A, et al. The impact and consequences of partner abuse on partners. Partner Abuse. 2012;3:406-428.

17. Langhinrichsen-Rohling J, Selwyn C, Rohling ML. Rates of bidirectional versus unidirectional intimate partner violence across samples, sexual orientations, and race/ethnicities: a comprehensive review. Partner Abuse. 2012;3:199-230.

18. Langhinrichsen-Rohling J, McCullars A, Misra TA. Motivations for men and women’s intimate partner violence perpetration: a comprehensive review. Partner Abuse. 2012;3:429-468.

19. Anderson CA, Bushman BJ. Human aggression. Annu Rev Psychol. 2002;53:27-51.

20. Straus MA, Gozjolko KL. “Intimate terrorism” and gender differences in injury of dating partners by male and female university students. J Fam Violence. 2014;29:51-65.

21. Ferraro KJ, Johnson JM. How women experience battering: the process of victimization. Soc Probl. 1983;30:325-339.

22. Sugg NK, Inui T. Primary care physicians’ response to domestic violence: opening Pandora’s box. JAMA. 1992;267:3157-3160.

23. Morgan KJ, Williamson E, Hester M, et al. Asking men about domestic violence and abuse in a family medicine context: help seeking and views on the general practitioner role. Aggress Violent Behav. 2014;19:637-642.

24. MacMillan HL, Wathen CN, Jamieson E, et al; McMaster Violence Against Women Research Group. Approaches to screening for intimate partner violence in health care settings: a randomized trial. JAMA. 2006;296:530-536.

25. Thompson RS, Rivara FP, Thompson DC, et al. Identification and management of domestic violence: a randomized trial. Am J Prev Med. 2000;19:253-263.

26. Ard KL, Makadon HJ. Addressing intimate partner violence in lesbian, gay, bisexual, and transgender patients. J Gen Intern Med. 2011;26:930-933.

27. Rabin RF, Jennings JM, Campbell JC, et al. Intimate partner violence screening tools: a systematic review. Am J Prev Med. 2009;36:439-445.e4.

28. Madras BK, Compton WM, Avula D, et al. Screening, brief interventions, referral to treatment (SBIRT) for illicit drug and alcohol use at multiple healthcare sites: comparison at intake and 6 months later. Drug Alcohol Depend. 2009;99:280-295.

29. Sherin KM, Sinacore JM, Li XQ, et al. HITS: A short domestic violence screening tool for use in a family practice setting. Fam Med. 1998;30:508-512.

30. Peralta RL, Fleming MF. Screening for intimate partner violence in a primary care setting: the validity of “feeling safe at home” and prevalence results. J Am Board Fam Pract. 2003;16:525-532.

31. Capaldi DM, Knoble NB, Shortt JW, et al. A systematic review of risk factors for intimate partner violence. Partner Abuse. 2012;3:231-280.

32. Brownridge DA, Taillieu TL, Tyler KA, et al. Pregnancy and intimate partner violence: risk factors, severity, and health effects. Violence Against Women. 2011;17:858-881.

33. Messing JT, Campbell JC, Snider C. Validation and adaptation of the danger assessment-5: a brief intimate partner violence risk assessment. J Adv Nurs. 2017;73:3220-3230.

34. Grigsby N, Hartman BR. The Barriers Model: an integrated strategy for intervention with battered women. Psychotherapy: Theory, Research, Practice, Training. 1997;34:485-497.

35. Moyers TB, Rollnick S. A motivational interviewing perspective on resistance in psychotherapy. J Clin Psychol. 2002;58:185-193.

36. Belfrage H, Strand S, Storey JE, et al. Assessment and management of risk for intimate partner violence by police officers using the Spousal Assault Risk Assessment Guide. Law Hum Behav. 2012;36:60-67.

37. McCloskey LA, Lichter E, Williams C, et al. Assessing intimate partner violence in health care settings leads to women’s receipt of interventions and improved health. Publ Health Rep. 2006;121:435-444.

38. Eckhardt CI, Murphy CM, Whitaker DJ, et al. The effectiveness of intervention programs for perpetrators and victims of intimate partner violence. Partner Abuse. 2013;4:196-231.

39. Trabold N, McMahon J, Alsobrooks S, et al. A systematic review of intimate partner violence interventions: state of the field and implications for practitioners. Trauma Violence Abuse. January 2018:1524838018767934.

40. Kraanen FL, Vedel E, Scholing A, et al. The comparative effectiveness of Integrated treatment for Substance abuse and Partner violence (I-StoP) and substance abuse treatment alone: a randomized controlled trial. BMC Psychiatry. 2013;13:189.

Article PDF
Author and Disclosure Information

Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Ohio (Dr. Sprunger); Department of Psychiatry and Human Behavior (Drs. Schumacher and Coffey) and Department of Family Medicine (Dr. Norris), University of Mississippi Medical Center, Jackson
[email protected]

The authors reported no potential conflict of interest relevant to this article.

Issue
The Journal of Family Practice - 68(3)
Publications
Topics
Page Number
152-154,156-161A
Sections
Author and Disclosure Information

Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Ohio (Dr. Sprunger); Department of Psychiatry and Human Behavior (Drs. Schumacher and Coffey) and Department of Family Medicine (Dr. Norris), University of Mississippi Medical Center, Jackson
[email protected]

The authors reported no potential conflict of interest relevant to this article.

Author and Disclosure Information

Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Ohio (Dr. Sprunger); Department of Psychiatry and Human Behavior (Drs. Schumacher and Coffey) and Department of Family Medicine (Dr. Norris), University of Mississippi Medical Center, Jackson
[email protected]

The authors reported no potential conflict of interest relevant to this article.

Article PDF
Article PDF

Intimate partner violence (IPV) is a serious public health problem with considerable harmful health consequences. Decades of research have been dedicated to improving the identification of women in abusive heterosexual relationships and interventions that support healthier outcomes. A result of this work has been the recommendation of the US Preventive Services Task Force that all women of childbearing age be screened for IPV and provided with intervention or referral.1

The problem extends further, however: Epidemiologic studies and comprehensive reviews show: 1) a high rate of IPV victimization among heterosexual men and lesbian, gay, bisexual, and transsexual (LGBT) men and women2,3; 2) significant harmful effects on health and greater expectations of prejudice and discrimination among these populations4-6; and 3) evidence that screening and referral for IPV are likely to confer similar benefits for these populations.7 We argue that it is reasonable to ask all patients about abuse in their relationships while the research literature progresses.

We intend this article to serve a number of purposes:

  • support national standards for IPV screening of female patients
  • highlight the need for piloting universal IPV screening for all patients (ie, male and female, across the lifespan)
  • offer recommendations for navigating the process from IPV screening to referral, using insights gained from the substance abuse literature.

We also provide supplemental materials that facilitate establishment of screening and referral protocols for physicians across practice settings.

It’s time to start asking all patients about intimate partner violence
© Joe Gorman

What is intimate partner violence? How can you identify it?

Intimate partner violence includes physical and sexual violence and nonphysical forms of abuse, such as psychological aggression and emotional abuse, perpetrated by a current or former intimate partner.8 TABLE 19-14 provides definitions for each of these behavior categories and example behaviors. Nearly 25% of women and 20% of men report having experienced physical violence from a romantic partner and even higher rates of nonphysical IPV.15 Consequences of IPV victimization include acute and chronic medical illness, injury, and psychological problems, including depression, anxiety, and poor self-esteem.16

What is intimate partner violence?

Intimate partner violence is heterogenous, with differences in severity (eg, frequency and intensity of violence) and laterality (ie, is one partner violent? are both partners violent?).

Intimate partner violence is heterogeneous, with differences in severity (eg, frequency and intensity of violence) and laterality (ie, is one partner violent? are both partners violent?). A recent comprehensive review of the literature revealed that, for 49.2%-69.7% of partner-violent couples across diverse samples, IPV is perpetrated by both partners.17 Furthermore, this bidirectionality is not due entirely to aggression perpetrated in self-defense; rather, across diverse patient samples, that is the case for fewer than one-quarter of males and no more than approximately one-third of females.18 In the remaining cases, bidirectionality may be attributed to other motivations, such as a maladaptive emotional expression or a means by which to get a partner’s attention.18

Women are disproportionately susceptible to harmful outcomes as a result of severe violence, including physical injury, psychological distress (eg, depression and anxiety), and substance abuse.16,19 Some patients in unidirectionally violent relationships experience severe physical violence that may be, or become, life-threatening (0.4%-2.4% of couples in community samples)20—victimization that is traditionally known as “battering.”21

Continue to: These tools can facilitate screening for IPV

 

 

These tools can facilitate screening for IPV

Physicians might have reservations asking about IPV because of 1) concern whether there is sufficient time during an office visit to interview, screen, and refer, 2) feelings of powerlessness to stop violence by or toward a patient, and 3) general discomfort with the topic.22 Additionally, mandated reporting laws regarding IPV vary by state, making it crucial to know one’s own state laws on this issue to protect the safety of the patient and those around them.

Screening increases the likelihood of engaging the patient in supportive services, thus decreasing the isolation that is typical of abuse.

Research has shown that some patients prefer that their health care providers ask about relationship violence directly23; others are more willing to acknowledge IPV if asked using a paper-and-pencil measure, rather than face-to-face questions.24 Either way, screening increases the likelihood of engaging the patient in supportive services, thus decreasing the isolation that is typical of abuse.25 Based on this research, screening that utilizes face-valid items embedded within paperwork completed in the waiting room is recommended as an important first step toward identifying and helping patients who are experiencing IPV. Even under these conditions, however, heterosexual men and sexual minorities might be less willing than heterosexual women to admit experiencing IPV.26,27

A brief vignette that depicts how quickly the screening and referral process can be applied is presented in “IPV screening and referral: A real-world vignette." The vignette is a de-identified composite of heterosexual men experiencing IPV whom we have counseled.

SIDEBAR
IPV screening and referral: A real-world vignette

Physician: Before we wrap up: I noticed on your screening that you have been hurt and threatened a fair amount in the past year. Would it be OK if we spoke about that more?

Patient: My wife is emotional. Sometimes she gets really stressed out and just starts screaming and punching me. That’s just how she is.

Physician: Do you ever feel concerned for your safety?

Patient: Not really. She’s smaller than me and I can generally calm her down. I keep the guns locked up, so she can’t grab those any more. Mostly she just screams at me.

Physician: This may or may not fit with your perception but, based on what you are reporting, your relationship is what is called “at risk”—meaning you are at risk for having your physical or mental health negatively impacted. This actually happens to a lot of men, and there’s a brochure I can give you that has a lot more information about the risks and consequences of being hurt or threatened by a partner. Would you be willing to take a look at it?

Patient: I guess so.

Physician: OK. I’ll have the nurse bring you that brochure, and we can talk more about it next time you come in for an appointment. Would it be OK if we get you back in here 6 months from now?

Patient: Yeah, that could work.

Physician: Great. Let’s do that. Don’t hesitate to give me a call if your situation changes in any way in the meantime.

One model that provides a useful framework for IPV assessment is the Screening, Brief Intervention, and Referral to Treatment (SBIRT) model, which was developed to facilitate assessment of, and referral for, substance abuse—another heavily stigmatized health care problem. The SBIRT approach for substance abuse screening is associated with significant reduction in alcohol and drug abuse 6 months postintervention, as well as improvements in well-being, mental health, and functioning across gender, race and ethnicity, and age.28

IPASSPRT. Inspired by the SBIRT model for substance abuse, we created the Intimate Partner Aggression Screening, Safety Planning, and Referral to Treatment, or IPASSPRT (spoken as “i-passport”) project to provide tools that make IPV screening and referral accessible to a range of health care providers. These tools include a script and safety plan that guide providers through screening, safety planning, and referral in a manner that is collaborative and grounded in the spirit of motivational interviewing. We have made these tools available on the Web for ease of distribution (http://bit.ly/ipassprt; open by linking through “IPASSPRT-Script”).

Continue to: The IPASSPRT script appears lengthy...

 

 

The IPASSPRT script appears lengthy, but progress through its sections is directed by patient need; most patients will not require that all parts be completed. For example, a patient whose screen for IPV is negative and who feels safe in their relationship does not need assessment beyond page 2; on the other hand, the physician might need more information from a patient who is at greater risk for IPV. This response-based progression through the script makes the screening process dynamic, data-driven, and tailored to the patient’s needs—an approach that aids rapport and optimizes the physician’s limited time during the appointment.

In the sections that follow, we describe key components of this script.

What aggression, if any, is present? From whom? The Hurt, Insult, Threaten, and Scream inventory (HITS) (TABLE 2)29 is a widely used screen for IPV that has been validated for use in family medicine. A 4-item scale asks patients to report how often their partner physically hurts, insults, threatens, and screams at them using a 5-point scale (1 point, “never,” to 5 points, “frequently”). Although a score > 10 is indicative of IPV, item-level analysis is encouraged. Attending to which items the patient acknowledges and how often these behaviors occur yields a richer assessment than a summary score. In regard to simply asking a patient, “Do you feel safe at home?” (sensitivity of this question, 8.8%; specificity, 91.2%), the HITS better detects IPV with male and female patient populations in family practice and emergency care settings (sensitivity, 30%-100%; specificity, 86%-99%).27,30

HITS: The Hurt, Insult, Threaten, and Scream Inventory

What contextual factors and related concerns are present? It is important to understand proximal factors that might influence IPV risk to determine what kind of referral or treatment is appropriate—particularly for patients experiencing or engaging in infrequent, noninjurious, and bidirectional forms of IPV. Environmental and contextual stressors, such as financial hardship, unemployment, pregnancy, and discussion of divorce, can increase the risk for IPV.31,32 Situational influences, such as alcohol and drug intoxication, can also increase the risk for IPV. Victims of partner violence are at greater risk for mental health problems, including depression, anxiety, trauma- and stressor-related disorders, and substance use disorders. Risk goes both ways, however: Mental illness predicts subsequent IPV perpetration or victimization, and vice versa.31

Does the patient feel safe? Assessing the situation. Patient perception of safety in the relationship provides important information about the necessity of referral. Asking a patient if they feel unsafe because of the behavior of a current or former partner sheds light on the need for further safety assessment and immediate connection with appropriate resources.

Continue to: The Danger Assessment-5...

 

 

The Danger Assessment-5 (DA-5) (TABLE 333) is a useful 5-item tool for quickly assessing the risk for severe IPV.33 Patients respond to whether:

  • the frequency or severity of violence has increased in the past year
  • the partner has ever used, or threatened to use, a weapon
  • the patient believes the partner is capable of killing her (him)
  • the partner has ever tried to choke or strangle her (him)
  • the partner is violently and constantly jealous.

The Danger Assessment-5

Mental illness predicts subsequent IPV perpetration or victimization and vice versa.

Sensitivity and specificity analyses with a high-risk female sample suggested that 3 affirmative responses indicate a high risk for severe IPV and a need for adequate safety planning.

Brief motivational enhancement intervention. There are 3 components to this intervention.

  • Assess interest in making changes or seeking help. IPV is paradoxical: Many factors complicate the decision to leave or stay, and patients across the spectrum of victimization might have some motivation to stay with their partner. It is important to assess the patient’s motivation to make changes in their relationship.4,34
  • Provide feedback on screening. Sharing the results of screening with patients makes the assessment and referral process collaborative and transparent; collaborative engagement helps patients feel in control and invested in the follow-through.35 In the spirit of this endeavor, physicians are encouraged to refrain from providing raw or total scores from the measures; instead, share the interpretation of those scores, based on the participant’s responses to the screening items, in a matter-of-fact manner. At this point, elicit the patient’s response to this information, listen empathically, and answer questions before proceeding.

Consistent with screening for other serious health problems, we recommend that all patients be provided with information about abuse in romantic relationships. The National Center for Injury Prevention and Control Division of Violence Prevention has published a useful, easy-to-understand fact sheet (www.cdc.gov/violenceprevention/pdf/ipv-factsheet.pdf) that provides an overview of IPV-related behavior, how it influences health outcomes, who is at risk for IPV, and sources for support.

Continue to: Our IPASSPRT interview script...

 

 

Our IPASSPRT interview script (http://bit.ly/ipassprt) outlines how this information can be presented to patients as a typical part of the screening process. Providers are encouraged to share and review the information from the fact sheet with all patients and present it as part of the normal screening process to mitigate the potential for defensiveness on the part of the patient. For patients who screen positive for IPV, it might be important to brainstorm ideas for a safe, secure place to store this fact sheet and other resources from the brief intervention and referral process below (eg, a safety plan and specific referral information) so that the patient can access them quickly and easily, if needed.

For patients who screen negative for IPV, their screen and interview conclude at this point.

  • Provide recommendations based on the screen. Evidence suggests that collaborating with the patient on safety planning and referral can increase the likelihood of their engagement.7 Furthermore, failure to tailor the referral to the needs of the patient can be detrimental36—ie, overshooting the level of intervention might decrease the patient’s future treatment-seeking behavior and undermine their internal coping strategies, increasing the likelihood of future victimization. For that reason, we provide the following guidance on navigating the referral process for patients who screen positive for IPV.

Screening-based referral: A delicate and collaborative process

Referral for IPV victimization. Individual counseling, with or without an IPV focus, might be appropriate for patients at lower levels of risk; immediate connection with local IPV resources is strongly encouraged for patients at higher risk. This is a delicate, collaborative process, in which the physician offers recommendations for referral commensurate to the patient’s risk but must, ultimately, respect the patient’s autonomy by identifying referrals that fit the patient’s goals. We encourage providers to provide risk-informed recommendations and to elicit the patient’s thoughts about that information.

Several online resources are available to help physicians locate and connect with IPV-related resources in their community, including the National Health Resource Center on Domestic Violence (http://ipvhealth.org/), which provides a step-by-step guide to making such connections. We encourage physicians to develop these collaborative partnerships early to facilitate warm handoffs and increase the likelihood that a patient will follow through with the referral after screening.37

Referral for related concerns. As we’ve noted, IPV has numerous physical and mental health consequences, including depression, low self-esteem, trauma- and non-trauma-related anxiety, and substance abuse. In general, cognitive behavioral therapies appear most efficacious for treating these IPV-related consequences, but evidence is limited that such interventions diminish the likelihood of re-victimization.38 Intervention programs that foster problem-solving, solution-seeking, and cognitive restructuring for self-critical thoughts and misconceptions seem to produce the best physical and mental health outcomes.39 For patients who have a substance use disorder, treatment programs that target substance use have demonstrated a reduction in the rate of IPV recidivism.40 These findings indicate that establishing multiple treatment targets might reduce the risk for future aggression in relationships.

Continue to: The Substance Abuse and Mental Health Services Administration...

 

 

The Substance Abuse and Mental Health Services Administration of the US Department of Health and Human Services provides a useful online tool (https://findtreatment.samhsa.gov/) for locating local referrals that address behavioral health and substance-related concerns. The agency also provides a hotline (1-800-662-HELP [4357]) as an alternative resource for information and treatment referrals.

Safety planning can improve outcomes

For a patient who screens above low risk, safety planning with the patient is an important part of improving outcomes and can take several forms. Online resources, such as the Path to Safety interactive Web page (www.thehotline.org/help/path-to-safety/) maintained by The National Domestic Violence Hotline ([800]799-SAFE [7233]), provide information regarding important considerations for safety planning when:

  • living with an abusive partner
  • children are in the home
  • the patient is pregnant
  • pets are involved.

The Web site also provides information regarding legal options and resources related to IPV (eg, an order of protection) and steps for improving safety when leaving an abusive relationship. Patients at risk for IPV can explore the online tool and call the hotline.

For physicians who want to engage in provider-assisted safety planning, we’ve provided further guidance in the IPASSPRT screening script and safety plan (http://bit.ly/ipassprt) (TABLE 4).

Components of a safety plan: A patient guide

Goal: Affirm patients’ strengths and reinforce hope

Psychological aggression is the most common form of relationship aggression; repeated denigration might leave a person with little confidence in their ability to change their relationship or seek out identified resources. That’s why it’s useful to inquire—with genuine curiosity—about a time in the past when the patient accomplished something challenging. The physician’s enthusiastic reflection on this achievement can be a means of highlighting the patient’s ability to accomplish a meaningful goal; of reinforcing their hope; and of eliciting important resources within and around the patient that can facilitate action on their safety plan. (See “IPV-related resources for physicians and patients.”)

SIDEBAR
IPV-related resources for physicians and patients

Intimate Partner Aggression Screening, Safety Planning, and Referral to Treatment (IPASSPRT) Project
http://bit.ly/ipassprt
Online resource with tools designed by the authors, including an SBIRT-inspired script and safety plan template for IPV screening, safety planning, and referral

National Center for Injury Prevention and Control Division of Violence Prevention
www.cdc.gov/violenceprevention/pdf/ipv-factsheet.pdf
Overview of IPV-related behavior, influence on health outcomes, people at risk of IPV, and sources of support, all in a format easily understood by patients

National Health Resource Center on Domestic Violence
http://ipvhealth.org/
Includes guidance on connecting with IPV-related community resources; establishing such connections can facilitate warm handoffs and improve the likelihood that patients will follow through

Path to Safety, a service of The National Domestic Violence Hotline
www.thehotline.org/help/path-to-safety/
Extensive primer on safety plans for patients intending to stay in (or leave) an abusive relationship; includes important considerations for children, pets, and pregnancy, as well as emotional safety and legal options

The National Domestic Violence Hotline
› (800) 799-SAFE (7233)

Substance Abuse and Mental Health Services Administration
www.samhsa.gov/sbirt
Learning resources for the SBIRT protocol for substance abuse
https://findtreatment.samhsa.gov/
Search engine and resources for locating local referrals
› (800) 662-HELP (4357)
Hotline for information and assistance with locating local treatment referral

IPV, intimate partner violence; SBIRT, screening, brief intervention, and referral to treatment.
 

Continue to: Closing the screen and making a referral

 

 

Closing the screen and making a referral

The end of the interview should consist of a summary of topics discussed, including:

  • changes that the patient wants to make (if any)
  • their stated reasons for making those changes
  • the patient’s plan for accomplishing changes.

Physicians should also include their own role in next steps—whether providing a warm handoff to a local IPV referral, agreeing to a follow-up schedule with the patient, or making a call as a mandated reporter. To close out the interview, it is important to affirm respect for the patient’s autonomy in executing the plan.

It’s important to screen all patients—here’s why

A major impetus for this article has been to raise awareness about the need for expanded IPV screening across primary care settings. As mentioned, much of the literature on IPV victimization has focused on women; however, the few epidemiological investigations of victimization rates among men and members of LGBT couples show a high rate of victimization and considerable harmful health outcomes. Driven by stigma surrounding IPV, sex, and sexual minority status, patients might have expectations that they will be judged by a provider or “outed.”

Such barriers can lead many to suffer in silence until the problem can no longer be hidden or the danger becomes more emergent. Compassionate, nonjudgmental screening and collaborative safety planning—such as the approach we describe in this article—help ease the concerns of LGBT victims of IPV and improve the likelihood that conversations you have with them will occur earlier, rather than later, in care.*

Underassessment of IPV (ie, underreporting as well as under-inquiry) because of stigma, misconception, and other factors obscures an accurate estimate of the rate of partner violence and its consequences for all couples. As a consequence, we know little about the dynamics of IPV, best practices for screening, and appropriate referral for couples from these populations. Furthermore, few resources are available to these understudied and underserved groups (eg, shelters for men and for transgender people).

Continue to: Although our immediate approach to IPV screening...

 

 

Although our immediate approach to IPV screening, safety planning, and referral with understudied patient populations might be informed by what we have learned from the experiences of heterosexual women in abusive relationships, such a practice is unsustainable. Unless we expand our scope of screening to all patients, it is unlikely that we will develop the evidence base necessary to 1) warrant stronger IPV screening recommendations for patient groups apart from women of childbearing age, let alone 2) demonstrate the need for additional community resources, and 3) provide comprehensive care in family practice of comparable quality.

The benefits of screening go beyond the individual patient

Screening for violence in the relationship does not take long; the value of asking about its presence in a relationship might offer benefits beyond the individual patient by raising awareness and providing the field of study with more data to increase attention and resources for under-researched and underserved populations. Screening might also combat the stigma that perpetuates the silence of many who deserve access to care.

CORRESPONDENCE
Joel G. Sprunger, PhD, Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, 260 Stetson St, Suite 3200, Cincinnati OH 45219; [email protected].

ACKNOWLEDGMENTS
The authors thank Jeffrey M. Girard, PhD, and Daniel C. Williams, PhD, for their input on the design and content, respectively, of the IPASSPRT screening materials; the authors of the DA-5 and the HITS screening tools, particularly Jacquelyn Campbell, PhD, RN, FAAN, and Kevin Sherin, MD, MPH, MBA, respectively, for permission to include these measures in this article and for their support of its goals; and The Journal of Family Practice’s peer reviewers for their thoughtful feedback throughout the prepublication process.

Intimate partner violence (IPV) is a serious public health problem with considerable harmful health consequences. Decades of research have been dedicated to improving the identification of women in abusive heterosexual relationships and interventions that support healthier outcomes. A result of this work has been the recommendation of the US Preventive Services Task Force that all women of childbearing age be screened for IPV and provided with intervention or referral.1

The problem extends further, however: Epidemiologic studies and comprehensive reviews show: 1) a high rate of IPV victimization among heterosexual men and lesbian, gay, bisexual, and transsexual (LGBT) men and women2,3; 2) significant harmful effects on health and greater expectations of prejudice and discrimination among these populations4-6; and 3) evidence that screening and referral for IPV are likely to confer similar benefits for these populations.7 We argue that it is reasonable to ask all patients about abuse in their relationships while the research literature progresses.

We intend this article to serve a number of purposes:

  • support national standards for IPV screening of female patients
  • highlight the need for piloting universal IPV screening for all patients (ie, male and female, across the lifespan)
  • offer recommendations for navigating the process from IPV screening to referral, using insights gained from the substance abuse literature.

We also provide supplemental materials that facilitate establishment of screening and referral protocols for physicians across practice settings.

It’s time to start asking all patients about intimate partner violence
© Joe Gorman

What is intimate partner violence? How can you identify it?

Intimate partner violence includes physical and sexual violence and nonphysical forms of abuse, such as psychological aggression and emotional abuse, perpetrated by a current or former intimate partner.8 TABLE 19-14 provides definitions for each of these behavior categories and example behaviors. Nearly 25% of women and 20% of men report having experienced physical violence from a romantic partner and even higher rates of nonphysical IPV.15 Consequences of IPV victimization include acute and chronic medical illness, injury, and psychological problems, including depression, anxiety, and poor self-esteem.16

What is intimate partner violence?

Intimate partner violence is heterogenous, with differences in severity (eg, frequency and intensity of violence) and laterality (ie, is one partner violent? are both partners violent?).

Intimate partner violence is heterogeneous, with differences in severity (eg, frequency and intensity of violence) and laterality (ie, is one partner violent? are both partners violent?). A recent comprehensive review of the literature revealed that, for 49.2%-69.7% of partner-violent couples across diverse samples, IPV is perpetrated by both partners.17 Furthermore, this bidirectionality is not due entirely to aggression perpetrated in self-defense; rather, across diverse patient samples, that is the case for fewer than one-quarter of males and no more than approximately one-third of females.18 In the remaining cases, bidirectionality may be attributed to other motivations, such as a maladaptive emotional expression or a means by which to get a partner’s attention.18

Women are disproportionately susceptible to harmful outcomes as a result of severe violence, including physical injury, psychological distress (eg, depression and anxiety), and substance abuse.16,19 Some patients in unidirectionally violent relationships experience severe physical violence that may be, or become, life-threatening (0.4%-2.4% of couples in community samples)20—victimization that is traditionally known as “battering.”21

Continue to: These tools can facilitate screening for IPV

 

 

These tools can facilitate screening for IPV

Physicians might have reservations asking about IPV because of 1) concern whether there is sufficient time during an office visit to interview, screen, and refer, 2) feelings of powerlessness to stop violence by or toward a patient, and 3) general discomfort with the topic.22 Additionally, mandated reporting laws regarding IPV vary by state, making it crucial to know one’s own state laws on this issue to protect the safety of the patient and those around them.

Screening increases the likelihood of engaging the patient in supportive services, thus decreasing the isolation that is typical of abuse.

Research has shown that some patients prefer that their health care providers ask about relationship violence directly23; others are more willing to acknowledge IPV if asked using a paper-and-pencil measure, rather than face-to-face questions.24 Either way, screening increases the likelihood of engaging the patient in supportive services, thus decreasing the isolation that is typical of abuse.25 Based on this research, screening that utilizes face-valid items embedded within paperwork completed in the waiting room is recommended as an important first step toward identifying and helping patients who are experiencing IPV. Even under these conditions, however, heterosexual men and sexual minorities might be less willing than heterosexual women to admit experiencing IPV.26,27

A brief vignette that depicts how quickly the screening and referral process can be applied is presented in “IPV screening and referral: A real-world vignette." The vignette is a de-identified composite of heterosexual men experiencing IPV whom we have counseled.

SIDEBAR
IPV screening and referral: A real-world vignette

Physician: Before we wrap up: I noticed on your screening that you have been hurt and threatened a fair amount in the past year. Would it be OK if we spoke about that more?

Patient: My wife is emotional. Sometimes she gets really stressed out and just starts screaming and punching me. That’s just how she is.

Physician: Do you ever feel concerned for your safety?

Patient: Not really. She’s smaller than me and I can generally calm her down. I keep the guns locked up, so she can’t grab those any more. Mostly she just screams at me.

Physician: This may or may not fit with your perception but, based on what you are reporting, your relationship is what is called “at risk”—meaning you are at risk for having your physical or mental health negatively impacted. This actually happens to a lot of men, and there’s a brochure I can give you that has a lot more information about the risks and consequences of being hurt or threatened by a partner. Would you be willing to take a look at it?

Patient: I guess so.

Physician: OK. I’ll have the nurse bring you that brochure, and we can talk more about it next time you come in for an appointment. Would it be OK if we get you back in here 6 months from now?

Patient: Yeah, that could work.

Physician: Great. Let’s do that. Don’t hesitate to give me a call if your situation changes in any way in the meantime.

One model that provides a useful framework for IPV assessment is the Screening, Brief Intervention, and Referral to Treatment (SBIRT) model, which was developed to facilitate assessment of, and referral for, substance abuse—another heavily stigmatized health care problem. The SBIRT approach for substance abuse screening is associated with significant reduction in alcohol and drug abuse 6 months postintervention, as well as improvements in well-being, mental health, and functioning across gender, race and ethnicity, and age.28

IPASSPRT. Inspired by the SBIRT model for substance abuse, we created the Intimate Partner Aggression Screening, Safety Planning, and Referral to Treatment, or IPASSPRT (spoken as “i-passport”) project to provide tools that make IPV screening and referral accessible to a range of health care providers. These tools include a script and safety plan that guide providers through screening, safety planning, and referral in a manner that is collaborative and grounded in the spirit of motivational interviewing. We have made these tools available on the Web for ease of distribution (http://bit.ly/ipassprt; open by linking through “IPASSPRT-Script”).

Continue to: The IPASSPRT script appears lengthy...

 

 

The IPASSPRT script appears lengthy, but progress through its sections is directed by patient need; most patients will not require that all parts be completed. For example, a patient whose screen for IPV is negative and who feels safe in their relationship does not need assessment beyond page 2; on the other hand, the physician might need more information from a patient who is at greater risk for IPV. This response-based progression through the script makes the screening process dynamic, data-driven, and tailored to the patient’s needs—an approach that aids rapport and optimizes the physician’s limited time during the appointment.

In the sections that follow, we describe key components of this script.

What aggression, if any, is present? From whom? The Hurt, Insult, Threaten, and Scream inventory (HITS) (TABLE 2)29 is a widely used screen for IPV that has been validated for use in family medicine. A 4-item scale asks patients to report how often their partner physically hurts, insults, threatens, and screams at them using a 5-point scale (1 point, “never,” to 5 points, “frequently”). Although a score > 10 is indicative of IPV, item-level analysis is encouraged. Attending to which items the patient acknowledges and how often these behaviors occur yields a richer assessment than a summary score. In regard to simply asking a patient, “Do you feel safe at home?” (sensitivity of this question, 8.8%; specificity, 91.2%), the HITS better detects IPV with male and female patient populations in family practice and emergency care settings (sensitivity, 30%-100%; specificity, 86%-99%).27,30

HITS: The Hurt, Insult, Threaten, and Scream Inventory

What contextual factors and related concerns are present? It is important to understand proximal factors that might influence IPV risk to determine what kind of referral or treatment is appropriate—particularly for patients experiencing or engaging in infrequent, noninjurious, and bidirectional forms of IPV. Environmental and contextual stressors, such as financial hardship, unemployment, pregnancy, and discussion of divorce, can increase the risk for IPV.31,32 Situational influences, such as alcohol and drug intoxication, can also increase the risk for IPV. Victims of partner violence are at greater risk for mental health problems, including depression, anxiety, trauma- and stressor-related disorders, and substance use disorders. Risk goes both ways, however: Mental illness predicts subsequent IPV perpetration or victimization, and vice versa.31

Does the patient feel safe? Assessing the situation. Patient perception of safety in the relationship provides important information about the necessity of referral. Asking a patient if they feel unsafe because of the behavior of a current or former partner sheds light on the need for further safety assessment and immediate connection with appropriate resources.

Continue to: The Danger Assessment-5...

 

 

The Danger Assessment-5 (DA-5) (TABLE 333) is a useful 5-item tool for quickly assessing the risk for severe IPV.33 Patients respond to whether:

  • the frequency or severity of violence has increased in the past year
  • the partner has ever used, or threatened to use, a weapon
  • the patient believes the partner is capable of killing her (him)
  • the partner has ever tried to choke or strangle her (him)
  • the partner is violently and constantly jealous.

The Danger Assessment-5

Mental illness predicts subsequent IPV perpetration or victimization and vice versa.

Sensitivity and specificity analyses with a high-risk female sample suggested that 3 affirmative responses indicate a high risk for severe IPV and a need for adequate safety planning.

Brief motivational enhancement intervention. There are 3 components to this intervention.

  • Assess interest in making changes or seeking help. IPV is paradoxical: Many factors complicate the decision to leave or stay, and patients across the spectrum of victimization might have some motivation to stay with their partner. It is important to assess the patient’s motivation to make changes in their relationship.4,34
  • Provide feedback on screening. Sharing the results of screening with patients makes the assessment and referral process collaborative and transparent; collaborative engagement helps patients feel in control and invested in the follow-through.35 In the spirit of this endeavor, physicians are encouraged to refrain from providing raw or total scores from the measures; instead, share the interpretation of those scores, based on the participant’s responses to the screening items, in a matter-of-fact manner. At this point, elicit the patient’s response to this information, listen empathically, and answer questions before proceeding.

Consistent with screening for other serious health problems, we recommend that all patients be provided with information about abuse in romantic relationships. The National Center for Injury Prevention and Control Division of Violence Prevention has published a useful, easy-to-understand fact sheet (www.cdc.gov/violenceprevention/pdf/ipv-factsheet.pdf) that provides an overview of IPV-related behavior, how it influences health outcomes, who is at risk for IPV, and sources for support.

Continue to: Our IPASSPRT interview script...

 

 

Our IPASSPRT interview script (http://bit.ly/ipassprt) outlines how this information can be presented to patients as a typical part of the screening process. Providers are encouraged to share and review the information from the fact sheet with all patients and present it as part of the normal screening process to mitigate the potential for defensiveness on the part of the patient. For patients who screen positive for IPV, it might be important to brainstorm ideas for a safe, secure place to store this fact sheet and other resources from the brief intervention and referral process below (eg, a safety plan and specific referral information) so that the patient can access them quickly and easily, if needed.

For patients who screen negative for IPV, their screen and interview conclude at this point.

  • Provide recommendations based on the screen. Evidence suggests that collaborating with the patient on safety planning and referral can increase the likelihood of their engagement.7 Furthermore, failure to tailor the referral to the needs of the patient can be detrimental36—ie, overshooting the level of intervention might decrease the patient’s future treatment-seeking behavior and undermine their internal coping strategies, increasing the likelihood of future victimization. For that reason, we provide the following guidance on navigating the referral process for patients who screen positive for IPV.

Screening-based referral: A delicate and collaborative process

Referral for IPV victimization. Individual counseling, with or without an IPV focus, might be appropriate for patients at lower levels of risk; immediate connection with local IPV resources is strongly encouraged for patients at higher risk. This is a delicate, collaborative process, in which the physician offers recommendations for referral commensurate to the patient’s risk but must, ultimately, respect the patient’s autonomy by identifying referrals that fit the patient’s goals. We encourage providers to provide risk-informed recommendations and to elicit the patient’s thoughts about that information.

Several online resources are available to help physicians locate and connect with IPV-related resources in their community, including the National Health Resource Center on Domestic Violence (http://ipvhealth.org/), which provides a step-by-step guide to making such connections. We encourage physicians to develop these collaborative partnerships early to facilitate warm handoffs and increase the likelihood that a patient will follow through with the referral after screening.37

Referral for related concerns. As we’ve noted, IPV has numerous physical and mental health consequences, including depression, low self-esteem, trauma- and non-trauma-related anxiety, and substance abuse. In general, cognitive behavioral therapies appear most efficacious for treating these IPV-related consequences, but evidence is limited that such interventions diminish the likelihood of re-victimization.38 Intervention programs that foster problem-solving, solution-seeking, and cognitive restructuring for self-critical thoughts and misconceptions seem to produce the best physical and mental health outcomes.39 For patients who have a substance use disorder, treatment programs that target substance use have demonstrated a reduction in the rate of IPV recidivism.40 These findings indicate that establishing multiple treatment targets might reduce the risk for future aggression in relationships.

Continue to: The Substance Abuse and Mental Health Services Administration...

 

 

The Substance Abuse and Mental Health Services Administration of the US Department of Health and Human Services provides a useful online tool (https://findtreatment.samhsa.gov/) for locating local referrals that address behavioral health and substance-related concerns. The agency also provides a hotline (1-800-662-HELP [4357]) as an alternative resource for information and treatment referrals.

Safety planning can improve outcomes

For a patient who screens above low risk, safety planning with the patient is an important part of improving outcomes and can take several forms. Online resources, such as the Path to Safety interactive Web page (www.thehotline.org/help/path-to-safety/) maintained by The National Domestic Violence Hotline ([800]799-SAFE [7233]), provide information regarding important considerations for safety planning when:

  • living with an abusive partner
  • children are in the home
  • the patient is pregnant
  • pets are involved.

The Web site also provides information regarding legal options and resources related to IPV (eg, an order of protection) and steps for improving safety when leaving an abusive relationship. Patients at risk for IPV can explore the online tool and call the hotline.

For physicians who want to engage in provider-assisted safety planning, we’ve provided further guidance in the IPASSPRT screening script and safety plan (http://bit.ly/ipassprt) (TABLE 4).

Components of a safety plan: A patient guide

Goal: Affirm patients’ strengths and reinforce hope

Psychological aggression is the most common form of relationship aggression; repeated denigration might leave a person with little confidence in their ability to change their relationship or seek out identified resources. That’s why it’s useful to inquire—with genuine curiosity—about a time in the past when the patient accomplished something challenging. The physician’s enthusiastic reflection on this achievement can be a means of highlighting the patient’s ability to accomplish a meaningful goal; of reinforcing their hope; and of eliciting important resources within and around the patient that can facilitate action on their safety plan. (See “IPV-related resources for physicians and patients.”)

SIDEBAR
IPV-related resources for physicians and patients

Intimate Partner Aggression Screening, Safety Planning, and Referral to Treatment (IPASSPRT) Project
http://bit.ly/ipassprt
Online resource with tools designed by the authors, including an SBIRT-inspired script and safety plan template for IPV screening, safety planning, and referral

National Center for Injury Prevention and Control Division of Violence Prevention
www.cdc.gov/violenceprevention/pdf/ipv-factsheet.pdf
Overview of IPV-related behavior, influence on health outcomes, people at risk of IPV, and sources of support, all in a format easily understood by patients

National Health Resource Center on Domestic Violence
http://ipvhealth.org/
Includes guidance on connecting with IPV-related community resources; establishing such connections can facilitate warm handoffs and improve the likelihood that patients will follow through

Path to Safety, a service of The National Domestic Violence Hotline
www.thehotline.org/help/path-to-safety/
Extensive primer on safety plans for patients intending to stay in (or leave) an abusive relationship; includes important considerations for children, pets, and pregnancy, as well as emotional safety and legal options

The National Domestic Violence Hotline
› (800) 799-SAFE (7233)

Substance Abuse and Mental Health Services Administration
www.samhsa.gov/sbirt
Learning resources for the SBIRT protocol for substance abuse
https://findtreatment.samhsa.gov/
Search engine and resources for locating local referrals
› (800) 662-HELP (4357)
Hotline for information and assistance with locating local treatment referral

IPV, intimate partner violence; SBIRT, screening, brief intervention, and referral to treatment.
 

Continue to: Closing the screen and making a referral

 

 

Closing the screen and making a referral

The end of the interview should consist of a summary of topics discussed, including:

  • changes that the patient wants to make (if any)
  • their stated reasons for making those changes
  • the patient’s plan for accomplishing changes.

Physicians should also include their own role in next steps—whether providing a warm handoff to a local IPV referral, agreeing to a follow-up schedule with the patient, or making a call as a mandated reporter. To close out the interview, it is important to affirm respect for the patient’s autonomy in executing the plan.

It’s important to screen all patients—here’s why

A major impetus for this article has been to raise awareness about the need for expanded IPV screening across primary care settings. As mentioned, much of the literature on IPV victimization has focused on women; however, the few epidemiological investigations of victimization rates among men and members of LGBT couples show a high rate of victimization and considerable harmful health outcomes. Driven by stigma surrounding IPV, sex, and sexual minority status, patients might have expectations that they will be judged by a provider or “outed.”

Such barriers can lead many to suffer in silence until the problem can no longer be hidden or the danger becomes more emergent. Compassionate, nonjudgmental screening and collaborative safety planning—such as the approach we describe in this article—help ease the concerns of LGBT victims of IPV and improve the likelihood that conversations you have with them will occur earlier, rather than later, in care.*

Underassessment of IPV (ie, underreporting as well as under-inquiry) because of stigma, misconception, and other factors obscures an accurate estimate of the rate of partner violence and its consequences for all couples. As a consequence, we know little about the dynamics of IPV, best practices for screening, and appropriate referral for couples from these populations. Furthermore, few resources are available to these understudied and underserved groups (eg, shelters for men and for transgender people).

Continue to: Although our immediate approach to IPV screening...

 

 

Although our immediate approach to IPV screening, safety planning, and referral with understudied patient populations might be informed by what we have learned from the experiences of heterosexual women in abusive relationships, such a practice is unsustainable. Unless we expand our scope of screening to all patients, it is unlikely that we will develop the evidence base necessary to 1) warrant stronger IPV screening recommendations for patient groups apart from women of childbearing age, let alone 2) demonstrate the need for additional community resources, and 3) provide comprehensive care in family practice of comparable quality.

The benefits of screening go beyond the individual patient

Screening for violence in the relationship does not take long; the value of asking about its presence in a relationship might offer benefits beyond the individual patient by raising awareness and providing the field of study with more data to increase attention and resources for under-researched and underserved populations. Screening might also combat the stigma that perpetuates the silence of many who deserve access to care.

CORRESPONDENCE
Joel G. Sprunger, PhD, Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, 260 Stetson St, Suite 3200, Cincinnati OH 45219; [email protected].

ACKNOWLEDGMENTS
The authors thank Jeffrey M. Girard, PhD, and Daniel C. Williams, PhD, for their input on the design and content, respectively, of the IPASSPRT screening materials; the authors of the DA-5 and the HITS screening tools, particularly Jacquelyn Campbell, PhD, RN, FAAN, and Kevin Sherin, MD, MPH, MBA, respectively, for permission to include these measures in this article and for their support of its goals; and The Journal of Family Practice’s peer reviewers for their thoughtful feedback throughout the prepublication process.

References

1. Campos-Outcalt D. USPSTF: What’s recommended, what’s not. J Fam Pract. 2014;63:265-269.

2. Black MC, Basile KC, Breiding MJ, et al. National Intimate Partner and Sexual Violence Survey: 2010 Summary Report. Atlanta, GA: National Center for Injury Prevention and Control, Centers for Disease Control and Prevention; 2011:113. www.cdc.gov/violenceprevention/pdf/NISVS_Report2010-a.pdf. Accessed February 20, 2019.

3. West CM. Partner abuse in ethnic minority and gay, lesbian, bisexual, and transgender populations. Partner Abuse. 2012;3:336-357.

4. Hines DA, Malley-Morrison K. Psychological effects of partner abuse against men: a neglected research area. Psychology of Men & Masculinities. 2001;2:75-85.

5. Houston E, McKirnan DJ. Intimate partner abuse among gay and bisexual men: risk correlates and health outcomes. J Urban Health. 2007;84:681-690.

6. Carvalho AF, Lewis RJ, Derlega VJ, et al. Internalized sexual minority stressors and same-sex intimate partner violence. J Fam Violence. 2011;26:501-509.

7. Nicholls TL, Pritchard MM, Reeves KA, et al. Risk assessment in intimate partner violence: a systematic review of contemporary approaches. Partner Abuse. 2013;4:76-168.

8. Intimate partner violence: definitions. Atlanta, GA: National Center for Injury Prevention and Control, Division of Violence Prevention, Centers for Disease Control and Prevention, August 22, 2017. www.cdc.gov/violenceprevention/intimatepartnerviolence/definitions.html. Accessed February 20, 2019.

9. Archer J. Sex differences in aggression between heterosexual partners: a meta-analytic review. Psychol Bull. 2000;126:651-680.

10. Baron RA, Richardson DR. Human Aggression. New York, NY: Springer Science+Business Media; 2004.

11. Breiding MJ, Basile KC, Smith SG, et al. Intimate Partner Violence Surveillance: Uniform Definitions and Recommended Data Elements, Version 2.0. Atlanta, GA: National Center for Injury Prevention and Control, Centers for Disease Control and Prevention; 2015.

12. Murphy CM, Eckhardt CI. Treating the Abusive Partner: An Individualized Cognitive-Behavioral Approach. New York, NY: Guilford Press; 2005.

13. Straus MA, Hamby SL, Boney-McCoy S, et al. The revised Conflict Tactics Scales (CTS2): development and preliminary psychometric data. J Fam Issues. 1996;17:283-316.

14. West CM. Partner abuse in ethnic minority and gay, lesbian, bisexual, and transgender populations. Partner Abuse. 2012;3:336-357.

15. Desmarais SL, Reeves KA, Nicholls TL, et al. Prevalence of physical violence in intimate relationships. Part 1: rates of male and female victimization. Partner Abuse. 2012;3:140-169.

16. Lawrence E, Orengo-Aguayo R, Langer A, et al. The impact and consequences of partner abuse on partners. Partner Abuse. 2012;3:406-428.

17. Langhinrichsen-Rohling J, Selwyn C, Rohling ML. Rates of bidirectional versus unidirectional intimate partner violence across samples, sexual orientations, and race/ethnicities: a comprehensive review. Partner Abuse. 2012;3:199-230.

18. Langhinrichsen-Rohling J, McCullars A, Misra TA. Motivations for men and women’s intimate partner violence perpetration: a comprehensive review. Partner Abuse. 2012;3:429-468.

19. Anderson CA, Bushman BJ. Human aggression. Annu Rev Psychol. 2002;53:27-51.

20. Straus MA, Gozjolko KL. “Intimate terrorism” and gender differences in injury of dating partners by male and female university students. J Fam Violence. 2014;29:51-65.

21. Ferraro KJ, Johnson JM. How women experience battering: the process of victimization. Soc Probl. 1983;30:325-339.

22. Sugg NK, Inui T. Primary care physicians’ response to domestic violence: opening Pandora’s box. JAMA. 1992;267:3157-3160.

23. Morgan KJ, Williamson E, Hester M, et al. Asking men about domestic violence and abuse in a family medicine context: help seeking and views on the general practitioner role. Aggress Violent Behav. 2014;19:637-642.

24. MacMillan HL, Wathen CN, Jamieson E, et al; McMaster Violence Against Women Research Group. Approaches to screening for intimate partner violence in health care settings: a randomized trial. JAMA. 2006;296:530-536.

25. Thompson RS, Rivara FP, Thompson DC, et al. Identification and management of domestic violence: a randomized trial. Am J Prev Med. 2000;19:253-263.

26. Ard KL, Makadon HJ. Addressing intimate partner violence in lesbian, gay, bisexual, and transgender patients. J Gen Intern Med. 2011;26:930-933.

27. Rabin RF, Jennings JM, Campbell JC, et al. Intimate partner violence screening tools: a systematic review. Am J Prev Med. 2009;36:439-445.e4.

28. Madras BK, Compton WM, Avula D, et al. Screening, brief interventions, referral to treatment (SBIRT) for illicit drug and alcohol use at multiple healthcare sites: comparison at intake and 6 months later. Drug Alcohol Depend. 2009;99:280-295.

29. Sherin KM, Sinacore JM, Li XQ, et al. HITS: A short domestic violence screening tool for use in a family practice setting. Fam Med. 1998;30:508-512.

30. Peralta RL, Fleming MF. Screening for intimate partner violence in a primary care setting: the validity of “feeling safe at home” and prevalence results. J Am Board Fam Pract. 2003;16:525-532.

31. Capaldi DM, Knoble NB, Shortt JW, et al. A systematic review of risk factors for intimate partner violence. Partner Abuse. 2012;3:231-280.

32. Brownridge DA, Taillieu TL, Tyler KA, et al. Pregnancy and intimate partner violence: risk factors, severity, and health effects. Violence Against Women. 2011;17:858-881.

33. Messing JT, Campbell JC, Snider C. Validation and adaptation of the danger assessment-5: a brief intimate partner violence risk assessment. J Adv Nurs. 2017;73:3220-3230.

34. Grigsby N, Hartman BR. The Barriers Model: an integrated strategy for intervention with battered women. Psychotherapy: Theory, Research, Practice, Training. 1997;34:485-497.

35. Moyers TB, Rollnick S. A motivational interviewing perspective on resistance in psychotherapy. J Clin Psychol. 2002;58:185-193.

36. Belfrage H, Strand S, Storey JE, et al. Assessment and management of risk for intimate partner violence by police officers using the Spousal Assault Risk Assessment Guide. Law Hum Behav. 2012;36:60-67.

37. McCloskey LA, Lichter E, Williams C, et al. Assessing intimate partner violence in health care settings leads to women’s receipt of interventions and improved health. Publ Health Rep. 2006;121:435-444.

38. Eckhardt CI, Murphy CM, Whitaker DJ, et al. The effectiveness of intervention programs for perpetrators and victims of intimate partner violence. Partner Abuse. 2013;4:196-231.

39. Trabold N, McMahon J, Alsobrooks S, et al. A systematic review of intimate partner violence interventions: state of the field and implications for practitioners. Trauma Violence Abuse. January 2018:1524838018767934.

40. Kraanen FL, Vedel E, Scholing A, et al. The comparative effectiveness of Integrated treatment for Substance abuse and Partner violence (I-StoP) and substance abuse treatment alone: a randomized controlled trial. BMC Psychiatry. 2013;13:189.

References

1. Campos-Outcalt D. USPSTF: What’s recommended, what’s not. J Fam Pract. 2014;63:265-269.

2. Black MC, Basile KC, Breiding MJ, et al. National Intimate Partner and Sexual Violence Survey: 2010 Summary Report. Atlanta, GA: National Center for Injury Prevention and Control, Centers for Disease Control and Prevention; 2011:113. www.cdc.gov/violenceprevention/pdf/NISVS_Report2010-a.pdf. Accessed February 20, 2019.

3. West CM. Partner abuse in ethnic minority and gay, lesbian, bisexual, and transgender populations. Partner Abuse. 2012;3:336-357.

4. Hines DA, Malley-Morrison K. Psychological effects of partner abuse against men: a neglected research area. Psychology of Men & Masculinities. 2001;2:75-85.

5. Houston E, McKirnan DJ. Intimate partner abuse among gay and bisexual men: risk correlates and health outcomes. J Urban Health. 2007;84:681-690.

6. Carvalho AF, Lewis RJ, Derlega VJ, et al. Internalized sexual minority stressors and same-sex intimate partner violence. J Fam Violence. 2011;26:501-509.

7. Nicholls TL, Pritchard MM, Reeves KA, et al. Risk assessment in intimate partner violence: a systematic review of contemporary approaches. Partner Abuse. 2013;4:76-168.

8. Intimate partner violence: definitions. Atlanta, GA: National Center for Injury Prevention and Control, Division of Violence Prevention, Centers for Disease Control and Prevention, August 22, 2017. www.cdc.gov/violenceprevention/intimatepartnerviolence/definitions.html. Accessed February 20, 2019.

9. Archer J. Sex differences in aggression between heterosexual partners: a meta-analytic review. Psychol Bull. 2000;126:651-680.

10. Baron RA, Richardson DR. Human Aggression. New York, NY: Springer Science+Business Media; 2004.

11. Breiding MJ, Basile KC, Smith SG, et al. Intimate Partner Violence Surveillance: Uniform Definitions and Recommended Data Elements, Version 2.0. Atlanta, GA: National Center for Injury Prevention and Control, Centers for Disease Control and Prevention; 2015.

12. Murphy CM, Eckhardt CI. Treating the Abusive Partner: An Individualized Cognitive-Behavioral Approach. New York, NY: Guilford Press; 2005.

13. Straus MA, Hamby SL, Boney-McCoy S, et al. The revised Conflict Tactics Scales (CTS2): development and preliminary psychometric data. J Fam Issues. 1996;17:283-316.

14. West CM. Partner abuse in ethnic minority and gay, lesbian, bisexual, and transgender populations. Partner Abuse. 2012;3:336-357.

15. Desmarais SL, Reeves KA, Nicholls TL, et al. Prevalence of physical violence in intimate relationships. Part 1: rates of male and female victimization. Partner Abuse. 2012;3:140-169.

16. Lawrence E, Orengo-Aguayo R, Langer A, et al. The impact and consequences of partner abuse on partners. Partner Abuse. 2012;3:406-428.

17. Langhinrichsen-Rohling J, Selwyn C, Rohling ML. Rates of bidirectional versus unidirectional intimate partner violence across samples, sexual orientations, and race/ethnicities: a comprehensive review. Partner Abuse. 2012;3:199-230.

18. Langhinrichsen-Rohling J, McCullars A, Misra TA. Motivations for men and women’s intimate partner violence perpetration: a comprehensive review. Partner Abuse. 2012;3:429-468.

19. Anderson CA, Bushman BJ. Human aggression. Annu Rev Psychol. 2002;53:27-51.

20. Straus MA, Gozjolko KL. “Intimate terrorism” and gender differences in injury of dating partners by male and female university students. J Fam Violence. 2014;29:51-65.

21. Ferraro KJ, Johnson JM. How women experience battering: the process of victimization. Soc Probl. 1983;30:325-339.

22. Sugg NK, Inui T. Primary care physicians’ response to domestic violence: opening Pandora’s box. JAMA. 1992;267:3157-3160.

23. Morgan KJ, Williamson E, Hester M, et al. Asking men about domestic violence and abuse in a family medicine context: help seeking and views on the general practitioner role. Aggress Violent Behav. 2014;19:637-642.

24. MacMillan HL, Wathen CN, Jamieson E, et al; McMaster Violence Against Women Research Group. Approaches to screening for intimate partner violence in health care settings: a randomized trial. JAMA. 2006;296:530-536.

25. Thompson RS, Rivara FP, Thompson DC, et al. Identification and management of domestic violence: a randomized trial. Am J Prev Med. 2000;19:253-263.

26. Ard KL, Makadon HJ. Addressing intimate partner violence in lesbian, gay, bisexual, and transgender patients. J Gen Intern Med. 2011;26:930-933.

27. Rabin RF, Jennings JM, Campbell JC, et al. Intimate partner violence screening tools: a systematic review. Am J Prev Med. 2009;36:439-445.e4.

28. Madras BK, Compton WM, Avula D, et al. Screening, brief interventions, referral to treatment (SBIRT) for illicit drug and alcohol use at multiple healthcare sites: comparison at intake and 6 months later. Drug Alcohol Depend. 2009;99:280-295.

29. Sherin KM, Sinacore JM, Li XQ, et al. HITS: A short domestic violence screening tool for use in a family practice setting. Fam Med. 1998;30:508-512.

30. Peralta RL, Fleming MF. Screening for intimate partner violence in a primary care setting: the validity of “feeling safe at home” and prevalence results. J Am Board Fam Pract. 2003;16:525-532.

31. Capaldi DM, Knoble NB, Shortt JW, et al. A systematic review of risk factors for intimate partner violence. Partner Abuse. 2012;3:231-280.

32. Brownridge DA, Taillieu TL, Tyler KA, et al. Pregnancy and intimate partner violence: risk factors, severity, and health effects. Violence Against Women. 2011;17:858-881.

33. Messing JT, Campbell JC, Snider C. Validation and adaptation of the danger assessment-5: a brief intimate partner violence risk assessment. J Adv Nurs. 2017;73:3220-3230.

34. Grigsby N, Hartman BR. The Barriers Model: an integrated strategy for intervention with battered women. Psychotherapy: Theory, Research, Practice, Training. 1997;34:485-497.

35. Moyers TB, Rollnick S. A motivational interviewing perspective on resistance in psychotherapy. J Clin Psychol. 2002;58:185-193.

36. Belfrage H, Strand S, Storey JE, et al. Assessment and management of risk for intimate partner violence by police officers using the Spousal Assault Risk Assessment Guide. Law Hum Behav. 2012;36:60-67.

37. McCloskey LA, Lichter E, Williams C, et al. Assessing intimate partner violence in health care settings leads to women’s receipt of interventions and improved health. Publ Health Rep. 2006;121:435-444.

38. Eckhardt CI, Murphy CM, Whitaker DJ, et al. The effectiveness of intervention programs for perpetrators and victims of intimate partner violence. Partner Abuse. 2013;4:196-231.

39. Trabold N, McMahon J, Alsobrooks S, et al. A systematic review of intimate partner violence interventions: state of the field and implications for practitioners. Trauma Violence Abuse. January 2018:1524838018767934.

40. Kraanen FL, Vedel E, Scholing A, et al. The comparative effectiveness of Integrated treatment for Substance abuse and Partner violence (I-StoP) and substance abuse treatment alone: a randomized controlled trial. BMC Psychiatry. 2013;13:189.

Issue
The Journal of Family Practice - 68(3)
Issue
The Journal of Family Practice - 68(3)
Page Number
152-154,156-161A
Page Number
152-154,156-161A
Publications
Publications
Topics
Article Type
Display Headline
It’s time to start asking all patients about intimate partner violence
Display Headline
It’s time to start asking all patients about intimate partner violence
Sections
Inside the Article

PRACTICE RECOMMENDATIONS

› Perform annual screening for intimate partner violence of all female patients of childbearing age; strongly consider a pilot program of universal screening (all male and female patients, across the lifespan). B

› Establish a protocol for intimate partner violence screening and referral—possibly the most effective means of identifying intimate partner violence at early and severe stages. B

› Collaborate with the patient in the safety planning and referral process; benefits include improved likelihood that the patient will adhere to a safety plan and follow through with the referral. B

› Utilize online resources to 1) ease the process of establishing relationships with local intimate partner violence referrals and 2) facilitate warm handoffs to increase the likelihood of patient engagement. B

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
PubMed ID
31039212
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Article PDF Media

Parabens: The 2019 Nonallergen of the Year

Article Type
Changed
Thu, 05/16/2019 - 09:02
Display Headline
Parabens: The 2019 Nonallergen of the Year

Each year, the American Contact Dermatitis Society (ACDS) names an allergen of the year with the purpose of promoting greater awareness of a key allergen and its impact on patients. Often, the allergen of the year is an emerging allergen that may represent an underrecognized or novel cause of allergic contact dermatitis (ACD). In 2019, the ACDS chose parabens as the “nonallergen” of the year to draw attention to their low rate of associated ACD despite high public interest in limiting exposure to parabens.1

What types of products contain parabens?

Parabens are preservatives commonly found in many different categories of personal care products. Preservatives inhibit microbial growth and are necessary ingredients in water-based products. The 4 most common parabens used in personal care products are methylparaben, ethylparaben, propylparaben, and butylparaben.1 Parabens are metabolized to 4-hydroxybenzoic acid and are excreted in urine. When parabens are applied topically, there is minimal penetration through intact human skin.2 In the United States, parabens are allowed as preservatives in cosmetics at concentrations up to 0.4% when used alone or up to 0.8% when used in combination with other parabens.3

Consumers are exposed to parabens in a wide variety of personal care products. The Contact Allergen Management Program (CAMP) is a system owned and managed by the ACDS that typically is used to generate lists of safe personal care products for patients and also can be queried for the presence of individual chemicals in products. According to a 2018 query of the CAMP, parabens were found in 19% of all products.1 A more recent query of CAMP (http://www.contactderm.org/resources/acds-camp) in March 2019 showed parabens were present in 39.3% of makeup products, especially in eye products, foundations, and concealers; parabens also were found in 34% of moisturizers, 11.5% of soaps, and 19% of sunscreens. Notably, 14.8% of prescription topical steroids listed in the CAMP contained a paraben. Another method for evaluating chemical contents of personal care products is a review of the Voluntary Cosmetic Registration Program, a US Food and Drug Administration–based registry for cosmetic products. Survey data from the Voluntary Cosmetic Registration Program in 2018 documented methylparaben in 11,626 formulations.4 Other parabens included propylparaben (8885 products), butylparaben (3915 products), and ethylparaben (3860 products). Parabens were reported more frequently in leave-on rather than rinse-off products.4

In medications, parabens are recommended at concentrations of no more than 0.1%.1 Fransway et al1 compiled a list of medications that contain parabens, including commonly prescribed dermatologic topical medications such as corticosteroids, several acne preparations, eflornithine, fluorouracil, hydroquinone, imiquimod, urea, and sertaconazole. Oral and parenteral medications including local anesthetics and corticosteroids also may contain parabens.

Consumers also may be exposed to parabens through foodstuffs. Methylparaben and propylparaben have been classified as generally recognized as safe in foods by the US Food and Drug Administration.5 The acceptable daily intake of parabens in food is 0 to 10 mg/kg of body weight,1 and the estimated dietary intake for a typical adult is 307 mg/kg of body weight daily.6 Several studies on paraben content in foodstuffs have confirmed their presence in both natural and processed foods.1,6 Systemic contact dermatitis caused by ingestion of parabens is rare. In general, individuals with positive patch test reactions to parabens should not routinely avoid them in foods or oral medications,1 but they should, of course, be avoided in topical medications.

 

 

What is the rate of ACD with parabens?

One of the main reasons that parabens were designated as the ACDS nonallergen of the year is the very low rate of ACD associated with parabens. The North American Contact Dermatitis Group, a research group with members in the United States and Canada, reported a 0.6% positive reaction rate when patch testing with paraben mix 12%,7 which closely compares with a 0.8% positive reaction rate when patch testing with paraben mix 16% using the Mayo Clinic standard series.8 From the standpoint of ACD, this very low patch test reaction rate makes parabens one of the safest preservative options for use in cosmetic products.

Are there health risks associated with parabens?

The paraben controversy in the scientific literature and in the lay press centers around potential health risks and endocrine disruption. We will focus on the conversation regarding parabens and the risk for endocrine disruption and association with breast cancer.

Parabens have been reported to have estrogenic effects; however, the bulk of the data is limited to in vitro and animal studies, with less evidence of endocrine disruption in humans.2 In vitro studies have demonstrated that the estrogenic potency of parabens is much less than that of estrogen. In one study, parabens were shown to be 10,000-fold less potent than 17β-estradiol9; in a separate study, they had a maximum potency of only 1/4000 that of estrogen.10 Additionally, an in vitro study showed varying ability for parabens to bind estrogen receptors, with a greater ability to bind with longer alkyl side chains.11 The result is decreased or increased estrogen activity, dependent on side chain length and type of receptor.2 Finally, some studies add conflicting results that parabens may actually create an antiestrogenic effect in human breast cancer cells.12 From the standpoint of estrogen mimicry, there are no known studies in humans confirming harmful effects associated with paraben exposure.

The reported association between parabens and breast cancer is closely related to their theoretical estrogenic effects. The conversation regarding parabens and breast cancer has been fueled by the identification of parabens in human breast tumors and their presence in concentrations similar to what is needed to stimulate in vitro breast cancer cells.2 The existing data do not confirm causation. An association with parabens in topical axillary personal care products has been theorized but not confirmed; for example, it was shown that paraben levels were highest in the axillary region of breast cancer tissue, including women who had never used deodorant. It was concluded that the presence of axillary parabens was due to sources other than topical axillary personal care products.13 Another study confirmed there was not an increased risk for breast cancer in patients who applied personal care products to the axillary area within an hour of shaving.14 The existing data do not support topical paraben exposure as a risk for breast cancer.

Final Thoughts

Parabens are preservatives frequently found in personal care products and exhibit a very low rate of associated ACD. Consumers may be exposed to parabens through foods, cosmetics, and medications. Although there have been consumer concerns regarding endocrine disruption or carcinogenicity associated with parabens, definite evidence of their harm is lacking in the scientific literature, and many studies confirm their safety.2 With their high prevalence in personal care products and low rates of associated contact allergy, parabens remain ideal preservative agents.

Ultimately, contact dermatitis is a common yet often underrecognized dermatologic condition. To address this knowledge gap in clinical practice, we are proud to launch Final Interpretation, a new column in Cutis covering emerging trends in contact dermatitis. We will address pearls, pitfalls, and updates in contact dermatitis. Although our primary focus will be ACD, other important causes of contact dermatitis will be highlighted. Look for the inaugural column in the June 2019 issue of Cutis.

References
  1. Fransway AF, Fransway PJ, Belsito DV, et al. Parabens: contact (non)allergen of the year. Dermatitis. 2019;30:3-31.
  2. Fransway AF, Fransway PJ, Belsito DV, et al. Paraben toxicology. Dermatitis. 2019;30:32-45.
  3. Final amended report on the safety assessment of methylparaben, ethylparaben, propylparaben, isopropylparaben, butylparaben, isobutylparaben, and benzylparaben as used in cosmetic products. Int J Toxicol. 2008;27(suppl 4):1-82.
  4. Cosmetic Ingredient Review. Amended safety assessment of parabens as used in cosmetics. https://www.cir-safety.org/sites/default/files/Parabens.pdf. Published August 29, 2018. Accessed March 12, 2019.
  5. Methylparaben. Fed Regist. 2018;21(3):1490. To be codified at 21 CFR §184.
  6. Liao C, Liu F, Kannan K. Occurrence of and dietary exposure to parabens in foodstuffs from the United States. Environ Sci Technol. 2013;47:3918-3925.
  7. DeKoven JG, Warshaw EM, Zug KA, et al. North American Contact Dermatitis Group Patch Test Results: 2015-2016. Dermatitis. 2018;29:297-309.
  8. Veverka KK, Hall MR, Yiannias JA, et al. Trends in patch testing with the Mayo Clinic standard series, 2011-2015. Dermatitis. 2018;29:310-315.
  9. Routledge EJ, Parker J, Odum J, et al. Some alkyl hydroxy benzoate preservatives (parabens) are estrogenic. Toxicol Appl Pharmacol. 1998;153:12-19.
  10. Miller D, Brian B, Wheals BB, et al. Estrogenic activity of phenolic additives determined by an in vitro yeast bioassay. Environ Health Perspect. 2001;109:133-138.
  11. Blair RM, Fang H, Branham WS. The estrogen receptor relative binding affinities of 188 natural and xenochemicals: structural diversity of ligands. Toxicol Sci. 2000;54:138-153.
  12. van Meeuwen JA, van Son O, Piersma AH, et al. Aromatase inhibiting and combined estrogenic effects of parabens and estrogenic effects of other additives in cosmetics. Toxicol Appl Pharmacol. 2008;230:372-382.
  13. Barr L, Metaxas G, Harbach CA, et al. Measurement of paraben concentrations in human breast tissue at serial locations across the breast from axilla to sternum. J Appl Toxicol. 2012;32:219-232.
  14. Mirick DK, Davis S, Thomas DB. Antiperspirant use and the risk of breast cancer. J Natl Cancer Inst. 2002;94:1578-1580.
Article PDF
Author and Disclosure Information

Dr. Reeder is from the Department of Dermatology, University of Wisconsin School of Medicine and Public Health, Madison. Dr. Atwater is from the Department of Dermatology, Duke University School of Medicine, Durham, North Carolina.

Dr. Reeder reports no conflict of interest. Dr. Atwater received a Pfizer Inc independent grant but will not receive any compensation from this grant.

Correspondence: Margo Reeder, MD, One S Park St, 7th Floor, Madison, WI 53715 ([email protected]).

Issue
Cutis - 103(4)
Publications
Topics
Page Number
192-193
Sections
Author and Disclosure Information

Dr. Reeder is from the Department of Dermatology, University of Wisconsin School of Medicine and Public Health, Madison. Dr. Atwater is from the Department of Dermatology, Duke University School of Medicine, Durham, North Carolina.

Dr. Reeder reports no conflict of interest. Dr. Atwater received a Pfizer Inc independent grant but will not receive any compensation from this grant.

Correspondence: Margo Reeder, MD, One S Park St, 7th Floor, Madison, WI 53715 ([email protected]).

Author and Disclosure Information

Dr. Reeder is from the Department of Dermatology, University of Wisconsin School of Medicine and Public Health, Madison. Dr. Atwater is from the Department of Dermatology, Duke University School of Medicine, Durham, North Carolina.

Dr. Reeder reports no conflict of interest. Dr. Atwater received a Pfizer Inc independent grant but will not receive any compensation from this grant.

Correspondence: Margo Reeder, MD, One S Park St, 7th Floor, Madison, WI 53715 ([email protected]).

Article PDF
Article PDF

Each year, the American Contact Dermatitis Society (ACDS) names an allergen of the year with the purpose of promoting greater awareness of a key allergen and its impact on patients. Often, the allergen of the year is an emerging allergen that may represent an underrecognized or novel cause of allergic contact dermatitis (ACD). In 2019, the ACDS chose parabens as the “nonallergen” of the year to draw attention to their low rate of associated ACD despite high public interest in limiting exposure to parabens.1

What types of products contain parabens?

Parabens are preservatives commonly found in many different categories of personal care products. Preservatives inhibit microbial growth and are necessary ingredients in water-based products. The 4 most common parabens used in personal care products are methylparaben, ethylparaben, propylparaben, and butylparaben.1 Parabens are metabolized to 4-hydroxybenzoic acid and are excreted in urine. When parabens are applied topically, there is minimal penetration through intact human skin.2 In the United States, parabens are allowed as preservatives in cosmetics at concentrations up to 0.4% when used alone or up to 0.8% when used in combination with other parabens.3

Consumers are exposed to parabens in a wide variety of personal care products. The Contact Allergen Management Program (CAMP) is a system owned and managed by the ACDS that typically is used to generate lists of safe personal care products for patients and also can be queried for the presence of individual chemicals in products. According to a 2018 query of the CAMP, parabens were found in 19% of all products.1 A more recent query of CAMP (http://www.contactderm.org/resources/acds-camp) in March 2019 showed parabens were present in 39.3% of makeup products, especially in eye products, foundations, and concealers; parabens also were found in 34% of moisturizers, 11.5% of soaps, and 19% of sunscreens. Notably, 14.8% of prescription topical steroids listed in the CAMP contained a paraben. Another method for evaluating chemical contents of personal care products is a review of the Voluntary Cosmetic Registration Program, a US Food and Drug Administration–based registry for cosmetic products. Survey data from the Voluntary Cosmetic Registration Program in 2018 documented methylparaben in 11,626 formulations.4 Other parabens included propylparaben (8885 products), butylparaben (3915 products), and ethylparaben (3860 products). Parabens were reported more frequently in leave-on rather than rinse-off products.4

In medications, parabens are recommended at concentrations of no more than 0.1%.1 Fransway et al1 compiled a list of medications that contain parabens, including commonly prescribed dermatologic topical medications such as corticosteroids, several acne preparations, eflornithine, fluorouracil, hydroquinone, imiquimod, urea, and sertaconazole. Oral and parenteral medications including local anesthetics and corticosteroids also may contain parabens.

Consumers also may be exposed to parabens through foodstuffs. Methylparaben and propylparaben have been classified as generally recognized as safe in foods by the US Food and Drug Administration.5 The acceptable daily intake of parabens in food is 0 to 10 mg/kg of body weight,1 and the estimated dietary intake for a typical adult is 307 mg/kg of body weight daily.6 Several studies on paraben content in foodstuffs have confirmed their presence in both natural and processed foods.1,6 Systemic contact dermatitis caused by ingestion of parabens is rare. In general, individuals with positive patch test reactions to parabens should not routinely avoid them in foods or oral medications,1 but they should, of course, be avoided in topical medications.

 

 

What is the rate of ACD with parabens?

One of the main reasons that parabens were designated as the ACDS nonallergen of the year is the very low rate of ACD associated with parabens. The North American Contact Dermatitis Group, a research group with members in the United States and Canada, reported a 0.6% positive reaction rate when patch testing with paraben mix 12%,7 which closely compares with a 0.8% positive reaction rate when patch testing with paraben mix 16% using the Mayo Clinic standard series.8 From the standpoint of ACD, this very low patch test reaction rate makes parabens one of the safest preservative options for use in cosmetic products.

Are there health risks associated with parabens?

The paraben controversy in the scientific literature and in the lay press centers around potential health risks and endocrine disruption. We will focus on the conversation regarding parabens and the risk for endocrine disruption and association with breast cancer.

Parabens have been reported to have estrogenic effects; however, the bulk of the data is limited to in vitro and animal studies, with less evidence of endocrine disruption in humans.2 In vitro studies have demonstrated that the estrogenic potency of parabens is much less than that of estrogen. In one study, parabens were shown to be 10,000-fold less potent than 17β-estradiol9; in a separate study, they had a maximum potency of only 1/4000 that of estrogen.10 Additionally, an in vitro study showed varying ability for parabens to bind estrogen receptors, with a greater ability to bind with longer alkyl side chains.11 The result is decreased or increased estrogen activity, dependent on side chain length and type of receptor.2 Finally, some studies add conflicting results that parabens may actually create an antiestrogenic effect in human breast cancer cells.12 From the standpoint of estrogen mimicry, there are no known studies in humans confirming harmful effects associated with paraben exposure.

The reported association between parabens and breast cancer is closely related to their theoretical estrogenic effects. The conversation regarding parabens and breast cancer has been fueled by the identification of parabens in human breast tumors and their presence in concentrations similar to what is needed to stimulate in vitro breast cancer cells.2 The existing data do not confirm causation. An association with parabens in topical axillary personal care products has been theorized but not confirmed; for example, it was shown that paraben levels were highest in the axillary region of breast cancer tissue, including women who had never used deodorant. It was concluded that the presence of axillary parabens was due to sources other than topical axillary personal care products.13 Another study confirmed there was not an increased risk for breast cancer in patients who applied personal care products to the axillary area within an hour of shaving.14 The existing data do not support topical paraben exposure as a risk for breast cancer.

Final Thoughts

Parabens are preservatives frequently found in personal care products and exhibit a very low rate of associated ACD. Consumers may be exposed to parabens through foods, cosmetics, and medications. Although there have been consumer concerns regarding endocrine disruption or carcinogenicity associated with parabens, definite evidence of their harm is lacking in the scientific literature, and many studies confirm their safety.2 With their high prevalence in personal care products and low rates of associated contact allergy, parabens remain ideal preservative agents.

Ultimately, contact dermatitis is a common yet often underrecognized dermatologic condition. To address this knowledge gap in clinical practice, we are proud to launch Final Interpretation, a new column in Cutis covering emerging trends in contact dermatitis. We will address pearls, pitfalls, and updates in contact dermatitis. Although our primary focus will be ACD, other important causes of contact dermatitis will be highlighted. Look for the inaugural column in the June 2019 issue of Cutis.

Each year, the American Contact Dermatitis Society (ACDS) names an allergen of the year with the purpose of promoting greater awareness of a key allergen and its impact on patients. Often, the allergen of the year is an emerging allergen that may represent an underrecognized or novel cause of allergic contact dermatitis (ACD). In 2019, the ACDS chose parabens as the “nonallergen” of the year to draw attention to their low rate of associated ACD despite high public interest in limiting exposure to parabens.1

What types of products contain parabens?

Parabens are preservatives commonly found in many different categories of personal care products. Preservatives inhibit microbial growth and are necessary ingredients in water-based products. The 4 most common parabens used in personal care products are methylparaben, ethylparaben, propylparaben, and butylparaben.1 Parabens are metabolized to 4-hydroxybenzoic acid and are excreted in urine. When parabens are applied topically, there is minimal penetration through intact human skin.2 In the United States, parabens are allowed as preservatives in cosmetics at concentrations up to 0.4% when used alone or up to 0.8% when used in combination with other parabens.3

Consumers are exposed to parabens in a wide variety of personal care products. The Contact Allergen Management Program (CAMP) is a system owned and managed by the ACDS that typically is used to generate lists of safe personal care products for patients and also can be queried for the presence of individual chemicals in products. According to a 2018 query of the CAMP, parabens were found in 19% of all products.1 A more recent query of CAMP (http://www.contactderm.org/resources/acds-camp) in March 2019 showed parabens were present in 39.3% of makeup products, especially in eye products, foundations, and concealers; parabens also were found in 34% of moisturizers, 11.5% of soaps, and 19% of sunscreens. Notably, 14.8% of prescription topical steroids listed in the CAMP contained a paraben. Another method for evaluating chemical contents of personal care products is a review of the Voluntary Cosmetic Registration Program, a US Food and Drug Administration–based registry for cosmetic products. Survey data from the Voluntary Cosmetic Registration Program in 2018 documented methylparaben in 11,626 formulations.4 Other parabens included propylparaben (8885 products), butylparaben (3915 products), and ethylparaben (3860 products). Parabens were reported more frequently in leave-on rather than rinse-off products.4

In medications, parabens are recommended at concentrations of no more than 0.1%.1 Fransway et al1 compiled a list of medications that contain parabens, including commonly prescribed dermatologic topical medications such as corticosteroids, several acne preparations, eflornithine, fluorouracil, hydroquinone, imiquimod, urea, and sertaconazole. Oral and parenteral medications including local anesthetics and corticosteroids also may contain parabens.

Consumers also may be exposed to parabens through foodstuffs. Methylparaben and propylparaben have been classified as generally recognized as safe in foods by the US Food and Drug Administration.5 The acceptable daily intake of parabens in food is 0 to 10 mg/kg of body weight,1 and the estimated dietary intake for a typical adult is 307 mg/kg of body weight daily.6 Several studies on paraben content in foodstuffs have confirmed their presence in both natural and processed foods.1,6 Systemic contact dermatitis caused by ingestion of parabens is rare. In general, individuals with positive patch test reactions to parabens should not routinely avoid them in foods or oral medications,1 but they should, of course, be avoided in topical medications.

 

 

What is the rate of ACD with parabens?

One of the main reasons that parabens were designated as the ACDS nonallergen of the year is the very low rate of ACD associated with parabens. The North American Contact Dermatitis Group, a research group with members in the United States and Canada, reported a 0.6% positive reaction rate when patch testing with paraben mix 12%,7 which closely compares with a 0.8% positive reaction rate when patch testing with paraben mix 16% using the Mayo Clinic standard series.8 From the standpoint of ACD, this very low patch test reaction rate makes parabens one of the safest preservative options for use in cosmetic products.

Are there health risks associated with parabens?

The paraben controversy in the scientific literature and in the lay press centers around potential health risks and endocrine disruption. We will focus on the conversation regarding parabens and the risk for endocrine disruption and association with breast cancer.

Parabens have been reported to have estrogenic effects; however, the bulk of the data is limited to in vitro and animal studies, with less evidence of endocrine disruption in humans.2 In vitro studies have demonstrated that the estrogenic potency of parabens is much less than that of estrogen. In one study, parabens were shown to be 10,000-fold less potent than 17β-estradiol9; in a separate study, they had a maximum potency of only 1/4000 that of estrogen.10 Additionally, an in vitro study showed varying ability for parabens to bind estrogen receptors, with a greater ability to bind with longer alkyl side chains.11 The result is decreased or increased estrogen activity, dependent on side chain length and type of receptor.2 Finally, some studies add conflicting results that parabens may actually create an antiestrogenic effect in human breast cancer cells.12 From the standpoint of estrogen mimicry, there are no known studies in humans confirming harmful effects associated with paraben exposure.

The reported association between parabens and breast cancer is closely related to their theoretical estrogenic effects. The conversation regarding parabens and breast cancer has been fueled by the identification of parabens in human breast tumors and their presence in concentrations similar to what is needed to stimulate in vitro breast cancer cells.2 The existing data do not confirm causation. An association with parabens in topical axillary personal care products has been theorized but not confirmed; for example, it was shown that paraben levels were highest in the axillary region of breast cancer tissue, including women who had never used deodorant. It was concluded that the presence of axillary parabens was due to sources other than topical axillary personal care products.13 Another study confirmed there was not an increased risk for breast cancer in patients who applied personal care products to the axillary area within an hour of shaving.14 The existing data do not support topical paraben exposure as a risk for breast cancer.

Final Thoughts

Parabens are preservatives frequently found in personal care products and exhibit a very low rate of associated ACD. Consumers may be exposed to parabens through foods, cosmetics, and medications. Although there have been consumer concerns regarding endocrine disruption or carcinogenicity associated with parabens, definite evidence of their harm is lacking in the scientific literature, and many studies confirm their safety.2 With their high prevalence in personal care products and low rates of associated contact allergy, parabens remain ideal preservative agents.

Ultimately, contact dermatitis is a common yet often underrecognized dermatologic condition. To address this knowledge gap in clinical practice, we are proud to launch Final Interpretation, a new column in Cutis covering emerging trends in contact dermatitis. We will address pearls, pitfalls, and updates in contact dermatitis. Although our primary focus will be ACD, other important causes of contact dermatitis will be highlighted. Look for the inaugural column in the June 2019 issue of Cutis.

References
  1. Fransway AF, Fransway PJ, Belsito DV, et al. Parabens: contact (non)allergen of the year. Dermatitis. 2019;30:3-31.
  2. Fransway AF, Fransway PJ, Belsito DV, et al. Paraben toxicology. Dermatitis. 2019;30:32-45.
  3. Final amended report on the safety assessment of methylparaben, ethylparaben, propylparaben, isopropylparaben, butylparaben, isobutylparaben, and benzylparaben as used in cosmetic products. Int J Toxicol. 2008;27(suppl 4):1-82.
  4. Cosmetic Ingredient Review. Amended safety assessment of parabens as used in cosmetics. https://www.cir-safety.org/sites/default/files/Parabens.pdf. Published August 29, 2018. Accessed March 12, 2019.
  5. Methylparaben. Fed Regist. 2018;21(3):1490. To be codified at 21 CFR §184.
  6. Liao C, Liu F, Kannan K. Occurrence of and dietary exposure to parabens in foodstuffs from the United States. Environ Sci Technol. 2013;47:3918-3925.
  7. DeKoven JG, Warshaw EM, Zug KA, et al. North American Contact Dermatitis Group Patch Test Results: 2015-2016. Dermatitis. 2018;29:297-309.
  8. Veverka KK, Hall MR, Yiannias JA, et al. Trends in patch testing with the Mayo Clinic standard series, 2011-2015. Dermatitis. 2018;29:310-315.
  9. Routledge EJ, Parker J, Odum J, et al. Some alkyl hydroxy benzoate preservatives (parabens) are estrogenic. Toxicol Appl Pharmacol. 1998;153:12-19.
  10. Miller D, Brian B, Wheals BB, et al. Estrogenic activity of phenolic additives determined by an in vitro yeast bioassay. Environ Health Perspect. 2001;109:133-138.
  11. Blair RM, Fang H, Branham WS. The estrogen receptor relative binding affinities of 188 natural and xenochemicals: structural diversity of ligands. Toxicol Sci. 2000;54:138-153.
  12. van Meeuwen JA, van Son O, Piersma AH, et al. Aromatase inhibiting and combined estrogenic effects of parabens and estrogenic effects of other additives in cosmetics. Toxicol Appl Pharmacol. 2008;230:372-382.
  13. Barr L, Metaxas G, Harbach CA, et al. Measurement of paraben concentrations in human breast tissue at serial locations across the breast from axilla to sternum. J Appl Toxicol. 2012;32:219-232.
  14. Mirick DK, Davis S, Thomas DB. Antiperspirant use and the risk of breast cancer. J Natl Cancer Inst. 2002;94:1578-1580.
References
  1. Fransway AF, Fransway PJ, Belsito DV, et al. Parabens: contact (non)allergen of the year. Dermatitis. 2019;30:3-31.
  2. Fransway AF, Fransway PJ, Belsito DV, et al. Paraben toxicology. Dermatitis. 2019;30:32-45.
  3. Final amended report on the safety assessment of methylparaben, ethylparaben, propylparaben, isopropylparaben, butylparaben, isobutylparaben, and benzylparaben as used in cosmetic products. Int J Toxicol. 2008;27(suppl 4):1-82.
  4. Cosmetic Ingredient Review. Amended safety assessment of parabens as used in cosmetics. https://www.cir-safety.org/sites/default/files/Parabens.pdf. Published August 29, 2018. Accessed March 12, 2019.
  5. Methylparaben. Fed Regist. 2018;21(3):1490. To be codified at 21 CFR §184.
  6. Liao C, Liu F, Kannan K. Occurrence of and dietary exposure to parabens in foodstuffs from the United States. Environ Sci Technol. 2013;47:3918-3925.
  7. DeKoven JG, Warshaw EM, Zug KA, et al. North American Contact Dermatitis Group Patch Test Results: 2015-2016. Dermatitis. 2018;29:297-309.
  8. Veverka KK, Hall MR, Yiannias JA, et al. Trends in patch testing with the Mayo Clinic standard series, 2011-2015. Dermatitis. 2018;29:310-315.
  9. Routledge EJ, Parker J, Odum J, et al. Some alkyl hydroxy benzoate preservatives (parabens) are estrogenic. Toxicol Appl Pharmacol. 1998;153:12-19.
  10. Miller D, Brian B, Wheals BB, et al. Estrogenic activity of phenolic additives determined by an in vitro yeast bioassay. Environ Health Perspect. 2001;109:133-138.
  11. Blair RM, Fang H, Branham WS. The estrogen receptor relative binding affinities of 188 natural and xenochemicals: structural diversity of ligands. Toxicol Sci. 2000;54:138-153.
  12. van Meeuwen JA, van Son O, Piersma AH, et al. Aromatase inhibiting and combined estrogenic effects of parabens and estrogenic effects of other additives in cosmetics. Toxicol Appl Pharmacol. 2008;230:372-382.
  13. Barr L, Metaxas G, Harbach CA, et al. Measurement of paraben concentrations in human breast tissue at serial locations across the breast from axilla to sternum. J Appl Toxicol. 2012;32:219-232.
  14. Mirick DK, Davis S, Thomas DB. Antiperspirant use and the risk of breast cancer. J Natl Cancer Inst. 2002;94:1578-1580.
Issue
Cutis - 103(4)
Issue
Cutis - 103(4)
Page Number
192-193
Page Number
192-193
Publications
Publications
Topics
Article Type
Display Headline
Parabens: The 2019 Nonallergen of the Year
Display Headline
Parabens: The 2019 Nonallergen of the Year
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Article PDF Media

No further amplification of signal for benefit from ultrathin stent at 3 years

Article Type
Changed
Tue, 05/21/2019 - 12:33

 

– In the latest analysis of data from a randomized trial comparing three different thin polymer-coated drug-eluting stents, the signal at 1 year that the thinnest device might reduce risk of target lesion revascularization has been lost at 3 years, according to an update of results from the BIO-RESORT trial presented at CRT 2019 sponsored by MedStar Heart & Vascular Institute.

Ted Bosworth/MDedge News
Dr. Clemons von Birgelen

“At 3-year follow-up, all three drug-eluting stents were associated with favorable outcomes and both very thin strut polymer-coated devices showed safety and patency similar to the thin-strut durable polymer drug-eluting stent,” reported Clemons von Birgelen, MD, PhD, professor of cardiology, University of Twente, Enschede, the Netherlands.

In order of strut thickness, the stents tested in BIO-RESORT were Orsiro (60 mcm), Synergy (74 mcm), and Resolute Integrity (90 mcm). Although the study had a noninferiority design, the potential for the biodegradable polymer coatings of the two thinner stents to provide faster healing than the durable polymer of the Resolute stent was one of the driving hypotheses of the trial (Lancet. 2016 Nov 26;388[10060]:2607-17).

Some support for this hypothesis was provided by 2-year results presented at EuroPCR 2018 last year. At that time, it was reported that the risk of target lesion revascularization between the end of year 1 and end of year 2 was significantly lower for the Orsiro stent (1.3%) than the Resolute stent (2.3%). Target lesion revascularization also was lower in the Synergy stent group (1.8%), but this rate did not differ significantly from that of the other two stents in the trial.

Now, reassessed at 3 years, the target lesion revascularization rates are 2.9%, 3.3%, and 3.8% for the Orsiro, Synergy, and Resolute stents, respectively. Although the numerical hierarchy is preserved, the differences are no longer significant.

Other outcomes, including the primary outcome of target lesion failure, show the same numerical hierarchy but, again, without differences reaching significance. For target lesion failure, these rates are 8.5%, 8.8%, and 10.0%, respectively.

The difference in the rates of stent thrombosis at 3 years was even smaller with rates of less than 1% for all three stents. A catch-up phenomenon between years 2 and 3 of follow-up largely eliminated a numerical advantage seen earlier for the Orsiro stent.

The BIO-RESORT trial randomized 3,514 patients, of whom 70% had an acute coronary syndrome. Nearly one-third had an ST-elevated myocardial infarction. Dr. von Birgelen emphasized that this was “a very complex study population.” For example, roughly 20% had severely calcified lesions. Follow-up data were available on 97% of the randomized patients at 3 years.

There are differences between these stents other than thickness and the durability of the polymer. In particular, Orsiro is coated with sirolimus, Synergy with everolimus, and Resolute with zotarolimus. While the metals of the frame also differ, the estimated time to resorption of the polymer is faster with the Synergy stent (4 months) than the Orsiro stent (24 months).

Despite the loss of a difference in target vessel revascularization in the most recent follow-up, the potential for the differences in designs and materials to influence risk of late complications, including revascularization and thrombosis, persists.

“Follow-up beyond 3 years is of interest to definitely answer the question of whether one of these drug-eluting stents might improve outcome at a later stage,” Dr. von Birgelen said.

Meeting/Event
Publications
Topics
Sections
Meeting/Event
Meeting/Event

 

– In the latest analysis of data from a randomized trial comparing three different thin polymer-coated drug-eluting stents, the signal at 1 year that the thinnest device might reduce risk of target lesion revascularization has been lost at 3 years, according to an update of results from the BIO-RESORT trial presented at CRT 2019 sponsored by MedStar Heart & Vascular Institute.

Ted Bosworth/MDedge News
Dr. Clemons von Birgelen

“At 3-year follow-up, all three drug-eluting stents were associated with favorable outcomes and both very thin strut polymer-coated devices showed safety and patency similar to the thin-strut durable polymer drug-eluting stent,” reported Clemons von Birgelen, MD, PhD, professor of cardiology, University of Twente, Enschede, the Netherlands.

In order of strut thickness, the stents tested in BIO-RESORT were Orsiro (60 mcm), Synergy (74 mcm), and Resolute Integrity (90 mcm). Although the study had a noninferiority design, the potential for the biodegradable polymer coatings of the two thinner stents to provide faster healing than the durable polymer of the Resolute stent was one of the driving hypotheses of the trial (Lancet. 2016 Nov 26;388[10060]:2607-17).

Some support for this hypothesis was provided by 2-year results presented at EuroPCR 2018 last year. At that time, it was reported that the risk of target lesion revascularization between the end of year 1 and end of year 2 was significantly lower for the Orsiro stent (1.3%) than the Resolute stent (2.3%). Target lesion revascularization also was lower in the Synergy stent group (1.8%), but this rate did not differ significantly from that of the other two stents in the trial.

Now, reassessed at 3 years, the target lesion revascularization rates are 2.9%, 3.3%, and 3.8% for the Orsiro, Synergy, and Resolute stents, respectively. Although the numerical hierarchy is preserved, the differences are no longer significant.

Other outcomes, including the primary outcome of target lesion failure, show the same numerical hierarchy but, again, without differences reaching significance. For target lesion failure, these rates are 8.5%, 8.8%, and 10.0%, respectively.

The difference in the rates of stent thrombosis at 3 years was even smaller with rates of less than 1% for all three stents. A catch-up phenomenon between years 2 and 3 of follow-up largely eliminated a numerical advantage seen earlier for the Orsiro stent.

The BIO-RESORT trial randomized 3,514 patients, of whom 70% had an acute coronary syndrome. Nearly one-third had an ST-elevated myocardial infarction. Dr. von Birgelen emphasized that this was “a very complex study population.” For example, roughly 20% had severely calcified lesions. Follow-up data were available on 97% of the randomized patients at 3 years.

There are differences between these stents other than thickness and the durability of the polymer. In particular, Orsiro is coated with sirolimus, Synergy with everolimus, and Resolute with zotarolimus. While the metals of the frame also differ, the estimated time to resorption of the polymer is faster with the Synergy stent (4 months) than the Orsiro stent (24 months).

Despite the loss of a difference in target vessel revascularization in the most recent follow-up, the potential for the differences in designs and materials to influence risk of late complications, including revascularization and thrombosis, persists.

“Follow-up beyond 3 years is of interest to definitely answer the question of whether one of these drug-eluting stents might improve outcome at a later stage,” Dr. von Birgelen said.

 

– In the latest analysis of data from a randomized trial comparing three different thin polymer-coated drug-eluting stents, the signal at 1 year that the thinnest device might reduce risk of target lesion revascularization has been lost at 3 years, according to an update of results from the BIO-RESORT trial presented at CRT 2019 sponsored by MedStar Heart & Vascular Institute.

Ted Bosworth/MDedge News
Dr. Clemons von Birgelen

“At 3-year follow-up, all three drug-eluting stents were associated with favorable outcomes and both very thin strut polymer-coated devices showed safety and patency similar to the thin-strut durable polymer drug-eluting stent,” reported Clemons von Birgelen, MD, PhD, professor of cardiology, University of Twente, Enschede, the Netherlands.

In order of strut thickness, the stents tested in BIO-RESORT were Orsiro (60 mcm), Synergy (74 mcm), and Resolute Integrity (90 mcm). Although the study had a noninferiority design, the potential for the biodegradable polymer coatings of the two thinner stents to provide faster healing than the durable polymer of the Resolute stent was one of the driving hypotheses of the trial (Lancet. 2016 Nov 26;388[10060]:2607-17).

Some support for this hypothesis was provided by 2-year results presented at EuroPCR 2018 last year. At that time, it was reported that the risk of target lesion revascularization between the end of year 1 and end of year 2 was significantly lower for the Orsiro stent (1.3%) than the Resolute stent (2.3%). Target lesion revascularization also was lower in the Synergy stent group (1.8%), but this rate did not differ significantly from that of the other two stents in the trial.

Now, reassessed at 3 years, the target lesion revascularization rates are 2.9%, 3.3%, and 3.8% for the Orsiro, Synergy, and Resolute stents, respectively. Although the numerical hierarchy is preserved, the differences are no longer significant.

Other outcomes, including the primary outcome of target lesion failure, show the same numerical hierarchy but, again, without differences reaching significance. For target lesion failure, these rates are 8.5%, 8.8%, and 10.0%, respectively.

The difference in the rates of stent thrombosis at 3 years was even smaller with rates of less than 1% for all three stents. A catch-up phenomenon between years 2 and 3 of follow-up largely eliminated a numerical advantage seen earlier for the Orsiro stent.

The BIO-RESORT trial randomized 3,514 patients, of whom 70% had an acute coronary syndrome. Nearly one-third had an ST-elevated myocardial infarction. Dr. von Birgelen emphasized that this was “a very complex study population.” For example, roughly 20% had severely calcified lesions. Follow-up data were available on 97% of the randomized patients at 3 years.

There are differences between these stents other than thickness and the durability of the polymer. In particular, Orsiro is coated with sirolimus, Synergy with everolimus, and Resolute with zotarolimus. While the metals of the frame also differ, the estimated time to resorption of the polymer is faster with the Synergy stent (4 months) than the Orsiro stent (24 months).

Despite the loss of a difference in target vessel revascularization in the most recent follow-up, the potential for the differences in designs and materials to influence risk of late complications, including revascularization and thrombosis, persists.

“Follow-up beyond 3 years is of interest to definitely answer the question of whether one of these drug-eluting stents might improve outcome at a later stage,” Dr. von Birgelen said.

Publications
Publications
Topics
Article Type
Sections
Article Source

REPORTING FROM CRT 2019

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.

HM19 Day One highlights: Plenary and sepsis updates (VIDEO)

Article Type
Changed
Thu, 04/04/2019 - 12:47
Vidyard Video

Dr. Kranthi Sitammagari of Atrium Health in Monroe, N.C., and Dr. Marina Farah of Farah MD Consulting in Corvallis, Ore., offer their expert analysis of the plenary session and Updates on Sepsis session at HM19.

Meeting/Event
Publications
Sections
Meeting/Event
Meeting/Event
Vidyard Video

Dr. Kranthi Sitammagari of Atrium Health in Monroe, N.C., and Dr. Marina Farah of Farah MD Consulting in Corvallis, Ore., offer their expert analysis of the plenary session and Updates on Sepsis session at HM19.

Vidyard Video

Dr. Kranthi Sitammagari of Atrium Health in Monroe, N.C., and Dr. Marina Farah of Farah MD Consulting in Corvallis, Ore., offer their expert analysis of the plenary session and Updates on Sepsis session at HM19.

Publications
Publications
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.

Scurvy Masquerading as Reactive Arthritis

Article Type
Changed
Wed, 04/03/2019 - 16:02
Display Headline
Scurvy Masquerading as Reactive Arthritis

To the Editor:

A 28-year-old recently homeless white man with a history of heroin abuse was admitted with a worsening rash and left ankle pain of 1 week’s duration, as well as subjective fever after 3 weeks of a productive cough, sore throat, hoarse voice, and general malaise. Six days prior to presentation, he developed redness and swelling of the dorsal aspects of both hands with accompanying rash, and 2 days prior to presentation he developed a similar rash on the legs with associated left ankle pain, redness, and swelling. He also reported eye redness, pain, photophobia, crusty eye discharge, and a pins and needles sensation on the soles of both feet. Additionally, he had noted difficulty with urination over several days. He had been homeless for less than 1 month prior to admission.

On physical examination, the patient appeared to be well nourished. Skin examination was notable for scattered perifollicular hemorrhagic and hyperkeratotic papules ranging in size from 3 to 6 mm with associated nummular alopecia of the bilateral medial thighs (Figure); well-demarcated desquamated patches on the weight-bearing aspects of the plantar feet; and a 2.0-cm, well-demarcated, thinly raised erythematous patch of the inferolateral penile shaft. Oral examination was notable for multiple discrete areas of ulceration on the lateral aspects of the tongue. Ophthalmic examination revealed conjunctival injection and photophobia. The ankles were edematous and tender (the left ankle more than the right), and range of passive motion was limited by pain.

A and B, Scattered perifollicular hemorrhagic and hyperkeratotic papules with associated alopecia on the thighs.


Laboratory values were remarkable for a hemoglobin count of 13.1 g/dL (reference range, 14.2–18 g/dL), erythrocyte sedimentation rate of 31 mm/h (reference range, 0–10 mm/h), and C-reactive protein level of 5.4 mg/dL (reference range, 0–0.8 mg/dL). Urinalysis was unremarkable, blood cultures were negative, and a chest radiograph was normal. Human immunodeficiency virus and rapid plasma reagin tests were negative, with normal levels of IgG, IgA, and IgM. IgE was elevated at 572 IU/mL (reference range, 0–100 IU/mL). Ultrasonography of the leg was negative for deep vein thrombosis, and a left ankle radiograph was negative for fracture. The patient previously was found to have antinuclear antibodies of 1:40 and negative antineutrophil cytoplasmic antibodies, anti–double-stranded DNA, anti–Sjögren syndrome antigens A and B, and cryoglobulins, as well as normal complement levels. The constellation of rash, arthritis, conjunctivitis, and difficulty with urination raised a high suspicion for reactive arthritis; however, the patient was found to be HLA-B27 negative with a negative urine chlamydia test.

The patient was mildly hypokalemic at 2.9 mmol/L (reference range, 3.5–5.0 mmol/L) and hypoalbuminemic at 3.6 g/dL (reference range, 3.9–5.0 g/dL). He had a slightly elevated international normalized ratio of 1.4 (reference range, 0.9–1.2). Further questioning revealed that his diet consisted mostly of soda and energy drinks; his vitamin C level was subsequently checked and found to be 0 mg/dL (reference range, 0.2–2.0 mg/dL). A diagnosis of scurvy was made, and his symptoms improved at the hospital while maintaining a diet with normal levels of vitamin C. His rash had markedly improved by hospital day 2, joint swelling decreased, and the conjunctival injection and eye pain had resolved. Upon outpatient follow-up, his rash and joint swelling continued to improve, and he had not experienced any further areas of hair loss.

Scurvy, a condition caused by vitamin C deficiency, is a disease of historical importance, as it ravaged ships full of sailors in days past; however, its incidence has decreased drastically since Lind1 first described its treatment using citrus fruits in 1753. Nonetheless, even with modern day access to foods rich in vitamin C, scurvy is far more common than expected in the developed world.



Vitamin C (ascorbic acid) plays a crucial role in human biochemistry. Although many plants and animals can synthesize ascorbic acid, humans and other animals such as guinea pigs lack the required enzyme, making vitamin C an essential nutrient required in dietary intake.­2-4 Hypovitaminosis C leads to scurvy when collagen production becomes impaired due to lack of ascorbic acid as a required cofactor for its synthesis, which leads to tissue and capillary fragility, causing hemorrhage and perivascular edema.4 The diagnosis of scurvy is clinical and typically is based on signs such as perivascular hemorrhage, bleeding gums, anemia, impaired wound healing, and ecchymoses in the setting of vitamin C deficiency (<11 μmol/L or <0.2 mg/dL) with rapid resolution upon vitamin C supplementation.5

 

 

Important sources of vitamin C include citrus fruits, strawberries, broccoli, spinach, and potatoes. Recommended daily intake is 75 to 90 mg, with smokers requiring 110 to 125 mg daily because of increased oxidative stress.6-9 Although access to these foods in the modern United States is high, as many as 10% of males and 6.9% of females are vitamin C deficient, and in the subset of generally healthy middle-class Americans, as many as 6% are deficient.8,10 The highest risk groups tend to be smokers and individuals with low incomes.8 Although vitamin C deficiency does not automatically equate to scurvy, early studies on experimentally induced scurvy in prisoners showed that signs of scurvy may begin to develop in as few as 29 days of complete vitamin C deprivation, with overt scurvy developing after approximately 40 to 90 days.11,12

Patients with scurvy often pose a diagnostic dilemma for physicians because their presenting symptoms, such as fatigue, anemia, and rash, are nonspecific and can lead physicians down a laborious and costly road of unnecessary tests including vasculitic, infectious, and rheumatologic workups to determine the cause of the symptoms. Increased awareness of the current prevalence of hypovitaminosis C may help to decrease these unnecessary costs by putting scurvy higher on the differential for patients with this spectrum of symptoms.



Scurvy has been called the eternal masquerader because its nonspecific signs and symptoms have often led to misdiagnosis.13 Cases of scurvy mimicking diseases ranging from bone tumors14 to spondyloarthritis15 and vasculitis16 have been reported. The typical patient at risk for scurvy tends to fall in one of the following categories: psychiatric illness, gastrointestinal disorders, malnourishment, chronic alcoholism, drug use, elderly age, infants, restrictive dietary habits or food allergies, or those in developing countries.17-20 Our patient did not fit particularly well into any of the aforementioned high-risk categories; he had only recently become homeless and had a history of intravenous drug use but had not been using drugs in the months prior to the development of scurvy. Additionally, his salient symptoms were more consistent with reactive arthritis than with classic scurvy.

Although he had many symptoms consistent with scurvy such as generalized malaise, perifollicular hemorrhage and hyperkeratosis, spongy edema of the joints, and mild anemia on laboratory testing, he was missing several classic scurvy symptoms. Unlike many patients with scurvy, our patient did not describe any history of bruising easily or dental concerns, and examination was notably absent of ecchymoses as well as spongy or bleeding gums. He did, however, present with eye irritation and photophobia. These symptoms, consistent with keratoconjunctivitis sicca, are lesser known because ocular findings are rarely found in scurvy.21 Patients with scurvy can report eye burning and irritation, redness, blurry vision, and sensitivity to bright light secondary to increased dryness of the corneal surfaces. Horrobin et al22 postulated that this symptom may be mediated by regulation of prostaglandin E1 by vitamin C.

Another less common sign of scurvy found in our patient was patchy alopecia. Alopecia most often is seen in association with concomitant Sjögren syndrome.11,23 The etiology of the hair loss stems from the role of ascorbic acid in disulfide bonding during hair formation. The hair may fracture, coil into a corkscrew hair, or bend in several places, leading to a swan-neck deformity. Although a skin biopsy was not performed in our patient, results typically demonstrate a coiled hair in its follicle.24,25

We present the case of an otherwise generally healthy patient who developed vitamin C deficiency due to a diet consisting mostly of soda and energy drinks. His case presented a diagnostic dilemma, as his symptoms at first seemed most consistent with reactive arthritis and he was missing several of the risk factors and symptoms that would have led to an early diagnosis of scurvy. Vitamin C deficiency is not as uncommon as expected in the developed world; practitioners must be aware of the common as well as the unusual signs of scurvy.

References
  1. Lind J. A Treatise of the Scurvy. Edinburgh, Scotland: Sands, Murray, and Cochran; 1753.
  2. Levine M, Rumsey SC, Daruwala R, et al. Criteria and recommendations for vitamin C intake. JAMA. 1999;281:1415-1423.
  3. Jacob RA. Vitamin C. In: Shils ME, Olson JA, Shike M, et al, eds. Modern Nutrition in Health and Disease. Baltimore, MD: William & Wilkins; 1999:467-483.
  4. Levine M. New concepts in the biology and biochemistry of ascorbic acid. N Engl J Med. 1986;314:892-902.
  5. Hirschman JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol. 1999;41:895-906.
  6. Bardnard ND, Weissinger R, Jaster BJ, et al, eds. Nutrition Guide for Clinicians. 2nd ed. Washington, DC: Physician’s Committee For Responsible Medicine; 2009:33.
  7. Institute of Medicine. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington DC: National Academic Press; 2000.
  8. Schleicher RL, Carroll MD, Ford ES, et al. Serum vitamin C and the prevalence of vitamin C deficiency in the United States: 2003-2004 National Health and Nutrition Examination Survey (NHANES). Am J Clin Nutr. 2009;90:1252-1263.
  9. Schectman G, Byrd JC, Gruchow HW. The influence of smoking on vitamin C status in adults. Am J Public Health. 1989;79:158-162.
  10. Johnston CS, Thompson LL. Vitamin C status of an outpatient population. J Am Coll Nutr. 1998;17:366-370.
  11. Hodges RE, Baker EM, Hood J, et al. Experimental scurvy in man. Am J Clin Nutr. 1969;22:535-548.
  12. Hodges RE, Hood J, Canham JE, et al. Clinical manifestations of ascorbic acid deficiency in man. Am J Clin Nutr. 1971;24:432-443.
  13. Gupta P, Taneja K, Iyer PU, et al. Scurvy—the eternal masquerader. Ann Trop Paediatr. 1989;9:118-121.
  14. Haq RU, Dhammi IK, Jain AK, et al. Infantile scurvy masquerading as bone tumour. Ann Acad Med Singapore. 2013;42:363-365.
  15. Pazzola G, Possemato N, Germanò G, et al. Scurvy mimicking spondyloarthritis in a young man. Clin Exp Rheumatol. 2013;31:795.
  16. Friesgaard Christensen A, Clemmensen O, Junker P. Palpable purpura with an unexpected outcome. Case Rep Rheumatol. 2013;2013:678427.
  17. Des Roches A, Paradis L, Paradis J, et al. Food allergy as a new risk factor for scurvy. Allergy. 2006;61:1487-1488.
  18. Pimentel L. Scurvy: historical review and current diagnostic approach. Am J Emerg Med. 2003;21:328-332.
  19. Codreanu F, Jarlot S, Astier C, et al. An apple a day...chronic glossitis in a 4-year-old boy. Eur Ann Allergy Clin Immunol. 2012;44:86-88.
  20. Stephen R, Utecht T. Scurvy identified in the emergency department: a case report. J Emerg Med. 2001;21:235-237.
  21. Hood J, Hodges RE. Ocular lesions in scurvy. Am J Clin Nutr. 1969;22:559-567.
  22. Horrobin DF, Oka M, Manku MS. The regulation of prostaglandin E1 formation: a candidate for one of the fundamental mechanisms involved in the actions of vitamin C. Med Hypotheses. 1979;5:849-858.
  23. Hood J, Burns CA, Hodges RE. Sjogren’s syndrome in scurvy. N Engl J Med. 1970;282:1120-1124.
  24. Walter JF. Scurvy resulting from a self-imposed diet. West J Med. 1979;130:177-179.
  25. Velandia B, Centor RM, McConnell V, et al. Scurvy is still present in developed countries. J Gen Intern Med. 2008;23:1281-1284.
Article PDF
Author and Disclosure Information

Drs. Christopher and Fathi are from and Dr. Menachof was from the University of Colorado, Denver. Dr. Christopher is from the Department of Ophthalmology and Dr. Fathi is from the Department of Dermatology. Dr. Menachof currently is from The Indian Health Service, Rockville, Maryland.

The authors report no conflict of interest.

Correspondence: Karen L. Christopher, MD, 1675 Aurora Ct, F731, Aurora, CO 80045 ([email protected]).

Issue
Cutis - 103(3)
Publications
Topics
Page Number
E21-23
Sections
Author and Disclosure Information

Drs. Christopher and Fathi are from and Dr. Menachof was from the University of Colorado, Denver. Dr. Christopher is from the Department of Ophthalmology and Dr. Fathi is from the Department of Dermatology. Dr. Menachof currently is from The Indian Health Service, Rockville, Maryland.

The authors report no conflict of interest.

Correspondence: Karen L. Christopher, MD, 1675 Aurora Ct, F731, Aurora, CO 80045 ([email protected]).

Author and Disclosure Information

Drs. Christopher and Fathi are from and Dr. Menachof was from the University of Colorado, Denver. Dr. Christopher is from the Department of Ophthalmology and Dr. Fathi is from the Department of Dermatology. Dr. Menachof currently is from The Indian Health Service, Rockville, Maryland.

The authors report no conflict of interest.

Correspondence: Karen L. Christopher, MD, 1675 Aurora Ct, F731, Aurora, CO 80045 ([email protected]).

Article PDF
Article PDF

To the Editor:

A 28-year-old recently homeless white man with a history of heroin abuse was admitted with a worsening rash and left ankle pain of 1 week’s duration, as well as subjective fever after 3 weeks of a productive cough, sore throat, hoarse voice, and general malaise. Six days prior to presentation, he developed redness and swelling of the dorsal aspects of both hands with accompanying rash, and 2 days prior to presentation he developed a similar rash on the legs with associated left ankle pain, redness, and swelling. He also reported eye redness, pain, photophobia, crusty eye discharge, and a pins and needles sensation on the soles of both feet. Additionally, he had noted difficulty with urination over several days. He had been homeless for less than 1 month prior to admission.

On physical examination, the patient appeared to be well nourished. Skin examination was notable for scattered perifollicular hemorrhagic and hyperkeratotic papules ranging in size from 3 to 6 mm with associated nummular alopecia of the bilateral medial thighs (Figure); well-demarcated desquamated patches on the weight-bearing aspects of the plantar feet; and a 2.0-cm, well-demarcated, thinly raised erythematous patch of the inferolateral penile shaft. Oral examination was notable for multiple discrete areas of ulceration on the lateral aspects of the tongue. Ophthalmic examination revealed conjunctival injection and photophobia. The ankles were edematous and tender (the left ankle more than the right), and range of passive motion was limited by pain.

A and B, Scattered perifollicular hemorrhagic and hyperkeratotic papules with associated alopecia on the thighs.


Laboratory values were remarkable for a hemoglobin count of 13.1 g/dL (reference range, 14.2–18 g/dL), erythrocyte sedimentation rate of 31 mm/h (reference range, 0–10 mm/h), and C-reactive protein level of 5.4 mg/dL (reference range, 0–0.8 mg/dL). Urinalysis was unremarkable, blood cultures were negative, and a chest radiograph was normal. Human immunodeficiency virus and rapid plasma reagin tests were negative, with normal levels of IgG, IgA, and IgM. IgE was elevated at 572 IU/mL (reference range, 0–100 IU/mL). Ultrasonography of the leg was negative for deep vein thrombosis, and a left ankle radiograph was negative for fracture. The patient previously was found to have antinuclear antibodies of 1:40 and negative antineutrophil cytoplasmic antibodies, anti–double-stranded DNA, anti–Sjögren syndrome antigens A and B, and cryoglobulins, as well as normal complement levels. The constellation of rash, arthritis, conjunctivitis, and difficulty with urination raised a high suspicion for reactive arthritis; however, the patient was found to be HLA-B27 negative with a negative urine chlamydia test.

The patient was mildly hypokalemic at 2.9 mmol/L (reference range, 3.5–5.0 mmol/L) and hypoalbuminemic at 3.6 g/dL (reference range, 3.9–5.0 g/dL). He had a slightly elevated international normalized ratio of 1.4 (reference range, 0.9–1.2). Further questioning revealed that his diet consisted mostly of soda and energy drinks; his vitamin C level was subsequently checked and found to be 0 mg/dL (reference range, 0.2–2.0 mg/dL). A diagnosis of scurvy was made, and his symptoms improved at the hospital while maintaining a diet with normal levels of vitamin C. His rash had markedly improved by hospital day 2, joint swelling decreased, and the conjunctival injection and eye pain had resolved. Upon outpatient follow-up, his rash and joint swelling continued to improve, and he had not experienced any further areas of hair loss.

Scurvy, a condition caused by vitamin C deficiency, is a disease of historical importance, as it ravaged ships full of sailors in days past; however, its incidence has decreased drastically since Lind1 first described its treatment using citrus fruits in 1753. Nonetheless, even with modern day access to foods rich in vitamin C, scurvy is far more common than expected in the developed world.



Vitamin C (ascorbic acid) plays a crucial role in human biochemistry. Although many plants and animals can synthesize ascorbic acid, humans and other animals such as guinea pigs lack the required enzyme, making vitamin C an essential nutrient required in dietary intake.­2-4 Hypovitaminosis C leads to scurvy when collagen production becomes impaired due to lack of ascorbic acid as a required cofactor for its synthesis, which leads to tissue and capillary fragility, causing hemorrhage and perivascular edema.4 The diagnosis of scurvy is clinical and typically is based on signs such as perivascular hemorrhage, bleeding gums, anemia, impaired wound healing, and ecchymoses in the setting of vitamin C deficiency (<11 μmol/L or <0.2 mg/dL) with rapid resolution upon vitamin C supplementation.5

 

 

Important sources of vitamin C include citrus fruits, strawberries, broccoli, spinach, and potatoes. Recommended daily intake is 75 to 90 mg, with smokers requiring 110 to 125 mg daily because of increased oxidative stress.6-9 Although access to these foods in the modern United States is high, as many as 10% of males and 6.9% of females are vitamin C deficient, and in the subset of generally healthy middle-class Americans, as many as 6% are deficient.8,10 The highest risk groups tend to be smokers and individuals with low incomes.8 Although vitamin C deficiency does not automatically equate to scurvy, early studies on experimentally induced scurvy in prisoners showed that signs of scurvy may begin to develop in as few as 29 days of complete vitamin C deprivation, with overt scurvy developing after approximately 40 to 90 days.11,12

Patients with scurvy often pose a diagnostic dilemma for physicians because their presenting symptoms, such as fatigue, anemia, and rash, are nonspecific and can lead physicians down a laborious and costly road of unnecessary tests including vasculitic, infectious, and rheumatologic workups to determine the cause of the symptoms. Increased awareness of the current prevalence of hypovitaminosis C may help to decrease these unnecessary costs by putting scurvy higher on the differential for patients with this spectrum of symptoms.



Scurvy has been called the eternal masquerader because its nonspecific signs and symptoms have often led to misdiagnosis.13 Cases of scurvy mimicking diseases ranging from bone tumors14 to spondyloarthritis15 and vasculitis16 have been reported. The typical patient at risk for scurvy tends to fall in one of the following categories: psychiatric illness, gastrointestinal disorders, malnourishment, chronic alcoholism, drug use, elderly age, infants, restrictive dietary habits or food allergies, or those in developing countries.17-20 Our patient did not fit particularly well into any of the aforementioned high-risk categories; he had only recently become homeless and had a history of intravenous drug use but had not been using drugs in the months prior to the development of scurvy. Additionally, his salient symptoms were more consistent with reactive arthritis than with classic scurvy.

Although he had many symptoms consistent with scurvy such as generalized malaise, perifollicular hemorrhage and hyperkeratosis, spongy edema of the joints, and mild anemia on laboratory testing, he was missing several classic scurvy symptoms. Unlike many patients with scurvy, our patient did not describe any history of bruising easily or dental concerns, and examination was notably absent of ecchymoses as well as spongy or bleeding gums. He did, however, present with eye irritation and photophobia. These symptoms, consistent with keratoconjunctivitis sicca, are lesser known because ocular findings are rarely found in scurvy.21 Patients with scurvy can report eye burning and irritation, redness, blurry vision, and sensitivity to bright light secondary to increased dryness of the corneal surfaces. Horrobin et al22 postulated that this symptom may be mediated by regulation of prostaglandin E1 by vitamin C.

Another less common sign of scurvy found in our patient was patchy alopecia. Alopecia most often is seen in association with concomitant Sjögren syndrome.11,23 The etiology of the hair loss stems from the role of ascorbic acid in disulfide bonding during hair formation. The hair may fracture, coil into a corkscrew hair, or bend in several places, leading to a swan-neck deformity. Although a skin biopsy was not performed in our patient, results typically demonstrate a coiled hair in its follicle.24,25

We present the case of an otherwise generally healthy patient who developed vitamin C deficiency due to a diet consisting mostly of soda and energy drinks. His case presented a diagnostic dilemma, as his symptoms at first seemed most consistent with reactive arthritis and he was missing several of the risk factors and symptoms that would have led to an early diagnosis of scurvy. Vitamin C deficiency is not as uncommon as expected in the developed world; practitioners must be aware of the common as well as the unusual signs of scurvy.

To the Editor:

A 28-year-old recently homeless white man with a history of heroin abuse was admitted with a worsening rash and left ankle pain of 1 week’s duration, as well as subjective fever after 3 weeks of a productive cough, sore throat, hoarse voice, and general malaise. Six days prior to presentation, he developed redness and swelling of the dorsal aspects of both hands with accompanying rash, and 2 days prior to presentation he developed a similar rash on the legs with associated left ankle pain, redness, and swelling. He also reported eye redness, pain, photophobia, crusty eye discharge, and a pins and needles sensation on the soles of both feet. Additionally, he had noted difficulty with urination over several days. He had been homeless for less than 1 month prior to admission.

On physical examination, the patient appeared to be well nourished. Skin examination was notable for scattered perifollicular hemorrhagic and hyperkeratotic papules ranging in size from 3 to 6 mm with associated nummular alopecia of the bilateral medial thighs (Figure); well-demarcated desquamated patches on the weight-bearing aspects of the plantar feet; and a 2.0-cm, well-demarcated, thinly raised erythematous patch of the inferolateral penile shaft. Oral examination was notable for multiple discrete areas of ulceration on the lateral aspects of the tongue. Ophthalmic examination revealed conjunctival injection and photophobia. The ankles were edematous and tender (the left ankle more than the right), and range of passive motion was limited by pain.

A and B, Scattered perifollicular hemorrhagic and hyperkeratotic papules with associated alopecia on the thighs.


Laboratory values were remarkable for a hemoglobin count of 13.1 g/dL (reference range, 14.2–18 g/dL), erythrocyte sedimentation rate of 31 mm/h (reference range, 0–10 mm/h), and C-reactive protein level of 5.4 mg/dL (reference range, 0–0.8 mg/dL). Urinalysis was unremarkable, blood cultures were negative, and a chest radiograph was normal. Human immunodeficiency virus and rapid plasma reagin tests were negative, with normal levels of IgG, IgA, and IgM. IgE was elevated at 572 IU/mL (reference range, 0–100 IU/mL). Ultrasonography of the leg was negative for deep vein thrombosis, and a left ankle radiograph was negative for fracture. The patient previously was found to have antinuclear antibodies of 1:40 and negative antineutrophil cytoplasmic antibodies, anti–double-stranded DNA, anti–Sjögren syndrome antigens A and B, and cryoglobulins, as well as normal complement levels. The constellation of rash, arthritis, conjunctivitis, and difficulty with urination raised a high suspicion for reactive arthritis; however, the patient was found to be HLA-B27 negative with a negative urine chlamydia test.

The patient was mildly hypokalemic at 2.9 mmol/L (reference range, 3.5–5.0 mmol/L) and hypoalbuminemic at 3.6 g/dL (reference range, 3.9–5.0 g/dL). He had a slightly elevated international normalized ratio of 1.4 (reference range, 0.9–1.2). Further questioning revealed that his diet consisted mostly of soda and energy drinks; his vitamin C level was subsequently checked and found to be 0 mg/dL (reference range, 0.2–2.0 mg/dL). A diagnosis of scurvy was made, and his symptoms improved at the hospital while maintaining a diet with normal levels of vitamin C. His rash had markedly improved by hospital day 2, joint swelling decreased, and the conjunctival injection and eye pain had resolved. Upon outpatient follow-up, his rash and joint swelling continued to improve, and he had not experienced any further areas of hair loss.

Scurvy, a condition caused by vitamin C deficiency, is a disease of historical importance, as it ravaged ships full of sailors in days past; however, its incidence has decreased drastically since Lind1 first described its treatment using citrus fruits in 1753. Nonetheless, even with modern day access to foods rich in vitamin C, scurvy is far more common than expected in the developed world.



Vitamin C (ascorbic acid) plays a crucial role in human biochemistry. Although many plants and animals can synthesize ascorbic acid, humans and other animals such as guinea pigs lack the required enzyme, making vitamin C an essential nutrient required in dietary intake.­2-4 Hypovitaminosis C leads to scurvy when collagen production becomes impaired due to lack of ascorbic acid as a required cofactor for its synthesis, which leads to tissue and capillary fragility, causing hemorrhage and perivascular edema.4 The diagnosis of scurvy is clinical and typically is based on signs such as perivascular hemorrhage, bleeding gums, anemia, impaired wound healing, and ecchymoses in the setting of vitamin C deficiency (<11 μmol/L or <0.2 mg/dL) with rapid resolution upon vitamin C supplementation.5

 

 

Important sources of vitamin C include citrus fruits, strawberries, broccoli, spinach, and potatoes. Recommended daily intake is 75 to 90 mg, with smokers requiring 110 to 125 mg daily because of increased oxidative stress.6-9 Although access to these foods in the modern United States is high, as many as 10% of males and 6.9% of females are vitamin C deficient, and in the subset of generally healthy middle-class Americans, as many as 6% are deficient.8,10 The highest risk groups tend to be smokers and individuals with low incomes.8 Although vitamin C deficiency does not automatically equate to scurvy, early studies on experimentally induced scurvy in prisoners showed that signs of scurvy may begin to develop in as few as 29 days of complete vitamin C deprivation, with overt scurvy developing after approximately 40 to 90 days.11,12

Patients with scurvy often pose a diagnostic dilemma for physicians because their presenting symptoms, such as fatigue, anemia, and rash, are nonspecific and can lead physicians down a laborious and costly road of unnecessary tests including vasculitic, infectious, and rheumatologic workups to determine the cause of the symptoms. Increased awareness of the current prevalence of hypovitaminosis C may help to decrease these unnecessary costs by putting scurvy higher on the differential for patients with this spectrum of symptoms.



Scurvy has been called the eternal masquerader because its nonspecific signs and symptoms have often led to misdiagnosis.13 Cases of scurvy mimicking diseases ranging from bone tumors14 to spondyloarthritis15 and vasculitis16 have been reported. The typical patient at risk for scurvy tends to fall in one of the following categories: psychiatric illness, gastrointestinal disorders, malnourishment, chronic alcoholism, drug use, elderly age, infants, restrictive dietary habits or food allergies, or those in developing countries.17-20 Our patient did not fit particularly well into any of the aforementioned high-risk categories; he had only recently become homeless and had a history of intravenous drug use but had not been using drugs in the months prior to the development of scurvy. Additionally, his salient symptoms were more consistent with reactive arthritis than with classic scurvy.

Although he had many symptoms consistent with scurvy such as generalized malaise, perifollicular hemorrhage and hyperkeratosis, spongy edema of the joints, and mild anemia on laboratory testing, he was missing several classic scurvy symptoms. Unlike many patients with scurvy, our patient did not describe any history of bruising easily or dental concerns, and examination was notably absent of ecchymoses as well as spongy or bleeding gums. He did, however, present with eye irritation and photophobia. These symptoms, consistent with keratoconjunctivitis sicca, are lesser known because ocular findings are rarely found in scurvy.21 Patients with scurvy can report eye burning and irritation, redness, blurry vision, and sensitivity to bright light secondary to increased dryness of the corneal surfaces. Horrobin et al22 postulated that this symptom may be mediated by regulation of prostaglandin E1 by vitamin C.

Another less common sign of scurvy found in our patient was patchy alopecia. Alopecia most often is seen in association with concomitant Sjögren syndrome.11,23 The etiology of the hair loss stems from the role of ascorbic acid in disulfide bonding during hair formation. The hair may fracture, coil into a corkscrew hair, or bend in several places, leading to a swan-neck deformity. Although a skin biopsy was not performed in our patient, results typically demonstrate a coiled hair in its follicle.24,25

We present the case of an otherwise generally healthy patient who developed vitamin C deficiency due to a diet consisting mostly of soda and energy drinks. His case presented a diagnostic dilemma, as his symptoms at first seemed most consistent with reactive arthritis and he was missing several of the risk factors and symptoms that would have led to an early diagnosis of scurvy. Vitamin C deficiency is not as uncommon as expected in the developed world; practitioners must be aware of the common as well as the unusual signs of scurvy.

References
  1. Lind J. A Treatise of the Scurvy. Edinburgh, Scotland: Sands, Murray, and Cochran; 1753.
  2. Levine M, Rumsey SC, Daruwala R, et al. Criteria and recommendations for vitamin C intake. JAMA. 1999;281:1415-1423.
  3. Jacob RA. Vitamin C. In: Shils ME, Olson JA, Shike M, et al, eds. Modern Nutrition in Health and Disease. Baltimore, MD: William & Wilkins; 1999:467-483.
  4. Levine M. New concepts in the biology and biochemistry of ascorbic acid. N Engl J Med. 1986;314:892-902.
  5. Hirschman JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol. 1999;41:895-906.
  6. Bardnard ND, Weissinger R, Jaster BJ, et al, eds. Nutrition Guide for Clinicians. 2nd ed. Washington, DC: Physician’s Committee For Responsible Medicine; 2009:33.
  7. Institute of Medicine. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington DC: National Academic Press; 2000.
  8. Schleicher RL, Carroll MD, Ford ES, et al. Serum vitamin C and the prevalence of vitamin C deficiency in the United States: 2003-2004 National Health and Nutrition Examination Survey (NHANES). Am J Clin Nutr. 2009;90:1252-1263.
  9. Schectman G, Byrd JC, Gruchow HW. The influence of smoking on vitamin C status in adults. Am J Public Health. 1989;79:158-162.
  10. Johnston CS, Thompson LL. Vitamin C status of an outpatient population. J Am Coll Nutr. 1998;17:366-370.
  11. Hodges RE, Baker EM, Hood J, et al. Experimental scurvy in man. Am J Clin Nutr. 1969;22:535-548.
  12. Hodges RE, Hood J, Canham JE, et al. Clinical manifestations of ascorbic acid deficiency in man. Am J Clin Nutr. 1971;24:432-443.
  13. Gupta P, Taneja K, Iyer PU, et al. Scurvy—the eternal masquerader. Ann Trop Paediatr. 1989;9:118-121.
  14. Haq RU, Dhammi IK, Jain AK, et al. Infantile scurvy masquerading as bone tumour. Ann Acad Med Singapore. 2013;42:363-365.
  15. Pazzola G, Possemato N, Germanò G, et al. Scurvy mimicking spondyloarthritis in a young man. Clin Exp Rheumatol. 2013;31:795.
  16. Friesgaard Christensen A, Clemmensen O, Junker P. Palpable purpura with an unexpected outcome. Case Rep Rheumatol. 2013;2013:678427.
  17. Des Roches A, Paradis L, Paradis J, et al. Food allergy as a new risk factor for scurvy. Allergy. 2006;61:1487-1488.
  18. Pimentel L. Scurvy: historical review and current diagnostic approach. Am J Emerg Med. 2003;21:328-332.
  19. Codreanu F, Jarlot S, Astier C, et al. An apple a day...chronic glossitis in a 4-year-old boy. Eur Ann Allergy Clin Immunol. 2012;44:86-88.
  20. Stephen R, Utecht T. Scurvy identified in the emergency department: a case report. J Emerg Med. 2001;21:235-237.
  21. Hood J, Hodges RE. Ocular lesions in scurvy. Am J Clin Nutr. 1969;22:559-567.
  22. Horrobin DF, Oka M, Manku MS. The regulation of prostaglandin E1 formation: a candidate for one of the fundamental mechanisms involved in the actions of vitamin C. Med Hypotheses. 1979;5:849-858.
  23. Hood J, Burns CA, Hodges RE. Sjogren’s syndrome in scurvy. N Engl J Med. 1970;282:1120-1124.
  24. Walter JF. Scurvy resulting from a self-imposed diet. West J Med. 1979;130:177-179.
  25. Velandia B, Centor RM, McConnell V, et al. Scurvy is still present in developed countries. J Gen Intern Med. 2008;23:1281-1284.
References
  1. Lind J. A Treatise of the Scurvy. Edinburgh, Scotland: Sands, Murray, and Cochran; 1753.
  2. Levine M, Rumsey SC, Daruwala R, et al. Criteria and recommendations for vitamin C intake. JAMA. 1999;281:1415-1423.
  3. Jacob RA. Vitamin C. In: Shils ME, Olson JA, Shike M, et al, eds. Modern Nutrition in Health and Disease. Baltimore, MD: William & Wilkins; 1999:467-483.
  4. Levine M. New concepts in the biology and biochemistry of ascorbic acid. N Engl J Med. 1986;314:892-902.
  5. Hirschman JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol. 1999;41:895-906.
  6. Bardnard ND, Weissinger R, Jaster BJ, et al, eds. Nutrition Guide for Clinicians. 2nd ed. Washington, DC: Physician’s Committee For Responsible Medicine; 2009:33.
  7. Institute of Medicine. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington DC: National Academic Press; 2000.
  8. Schleicher RL, Carroll MD, Ford ES, et al. Serum vitamin C and the prevalence of vitamin C deficiency in the United States: 2003-2004 National Health and Nutrition Examination Survey (NHANES). Am J Clin Nutr. 2009;90:1252-1263.
  9. Schectman G, Byrd JC, Gruchow HW. The influence of smoking on vitamin C status in adults. Am J Public Health. 1989;79:158-162.
  10. Johnston CS, Thompson LL. Vitamin C status of an outpatient population. J Am Coll Nutr. 1998;17:366-370.
  11. Hodges RE, Baker EM, Hood J, et al. Experimental scurvy in man. Am J Clin Nutr. 1969;22:535-548.
  12. Hodges RE, Hood J, Canham JE, et al. Clinical manifestations of ascorbic acid deficiency in man. Am J Clin Nutr. 1971;24:432-443.
  13. Gupta P, Taneja K, Iyer PU, et al. Scurvy—the eternal masquerader. Ann Trop Paediatr. 1989;9:118-121.
  14. Haq RU, Dhammi IK, Jain AK, et al. Infantile scurvy masquerading as bone tumour. Ann Acad Med Singapore. 2013;42:363-365.
  15. Pazzola G, Possemato N, Germanò G, et al. Scurvy mimicking spondyloarthritis in a young man. Clin Exp Rheumatol. 2013;31:795.
  16. Friesgaard Christensen A, Clemmensen O, Junker P. Palpable purpura with an unexpected outcome. Case Rep Rheumatol. 2013;2013:678427.
  17. Des Roches A, Paradis L, Paradis J, et al. Food allergy as a new risk factor for scurvy. Allergy. 2006;61:1487-1488.
  18. Pimentel L. Scurvy: historical review and current diagnostic approach. Am J Emerg Med. 2003;21:328-332.
  19. Codreanu F, Jarlot S, Astier C, et al. An apple a day...chronic glossitis in a 4-year-old boy. Eur Ann Allergy Clin Immunol. 2012;44:86-88.
  20. Stephen R, Utecht T. Scurvy identified in the emergency department: a case report. J Emerg Med. 2001;21:235-237.
  21. Hood J, Hodges RE. Ocular lesions in scurvy. Am J Clin Nutr. 1969;22:559-567.
  22. Horrobin DF, Oka M, Manku MS. The regulation of prostaglandin E1 formation: a candidate for one of the fundamental mechanisms involved in the actions of vitamin C. Med Hypotheses. 1979;5:849-858.
  23. Hood J, Burns CA, Hodges RE. Sjogren’s syndrome in scurvy. N Engl J Med. 1970;282:1120-1124.
  24. Walter JF. Scurvy resulting from a self-imposed diet. West J Med. 1979;130:177-179.
  25. Velandia B, Centor RM, McConnell V, et al. Scurvy is still present in developed countries. J Gen Intern Med. 2008;23:1281-1284.
Issue
Cutis - 103(3)
Issue
Cutis - 103(3)
Page Number
E21-23
Page Number
E21-23
Publications
Publications
Topics
Article Type
Display Headline
Scurvy Masquerading as Reactive Arthritis
Display Headline
Scurvy Masquerading as Reactive Arthritis
Sections
Inside the Article

Practice Points

  • Patients with scurvy often pose a diagnostic dilemma because their presenting symptoms can lead physicians down a laborious and costly road of unnecessary tests including vasculitic, infectious, and rheumatologic workups.
  • The diagnosis of scurvy is clinical and typically is based on signs such as perivascular hemorrhage, bleeding gums, anemia, impaired wound healing, and ecchymoses in the setting of vitamin C deficiency with rapid resolution upon vitamin C supplementation.
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Article PDF Media

Genetic data boost HIV surveillance efforts

Article Type
Changed
Mon, 04/08/2019 - 09:54

 

– Advances in genetic sequencing are boosting efforts to identify new clusters of HIV infections and guiding public health interventions to address them. The method relies on resistance testing at diagnosis and virologic failure and allows public health researchers to determine the genetic relatedness of viruses responsible for new infections. If the viruses are genetically, geographically, and temporally associated, it indicates a previously unknown transmission cluster.

copyright Kativ/iStockphoto

“The presence of a cluster indicates gaps in our preventative services, which we must address to improve service delivery and stop transmission,” Alexandra M. Oster, MD, Division of HIV/AIDS Prevention, Surveillance, and Epidemiology at the Centers for Disease Control and Prevention, Atlanta, said during a talk at the Conference on Retroviruses and Opportunistic Infections.

She noted that HIV brings special challenges to outbreak detection. The median delay between infection and diagnosis is 3 years. Individuals are highly mobile, and signals of new outbreaks can be quickly drowned out in high-burden areas. But these challenges aren’t unique. Tuberculosis has a similarly lengthy latency period, yet more than 75% of new TB outbreaks are now identified through the use of genetic data. Sequencing also is used to track food-borne illness. The CDC’s PulseNet is a network of laboratories that examines DNA sequences from bacterial infections in search of previously unrecognized outbreaks.

In the HIV setting, molecular surveillance has great potential in identifying and intervening in evolving networks of HIV transmission, but also carries ethical and other challenges.

Nevertheless, “I hope to make the case that cluster detection and response [using molecular surveillance] can help bring the nation closer to ending the HIV epidemic,” said Dr. Oster.

Molecular surveillance obtains most of its data from drug resistance testing, both at entry to care and after virologic failure, which then gets passed to the U.S. National HIV Surveillance System. The data are then stripped of patient identifying information and submitted to the CDC.

With data from multiple individuals in hand, researchers create a phylogenetic tree, in which closely-related viruses appear as close neighbors on a branch. “By tracing back along the tree, you can see the inferred ancestor of [individual strains], and also the inferred ancestor of all strains on the tree,” said Dr. Oster. Together with geographical data, that information allows researchers to identify clusters of patients connected in a transmission network, and that information can be passed along to federal, state, and local agencies to prevent infections and improve care.

From 1997 through 2012, the CDC’s molecular surveillance program focused on drug resistance patterns, but in 2013 the agency decided to expand to include transmission clusters. It now uses a tool called HIV Trace, which helps public health workers with no background in bioinformatics to visualize the DNA sequences and potential clusters, though Dr. Oster cautioned against overinterpretation of the results. “The links shown can easily be misinterpreted as actual social connections,” she said.

As proof of the approach’s potential, an analysis of the clusters identified showed their potential for HIV spread. On average in the United States, four new HIV infections occur per 100 people living with HIV. In the first 13 clusters that CDC identified, the number of infections was 33 per 100 person-years. The first 60 clusters had an average of 44 transmissions per 100 person-years. “None of these clusters had been found by [standard] epidemiologic methods, demonstrating that rapid transmission can be hard to detect without molecular data,” said Dr. Oster.

In 2018, all health departments began collecting sequencing data, and almost 40% of newly diagnosed patients have had sequencing data reported, more than 340,000 patients in total. Researchers have identified 145 priority clusters.

But use of molecular data is not the only method available. The CDC monitors increases in diagnoses in specific areas and conducts time-space analyses. These more traditional methods are particularly useful in areas with small populations or low HIV burden.

With a cluster identified, public health officials can attempt to identify all of the members of the network and help them to access services, such as testing, preexposure prophylaxis (PrEP), syringe service programs, and linkage to care.

In San Antonio, Tex., an analysis identified a cluster of 24 gay and bisexual men, and further analysis revealed an extended network of 87 sexual or needle-sharing partners. Researchers also identified missed opportunities for diagnosis of acute infection as well as low access to PrEP, so the health department sent out an alert clarifying diagnosis testing guidelines, highlighting the concern over acute infection, and containing PrEP educational material.

Analysis of another network in Michigan found that all identified individuals were virally suppressed, even though the network continued to grow. That suggested that there were unidentified individuals who were contributing to transmission, which prompted efforts by providers to encourage testing, linkage to care, and prevention.

All of these developments are good news for efforts to eradicate HIV, but they come with pitfalls. Local communities have expressed concerned that molecular data could be used to identify direction of transmission and for prosecution, since there are HIV laws that criminalize lack of disclosure and potential exposure to the virus, even when transmission doesn’t occur. “These laws are not aligned with current science and have not been found to help curb HIV,” said Dr. Oster.

She noted that current molecular methods are incapable of identifying direction of transmission. Still, the CDC is reemphasizing efforts to protect public health data from nonpublic health use. “CDC and health departments implement unprecedented policies and procedures to ensure confidentiality and security of the data,” Dr. Oster said.

She reported having no relevant disclosures.

Meeting/Event
Publications
Topics
Sections
Meeting/Event
Meeting/Event

 

– Advances in genetic sequencing are boosting efforts to identify new clusters of HIV infections and guiding public health interventions to address them. The method relies on resistance testing at diagnosis and virologic failure and allows public health researchers to determine the genetic relatedness of viruses responsible for new infections. If the viruses are genetically, geographically, and temporally associated, it indicates a previously unknown transmission cluster.

copyright Kativ/iStockphoto

“The presence of a cluster indicates gaps in our preventative services, which we must address to improve service delivery and stop transmission,” Alexandra M. Oster, MD, Division of HIV/AIDS Prevention, Surveillance, and Epidemiology at the Centers for Disease Control and Prevention, Atlanta, said during a talk at the Conference on Retroviruses and Opportunistic Infections.

She noted that HIV brings special challenges to outbreak detection. The median delay between infection and diagnosis is 3 years. Individuals are highly mobile, and signals of new outbreaks can be quickly drowned out in high-burden areas. But these challenges aren’t unique. Tuberculosis has a similarly lengthy latency period, yet more than 75% of new TB outbreaks are now identified through the use of genetic data. Sequencing also is used to track food-borne illness. The CDC’s PulseNet is a network of laboratories that examines DNA sequences from bacterial infections in search of previously unrecognized outbreaks.

In the HIV setting, molecular surveillance has great potential in identifying and intervening in evolving networks of HIV transmission, but also carries ethical and other challenges.

Nevertheless, “I hope to make the case that cluster detection and response [using molecular surveillance] can help bring the nation closer to ending the HIV epidemic,” said Dr. Oster.

Molecular surveillance obtains most of its data from drug resistance testing, both at entry to care and after virologic failure, which then gets passed to the U.S. National HIV Surveillance System. The data are then stripped of patient identifying information and submitted to the CDC.

With data from multiple individuals in hand, researchers create a phylogenetic tree, in which closely-related viruses appear as close neighbors on a branch. “By tracing back along the tree, you can see the inferred ancestor of [individual strains], and also the inferred ancestor of all strains on the tree,” said Dr. Oster. Together with geographical data, that information allows researchers to identify clusters of patients connected in a transmission network, and that information can be passed along to federal, state, and local agencies to prevent infections and improve care.

From 1997 through 2012, the CDC’s molecular surveillance program focused on drug resistance patterns, but in 2013 the agency decided to expand to include transmission clusters. It now uses a tool called HIV Trace, which helps public health workers with no background in bioinformatics to visualize the DNA sequences and potential clusters, though Dr. Oster cautioned against overinterpretation of the results. “The links shown can easily be misinterpreted as actual social connections,” she said.

As proof of the approach’s potential, an analysis of the clusters identified showed their potential for HIV spread. On average in the United States, four new HIV infections occur per 100 people living with HIV. In the first 13 clusters that CDC identified, the number of infections was 33 per 100 person-years. The first 60 clusters had an average of 44 transmissions per 100 person-years. “None of these clusters had been found by [standard] epidemiologic methods, demonstrating that rapid transmission can be hard to detect without molecular data,” said Dr. Oster.

In 2018, all health departments began collecting sequencing data, and almost 40% of newly diagnosed patients have had sequencing data reported, more than 340,000 patients in total. Researchers have identified 145 priority clusters.

But use of molecular data is not the only method available. The CDC monitors increases in diagnoses in specific areas and conducts time-space analyses. These more traditional methods are particularly useful in areas with small populations or low HIV burden.

With a cluster identified, public health officials can attempt to identify all of the members of the network and help them to access services, such as testing, preexposure prophylaxis (PrEP), syringe service programs, and linkage to care.

In San Antonio, Tex., an analysis identified a cluster of 24 gay and bisexual men, and further analysis revealed an extended network of 87 sexual or needle-sharing partners. Researchers also identified missed opportunities for diagnosis of acute infection as well as low access to PrEP, so the health department sent out an alert clarifying diagnosis testing guidelines, highlighting the concern over acute infection, and containing PrEP educational material.

Analysis of another network in Michigan found that all identified individuals were virally suppressed, even though the network continued to grow. That suggested that there were unidentified individuals who were contributing to transmission, which prompted efforts by providers to encourage testing, linkage to care, and prevention.

All of these developments are good news for efforts to eradicate HIV, but they come with pitfalls. Local communities have expressed concerned that molecular data could be used to identify direction of transmission and for prosecution, since there are HIV laws that criminalize lack of disclosure and potential exposure to the virus, even when transmission doesn’t occur. “These laws are not aligned with current science and have not been found to help curb HIV,” said Dr. Oster.

She noted that current molecular methods are incapable of identifying direction of transmission. Still, the CDC is reemphasizing efforts to protect public health data from nonpublic health use. “CDC and health departments implement unprecedented policies and procedures to ensure confidentiality and security of the data,” Dr. Oster said.

She reported having no relevant disclosures.

 

– Advances in genetic sequencing are boosting efforts to identify new clusters of HIV infections and guiding public health interventions to address them. The method relies on resistance testing at diagnosis and virologic failure and allows public health researchers to determine the genetic relatedness of viruses responsible for new infections. If the viruses are genetically, geographically, and temporally associated, it indicates a previously unknown transmission cluster.

copyright Kativ/iStockphoto

“The presence of a cluster indicates gaps in our preventative services, which we must address to improve service delivery and stop transmission,” Alexandra M. Oster, MD, Division of HIV/AIDS Prevention, Surveillance, and Epidemiology at the Centers for Disease Control and Prevention, Atlanta, said during a talk at the Conference on Retroviruses and Opportunistic Infections.

She noted that HIV brings special challenges to outbreak detection. The median delay between infection and diagnosis is 3 years. Individuals are highly mobile, and signals of new outbreaks can be quickly drowned out in high-burden areas. But these challenges aren’t unique. Tuberculosis has a similarly lengthy latency period, yet more than 75% of new TB outbreaks are now identified through the use of genetic data. Sequencing also is used to track food-borne illness. The CDC’s PulseNet is a network of laboratories that examines DNA sequences from bacterial infections in search of previously unrecognized outbreaks.

In the HIV setting, molecular surveillance has great potential in identifying and intervening in evolving networks of HIV transmission, but also carries ethical and other challenges.

Nevertheless, “I hope to make the case that cluster detection and response [using molecular surveillance] can help bring the nation closer to ending the HIV epidemic,” said Dr. Oster.

Molecular surveillance obtains most of its data from drug resistance testing, both at entry to care and after virologic failure, which then gets passed to the U.S. National HIV Surveillance System. The data are then stripped of patient identifying information and submitted to the CDC.

With data from multiple individuals in hand, researchers create a phylogenetic tree, in which closely-related viruses appear as close neighbors on a branch. “By tracing back along the tree, you can see the inferred ancestor of [individual strains], and also the inferred ancestor of all strains on the tree,” said Dr. Oster. Together with geographical data, that information allows researchers to identify clusters of patients connected in a transmission network, and that information can be passed along to federal, state, and local agencies to prevent infections and improve care.

From 1997 through 2012, the CDC’s molecular surveillance program focused on drug resistance patterns, but in 2013 the agency decided to expand to include transmission clusters. It now uses a tool called HIV Trace, which helps public health workers with no background in bioinformatics to visualize the DNA sequences and potential clusters, though Dr. Oster cautioned against overinterpretation of the results. “The links shown can easily be misinterpreted as actual social connections,” she said.

As proof of the approach’s potential, an analysis of the clusters identified showed their potential for HIV spread. On average in the United States, four new HIV infections occur per 100 people living with HIV. In the first 13 clusters that CDC identified, the number of infections was 33 per 100 person-years. The first 60 clusters had an average of 44 transmissions per 100 person-years. “None of these clusters had been found by [standard] epidemiologic methods, demonstrating that rapid transmission can be hard to detect without molecular data,” said Dr. Oster.

In 2018, all health departments began collecting sequencing data, and almost 40% of newly diagnosed patients have had sequencing data reported, more than 340,000 patients in total. Researchers have identified 145 priority clusters.

But use of molecular data is not the only method available. The CDC monitors increases in diagnoses in specific areas and conducts time-space analyses. These more traditional methods are particularly useful in areas with small populations or low HIV burden.

With a cluster identified, public health officials can attempt to identify all of the members of the network and help them to access services, such as testing, preexposure prophylaxis (PrEP), syringe service programs, and linkage to care.

In San Antonio, Tex., an analysis identified a cluster of 24 gay and bisexual men, and further analysis revealed an extended network of 87 sexual or needle-sharing partners. Researchers also identified missed opportunities for diagnosis of acute infection as well as low access to PrEP, so the health department sent out an alert clarifying diagnosis testing guidelines, highlighting the concern over acute infection, and containing PrEP educational material.

Analysis of another network in Michigan found that all identified individuals were virally suppressed, even though the network continued to grow. That suggested that there were unidentified individuals who were contributing to transmission, which prompted efforts by providers to encourage testing, linkage to care, and prevention.

All of these developments are good news for efforts to eradicate HIV, but they come with pitfalls. Local communities have expressed concerned that molecular data could be used to identify direction of transmission and for prosecution, since there are HIV laws that criminalize lack of disclosure and potential exposure to the virus, even when transmission doesn’t occur. “These laws are not aligned with current science and have not been found to help curb HIV,” said Dr. Oster.

She noted that current molecular methods are incapable of identifying direction of transmission. Still, the CDC is reemphasizing efforts to protect public health data from nonpublic health use. “CDC and health departments implement unprecedented policies and procedures to ensure confidentiality and security of the data,” Dr. Oster said.

She reported having no relevant disclosures.

Publications
Publications
Topics
Article Type
Sections
Article Source

EXPERT ANALYSIS FROM CROI 2019

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.

FDA concerned about e-cigs/seizures in youth

Article Type
Changed
Wed, 04/03/2019 - 15:56

 

The Food and Drug Administration has received reports about people who use e-cigarettes experiencing seizures, and a “recent uptick in voluntary reports” may signal the potential for an emerging safety concern, the agency announced April 3.

mauro grigollo/Thinkstock

Between 2010 and early 2019, the FDA and poison control centers received 35 reports of seizures that mentioned the use of e-cigarettes. Most reports involved youth or young adults, and the reports have increased slightly since June 2018, the announcement says.

“We want to be clear that we don’t yet know if there’s a direct relationship between the use of e-cigarettes and a risk of seizure,” said FDA Commissioner Scott Gottlieb, MD, and Principal Deputy Commissioner Amy Abernethy, MD, PhD, in a statement. “We believe these 35 cases warrant scientific investigation into whether there is in fact a connection.”

In addition, the FDA is trying to determine whether any e-cigarette product-specific factors may be associated with the risk of seizures.

Seizures have been reported after a few puffs or up to 1 day after e-cigarette use and among first-time and experienced users. A few patients had a prior history of seizures or also used other substances, such as marijuana or amphetamines.

“While 35 cases may not seem like much compared to the total number of people using e-cigarettes, we are nonetheless concerned by these reported cases. We also recognized that not all of the cases may be reported,” Dr. Gottlieb and Dr. Abernethy said.

Although seizures are known side effects of nicotine toxicity and have been reported in the context of intentional or accidental swallowing of e-cigarette liquid, the voluntary reports of seizures occurring with vaping could represent a new safety issue, the FDA said.

The agency encouraged people to report cases via an online safety reporting portal. It also provided redacted case reports that involve vaping and seizures.
 

Publications
Topics
Sections

 

The Food and Drug Administration has received reports about people who use e-cigarettes experiencing seizures, and a “recent uptick in voluntary reports” may signal the potential for an emerging safety concern, the agency announced April 3.

mauro grigollo/Thinkstock

Between 2010 and early 2019, the FDA and poison control centers received 35 reports of seizures that mentioned the use of e-cigarettes. Most reports involved youth or young adults, and the reports have increased slightly since June 2018, the announcement says.

“We want to be clear that we don’t yet know if there’s a direct relationship between the use of e-cigarettes and a risk of seizure,” said FDA Commissioner Scott Gottlieb, MD, and Principal Deputy Commissioner Amy Abernethy, MD, PhD, in a statement. “We believe these 35 cases warrant scientific investigation into whether there is in fact a connection.”

In addition, the FDA is trying to determine whether any e-cigarette product-specific factors may be associated with the risk of seizures.

Seizures have been reported after a few puffs or up to 1 day after e-cigarette use and among first-time and experienced users. A few patients had a prior history of seizures or also used other substances, such as marijuana or amphetamines.

“While 35 cases may not seem like much compared to the total number of people using e-cigarettes, we are nonetheless concerned by these reported cases. We also recognized that not all of the cases may be reported,” Dr. Gottlieb and Dr. Abernethy said.

Although seizures are known side effects of nicotine toxicity and have been reported in the context of intentional or accidental swallowing of e-cigarette liquid, the voluntary reports of seizures occurring with vaping could represent a new safety issue, the FDA said.

The agency encouraged people to report cases via an online safety reporting portal. It also provided redacted case reports that involve vaping and seizures.
 

 

The Food and Drug Administration has received reports about people who use e-cigarettes experiencing seizures, and a “recent uptick in voluntary reports” may signal the potential for an emerging safety concern, the agency announced April 3.

mauro grigollo/Thinkstock

Between 2010 and early 2019, the FDA and poison control centers received 35 reports of seizures that mentioned the use of e-cigarettes. Most reports involved youth or young adults, and the reports have increased slightly since June 2018, the announcement says.

“We want to be clear that we don’t yet know if there’s a direct relationship between the use of e-cigarettes and a risk of seizure,” said FDA Commissioner Scott Gottlieb, MD, and Principal Deputy Commissioner Amy Abernethy, MD, PhD, in a statement. “We believe these 35 cases warrant scientific investigation into whether there is in fact a connection.”

In addition, the FDA is trying to determine whether any e-cigarette product-specific factors may be associated with the risk of seizures.

Seizures have been reported after a few puffs or up to 1 day after e-cigarette use and among first-time and experienced users. A few patients had a prior history of seizures or also used other substances, such as marijuana or amphetamines.

“While 35 cases may not seem like much compared to the total number of people using e-cigarettes, we are nonetheless concerned by these reported cases. We also recognized that not all of the cases may be reported,” Dr. Gottlieb and Dr. Abernethy said.

Although seizures are known side effects of nicotine toxicity and have been reported in the context of intentional or accidental swallowing of e-cigarette liquid, the voluntary reports of seizures occurring with vaping could represent a new safety issue, the FDA said.

The agency encouraged people to report cases via an online safety reporting portal. It also provided redacted case reports that involve vaping and seizures.
 

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.

Marcela Romero-Reyes, DDS, PhD, Comments on Peripheral and Central Headache Challenges

Article Type
Changed
Thu, 12/15/2022 - 14:42
Display Headline
Marcela Romero-Reyes, DDS, PhD, Comments on Peripheral and Central Headache Challenges

Neurology Reviews recently published an article about the headache treatment challenges that occur when both central and peripheral symptoms are involved. In follow up, Dr. Alan M. Rapoport, Migraine Resource Center editor-in-chief, asked Dr. Marcela Romero Reyes, Clinical Associate Professor and Clinical Director of the Brotman Facial Pain Clinic at the University of Maryland and chair of the Special Interest Section of TMD, Cervical Spine and Orofacial Pain of the American Headache Society, to weigh in on how she addresses these challenges in practice as well as the importance of a multi-specialty approach.

###

 

Dr. Rapoport: Do you commonly see patients who present with symptoms of both central and peripheral symptoms in practice?

 

Dr. Romero-Reyes: Yes, I see patients that present with temporomandibular disorders (TMD) and headache comorbidity, as well as patients with migraine, tension-type headache, and cervicogenic headache with myofascial pain.

 

Dr. Rapoport: Why do you think this condition is so challenging to treat?

 

Dr. Romero-Reyes: I think this is because of the lack of understanding and awareness that in addition to the multifactorial nature of headache disorders, other types of disorders that are not neurovascular in origin may influence trigeminovascular nociception, and these types of non-neurovascular disorders involve the skill and knowledge of other expertise.

 

Headaches receiving inputs from extracranial structures such as in TMD (temporomandibular joint [TMJ] and muscles of mastication) and/or cervical structures (cervical spine, cervical muscles) require multidisciplinary evaluation and management. In these cases, the management should involve a neurologist specialized in headache disorders, a dentist trained in TMD and orofacial pain disorders, and a physical therapist with special training in craniofacial and cervical Therapeutics. Multidisciplinary communication is key for successful management.

 

Another reason is that myofascial pain (MFP) is often overlooked in patients with headache disorders. In my experience, patients with episodic and chronic migraine, episodic and chronic tension-type headache, cervicogenic headache, and patients presenting TMD and headache comorbidity can present trigger points in the craniofacial and cervical muscles, an indication of MFP. It has been reported that these patients present a higher disability impact. The presence of MFP may be contributing to the activation of the trigeminovascular system and therefore facilitate, exacerbate, and perpetuate headache symptomatology and may accelerate the progression to a more chronic form of the disorder.

 

Dr. Rapoport: In your opinion, is this considered a controversial topic? Why or why not?
 

Dr. Romero-Reyes: Yes, I think it is necessary to clarify that tenderness in the back of the head or of neck muscles present in headache patients does not necessarily imply that it is due to a nerve compression. This could also be caused by local myalgia but more commonly, from latent or active myofascial trigger points present in the muscles of the area being palpated, or by referred pain beyond the area of the muscle being palpated. Suboccipital muscles (in the occiput area) are not the only muscle group that is associated with headache and neck pain symptomatology. For example, the trapezius muscle, which is an overlooked source of tension- type and cervicogenic headache, can present trigger points that can refer pain to the shoulder, neck, head, face and the eye. In addition, other craniofacial and cervical muscles such as the sternocleidomastoid (SCM) and temporalis muscles have been shown to be associated with headache symptomatology in the migraineur, as well as the chronic tension-type headache patient. Other muscles that also refer to the craniofacial area and can elicit headache and neck pain symptomatology include the masseter, occipitofrontalis, splenius capitis, splenius cervicis, semispinalis capitis, semispinalis cervicis and multifidi (cervical). The presence of trigger points in these muscles do not support or warrant the need to be removed or managed with non-conservative approaches.

 

Myofascial trigger points can result from muscle injury and overload, parafunctional activity, and poor head and neck posture. MFP is characterized by a regional pain and presence of localized tender areas (trigger points) in muscle, fascia or tendons that reproduce pain when palpated, and produce a pattern of regional pain spreading along the muscle palpated, or beyond the location boundary of the muscle palpated. It has been shown by microdyalisis that inflammatory mediators and neuropeptides are present in the area of an active trigger point. In addition, an increase of electromyography activity has been shown in trigger points in patients with chronic tension-type headache when compared with controls.

 

The importance of an evaluation by a skilled clinician in the craniofacial and cervical area to verify the source of pain is critical.  The patient may be reporting pain in one area, but the source of the pain is in another area, and this is typical symptomatology present when there are active trigger points. In addition, an assessment of any contributing factors arising from the cervical spine (eg, poor posture) and craniofacial area (eg, TMD) that may exacerbate headache symptomatology is vital to proper diagnosis.

 

In my experience, patients with migraine, tension-type headache, cervicogenic headache, and TMD and headache comorbidity present MFP perpetuating headache symptomatology. MFP is not managed by surgical interventions. This perpetuating factor can be managed effectively with conservative measures. The plan is tailored for each patient’s needs. In general, the plan of management may include trigger point injections in the muscle with anesthetics, dry needling, and a physical therapy plan that may include education regarding habits and posture, exercises and physical therapy modalities, which are crucial to relieve pain and increase function. In cases of TMD and headache comorbidity, an occlusal appliance (stabilization appliance) can be included if necessary. We should also consider behavioral therapies (especially EMG biofeedback training) and some oral anti-inflammatories or muscle relaxants in the beginning of management, together with the plan of management mentioned above.

 

With these approaches to manage the MFP component in headache patients, I have been able to see that in migraineurs with MFP, the frequency and severity of the attacks decrease significantly. The patient may still experience migraine attacks, but feel happy to have the possibility to reduce medication intake and be in more control of their pain. In patients with tension-type headache, I have seen this even more dramatically.

 

This is telling us that headache pathophysiology involves a “conversation” between the peripheral and central nervous system, which influence each other. Peripheral nociceptive input coming from extracranial structures can induce trigeminovascular activation and therefore exacerbate a headache disorder and vice versa.  Chronic myofascial pain may be the result of central sensitization due to the protracted peripheral nociceptive input (eg, poor posture, neck strain, parafunctional activity), therefore perpetuating the headache disorder even more.

 

Dr. Rapoport: Do you have any other comments about the article Treatment Challenges When Headache Has Central and Peripheral Involvement that you would like to share with our readers?

 

Dr. Romero-Reyes: It is simplistic to say migraine is either a peripheral or a central disorder, or that symptoms are either peripheral or central. Beyond thinking about migraine pain, migraine is fundamentally a brain (central) disorder. Its associated symptoms (nausea, phonophobia, photophobia) tell us this. Migraine headache is complex, and most likely the result of central mechanisms that can be influenced by peripheral inputs from the craniofacial and cervical region.

 

Embarking on surgical interventions for the management of headache disorders warrants a caution since it is still an experimental research question and the need of such therapies should be evaluated against conservative management. We are in a very exciting and hopeful time for migraine management. New evidence-based options from biological agents, such as anti-calcitonin gene-related peptide (CGRP) therapies, to non-pharmacological approaches, such as neuromodulation, can be offered to the patients. If the patient is experiencing pain in the neck area or other craniofacial area, it is recommended to have a thorough evaluation by a physical therapist with special training in cervical and craniofacial therapeutics and/or a dentist trained in TMD and orofacial pain disorders to work in consultation with a neurologist to elaborate a personalized management plan. Do not overlook the contribution of myofascial pain (trigger points) as well as TMD in the symptomatology of headache disorders. Few patients need to undergo surgical measures of peripheral nerves and muscles for improvement. An exhaustive evaluation must be undertaken first.

 

Resources for patients:

 

AHS

https://americanheadachesociety.org/

 

https://americanheadachesociety.org/wp-content/uploads/2018/06/Choosing-Wisely-Flyer.pdf

 

AAOP

https://aaop.clubexpress.com/content.aspx?sl=1152088466

 

PTBCTT

https://ptbcct.org/

Publications
Topics
Sections

Neurology Reviews recently published an article about the headache treatment challenges that occur when both central and peripheral symptoms are involved. In follow up, Dr. Alan M. Rapoport, Migraine Resource Center editor-in-chief, asked Dr. Marcela Romero Reyes, Clinical Associate Professor and Clinical Director of the Brotman Facial Pain Clinic at the University of Maryland and chair of the Special Interest Section of TMD, Cervical Spine and Orofacial Pain of the American Headache Society, to weigh in on how she addresses these challenges in practice as well as the importance of a multi-specialty approach.

###

 

Dr. Rapoport: Do you commonly see patients who present with symptoms of both central and peripheral symptoms in practice?

 

Dr. Romero-Reyes: Yes, I see patients that present with temporomandibular disorders (TMD) and headache comorbidity, as well as patients with migraine, tension-type headache, and cervicogenic headache with myofascial pain.

 

Dr. Rapoport: Why do you think this condition is so challenging to treat?

 

Dr. Romero-Reyes: I think this is because of the lack of understanding and awareness that in addition to the multifactorial nature of headache disorders, other types of disorders that are not neurovascular in origin may influence trigeminovascular nociception, and these types of non-neurovascular disorders involve the skill and knowledge of other expertise.

 

Headaches receiving inputs from extracranial structures such as in TMD (temporomandibular joint [TMJ] and muscles of mastication) and/or cervical structures (cervical spine, cervical muscles) require multidisciplinary evaluation and management. In these cases, the management should involve a neurologist specialized in headache disorders, a dentist trained in TMD and orofacial pain disorders, and a physical therapist with special training in craniofacial and cervical Therapeutics. Multidisciplinary communication is key for successful management.

 

Another reason is that myofascial pain (MFP) is often overlooked in patients with headache disorders. In my experience, patients with episodic and chronic migraine, episodic and chronic tension-type headache, cervicogenic headache, and patients presenting TMD and headache comorbidity can present trigger points in the craniofacial and cervical muscles, an indication of MFP. It has been reported that these patients present a higher disability impact. The presence of MFP may be contributing to the activation of the trigeminovascular system and therefore facilitate, exacerbate, and perpetuate headache symptomatology and may accelerate the progression to a more chronic form of the disorder.

 

Dr. Rapoport: In your opinion, is this considered a controversial topic? Why or why not?
 

Dr. Romero-Reyes: Yes, I think it is necessary to clarify that tenderness in the back of the head or of neck muscles present in headache patients does not necessarily imply that it is due to a nerve compression. This could also be caused by local myalgia but more commonly, from latent or active myofascial trigger points present in the muscles of the area being palpated, or by referred pain beyond the area of the muscle being palpated. Suboccipital muscles (in the occiput area) are not the only muscle group that is associated with headache and neck pain symptomatology. For example, the trapezius muscle, which is an overlooked source of tension- type and cervicogenic headache, can present trigger points that can refer pain to the shoulder, neck, head, face and the eye. In addition, other craniofacial and cervical muscles such as the sternocleidomastoid (SCM) and temporalis muscles have been shown to be associated with headache symptomatology in the migraineur, as well as the chronic tension-type headache patient. Other muscles that also refer to the craniofacial area and can elicit headache and neck pain symptomatology include the masseter, occipitofrontalis, splenius capitis, splenius cervicis, semispinalis capitis, semispinalis cervicis and multifidi (cervical). The presence of trigger points in these muscles do not support or warrant the need to be removed or managed with non-conservative approaches.

 

Myofascial trigger points can result from muscle injury and overload, parafunctional activity, and poor head and neck posture. MFP is characterized by a regional pain and presence of localized tender areas (trigger points) in muscle, fascia or tendons that reproduce pain when palpated, and produce a pattern of regional pain spreading along the muscle palpated, or beyond the location boundary of the muscle palpated. It has been shown by microdyalisis that inflammatory mediators and neuropeptides are present in the area of an active trigger point. In addition, an increase of electromyography activity has been shown in trigger points in patients with chronic tension-type headache when compared with controls.

 

The importance of an evaluation by a skilled clinician in the craniofacial and cervical area to verify the source of pain is critical.  The patient may be reporting pain in one area, but the source of the pain is in another area, and this is typical symptomatology present when there are active trigger points. In addition, an assessment of any contributing factors arising from the cervical spine (eg, poor posture) and craniofacial area (eg, TMD) that may exacerbate headache symptomatology is vital to proper diagnosis.

 

In my experience, patients with migraine, tension-type headache, cervicogenic headache, and TMD and headache comorbidity present MFP perpetuating headache symptomatology. MFP is not managed by surgical interventions. This perpetuating factor can be managed effectively with conservative measures. The plan is tailored for each patient’s needs. In general, the plan of management may include trigger point injections in the muscle with anesthetics, dry needling, and a physical therapy plan that may include education regarding habits and posture, exercises and physical therapy modalities, which are crucial to relieve pain and increase function. In cases of TMD and headache comorbidity, an occlusal appliance (stabilization appliance) can be included if necessary. We should also consider behavioral therapies (especially EMG biofeedback training) and some oral anti-inflammatories or muscle relaxants in the beginning of management, together with the plan of management mentioned above.

 

With these approaches to manage the MFP component in headache patients, I have been able to see that in migraineurs with MFP, the frequency and severity of the attacks decrease significantly. The patient may still experience migraine attacks, but feel happy to have the possibility to reduce medication intake and be in more control of their pain. In patients with tension-type headache, I have seen this even more dramatically.

 

This is telling us that headache pathophysiology involves a “conversation” between the peripheral and central nervous system, which influence each other. Peripheral nociceptive input coming from extracranial structures can induce trigeminovascular activation and therefore exacerbate a headache disorder and vice versa.  Chronic myofascial pain may be the result of central sensitization due to the protracted peripheral nociceptive input (eg, poor posture, neck strain, parafunctional activity), therefore perpetuating the headache disorder even more.

 

Dr. Rapoport: Do you have any other comments about the article Treatment Challenges When Headache Has Central and Peripheral Involvement that you would like to share with our readers?

 

Dr. Romero-Reyes: It is simplistic to say migraine is either a peripheral or a central disorder, or that symptoms are either peripheral or central. Beyond thinking about migraine pain, migraine is fundamentally a brain (central) disorder. Its associated symptoms (nausea, phonophobia, photophobia) tell us this. Migraine headache is complex, and most likely the result of central mechanisms that can be influenced by peripheral inputs from the craniofacial and cervical region.

 

Embarking on surgical interventions for the management of headache disorders warrants a caution since it is still an experimental research question and the need of such therapies should be evaluated against conservative management. We are in a very exciting and hopeful time for migraine management. New evidence-based options from biological agents, such as anti-calcitonin gene-related peptide (CGRP) therapies, to non-pharmacological approaches, such as neuromodulation, can be offered to the patients. If the patient is experiencing pain in the neck area or other craniofacial area, it is recommended to have a thorough evaluation by a physical therapist with special training in cervical and craniofacial therapeutics and/or a dentist trained in TMD and orofacial pain disorders to work in consultation with a neurologist to elaborate a personalized management plan. Do not overlook the contribution of myofascial pain (trigger points) as well as TMD in the symptomatology of headache disorders. Few patients need to undergo surgical measures of peripheral nerves and muscles for improvement. An exhaustive evaluation must be undertaken first.

 

Resources for patients:

 

AHS

https://americanheadachesociety.org/

 

https://americanheadachesociety.org/wp-content/uploads/2018/06/Choosing-Wisely-Flyer.pdf

 

AAOP

https://aaop.clubexpress.com/content.aspx?sl=1152088466

 

PTBCTT

https://ptbcct.org/

Neurology Reviews recently published an article about the headache treatment challenges that occur when both central and peripheral symptoms are involved. In follow up, Dr. Alan M. Rapoport, Migraine Resource Center editor-in-chief, asked Dr. Marcela Romero Reyes, Clinical Associate Professor and Clinical Director of the Brotman Facial Pain Clinic at the University of Maryland and chair of the Special Interest Section of TMD, Cervical Spine and Orofacial Pain of the American Headache Society, to weigh in on how she addresses these challenges in practice as well as the importance of a multi-specialty approach.

###

 

Dr. Rapoport: Do you commonly see patients who present with symptoms of both central and peripheral symptoms in practice?

 

Dr. Romero-Reyes: Yes, I see patients that present with temporomandibular disorders (TMD) and headache comorbidity, as well as patients with migraine, tension-type headache, and cervicogenic headache with myofascial pain.

 

Dr. Rapoport: Why do you think this condition is so challenging to treat?

 

Dr. Romero-Reyes: I think this is because of the lack of understanding and awareness that in addition to the multifactorial nature of headache disorders, other types of disorders that are not neurovascular in origin may influence trigeminovascular nociception, and these types of non-neurovascular disorders involve the skill and knowledge of other expertise.

 

Headaches receiving inputs from extracranial structures such as in TMD (temporomandibular joint [TMJ] and muscles of mastication) and/or cervical structures (cervical spine, cervical muscles) require multidisciplinary evaluation and management. In these cases, the management should involve a neurologist specialized in headache disorders, a dentist trained in TMD and orofacial pain disorders, and a physical therapist with special training in craniofacial and cervical Therapeutics. Multidisciplinary communication is key for successful management.

 

Another reason is that myofascial pain (MFP) is often overlooked in patients with headache disorders. In my experience, patients with episodic and chronic migraine, episodic and chronic tension-type headache, cervicogenic headache, and patients presenting TMD and headache comorbidity can present trigger points in the craniofacial and cervical muscles, an indication of MFP. It has been reported that these patients present a higher disability impact. The presence of MFP may be contributing to the activation of the trigeminovascular system and therefore facilitate, exacerbate, and perpetuate headache symptomatology and may accelerate the progression to a more chronic form of the disorder.

 

Dr. Rapoport: In your opinion, is this considered a controversial topic? Why or why not?
 

Dr. Romero-Reyes: Yes, I think it is necessary to clarify that tenderness in the back of the head or of neck muscles present in headache patients does not necessarily imply that it is due to a nerve compression. This could also be caused by local myalgia but more commonly, from latent or active myofascial trigger points present in the muscles of the area being palpated, or by referred pain beyond the area of the muscle being palpated. Suboccipital muscles (in the occiput area) are not the only muscle group that is associated with headache and neck pain symptomatology. For example, the trapezius muscle, which is an overlooked source of tension- type and cervicogenic headache, can present trigger points that can refer pain to the shoulder, neck, head, face and the eye. In addition, other craniofacial and cervical muscles such as the sternocleidomastoid (SCM) and temporalis muscles have been shown to be associated with headache symptomatology in the migraineur, as well as the chronic tension-type headache patient. Other muscles that also refer to the craniofacial area and can elicit headache and neck pain symptomatology include the masseter, occipitofrontalis, splenius capitis, splenius cervicis, semispinalis capitis, semispinalis cervicis and multifidi (cervical). The presence of trigger points in these muscles do not support or warrant the need to be removed or managed with non-conservative approaches.

 

Myofascial trigger points can result from muscle injury and overload, parafunctional activity, and poor head and neck posture. MFP is characterized by a regional pain and presence of localized tender areas (trigger points) in muscle, fascia or tendons that reproduce pain when palpated, and produce a pattern of regional pain spreading along the muscle palpated, or beyond the location boundary of the muscle palpated. It has been shown by microdyalisis that inflammatory mediators and neuropeptides are present in the area of an active trigger point. In addition, an increase of electromyography activity has been shown in trigger points in patients with chronic tension-type headache when compared with controls.

 

The importance of an evaluation by a skilled clinician in the craniofacial and cervical area to verify the source of pain is critical.  The patient may be reporting pain in one area, but the source of the pain is in another area, and this is typical symptomatology present when there are active trigger points. In addition, an assessment of any contributing factors arising from the cervical spine (eg, poor posture) and craniofacial area (eg, TMD) that may exacerbate headache symptomatology is vital to proper diagnosis.

 

In my experience, patients with migraine, tension-type headache, cervicogenic headache, and TMD and headache comorbidity present MFP perpetuating headache symptomatology. MFP is not managed by surgical interventions. This perpetuating factor can be managed effectively with conservative measures. The plan is tailored for each patient’s needs. In general, the plan of management may include trigger point injections in the muscle with anesthetics, dry needling, and a physical therapy plan that may include education regarding habits and posture, exercises and physical therapy modalities, which are crucial to relieve pain and increase function. In cases of TMD and headache comorbidity, an occlusal appliance (stabilization appliance) can be included if necessary. We should also consider behavioral therapies (especially EMG biofeedback training) and some oral anti-inflammatories or muscle relaxants in the beginning of management, together with the plan of management mentioned above.

 

With these approaches to manage the MFP component in headache patients, I have been able to see that in migraineurs with MFP, the frequency and severity of the attacks decrease significantly. The patient may still experience migraine attacks, but feel happy to have the possibility to reduce medication intake and be in more control of their pain. In patients with tension-type headache, I have seen this even more dramatically.

 

This is telling us that headache pathophysiology involves a “conversation” between the peripheral and central nervous system, which influence each other. Peripheral nociceptive input coming from extracranial structures can induce trigeminovascular activation and therefore exacerbate a headache disorder and vice versa.  Chronic myofascial pain may be the result of central sensitization due to the protracted peripheral nociceptive input (eg, poor posture, neck strain, parafunctional activity), therefore perpetuating the headache disorder even more.

 

Dr. Rapoport: Do you have any other comments about the article Treatment Challenges When Headache Has Central and Peripheral Involvement that you would like to share with our readers?

 

Dr. Romero-Reyes: It is simplistic to say migraine is either a peripheral or a central disorder, or that symptoms are either peripheral or central. Beyond thinking about migraine pain, migraine is fundamentally a brain (central) disorder. Its associated symptoms (nausea, phonophobia, photophobia) tell us this. Migraine headache is complex, and most likely the result of central mechanisms that can be influenced by peripheral inputs from the craniofacial and cervical region.

 

Embarking on surgical interventions for the management of headache disorders warrants a caution since it is still an experimental research question and the need of such therapies should be evaluated against conservative management. We are in a very exciting and hopeful time for migraine management. New evidence-based options from biological agents, such as anti-calcitonin gene-related peptide (CGRP) therapies, to non-pharmacological approaches, such as neuromodulation, can be offered to the patients. If the patient is experiencing pain in the neck area or other craniofacial area, it is recommended to have a thorough evaluation by a physical therapist with special training in cervical and craniofacial therapeutics and/or a dentist trained in TMD and orofacial pain disorders to work in consultation with a neurologist to elaborate a personalized management plan. Do not overlook the contribution of myofascial pain (trigger points) as well as TMD in the symptomatology of headache disorders. Few patients need to undergo surgical measures of peripheral nerves and muscles for improvement. An exhaustive evaluation must be undertaken first.

 

Resources for patients:

 

AHS

https://americanheadachesociety.org/

 

https://americanheadachesociety.org/wp-content/uploads/2018/06/Choosing-Wisely-Flyer.pdf

 

AAOP

https://aaop.clubexpress.com/content.aspx?sl=1152088466

 

PTBCTT

https://ptbcct.org/

Publications
Publications
Topics
Article Type
Display Headline
Marcela Romero-Reyes, DDS, PhD, Comments on Peripheral and Central Headache Challenges
Display Headline
Marcela Romero-Reyes, DDS, PhD, Comments on Peripheral and Central Headache Challenges
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Gate On Date
Wed, 04/03/2019 - 12:30
Un-Gate On Date
Wed, 04/03/2019 - 12:30
Use ProPublica
CFC Schedule Remove Status
Wed, 04/03/2019 - 12:30
Hide sidebar & use full width
render the right sidebar.

STIs pose complex challenge to HIV efforts

Article Type
Changed
Mon, 04/08/2019 - 09:47

– Sexually-transmitted infections (STIs) such as gonorrhea, chlamydia, and syphilis are on the rise among HIV-infected individuals, and emerging antimicrobial resistance in these organisms is presenting serious challenges to physicians. The issue may be traceable to the introduction of preexposure prophylaxis (PrEP) in 2011, which previous studies have shown to be associated with less condom use.

CDC
This photomicrograph reveals the histopathology in an acute case of gonococcal urethritis using Gram-stain technique.

In the United States, a 2017 report by the Centers for Disease Control and Prevention showed rising incidences of chlamydia (+5% from 2015 to 2017), gonorrhea (+19%), and syphilis (+18%). “We have an incidence among men who have sex with men [MSM] that is above the pre-AIDS era estimates, and we have evidence of spread into heterosexual networks, and a very scary collision with the methamphetamine and heroine using networks,” said Jeanne Marrazzo, MD, professor of infectious diseases at the University of Alabama at Birmingham.

But the numbers alone don’t tell the whole story. “It’s not just the burden of these infections. What’s characterizing these trends is that we have continuing evolution of microbial resistance, which is really a crisis,” Dr. Marrazzo added during a plenary she delivered at the Conference on Retroviruses & Opportunistic Infections.

These infections also remain intricately linked with HIV. An analysis of syphilis cases found that 88% occurred in men. Of those, 80% were MSM. Of the cases in MSM, 46% were coinfected with HIV. “Those are incredible rates,” said Dr. Marrazzo. Among women, the trends are even more alarming. There has been a greater than 150% increase in primary/secondary and congenital syphilis between 2013 and 2017.

Resistance to ceftriaxone and azithromycin remains on the rise in gonorrhea, with 24% of countries reporting at least a 5% incidence of strains that are less susceptible or resistant to ceftriaxone, and 81% of countries reporting similar trends with azithromycin.

In the absence of new drugs to overcome that resistance, or vaccines that can prevent gonorrhea and other infections, what are clinicians to do?

One option may be postexposure doxycycline. One trial in MSM showed that a 200-mg dose taken 24-72 hours after sex was associated with about a 70% increase in both time to first chlamydia and time to first syphilis infection, though no effect was seen on gonorrhea infections. “We shouldn’t be surprised. We know that gonorrhea is classically resistant to tetracyclines, and the MSM population has the highest prevalence of antimicrobial resistance in gonorrhea,” said Dr. Marrazzo.

There are pros and cons to this strategy, of course. On the one hand, doxycycline works for chlamydia and syphilis, it’s safe, and it’s easy to administer. “We’re up a tree when it comes to syphilis, so why not?” opined Dr. Marrazzo. In fact, some MSM have read the literature and are already using it prophylactically. But there are downsides, including adverse effects such as esophagitis/ulceration and photosensitivity, and it is contraindicated in pregnant women. And then there’s the potential for evolving greater resistance. “The horse is out of the barn with respect to gonorrhea, but I think it’s worth thinking about resistance to other pathogens, where we still rely on doxycycline [to treat] in rare cases,” said Dr. Marrazzo.

Finally, Dr. Marrazzo discussed the role of STI treatment in the effort to eradicate HIV. Should the Getting to 0 strategies include aggressive prevention and treatment of STIs? Despite the potentiating role of some STIs in the spread HIV, some urban areas are approaching zero new infections even as other STIs remain a problem. It could be that undetectable = untransmittable, regardless of the presence an STI. Some view targeting STIs as a regressive practice in a setting where the U=U mantra has opened up an era of sexual freedom living with or at risk of HIV.

On the other hand, there are also good arguments to target STIs while trying to eliminate HIV. Results from high-resource locales such as San Francisco and New York City are unlikely to be replicated in places like Sub-Saharan Africa. The public health burden of STIs is extensive, and antibiotic resistance and antibiotic shortages can make treatment difficult. The situation is also different for women, who may experience impacts on fertility or pregnancies, and do not have the same freedom as men in many countries. “Stigma is highly operative and I would wager that sexual pleasure and freedom remain a very elusive goal for women across the globe,” said Dr. Marrazzo.

Dr. Marrazzo has a research grant/grant pending from Cepheid, and is on the advisory panels of BioFire and Gilead.

Meeting/Event
Publications
Topics
Sections
Meeting/Event
Meeting/Event

– Sexually-transmitted infections (STIs) such as gonorrhea, chlamydia, and syphilis are on the rise among HIV-infected individuals, and emerging antimicrobial resistance in these organisms is presenting serious challenges to physicians. The issue may be traceable to the introduction of preexposure prophylaxis (PrEP) in 2011, which previous studies have shown to be associated with less condom use.

CDC
This photomicrograph reveals the histopathology in an acute case of gonococcal urethritis using Gram-stain technique.

In the United States, a 2017 report by the Centers for Disease Control and Prevention showed rising incidences of chlamydia (+5% from 2015 to 2017), gonorrhea (+19%), and syphilis (+18%). “We have an incidence among men who have sex with men [MSM] that is above the pre-AIDS era estimates, and we have evidence of spread into heterosexual networks, and a very scary collision with the methamphetamine and heroine using networks,” said Jeanne Marrazzo, MD, professor of infectious diseases at the University of Alabama at Birmingham.

But the numbers alone don’t tell the whole story. “It’s not just the burden of these infections. What’s characterizing these trends is that we have continuing evolution of microbial resistance, which is really a crisis,” Dr. Marrazzo added during a plenary she delivered at the Conference on Retroviruses & Opportunistic Infections.

These infections also remain intricately linked with HIV. An analysis of syphilis cases found that 88% occurred in men. Of those, 80% were MSM. Of the cases in MSM, 46% were coinfected with HIV. “Those are incredible rates,” said Dr. Marrazzo. Among women, the trends are even more alarming. There has been a greater than 150% increase in primary/secondary and congenital syphilis between 2013 and 2017.

Resistance to ceftriaxone and azithromycin remains on the rise in gonorrhea, with 24% of countries reporting at least a 5% incidence of strains that are less susceptible or resistant to ceftriaxone, and 81% of countries reporting similar trends with azithromycin.

In the absence of new drugs to overcome that resistance, or vaccines that can prevent gonorrhea and other infections, what are clinicians to do?

One option may be postexposure doxycycline. One trial in MSM showed that a 200-mg dose taken 24-72 hours after sex was associated with about a 70% increase in both time to first chlamydia and time to first syphilis infection, though no effect was seen on gonorrhea infections. “We shouldn’t be surprised. We know that gonorrhea is classically resistant to tetracyclines, and the MSM population has the highest prevalence of antimicrobial resistance in gonorrhea,” said Dr. Marrazzo.

There are pros and cons to this strategy, of course. On the one hand, doxycycline works for chlamydia and syphilis, it’s safe, and it’s easy to administer. “We’re up a tree when it comes to syphilis, so why not?” opined Dr. Marrazzo. In fact, some MSM have read the literature and are already using it prophylactically. But there are downsides, including adverse effects such as esophagitis/ulceration and photosensitivity, and it is contraindicated in pregnant women. And then there’s the potential for evolving greater resistance. “The horse is out of the barn with respect to gonorrhea, but I think it’s worth thinking about resistance to other pathogens, where we still rely on doxycycline [to treat] in rare cases,” said Dr. Marrazzo.

Finally, Dr. Marrazzo discussed the role of STI treatment in the effort to eradicate HIV. Should the Getting to 0 strategies include aggressive prevention and treatment of STIs? Despite the potentiating role of some STIs in the spread HIV, some urban areas are approaching zero new infections even as other STIs remain a problem. It could be that undetectable = untransmittable, regardless of the presence an STI. Some view targeting STIs as a regressive practice in a setting where the U=U mantra has opened up an era of sexual freedom living with or at risk of HIV.

On the other hand, there are also good arguments to target STIs while trying to eliminate HIV. Results from high-resource locales such as San Francisco and New York City are unlikely to be replicated in places like Sub-Saharan Africa. The public health burden of STIs is extensive, and antibiotic resistance and antibiotic shortages can make treatment difficult. The situation is also different for women, who may experience impacts on fertility or pregnancies, and do not have the same freedom as men in many countries. “Stigma is highly operative and I would wager that sexual pleasure and freedom remain a very elusive goal for women across the globe,” said Dr. Marrazzo.

Dr. Marrazzo has a research grant/grant pending from Cepheid, and is on the advisory panels of BioFire and Gilead.

– Sexually-transmitted infections (STIs) such as gonorrhea, chlamydia, and syphilis are on the rise among HIV-infected individuals, and emerging antimicrobial resistance in these organisms is presenting serious challenges to physicians. The issue may be traceable to the introduction of preexposure prophylaxis (PrEP) in 2011, which previous studies have shown to be associated with less condom use.

CDC
This photomicrograph reveals the histopathology in an acute case of gonococcal urethritis using Gram-stain technique.

In the United States, a 2017 report by the Centers for Disease Control and Prevention showed rising incidences of chlamydia (+5% from 2015 to 2017), gonorrhea (+19%), and syphilis (+18%). “We have an incidence among men who have sex with men [MSM] that is above the pre-AIDS era estimates, and we have evidence of spread into heterosexual networks, and a very scary collision with the methamphetamine and heroine using networks,” said Jeanne Marrazzo, MD, professor of infectious diseases at the University of Alabama at Birmingham.

But the numbers alone don’t tell the whole story. “It’s not just the burden of these infections. What’s characterizing these trends is that we have continuing evolution of microbial resistance, which is really a crisis,” Dr. Marrazzo added during a plenary she delivered at the Conference on Retroviruses & Opportunistic Infections.

These infections also remain intricately linked with HIV. An analysis of syphilis cases found that 88% occurred in men. Of those, 80% were MSM. Of the cases in MSM, 46% were coinfected with HIV. “Those are incredible rates,” said Dr. Marrazzo. Among women, the trends are even more alarming. There has been a greater than 150% increase in primary/secondary and congenital syphilis between 2013 and 2017.

Resistance to ceftriaxone and azithromycin remains on the rise in gonorrhea, with 24% of countries reporting at least a 5% incidence of strains that are less susceptible or resistant to ceftriaxone, and 81% of countries reporting similar trends with azithromycin.

In the absence of new drugs to overcome that resistance, or vaccines that can prevent gonorrhea and other infections, what are clinicians to do?

One option may be postexposure doxycycline. One trial in MSM showed that a 200-mg dose taken 24-72 hours after sex was associated with about a 70% increase in both time to first chlamydia and time to first syphilis infection, though no effect was seen on gonorrhea infections. “We shouldn’t be surprised. We know that gonorrhea is classically resistant to tetracyclines, and the MSM population has the highest prevalence of antimicrobial resistance in gonorrhea,” said Dr. Marrazzo.

There are pros and cons to this strategy, of course. On the one hand, doxycycline works for chlamydia and syphilis, it’s safe, and it’s easy to administer. “We’re up a tree when it comes to syphilis, so why not?” opined Dr. Marrazzo. In fact, some MSM have read the literature and are already using it prophylactically. But there are downsides, including adverse effects such as esophagitis/ulceration and photosensitivity, and it is contraindicated in pregnant women. And then there’s the potential for evolving greater resistance. “The horse is out of the barn with respect to gonorrhea, but I think it’s worth thinking about resistance to other pathogens, where we still rely on doxycycline [to treat] in rare cases,” said Dr. Marrazzo.

Finally, Dr. Marrazzo discussed the role of STI treatment in the effort to eradicate HIV. Should the Getting to 0 strategies include aggressive prevention and treatment of STIs? Despite the potentiating role of some STIs in the spread HIV, some urban areas are approaching zero new infections even as other STIs remain a problem. It could be that undetectable = untransmittable, regardless of the presence an STI. Some view targeting STIs as a regressive practice in a setting where the U=U mantra has opened up an era of sexual freedom living with or at risk of HIV.

On the other hand, there are also good arguments to target STIs while trying to eliminate HIV. Results from high-resource locales such as San Francisco and New York City are unlikely to be replicated in places like Sub-Saharan Africa. The public health burden of STIs is extensive, and antibiotic resistance and antibiotic shortages can make treatment difficult. The situation is also different for women, who may experience impacts on fertility or pregnancies, and do not have the same freedom as men in many countries. “Stigma is highly operative and I would wager that sexual pleasure and freedom remain a very elusive goal for women across the globe,” said Dr. Marrazzo.

Dr. Marrazzo has a research grant/grant pending from Cepheid, and is on the advisory panels of BioFire and Gilead.

Publications
Publications
Topics
Article Type
Sections
Article Source

EXPERT ANALYSIS FROM CROI 2019

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.

Anterior, apical, posterior: Vaginal anatomy for the gynecologic surgeon

Article Type
Changed
Mon, 05/20/2019 - 10:22

CASE 1 Defining anatomic structures to assure surgical precision

A 44-year-old woman is scheduled for a vaginal hysterectomy and bilateral salpingectomy for abnormal uterine bleeding. In your academic practice, a resident routinely operates with you and is accompanied by a medical student. As this is your first case with each learner, you review the steps of the procedure along with pertinent anatomy. During this discussion, numerous anatomic terms are used to describe anterior cul-de-sac entry, including pubocervical fascia, vesicouterine fold, and vesicovaginal space. Which of these terms, if any, are correct? Is there a preferred term that should be used to teach future learners so we can all “speak” the same language?

What’s in a name?

ObGyns must thoroughly understand pelvic anatomy, since much of our patient care relates to structures in that region. We also must understand the terminology that most appropriately describes each pelvic structure so that we can communicate effectively with colleagues and other providers. The case described above lists several terms that are commonly found in gynecologic textbooks and surgical atlases to describe dissection for vaginal hysterectomy. Lack of a standardized vocabulary, however, often confuses teachers and learners alike, and it highlights the importance of having a universal language to ensure the safe, effective performance of surgical procedures.1

At first glance, it may seem that anatomic terms are inherently descriptive of the structure they represent; for example, the terms uterus and vagina seem rather obvious. However, many anatomic terms convey ambiguity. Which muscles, for example, constitute the levator ani: pubococcygeus, pubovisceral, pubovisceralis, puboperinealis, puboanalis, pubovaginalis, puborectalis, puborectal, iliococcygeus, ischiococcygeus? Do any of these terms redundantly describe the same structure, or does each term refer to an independent structure?

Standard terminology is essential

Anatomists long have recognized the need for standardized terminology to facilitate clear communication. To provide historical background, the term anatomy is derived from the Greek word for “dissection” or “to cut open.”2 Records on the scientific study of human anatomy date back thousands of years.

A brief review of current standardized terminology can be traced back to 1895, with the publication of Basle Terminologia Anatomica.3 That work was intended to provide a consolidated reference with clear direction regarding which anatomic terms should be used. It was updated several times during the ensuing century and was later published as Nomina Anatomica.

In 1990, an international committee was formed with representatives from many anatomical organizations, again with the intention of providing standardized anatomic terminology. Those efforts resulted in the publication of Terminologia Anatomica: International Anatomical Terminology, commonly referred to as TA, in 1998. TA continues to be the referent standard for human anatomic terminology; it was most recently updated in 2011.4

CASE 2 Conveying details of mesh erosion

A 52-year-old woman presents to the general gynecology clinic with a 10-year history of pelvic pain and dyspareunia after undergoing vaginal mesh surgery for prolapse and urinary incontinence. On examination, there is a visible ridge of mesh extending from the left side of the midurethra along the anterior and lateral vagina for a length of 1.5 cm. There also is a palpable tight band on the right vaginal wall near the ischial spine that reproduces her pain and causes spasm of the levator ani. You believe the patient needs a urogynecology referral for complications of vaginal mesh. How do you best describe your findings to your urogynecology colleague?

Continue to: Pelvic anatomy from the SGS perspective...

 

 

Pelvic anatomy from the SGS perspective

The Society of Gynecologic Surgeons (SGS) recognized the importance of standardizing terminology specific to the pelvis. The SGS Pelvic Anatomy Group thus was organized in 2016. The Pelvic Anatomy Group’s purpose is to help educate physicians about pelvic anatomy, with the overarching goal of compiling instructional materials, primarily from dissections (surgical or cadaveric), and radiologic imaging for all pelvic structures. Throughout the discussions on this initiative, it became clear that standardized terms needed to be established and used for pelvic structures.

While TA is an excellent reference work, it does not include all of the clinically relevant structures for gynecologic surgeons. As physicians, surgeons, and women’s health care providers, we read about and discuss pelvic anatomy structures in medical textbooks, medical literature, and clinical settings that are not necessarily included in TA. In addition, advances in information technology have facilitated the creation of clinically oriented computer-based anatomy programs and expanded the number and availability of electronic publications on surgical and clinical anatomy.5 As a result, there is a need not only to standardize nomenclature but also to continually revise and update terminology and integrate new terms, both from an anatomic and a clinical perspective.

The Pelvic Anatomy Group developed a novel approach to anatomic terminology. We decided to review the medical literature, identify the terms used, adjudicate the terms with current TA terms, and provide consensus for the terms and structures in the pelvis. Because of the volume of literature available and the existing number of terms, we divided the pelvis into 4 regions—anterior, apical, posterior, and vulvar—to improve the feasibility of reviewing the medical literature for the entire female pelvis.

Our process for tackling terminology

Our literature review started with the anterior compartment. (For complete details, see our prior publication.3) Modeled on a systematic review, we searched the MEDLINE database for terms related to the anterior pelvis, screened all associated abstracts, and then extracted terms from appropriate papers. We also identified several book chapters from various disciplines (anatomy, gynecology, urology, and radiology) to ensure wide representation of disciplines. We then extracted all terms pertinent to the anterior pelvis.

We organized the terms, with terms that referred to the same anatomic structure grouped together. Whenever possible, we used TA terms as the preferred terms. In this process, however, we identified several clinically relevant terms that were not included in TA: pelvic sidewall, pelvic bones, anterior compartment, pubourethral ligament, vaginal sulcus, and levator hiatus, among others. The new terms were then proposed and agreed on by members of the SGS Pelvic Anatomy Group and accepted by SGS members. We currently are completing a similar process for the apical pelvis, posterior pelvis, and vulvar regions.

TA code numbers pinpoint the nomenclature

As we move forward, we suggest that physicians use TA or other approved terms for patient and research communication. Such use will help standardize anatomic terms and also will improve communication between providers and education for learners.

Continue to: TA includes approved options...

 

 

TA includes approved options in English and Latin and lists a unique identification number for each term (shown in parentheses in the examples that follow). For instance, to answer the question posed earlier, the levator ani (A04.5.04.002) is comprised of the pubococcygeus (A04.5.04.003), puborectalis (A04.5.04.007), and iliococcygeus (A04.5.04.008) muscles (FIGURE 1).The terms pubovisceral and pubovisceralis are used synonymously in the literature with pubococcygeus (A04.5.04.003).3 The additional terms puboperinealis (A04.5.04.004), pubovaginalis (A04.5.04.005), and puboanalis (A04.5.04.006) are subcomponents of the pubococcygeus (A04.5.04.003), and this relationship is indicated in TA by indentation formatting.4 Finally, the ischiococcygeus (A04.5.04.011) muscle is not considered part of the levator ani (A04.5.04.002).

Revisiting the mesh erosion case: Reporting your findings

After reviewing the recommended terminology for the anterior pelvis,3,4 you might draft a report as follows: “A mesh erosion was visualized in anterior vaginal wall (A09.1.04.006) at the level of the mid-urethra extending into ‘anterior and lateral vaginal sulci’ (proposed term). In addition, there is a painful tight band in the ‘lateral vaginal wall’ (proposed term) near the ischial spine (A02.5.01.205). Palpation of this band reproduces the patient’s pain and causes secondary spasm of the levator ani (A04.5.04.002).” Certainly, TA identification numbers would not be expected to be included in medical communication; they are included here for reference.

From your description, your urogynecology colleague has a better understanding of the location of your patient’s vaginal mesh and requests her operative report from an outside facility. In the operative report, the surgeon described “placement of mesh into the vagina, dissection through the rectal spaces, and anchoring of the mesh into the levator/pelvic muscles, the cervix, and lastly to the paraurethral ligaments,” and “passage of trocars through the cave of Retzius at the level of the midurethra” (FIGURE 2).

Based on this description, the urogynecologist ascertains that the mesh is located in the anterior vaginal wall (A09.1.04.006), with passage of anchoring arms through the bilateral sacrospinous ligaments (A03.6.03.007) and retropubic space (A10.1.01.003). Exposed mesh is visible, extending from the midurethra to the “anterior and lateral vaginal sulci” (proposed term).

This case clearly demonstrates the importance of communication between providers for patient care, since understanding the patient’s anatomy and the location of the vaginal mesh is important for planning surgical excision of the exposed mesh.

Additional initiatives

Outlining standardized terminology is just the first step toward improving the anatomic “language” used among providers. Ongoing efforts from the SGS Pelvic Anatomy Group include a special imaging group’s review of imaging modalities (ultrasonography, magnetic resonance imaging, computerized tomography) to improve standardization on reporting clinical anatomy. In addition, SGS has developed a group to create educational content related to the structures identified by the terminology group from cadaveric or surgical dissections. Educational materials will be compiled to help physicians and learners expand their anatomic understanding and improve their communication.

Further details of the Pelvic Anatomy Group’s efforts can be found on the SGS website at https://www.sgsonline.org.

References
  1. American Association of Clinical Anatomists, Educational Affairs Committee. The clinical anatomy of several invasive procedures. Clin Anat. 1999;12:43-54. 
  2. Venes D, ed. Taber's Cyclopedic Medical Dictionary. 23rd ed. Philadelphia, PA: FA Davis Company; 2017. 
  3. Jeppson PC, Balgobin S, Washington BB, et al; for the Society of Gynecologic Surgeons Pelvic Anatomy Group. Recommended standardized terminology of the anterior female pelvis based on a structured medical literature review. Am J Obstet Gynecol. 2018;219:26-39. 
  4. Federative Committee on Anatomical Terminologies (FCAT). Terminologia Anatomica: International Anatomical Terminology. 2nd ed. Stuttgart, Germany: Thieme; 2011. 
  5. Rosse C. Terminologia Anatomica: considered from the perspective of next-generation knowledge sources. Clin Anat. 2001;14:120-133. 
     
Article PDF
Author and Disclosure Information

Peter C. Jeppson, MD; Audra Jolyn Hill, MD; Sunil Balgobin, MD

Dr. Jeppson is Assistant Professor, Division of Urogynecology, Department of Obstetrics and Gynecology, University of New Mexico School of Medicine, Albuquerque, New Mexico.

Dr. Hill is Assistant Professor, Division of Urogynecology, Department of Obstetrics and Gynecology, University of Utah School of Medicine, Salt Lake City, Utah.

Dr. Balgobin is Assistant Professor, Department of Obstetrics and Gynecology, Division of Female Pelvic Medicine and Reconstructive Surgery, University of Texas Southwestern Medical Center, Dallas Texas.

The authors report no financial relationships relevant to this article.

Issue
OBG Management - 31(4)
Publications
Topics
Page Number
SS4-SS7
Sections
Author and Disclosure Information

Peter C. Jeppson, MD; Audra Jolyn Hill, MD; Sunil Balgobin, MD

Dr. Jeppson is Assistant Professor, Division of Urogynecology, Department of Obstetrics and Gynecology, University of New Mexico School of Medicine, Albuquerque, New Mexico.

Dr. Hill is Assistant Professor, Division of Urogynecology, Department of Obstetrics and Gynecology, University of Utah School of Medicine, Salt Lake City, Utah.

Dr. Balgobin is Assistant Professor, Department of Obstetrics and Gynecology, Division of Female Pelvic Medicine and Reconstructive Surgery, University of Texas Southwestern Medical Center, Dallas Texas.

The authors report no financial relationships relevant to this article.

Author and Disclosure Information

Peter C. Jeppson, MD; Audra Jolyn Hill, MD; Sunil Balgobin, MD

Dr. Jeppson is Assistant Professor, Division of Urogynecology, Department of Obstetrics and Gynecology, University of New Mexico School of Medicine, Albuquerque, New Mexico.

Dr. Hill is Assistant Professor, Division of Urogynecology, Department of Obstetrics and Gynecology, University of Utah School of Medicine, Salt Lake City, Utah.

Dr. Balgobin is Assistant Professor, Department of Obstetrics and Gynecology, Division of Female Pelvic Medicine and Reconstructive Surgery, University of Texas Southwestern Medical Center, Dallas Texas.

The authors report no financial relationships relevant to this article.

Article PDF
Article PDF

CASE 1 Defining anatomic structures to assure surgical precision

A 44-year-old woman is scheduled for a vaginal hysterectomy and bilateral salpingectomy for abnormal uterine bleeding. In your academic practice, a resident routinely operates with you and is accompanied by a medical student. As this is your first case with each learner, you review the steps of the procedure along with pertinent anatomy. During this discussion, numerous anatomic terms are used to describe anterior cul-de-sac entry, including pubocervical fascia, vesicouterine fold, and vesicovaginal space. Which of these terms, if any, are correct? Is there a preferred term that should be used to teach future learners so we can all “speak” the same language?

What’s in a name?

ObGyns must thoroughly understand pelvic anatomy, since much of our patient care relates to structures in that region. We also must understand the terminology that most appropriately describes each pelvic structure so that we can communicate effectively with colleagues and other providers. The case described above lists several terms that are commonly found in gynecologic textbooks and surgical atlases to describe dissection for vaginal hysterectomy. Lack of a standardized vocabulary, however, often confuses teachers and learners alike, and it highlights the importance of having a universal language to ensure the safe, effective performance of surgical procedures.1

At first glance, it may seem that anatomic terms are inherently descriptive of the structure they represent; for example, the terms uterus and vagina seem rather obvious. However, many anatomic terms convey ambiguity. Which muscles, for example, constitute the levator ani: pubococcygeus, pubovisceral, pubovisceralis, puboperinealis, puboanalis, pubovaginalis, puborectalis, puborectal, iliococcygeus, ischiococcygeus? Do any of these terms redundantly describe the same structure, or does each term refer to an independent structure?

Standard terminology is essential

Anatomists long have recognized the need for standardized terminology to facilitate clear communication. To provide historical background, the term anatomy is derived from the Greek word for “dissection” or “to cut open.”2 Records on the scientific study of human anatomy date back thousands of years.

A brief review of current standardized terminology can be traced back to 1895, with the publication of Basle Terminologia Anatomica.3 That work was intended to provide a consolidated reference with clear direction regarding which anatomic terms should be used. It was updated several times during the ensuing century and was later published as Nomina Anatomica.

In 1990, an international committee was formed with representatives from many anatomical organizations, again with the intention of providing standardized anatomic terminology. Those efforts resulted in the publication of Terminologia Anatomica: International Anatomical Terminology, commonly referred to as TA, in 1998. TA continues to be the referent standard for human anatomic terminology; it was most recently updated in 2011.4

CASE 2 Conveying details of mesh erosion

A 52-year-old woman presents to the general gynecology clinic with a 10-year history of pelvic pain and dyspareunia after undergoing vaginal mesh surgery for prolapse and urinary incontinence. On examination, there is a visible ridge of mesh extending from the left side of the midurethra along the anterior and lateral vagina for a length of 1.5 cm. There also is a palpable tight band on the right vaginal wall near the ischial spine that reproduces her pain and causes spasm of the levator ani. You believe the patient needs a urogynecology referral for complications of vaginal mesh. How do you best describe your findings to your urogynecology colleague?

Continue to: Pelvic anatomy from the SGS perspective...

 

 

Pelvic anatomy from the SGS perspective

The Society of Gynecologic Surgeons (SGS) recognized the importance of standardizing terminology specific to the pelvis. The SGS Pelvic Anatomy Group thus was organized in 2016. The Pelvic Anatomy Group’s purpose is to help educate physicians about pelvic anatomy, with the overarching goal of compiling instructional materials, primarily from dissections (surgical or cadaveric), and radiologic imaging for all pelvic structures. Throughout the discussions on this initiative, it became clear that standardized terms needed to be established and used for pelvic structures.

While TA is an excellent reference work, it does not include all of the clinically relevant structures for gynecologic surgeons. As physicians, surgeons, and women’s health care providers, we read about and discuss pelvic anatomy structures in medical textbooks, medical literature, and clinical settings that are not necessarily included in TA. In addition, advances in information technology have facilitated the creation of clinically oriented computer-based anatomy programs and expanded the number and availability of electronic publications on surgical and clinical anatomy.5 As a result, there is a need not only to standardize nomenclature but also to continually revise and update terminology and integrate new terms, both from an anatomic and a clinical perspective.

The Pelvic Anatomy Group developed a novel approach to anatomic terminology. We decided to review the medical literature, identify the terms used, adjudicate the terms with current TA terms, and provide consensus for the terms and structures in the pelvis. Because of the volume of literature available and the existing number of terms, we divided the pelvis into 4 regions—anterior, apical, posterior, and vulvar—to improve the feasibility of reviewing the medical literature for the entire female pelvis.

Our process for tackling terminology

Our literature review started with the anterior compartment. (For complete details, see our prior publication.3) Modeled on a systematic review, we searched the MEDLINE database for terms related to the anterior pelvis, screened all associated abstracts, and then extracted terms from appropriate papers. We also identified several book chapters from various disciplines (anatomy, gynecology, urology, and radiology) to ensure wide representation of disciplines. We then extracted all terms pertinent to the anterior pelvis.

We organized the terms, with terms that referred to the same anatomic structure grouped together. Whenever possible, we used TA terms as the preferred terms. In this process, however, we identified several clinically relevant terms that were not included in TA: pelvic sidewall, pelvic bones, anterior compartment, pubourethral ligament, vaginal sulcus, and levator hiatus, among others. The new terms were then proposed and agreed on by members of the SGS Pelvic Anatomy Group and accepted by SGS members. We currently are completing a similar process for the apical pelvis, posterior pelvis, and vulvar regions.

TA code numbers pinpoint the nomenclature

As we move forward, we suggest that physicians use TA or other approved terms for patient and research communication. Such use will help standardize anatomic terms and also will improve communication between providers and education for learners.

Continue to: TA includes approved options...

 

 

TA includes approved options in English and Latin and lists a unique identification number for each term (shown in parentheses in the examples that follow). For instance, to answer the question posed earlier, the levator ani (A04.5.04.002) is comprised of the pubococcygeus (A04.5.04.003), puborectalis (A04.5.04.007), and iliococcygeus (A04.5.04.008) muscles (FIGURE 1).The terms pubovisceral and pubovisceralis are used synonymously in the literature with pubococcygeus (A04.5.04.003).3 The additional terms puboperinealis (A04.5.04.004), pubovaginalis (A04.5.04.005), and puboanalis (A04.5.04.006) are subcomponents of the pubococcygeus (A04.5.04.003), and this relationship is indicated in TA by indentation formatting.4 Finally, the ischiococcygeus (A04.5.04.011) muscle is not considered part of the levator ani (A04.5.04.002).

Revisiting the mesh erosion case: Reporting your findings

After reviewing the recommended terminology for the anterior pelvis,3,4 you might draft a report as follows: “A mesh erosion was visualized in anterior vaginal wall (A09.1.04.006) at the level of the mid-urethra extending into ‘anterior and lateral vaginal sulci’ (proposed term). In addition, there is a painful tight band in the ‘lateral vaginal wall’ (proposed term) near the ischial spine (A02.5.01.205). Palpation of this band reproduces the patient’s pain and causes secondary spasm of the levator ani (A04.5.04.002).” Certainly, TA identification numbers would not be expected to be included in medical communication; they are included here for reference.

From your description, your urogynecology colleague has a better understanding of the location of your patient’s vaginal mesh and requests her operative report from an outside facility. In the operative report, the surgeon described “placement of mesh into the vagina, dissection through the rectal spaces, and anchoring of the mesh into the levator/pelvic muscles, the cervix, and lastly to the paraurethral ligaments,” and “passage of trocars through the cave of Retzius at the level of the midurethra” (FIGURE 2).

Based on this description, the urogynecologist ascertains that the mesh is located in the anterior vaginal wall (A09.1.04.006), with passage of anchoring arms through the bilateral sacrospinous ligaments (A03.6.03.007) and retropubic space (A10.1.01.003). Exposed mesh is visible, extending from the midurethra to the “anterior and lateral vaginal sulci” (proposed term).

This case clearly demonstrates the importance of communication between providers for patient care, since understanding the patient’s anatomy and the location of the vaginal mesh is important for planning surgical excision of the exposed mesh.

Additional initiatives

Outlining standardized terminology is just the first step toward improving the anatomic “language” used among providers. Ongoing efforts from the SGS Pelvic Anatomy Group include a special imaging group’s review of imaging modalities (ultrasonography, magnetic resonance imaging, computerized tomography) to improve standardization on reporting clinical anatomy. In addition, SGS has developed a group to create educational content related to the structures identified by the terminology group from cadaveric or surgical dissections. Educational materials will be compiled to help physicians and learners expand their anatomic understanding and improve their communication.

Further details of the Pelvic Anatomy Group’s efforts can be found on the SGS website at https://www.sgsonline.org.

CASE 1 Defining anatomic structures to assure surgical precision

A 44-year-old woman is scheduled for a vaginal hysterectomy and bilateral salpingectomy for abnormal uterine bleeding. In your academic practice, a resident routinely operates with you and is accompanied by a medical student. As this is your first case with each learner, you review the steps of the procedure along with pertinent anatomy. During this discussion, numerous anatomic terms are used to describe anterior cul-de-sac entry, including pubocervical fascia, vesicouterine fold, and vesicovaginal space. Which of these terms, if any, are correct? Is there a preferred term that should be used to teach future learners so we can all “speak” the same language?

What’s in a name?

ObGyns must thoroughly understand pelvic anatomy, since much of our patient care relates to structures in that region. We also must understand the terminology that most appropriately describes each pelvic structure so that we can communicate effectively with colleagues and other providers. The case described above lists several terms that are commonly found in gynecologic textbooks and surgical atlases to describe dissection for vaginal hysterectomy. Lack of a standardized vocabulary, however, often confuses teachers and learners alike, and it highlights the importance of having a universal language to ensure the safe, effective performance of surgical procedures.1

At first glance, it may seem that anatomic terms are inherently descriptive of the structure they represent; for example, the terms uterus and vagina seem rather obvious. However, many anatomic terms convey ambiguity. Which muscles, for example, constitute the levator ani: pubococcygeus, pubovisceral, pubovisceralis, puboperinealis, puboanalis, pubovaginalis, puborectalis, puborectal, iliococcygeus, ischiococcygeus? Do any of these terms redundantly describe the same structure, or does each term refer to an independent structure?

Standard terminology is essential

Anatomists long have recognized the need for standardized terminology to facilitate clear communication. To provide historical background, the term anatomy is derived from the Greek word for “dissection” or “to cut open.”2 Records on the scientific study of human anatomy date back thousands of years.

A brief review of current standardized terminology can be traced back to 1895, with the publication of Basle Terminologia Anatomica.3 That work was intended to provide a consolidated reference with clear direction regarding which anatomic terms should be used. It was updated several times during the ensuing century and was later published as Nomina Anatomica.

In 1990, an international committee was formed with representatives from many anatomical organizations, again with the intention of providing standardized anatomic terminology. Those efforts resulted in the publication of Terminologia Anatomica: International Anatomical Terminology, commonly referred to as TA, in 1998. TA continues to be the referent standard for human anatomic terminology; it was most recently updated in 2011.4

CASE 2 Conveying details of mesh erosion

A 52-year-old woman presents to the general gynecology clinic with a 10-year history of pelvic pain and dyspareunia after undergoing vaginal mesh surgery for prolapse and urinary incontinence. On examination, there is a visible ridge of mesh extending from the left side of the midurethra along the anterior and lateral vagina for a length of 1.5 cm. There also is a palpable tight band on the right vaginal wall near the ischial spine that reproduces her pain and causes spasm of the levator ani. You believe the patient needs a urogynecology referral for complications of vaginal mesh. How do you best describe your findings to your urogynecology colleague?

Continue to: Pelvic anatomy from the SGS perspective...

 

 

Pelvic anatomy from the SGS perspective

The Society of Gynecologic Surgeons (SGS) recognized the importance of standardizing terminology specific to the pelvis. The SGS Pelvic Anatomy Group thus was organized in 2016. The Pelvic Anatomy Group’s purpose is to help educate physicians about pelvic anatomy, with the overarching goal of compiling instructional materials, primarily from dissections (surgical or cadaveric), and radiologic imaging for all pelvic structures. Throughout the discussions on this initiative, it became clear that standardized terms needed to be established and used for pelvic structures.

While TA is an excellent reference work, it does not include all of the clinically relevant structures for gynecologic surgeons. As physicians, surgeons, and women’s health care providers, we read about and discuss pelvic anatomy structures in medical textbooks, medical literature, and clinical settings that are not necessarily included in TA. In addition, advances in information technology have facilitated the creation of clinically oriented computer-based anatomy programs and expanded the number and availability of electronic publications on surgical and clinical anatomy.5 As a result, there is a need not only to standardize nomenclature but also to continually revise and update terminology and integrate new terms, both from an anatomic and a clinical perspective.

The Pelvic Anatomy Group developed a novel approach to anatomic terminology. We decided to review the medical literature, identify the terms used, adjudicate the terms with current TA terms, and provide consensus for the terms and structures in the pelvis. Because of the volume of literature available and the existing number of terms, we divided the pelvis into 4 regions—anterior, apical, posterior, and vulvar—to improve the feasibility of reviewing the medical literature for the entire female pelvis.

Our process for tackling terminology

Our literature review started with the anterior compartment. (For complete details, see our prior publication.3) Modeled on a systematic review, we searched the MEDLINE database for terms related to the anterior pelvis, screened all associated abstracts, and then extracted terms from appropriate papers. We also identified several book chapters from various disciplines (anatomy, gynecology, urology, and radiology) to ensure wide representation of disciplines. We then extracted all terms pertinent to the anterior pelvis.

We organized the terms, with terms that referred to the same anatomic structure grouped together. Whenever possible, we used TA terms as the preferred terms. In this process, however, we identified several clinically relevant terms that were not included in TA: pelvic sidewall, pelvic bones, anterior compartment, pubourethral ligament, vaginal sulcus, and levator hiatus, among others. The new terms were then proposed and agreed on by members of the SGS Pelvic Anatomy Group and accepted by SGS members. We currently are completing a similar process for the apical pelvis, posterior pelvis, and vulvar regions.

TA code numbers pinpoint the nomenclature

As we move forward, we suggest that physicians use TA or other approved terms for patient and research communication. Such use will help standardize anatomic terms and also will improve communication between providers and education for learners.

Continue to: TA includes approved options...

 

 

TA includes approved options in English and Latin and lists a unique identification number for each term (shown in parentheses in the examples that follow). For instance, to answer the question posed earlier, the levator ani (A04.5.04.002) is comprised of the pubococcygeus (A04.5.04.003), puborectalis (A04.5.04.007), and iliococcygeus (A04.5.04.008) muscles (FIGURE 1).The terms pubovisceral and pubovisceralis are used synonymously in the literature with pubococcygeus (A04.5.04.003).3 The additional terms puboperinealis (A04.5.04.004), pubovaginalis (A04.5.04.005), and puboanalis (A04.5.04.006) are subcomponents of the pubococcygeus (A04.5.04.003), and this relationship is indicated in TA by indentation formatting.4 Finally, the ischiococcygeus (A04.5.04.011) muscle is not considered part of the levator ani (A04.5.04.002).

Revisiting the mesh erosion case: Reporting your findings

After reviewing the recommended terminology for the anterior pelvis,3,4 you might draft a report as follows: “A mesh erosion was visualized in anterior vaginal wall (A09.1.04.006) at the level of the mid-urethra extending into ‘anterior and lateral vaginal sulci’ (proposed term). In addition, there is a painful tight band in the ‘lateral vaginal wall’ (proposed term) near the ischial spine (A02.5.01.205). Palpation of this band reproduces the patient’s pain and causes secondary spasm of the levator ani (A04.5.04.002).” Certainly, TA identification numbers would not be expected to be included in medical communication; they are included here for reference.

From your description, your urogynecology colleague has a better understanding of the location of your patient’s vaginal mesh and requests her operative report from an outside facility. In the operative report, the surgeon described “placement of mesh into the vagina, dissection through the rectal spaces, and anchoring of the mesh into the levator/pelvic muscles, the cervix, and lastly to the paraurethral ligaments,” and “passage of trocars through the cave of Retzius at the level of the midurethra” (FIGURE 2).

Based on this description, the urogynecologist ascertains that the mesh is located in the anterior vaginal wall (A09.1.04.006), with passage of anchoring arms through the bilateral sacrospinous ligaments (A03.6.03.007) and retropubic space (A10.1.01.003). Exposed mesh is visible, extending from the midurethra to the “anterior and lateral vaginal sulci” (proposed term).

This case clearly demonstrates the importance of communication between providers for patient care, since understanding the patient’s anatomy and the location of the vaginal mesh is important for planning surgical excision of the exposed mesh.

Additional initiatives

Outlining standardized terminology is just the first step toward improving the anatomic “language” used among providers. Ongoing efforts from the SGS Pelvic Anatomy Group include a special imaging group’s review of imaging modalities (ultrasonography, magnetic resonance imaging, computerized tomography) to improve standardization on reporting clinical anatomy. In addition, SGS has developed a group to create educational content related to the structures identified by the terminology group from cadaveric or surgical dissections. Educational materials will be compiled to help physicians and learners expand their anatomic understanding and improve their communication.

Further details of the Pelvic Anatomy Group’s efforts can be found on the SGS website at https://www.sgsonline.org.

References
  1. American Association of Clinical Anatomists, Educational Affairs Committee. The clinical anatomy of several invasive procedures. Clin Anat. 1999;12:43-54. 
  2. Venes D, ed. Taber's Cyclopedic Medical Dictionary. 23rd ed. Philadelphia, PA: FA Davis Company; 2017. 
  3. Jeppson PC, Balgobin S, Washington BB, et al; for the Society of Gynecologic Surgeons Pelvic Anatomy Group. Recommended standardized terminology of the anterior female pelvis based on a structured medical literature review. Am J Obstet Gynecol. 2018;219:26-39. 
  4. Federative Committee on Anatomical Terminologies (FCAT). Terminologia Anatomica: International Anatomical Terminology. 2nd ed. Stuttgart, Germany: Thieme; 2011. 
  5. Rosse C. Terminologia Anatomica: considered from the perspective of next-generation knowledge sources. Clin Anat. 2001;14:120-133. 
     
References
  1. American Association of Clinical Anatomists, Educational Affairs Committee. The clinical anatomy of several invasive procedures. Clin Anat. 1999;12:43-54. 
  2. Venes D, ed. Taber's Cyclopedic Medical Dictionary. 23rd ed. Philadelphia, PA: FA Davis Company; 2017. 
  3. Jeppson PC, Balgobin S, Washington BB, et al; for the Society of Gynecologic Surgeons Pelvic Anatomy Group. Recommended standardized terminology of the anterior female pelvis based on a structured medical literature review. Am J Obstet Gynecol. 2018;219:26-39. 
  4. Federative Committee on Anatomical Terminologies (FCAT). Terminologia Anatomica: International Anatomical Terminology. 2nd ed. Stuttgart, Germany: Thieme; 2011. 
  5. Rosse C. Terminologia Anatomica: considered from the perspective of next-generation knowledge sources. Clin Anat. 2001;14:120-133. 
     
Issue
OBG Management - 31(4)
Issue
OBG Management - 31(4)
Page Number
SS4-SS7
Page Number
SS4-SS7
Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Article PDF Media