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Urinary incontinence
Editor’s Note: This is the first installment of a six-part series that will review key concepts and articles that ob.gyns. can use to prepare for the American Board of Obstetrics and Gynecology Maintenance of Certification examination. The series is adapted from Ob/Gyn Board Master (obgynboardmaster.com), an online board review course created by Erudyte Inc. The series will cover key topics across the specialty, as well as general test-taking and study tips. This month’s edition of the Board Exam Corner focuses on urinary incontinence.
The literature
The American College of Obstetricians and Gynecologists and the American Urogynecologic Society recently published an updated Practice Bulletin regarding the diagnosis and management of urinary incontinence. Practice Bulletin No. 155 was also a maintenance of certification (MOC) assignment for 2016. The contents of this article are critical as urinary incontinence is a prevalent and treatable condition, and it will likely be part of this year’s board examination. This month’s Board Corner will review the key elements of the updated guidelines.
Let’s begin with a possible medical board question: An 80-year old patient has urinary leakage as a result of severe arthritis and poor vision, and is unable to reach the bathroom in time. What is the diagnosis?
A. Mixed urinary incontinence
B. Extraurethral incontinence
C. Functional incontinence
D. Postural incontinence
E. Ectopic ureter
The answer is C.
Functional incontinence occurs because of cognitive or mobility impairments in the presence of an intact lower urinary tract. The patient in the vignette has “restricted mobility” and a physical impairment that leads to urinary incontinence.
A is incorrect because mixed incontinence is an involuntary loss of urine associated with urgency and with physical exertion.
B and E are incorrect because extraurethral incontinence is urine leakage through channels other than the urethral meatus (e.g., vesicovaginal fistula or ectopic ureter).
D is incorrect because postural incontinence is the involuntary loss of urine associated with change in body positions (e.g., from sitting to standing).
The key points to remember are:
• Urinary incontinence is a prevalent condition that is treatable despite what many women believe.
• There are several types of incontinence but the main types are stress, urgency, and mixed incontinence.
• Basic office evaluation includes urinalysis and postvoid residual, but not urodynamics or cystoscopy.
• Treatment of stress incontinence includes weight loss, fluid management, pelvic floor muscle exercises (with or without assistance from a physical therapist), and suburethral sling or bulking agent injections.
• Treatment of urgency urinary incontinence includes bladder training, fluid management, decreasing caffeine, antimuscarinic and beta-3 agonists, and third-line treatments (botulinum toxin A injection, sacral neuromodulation, or tibial nerve stimulation).
• The mnemonic DIAPPERS is useful in remembering all of the reversible, nongenitourinary (i.e., functional) causes of incontinence. 
Test-taking tip of the month
If you finish the test early, take the time to go back to any question for which you made an educated guess. Reread the question carefully. Don’t change your answer unless there is a very good reason for doing so because your first impression is usually the right one. Don’t change an answer just because you have a gut feeling. However, there are good reasons to change your answers when you go back. For instance, consider changing your answer if rereading the question helped you to better understand what is being asked, if you reconsidered and conceptualized a better answer, if you remembered a new piece of information, or if you learned something from a later question that will help you better answer the earlier question.
Reference
Obstet Gynecol. 2015 Nov;126(5): e66-81.
Dr. Sam Siddighi is editor-in-chief of the Ob/Gyn Board Master and director of female pelvic medicine and reconstructive surgery and director of grand rounds at Loma Linda University Health in California. Ob.Gyn. News and Ob/Gyn Board Master are owned by the same parent company, Frontline Medical Communications.
Editor’s Note: This is the first installment of a six-part series that will review key concepts and articles that ob.gyns. can use to prepare for the American Board of Obstetrics and Gynecology Maintenance of Certification examination. The series is adapted from Ob/Gyn Board Master (obgynboardmaster.com), an online board review course created by Erudyte Inc. The series will cover key topics across the specialty, as well as general test-taking and study tips. This month’s edition of the Board Exam Corner focuses on urinary incontinence.
The literature
The American College of Obstetricians and Gynecologists and the American Urogynecologic Society recently published an updated Practice Bulletin regarding the diagnosis and management of urinary incontinence. Practice Bulletin No. 155 was also a maintenance of certification (MOC) assignment for 2016. The contents of this article are critical as urinary incontinence is a prevalent and treatable condition, and it will likely be part of this year’s board examination. This month’s Board Corner will review the key elements of the updated guidelines.
Let’s begin with a possible medical board question: An 80-year old patient has urinary leakage as a result of severe arthritis and poor vision, and is unable to reach the bathroom in time. What is the diagnosis?
A. Mixed urinary incontinence
B. Extraurethral incontinence
C. Functional incontinence
D. Postural incontinence
E. Ectopic ureter
The answer is C.
Functional incontinence occurs because of cognitive or mobility impairments in the presence of an intact lower urinary tract. The patient in the vignette has “restricted mobility” and a physical impairment that leads to urinary incontinence.
A is incorrect because mixed incontinence is an involuntary loss of urine associated with urgency and with physical exertion.
B and E are incorrect because extraurethral incontinence is urine leakage through channels other than the urethral meatus (e.g., vesicovaginal fistula or ectopic ureter).
D is incorrect because postural incontinence is the involuntary loss of urine associated with change in body positions (e.g., from sitting to standing).
The key points to remember are:
• Urinary incontinence is a prevalent condition that is treatable despite what many women believe.
• There are several types of incontinence but the main types are stress, urgency, and mixed incontinence.
• Basic office evaluation includes urinalysis and postvoid residual, but not urodynamics or cystoscopy.
• Treatment of stress incontinence includes weight loss, fluid management, pelvic floor muscle exercises (with or without assistance from a physical therapist), and suburethral sling or bulking agent injections.
• Treatment of urgency urinary incontinence includes bladder training, fluid management, decreasing caffeine, antimuscarinic and beta-3 agonists, and third-line treatments (botulinum toxin A injection, sacral neuromodulation, or tibial nerve stimulation).
• The mnemonic DIAPPERS is useful in remembering all of the reversible, nongenitourinary (i.e., functional) causes of incontinence.
Test-taking tip of the month
If you finish the test early, take the time to go back to any question for which you made an educated guess. Reread the question carefully. Don’t change your answer unless there is a very good reason for doing so because your first impression is usually the right one. Don’t change an answer just because you have a gut feeling. However, there are good reasons to change your answers when you go back. For instance, consider changing your answer if rereading the question helped you to better understand what is being asked, if you reconsidered and conceptualized a better answer, if you remembered a new piece of information, or if you learned something from a later question that will help you better answer the earlier question.
Reference
Obstet Gynecol. 2015 Nov;126(5): e66-81.
Dr. Sam Siddighi is editor-in-chief of the Ob/Gyn Board Master and director of female pelvic medicine and reconstructive surgery and director of grand rounds at Loma Linda University Health in California. Ob.Gyn. News and Ob/Gyn Board Master are owned by the same parent company, Frontline Medical Communications.
Editor’s Note: This is the first installment of a six-part series that will review key concepts and articles that ob.gyns. can use to prepare for the American Board of Obstetrics and Gynecology Maintenance of Certification examination. The series is adapted from Ob/Gyn Board Master (obgynboardmaster.com), an online board review course created by Erudyte Inc. The series will cover key topics across the specialty, as well as general test-taking and study tips. This month’s edition of the Board Exam Corner focuses on urinary incontinence.
The literature
The American College of Obstetricians and Gynecologists and the American Urogynecologic Society recently published an updated Practice Bulletin regarding the diagnosis and management of urinary incontinence. Practice Bulletin No. 155 was also a maintenance of certification (MOC) assignment for 2016. The contents of this article are critical as urinary incontinence is a prevalent and treatable condition, and it will likely be part of this year’s board examination. This month’s Board Corner will review the key elements of the updated guidelines.
Let’s begin with a possible medical board question: An 80-year old patient has urinary leakage as a result of severe arthritis and poor vision, and is unable to reach the bathroom in time. What is the diagnosis?
A. Mixed urinary incontinence
B. Extraurethral incontinence
C. Functional incontinence
D. Postural incontinence
E. Ectopic ureter
The answer is C.
Functional incontinence occurs because of cognitive or mobility impairments in the presence of an intact lower urinary tract. The patient in the vignette has “restricted mobility” and a physical impairment that leads to urinary incontinence.
A is incorrect because mixed incontinence is an involuntary loss of urine associated with urgency and with physical exertion.
B and E are incorrect because extraurethral incontinence is urine leakage through channels other than the urethral meatus (e.g., vesicovaginal fistula or ectopic ureter).
D is incorrect because postural incontinence is the involuntary loss of urine associated with change in body positions (e.g., from sitting to standing).
The key points to remember are:
• Urinary incontinence is a prevalent condition that is treatable despite what many women believe.
• There are several types of incontinence but the main types are stress, urgency, and mixed incontinence.
• Basic office evaluation includes urinalysis and postvoid residual, but not urodynamics or cystoscopy.
• Treatment of stress incontinence includes weight loss, fluid management, pelvic floor muscle exercises (with or without assistance from a physical therapist), and suburethral sling or bulking agent injections.
• Treatment of urgency urinary incontinence includes bladder training, fluid management, decreasing caffeine, antimuscarinic and beta-3 agonists, and third-line treatments (botulinum toxin A injection, sacral neuromodulation, or tibial nerve stimulation).
• The mnemonic DIAPPERS is useful in remembering all of the reversible, nongenitourinary (i.e., functional) causes of incontinence.
Test-taking tip of the month
If you finish the test early, take the time to go back to any question for which you made an educated guess. Reread the question carefully. Don’t change your answer unless there is a very good reason for doing so because your first impression is usually the right one. Don’t change an answer just because you have a gut feeling. However, there are good reasons to change your answers when you go back. For instance, consider changing your answer if rereading the question helped you to better understand what is being asked, if you reconsidered and conceptualized a better answer, if you remembered a new piece of information, or if you learned something from a later question that will help you better answer the earlier question.
Reference
Obstet Gynecol. 2015 Nov;126(5): e66-81.
Dr. Sam Siddighi is editor-in-chief of the Ob/Gyn Board Master and director of female pelvic medicine and reconstructive surgery and director of grand rounds at Loma Linda University Health in California. Ob.Gyn. News and Ob/Gyn Board Master are owned by the same parent company, Frontline Medical Communications.
VIDEO: New antisense inhibitor nets impressive reductions in lipids
NEW ORLEANS – A new antisense inhibitor to angiopoietinlike protein 3 (ANGPTL3) reduces lipids in healthy adults with elevated triglyceride levels, according to results of a phase I/IIa ascending-dose trial reported at the American Heart Association scientific sessions.
ANGPTL3 regulates lipid and possibly general metabolism through actions in the liver, gut, muscle, and adipose tissue, explained presenting author Sotirios Tsimikas, MD, an investigator with Ionis Pharmaceuticals, Carlsbad, Calif., and a professor of medicine and director of vascular medicine at the University of California, San Diego. Individuals having loss-of-function mutations in the gene encoding this protein have very low plasma levels of cholesterol and triglycerides.
In the trial, sponsored by Ionis Pharmaceuticals, 32 healthy volunteers with elevated triglyceride levels were treated with various doses of the antisense inhibitor, called IONIS-ANGPTL3-LRx, or a placebo, given by weekly subcutaneous injections for 6 weeks.
Results showed that participants treated at the higher-dose levels had a reduction from baseline of 66% in triglycerides, 68% in apoliprotein C-III (ApoC-III), 35% in LDL cholesterol, 36% in total cholesterol, and 40% in non-HDL cholesterol, as well as 25% in HDL cholesterol, Dr. Tsimikas reported. They also had reductions in apolipoprotein B (ApoB).
“All these lipid parameters are really going in the right direction in terms of postulating potential clinical benefit,” he commented.
Safety and tolerability results showed that only a single participant experienced a local injection site adverse event related to the inhibitor (erythema and pruritus). None experienced flulike symptoms, platelet reductions, or serious adverse events, and none left the study because of adverse events.
“Among all known therapies that lower triglycerides, this [IONIS-ANGPTL3-LRx] is also associated with a reduction not only in LDL cholesterol levels, but also in ApoB as well, which portends well for future outcomes trials,” noted Dr. Tsimikas.
“We think this is going to be a promising candidate for patients who have uncontrolled LDL cholesterol, elevated triglycerides, and possibly patients who have hepatic steatosis and NASH [nonalcoholic steatohepatitis],” he concluded.
Dr. Tsimikas, who is an employee of and shareholder in the trial’s sponsor, Ionis Pharmaceuticals, discussed his findings in a video interview.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
The trial shows a very clear proof of concept in regards to the effects on lipids.
In contrast to agents that increase LDL receptor levels (statins, proprotein convertase subtilisin/kexin type 9 [PCSK9] inhibitors, bile acid–binding resins, and ezetimibe), IONIS-ANGPTL3-LRx produces greater reductions in non-HDL cholesterol than in LDL cholesterol, suggesting different mechanisms are at work.
But the key issue at this point is to ascertain the longer-term safety of IONIS-ANGPTL3-LRx in the liver and other organs.
One of the most impressive aspects of the combination of biotechnology and genetics is how rapidly you can come to a proof of concept in humans, and this is unprecedented, compared with what we have seen over the last 20 or 30 years. Unfortunately, the determination of safety is not quite as rapid, and it takes large numbers and long duration of follow-up. Obviously, we need that in terms of understanding benefits and risks.
Christie M. Ballantyne, MD, director of the Center for Cardiovascular Disease Prevention at the Methodist DeBakey Heart Center, Baylor College of Medicine in Houston, made these comments as the invited discussant. He has been a consultant to and received research support from trial sponsor Ionis Pharmaceuticals.
The trial shows a very clear proof of concept in regards to the effects on lipids.
In contrast to agents that increase LDL receptor levels (statins, proprotein convertase subtilisin/kexin type 9 [PCSK9] inhibitors, bile acid–binding resins, and ezetimibe), IONIS-ANGPTL3-LRx produces greater reductions in non-HDL cholesterol than in LDL cholesterol, suggesting different mechanisms are at work.
But the key issue at this point is to ascertain the longer-term safety of IONIS-ANGPTL3-LRx in the liver and other organs.
One of the most impressive aspects of the combination of biotechnology and genetics is how rapidly you can come to a proof of concept in humans, and this is unprecedented, compared with what we have seen over the last 20 or 30 years. Unfortunately, the determination of safety is not quite as rapid, and it takes large numbers and long duration of follow-up. Obviously, we need that in terms of understanding benefits and risks.
Christie M. Ballantyne, MD, director of the Center for Cardiovascular Disease Prevention at the Methodist DeBakey Heart Center, Baylor College of Medicine in Houston, made these comments as the invited discussant. He has been a consultant to and received research support from trial sponsor Ionis Pharmaceuticals.
The trial shows a very clear proof of concept in regards to the effects on lipids.
In contrast to agents that increase LDL receptor levels (statins, proprotein convertase subtilisin/kexin type 9 [PCSK9] inhibitors, bile acid–binding resins, and ezetimibe), IONIS-ANGPTL3-LRx produces greater reductions in non-HDL cholesterol than in LDL cholesterol, suggesting different mechanisms are at work.
But the key issue at this point is to ascertain the longer-term safety of IONIS-ANGPTL3-LRx in the liver and other organs.
One of the most impressive aspects of the combination of biotechnology and genetics is how rapidly you can come to a proof of concept in humans, and this is unprecedented, compared with what we have seen over the last 20 or 30 years. Unfortunately, the determination of safety is not quite as rapid, and it takes large numbers and long duration of follow-up. Obviously, we need that in terms of understanding benefits and risks.
Christie M. Ballantyne, MD, director of the Center for Cardiovascular Disease Prevention at the Methodist DeBakey Heart Center, Baylor College of Medicine in Houston, made these comments as the invited discussant. He has been a consultant to and received research support from trial sponsor Ionis Pharmaceuticals.
NEW ORLEANS – A new antisense inhibitor to angiopoietinlike protein 3 (ANGPTL3) reduces lipids in healthy adults with elevated triglyceride levels, according to results of a phase I/IIa ascending-dose trial reported at the American Heart Association scientific sessions.
ANGPTL3 regulates lipid and possibly general metabolism through actions in the liver, gut, muscle, and adipose tissue, explained presenting author Sotirios Tsimikas, MD, an investigator with Ionis Pharmaceuticals, Carlsbad, Calif., and a professor of medicine and director of vascular medicine at the University of California, San Diego. Individuals having loss-of-function mutations in the gene encoding this protein have very low plasma levels of cholesterol and triglycerides.
In the trial, sponsored by Ionis Pharmaceuticals, 32 healthy volunteers with elevated triglyceride levels were treated with various doses of the antisense inhibitor, called IONIS-ANGPTL3-LRx, or a placebo, given by weekly subcutaneous injections for 6 weeks.
Results showed that participants treated at the higher-dose levels had a reduction from baseline of 66% in triglycerides, 68% in apoliprotein C-III (ApoC-III), 35% in LDL cholesterol, 36% in total cholesterol, and 40% in non-HDL cholesterol, as well as 25% in HDL cholesterol, Dr. Tsimikas reported. They also had reductions in apolipoprotein B (ApoB).
“All these lipid parameters are really going in the right direction in terms of postulating potential clinical benefit,” he commented.
Safety and tolerability results showed that only a single participant experienced a local injection site adverse event related to the inhibitor (erythema and pruritus). None experienced flulike symptoms, platelet reductions, or serious adverse events, and none left the study because of adverse events.
“Among all known therapies that lower triglycerides, this [IONIS-ANGPTL3-LRx] is also associated with a reduction not only in LDL cholesterol levels, but also in ApoB as well, which portends well for future outcomes trials,” noted Dr. Tsimikas.
“We think this is going to be a promising candidate for patients who have uncontrolled LDL cholesterol, elevated triglycerides, and possibly patients who have hepatic steatosis and NASH [nonalcoholic steatohepatitis],” he concluded.
Dr. Tsimikas, who is an employee of and shareholder in the trial’s sponsor, Ionis Pharmaceuticals, discussed his findings in a video interview.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
NEW ORLEANS – A new antisense inhibitor to angiopoietinlike protein 3 (ANGPTL3) reduces lipids in healthy adults with elevated triglyceride levels, according to results of a phase I/IIa ascending-dose trial reported at the American Heart Association scientific sessions.
ANGPTL3 regulates lipid and possibly general metabolism through actions in the liver, gut, muscle, and adipose tissue, explained presenting author Sotirios Tsimikas, MD, an investigator with Ionis Pharmaceuticals, Carlsbad, Calif., and a professor of medicine and director of vascular medicine at the University of California, San Diego. Individuals having loss-of-function mutations in the gene encoding this protein have very low plasma levels of cholesterol and triglycerides.
In the trial, sponsored by Ionis Pharmaceuticals, 32 healthy volunteers with elevated triglyceride levels were treated with various doses of the antisense inhibitor, called IONIS-ANGPTL3-LRx, or a placebo, given by weekly subcutaneous injections for 6 weeks.
Results showed that participants treated at the higher-dose levels had a reduction from baseline of 66% in triglycerides, 68% in apoliprotein C-III (ApoC-III), 35% in LDL cholesterol, 36% in total cholesterol, and 40% in non-HDL cholesterol, as well as 25% in HDL cholesterol, Dr. Tsimikas reported. They also had reductions in apolipoprotein B (ApoB).
“All these lipid parameters are really going in the right direction in terms of postulating potential clinical benefit,” he commented.
Safety and tolerability results showed that only a single participant experienced a local injection site adverse event related to the inhibitor (erythema and pruritus). None experienced flulike symptoms, platelet reductions, or serious adverse events, and none left the study because of adverse events.
“Among all known therapies that lower triglycerides, this [IONIS-ANGPTL3-LRx] is also associated with a reduction not only in LDL cholesterol levels, but also in ApoB as well, which portends well for future outcomes trials,” noted Dr. Tsimikas.
“We think this is going to be a promising candidate for patients who have uncontrolled LDL cholesterol, elevated triglycerides, and possibly patients who have hepatic steatosis and NASH [nonalcoholic steatohepatitis],” he concluded.
Dr. Tsimikas, who is an employee of and shareholder in the trial’s sponsor, Ionis Pharmaceuticals, discussed his findings in a video interview.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
AT THE AHA SCIENTIFIC SESSIONS
Key clinical point:
Major finding: Treatment was associated with reductions in levels of triglycerides (–66%), ApoC-III (–68%), LDL cholesterol (–35%), total cholesterol (–36%), and non-HDL cholesterol (–40%), as well as levels of HDL cholesterol (–25%).
Data source: A phase I/IIa ascending-dose trial among 32 healthy adults with hypertriglyceridemia.
Disclosures: Dr. Tsimikas is an employee of and shareholder in Ionis Pharmaceuticals, which sponsored the trial.
Addressing Sexual Health With Patients
Why start this new column on mental health with an article that focuses on sexual health? Surely that is the domain of family practice, urology, gynecology, endocrinology, or some other discipline. While it is true that all these disciplines and many others are central to the diagnosis and treatment of sexual health, mental health providers need to be an integral part of the conversations.
I have a problem with arbitrarily separating mental health and behavioral health from physical health. Mental health is directly affected by physical health and vice versa. If a woman has a urinary tract infection, she is not feeling mentally or sexually healthy. If a man has erectile dysfunction (ED), he seldom is at the top of his game emotionally. For our war-wounded who lack limbs or who have genitourinary injuries, optimal sexual functioning can be a challenge.
I am probably preaching to the choir here, so I will not belabor the point. However, I will develop this point by using lessons learned from combat-injured service members, the psychiatric adverse effects (AEs) of commonly used psychiatric medications, and most important, asking about sexual health as part of taking a mental health history.
The War-Wounded
Since 9/11, 2.7 million U.S. service members have served in wars. Much discussion has been focused on posttraumatic stress disorder (PTSD) and traumatic brain injury (TBI), the invisible wounds of war. Probably about 25% of service members who have been deployed have PTSD, and about 300,000 service members have TBI.1 About 50,000 have other physical injuries. These injuries directly affect intimate relationships.
The signature weapon of the wars in Iraq and Afghanistan was the bomb, or improvised explosive device. Motor vehicle accidents and gunshot wounds also have added to the myriad of injuries. Physical war wounds involve sexual functioning. These include, but are not limited to, lower extremity amputations, genitourinary injuries, and facial disfigurement or burns. All of these may involve multiple surgeries, pain, and disability and can significantly impact self-esteem.
One of the many lessons I have learned in putting together my most recent book, Intimacy Post Injury: Combat Trauma and Sexual Health, is that there is a void in the recent general medical and popular literature about optimizing sexual health in those with injuries or diseases.2 The majority of wounded warriors are men, but injuries happen to women service members as well. Of course, sexual assault causes severe harm to intimate relationships as well.
At this time, most injured personnel are still in the Military Health System (MHS) or have transitioned to the VHA. However, many service members also will be treated in the civilian health system.
Psychiatric Medications and Sexual Adverse Effects
The treatment of PTSD, depression, and other psychiatric conditions often involves medications that have sexual AEs. Sexual AEs usually refer to problems with erectile function (impotence), difficulties with ejaculation, lack of orgasm or desire, or lack of lubrication for women. Selective serotonin reuptake inhibitors (SSRIs) have a very high incidence of sexual AEs, ranging from 30% to 70%.3 When I speak with clinicians about their anecdotal experience, the percentage always is high, usually more than 50%. Other psychiatric medications, such as antipsychotics, older antidepressants, and stimulants also have sexual AEs, and narcotics are notorious for their sexual AEs.
Fortunately, many solutions exist. For SSRIs, the solutions include lowering the dose of the offending agent, switching to another agent, drug holidays, or adding other medications, such as bupropion or cyproheptadine. Family practice and other physicians are very familiar with phosphodiesterase inhibitors, such as sildenafil, tadalafil, and vardenafil. Although these medications have AEs and are very expensive, they work well for impotence.
Other solutions are nonpharmacologic: Setting aside time for intimacy can be crucial. Gels and creams can help with lubrication. Communication with providers and between partners and families is the most important ingredient.
Asking About Sexual Health
I encourage all medical personnel who treat active-duty service members or veterans to (1) discuss sexual health with their patients; (2) learn the basics of how to evaluate, treat, or refer ED, including SSRI AEs; and (3) understand how to discuss the effects of physical injury, pain, and disability on sexual functioning.
The conversation should touch on sexual activity, satisfaction with intimacy, exposure to sexually transmitted diseases, and if appropriate, previous sexual abuse. The appropriate time and place for a conversation about sexual health depends on the setting. In the outpatient setting, I bring up the subject after I ask about sleep and appetite and before I ask about suicidal and homicidal thoughts; others may choose elsewhere in the patient history. However, asking about sexual issues may or may not be appropriate in an emergency department situation.
Providers often are uncomfortable with asking about sexual issues, perhaps more so if they are young and female and the patient is older and male. Therefore, I encourage expanded training in medical school and throughout residency.
Sexual Difficulties and Suicide
In the military, the suicide rate has been rising from about 10 per 100,000 per year in 2004 to about 20 per 20,000 in this decade.4,5 According to the VA Office of Suicide Prevention, about 20 veterans die by suicide daily.6 One question that has received little attention is the relationship between sexual difficulties and suicide. Although there has been an important focus on causes of suicide in the military and veterans, little is known about the important issue of how many service members die by suicide because of impotence.
We do know a lot about the big picture as to why service members die by suicide. In about two-thirds of the completed suicides, there were relationship issues. In addition, there are often legal, occupational, and financial difficulties. About two-thirds of service members die by suicide using firearms. Jumping and strangulation are other common methods.4,5
But there is much we do not know. What percentage of relationship difficulties are related to sexual dysfunction? Is ED the straw that breaks the camel’s back and leads to the shot to the chest? Other subjects outside the scope of this column (but included in Intimacy Post Injury) include sexual therapy, fertility, adaptations for those with disabilities, reproductive AEs of toxin exposure, and surgeries that include penile transplantation.
My hypothesis is that sexual problems, specifically ED or impotence, contribute to feelings of failure and inadequacy and thus to suicidal or homicidal thoughts.
Conclusion
Health care providers do not always talk to patients about their sexual health and may barely mention the sexual AEs of psychiatric or other medications. In whatever setting you practice, you should not neglect asking questions about sexual health, as it is a critical issue for many of our patients and should be for us.
1. Committee on the Assessment of Ongoing Efforts in the Treatment of Posttraumatic Stress Disorder, Board of Health of Selected Populations. Treatment of Posttraumatic Stress Disorder in Military and Veteran Populations: Final Assessment. Washington, DC: National Academies Press; 2014.
2. Ritchie EC, ed. Intimacy Post-Injury: Combat Trauma and Sexual Health. New York: Oxford University Press; 2016.
3. Higgins A, Nash M, Lynch AM. Antidepressant-associated sexual dysfunction: impact, effects and treatment. Drug Healthc Patient Saf. 2010;2:141-150.
4. Black SA, Gallaway S, Bell MR, Ritchie EC. Prevalence and risk factors associated with suicides of army soldiers 2001-2009. Mil Psychol. 2011;23:433-451.
5. Ritchie EC. Suicides and the United States army: perspectives from the former psychiatry consultant to the army surgeon general. Cerebrum. 2012;2012:1.
6. U.S. Department of Veterans Affairs. Suicide among veterans and other Americans 2001-2014. http://www.mentalhealth.va.gov/docs/2016suicidedatareport.pdf. Published August 3, 2016. Accessed December 27, 2016.
Why start this new column on mental health with an article that focuses on sexual health? Surely that is the domain of family practice, urology, gynecology, endocrinology, or some other discipline. While it is true that all these disciplines and many others are central to the diagnosis and treatment of sexual health, mental health providers need to be an integral part of the conversations.
I have a problem with arbitrarily separating mental health and behavioral health from physical health. Mental health is directly affected by physical health and vice versa. If a woman has a urinary tract infection, she is not feeling mentally or sexually healthy. If a man has erectile dysfunction (ED), he seldom is at the top of his game emotionally. For our war-wounded who lack limbs or who have genitourinary injuries, optimal sexual functioning can be a challenge.
I am probably preaching to the choir here, so I will not belabor the point. However, I will develop this point by using lessons learned from combat-injured service members, the psychiatric adverse effects (AEs) of commonly used psychiatric medications, and most important, asking about sexual health as part of taking a mental health history.
The War-Wounded
Since 9/11, 2.7 million U.S. service members have served in wars. Much discussion has been focused on posttraumatic stress disorder (PTSD) and traumatic brain injury (TBI), the invisible wounds of war. Probably about 25% of service members who have been deployed have PTSD, and about 300,000 service members have TBI.1 About 50,000 have other physical injuries. These injuries directly affect intimate relationships.
The signature weapon of the wars in Iraq and Afghanistan was the bomb, or improvised explosive device. Motor vehicle accidents and gunshot wounds also have added to the myriad of injuries. Physical war wounds involve sexual functioning. These include, but are not limited to, lower extremity amputations, genitourinary injuries, and facial disfigurement or burns. All of these may involve multiple surgeries, pain, and disability and can significantly impact self-esteem.
One of the many lessons I have learned in putting together my most recent book, Intimacy Post Injury: Combat Trauma and Sexual Health, is that there is a void in the recent general medical and popular literature about optimizing sexual health in those with injuries or diseases.2 The majority of wounded warriors are men, but injuries happen to women service members as well. Of course, sexual assault causes severe harm to intimate relationships as well.
At this time, most injured personnel are still in the Military Health System (MHS) or have transitioned to the VHA. However, many service members also will be treated in the civilian health system.
Psychiatric Medications and Sexual Adverse Effects
The treatment of PTSD, depression, and other psychiatric conditions often involves medications that have sexual AEs. Sexual AEs usually refer to problems with erectile function (impotence), difficulties with ejaculation, lack of orgasm or desire, or lack of lubrication for women. Selective serotonin reuptake inhibitors (SSRIs) have a very high incidence of sexual AEs, ranging from 30% to 70%.3 When I speak with clinicians about their anecdotal experience, the percentage always is high, usually more than 50%. Other psychiatric medications, such as antipsychotics, older antidepressants, and stimulants also have sexual AEs, and narcotics are notorious for their sexual AEs.
Fortunately, many solutions exist. For SSRIs, the solutions include lowering the dose of the offending agent, switching to another agent, drug holidays, or adding other medications, such as bupropion or cyproheptadine. Family practice and other physicians are very familiar with phosphodiesterase inhibitors, such as sildenafil, tadalafil, and vardenafil. Although these medications have AEs and are very expensive, they work well for impotence.
Other solutions are nonpharmacologic: Setting aside time for intimacy can be crucial. Gels and creams can help with lubrication. Communication with providers and between partners and families is the most important ingredient.
Asking About Sexual Health
I encourage all medical personnel who treat active-duty service members or veterans to (1) discuss sexual health with their patients; (2) learn the basics of how to evaluate, treat, or refer ED, including SSRI AEs; and (3) understand how to discuss the effects of physical injury, pain, and disability on sexual functioning.
The conversation should touch on sexual activity, satisfaction with intimacy, exposure to sexually transmitted diseases, and if appropriate, previous sexual abuse. The appropriate time and place for a conversation about sexual health depends on the setting. In the outpatient setting, I bring up the subject after I ask about sleep and appetite and before I ask about suicidal and homicidal thoughts; others may choose elsewhere in the patient history. However, asking about sexual issues may or may not be appropriate in an emergency department situation.
Providers often are uncomfortable with asking about sexual issues, perhaps more so if they are young and female and the patient is older and male. Therefore, I encourage expanded training in medical school and throughout residency.
Sexual Difficulties and Suicide
In the military, the suicide rate has been rising from about 10 per 100,000 per year in 2004 to about 20 per 20,000 in this decade.4,5 According to the VA Office of Suicide Prevention, about 20 veterans die by suicide daily.6 One question that has received little attention is the relationship between sexual difficulties and suicide. Although there has been an important focus on causes of suicide in the military and veterans, little is known about the important issue of how many service members die by suicide because of impotence.
We do know a lot about the big picture as to why service members die by suicide. In about two-thirds of the completed suicides, there were relationship issues. In addition, there are often legal, occupational, and financial difficulties. About two-thirds of service members die by suicide using firearms. Jumping and strangulation are other common methods.4,5
But there is much we do not know. What percentage of relationship difficulties are related to sexual dysfunction? Is ED the straw that breaks the camel’s back and leads to the shot to the chest? Other subjects outside the scope of this column (but included in Intimacy Post Injury) include sexual therapy, fertility, adaptations for those with disabilities, reproductive AEs of toxin exposure, and surgeries that include penile transplantation.
My hypothesis is that sexual problems, specifically ED or impotence, contribute to feelings of failure and inadequacy and thus to suicidal or homicidal thoughts.
Conclusion
Health care providers do not always talk to patients about their sexual health and may barely mention the sexual AEs of psychiatric or other medications. In whatever setting you practice, you should not neglect asking questions about sexual health, as it is a critical issue for many of our patients and should be for us.
Why start this new column on mental health with an article that focuses on sexual health? Surely that is the domain of family practice, urology, gynecology, endocrinology, or some other discipline. While it is true that all these disciplines and many others are central to the diagnosis and treatment of sexual health, mental health providers need to be an integral part of the conversations.
I have a problem with arbitrarily separating mental health and behavioral health from physical health. Mental health is directly affected by physical health and vice versa. If a woman has a urinary tract infection, she is not feeling mentally or sexually healthy. If a man has erectile dysfunction (ED), he seldom is at the top of his game emotionally. For our war-wounded who lack limbs or who have genitourinary injuries, optimal sexual functioning can be a challenge.
I am probably preaching to the choir here, so I will not belabor the point. However, I will develop this point by using lessons learned from combat-injured service members, the psychiatric adverse effects (AEs) of commonly used psychiatric medications, and most important, asking about sexual health as part of taking a mental health history.
The War-Wounded
Since 9/11, 2.7 million U.S. service members have served in wars. Much discussion has been focused on posttraumatic stress disorder (PTSD) and traumatic brain injury (TBI), the invisible wounds of war. Probably about 25% of service members who have been deployed have PTSD, and about 300,000 service members have TBI.1 About 50,000 have other physical injuries. These injuries directly affect intimate relationships.
The signature weapon of the wars in Iraq and Afghanistan was the bomb, or improvised explosive device. Motor vehicle accidents and gunshot wounds also have added to the myriad of injuries. Physical war wounds involve sexual functioning. These include, but are not limited to, lower extremity amputations, genitourinary injuries, and facial disfigurement or burns. All of these may involve multiple surgeries, pain, and disability and can significantly impact self-esteem.
One of the many lessons I have learned in putting together my most recent book, Intimacy Post Injury: Combat Trauma and Sexual Health, is that there is a void in the recent general medical and popular literature about optimizing sexual health in those with injuries or diseases.2 The majority of wounded warriors are men, but injuries happen to women service members as well. Of course, sexual assault causes severe harm to intimate relationships as well.
At this time, most injured personnel are still in the Military Health System (MHS) or have transitioned to the VHA. However, many service members also will be treated in the civilian health system.
Psychiatric Medications and Sexual Adverse Effects
The treatment of PTSD, depression, and other psychiatric conditions often involves medications that have sexual AEs. Sexual AEs usually refer to problems with erectile function (impotence), difficulties with ejaculation, lack of orgasm or desire, or lack of lubrication for women. Selective serotonin reuptake inhibitors (SSRIs) have a very high incidence of sexual AEs, ranging from 30% to 70%.3 When I speak with clinicians about their anecdotal experience, the percentage always is high, usually more than 50%. Other psychiatric medications, such as antipsychotics, older antidepressants, and stimulants also have sexual AEs, and narcotics are notorious for their sexual AEs.
Fortunately, many solutions exist. For SSRIs, the solutions include lowering the dose of the offending agent, switching to another agent, drug holidays, or adding other medications, such as bupropion or cyproheptadine. Family practice and other physicians are very familiar with phosphodiesterase inhibitors, such as sildenafil, tadalafil, and vardenafil. Although these medications have AEs and are very expensive, they work well for impotence.
Other solutions are nonpharmacologic: Setting aside time for intimacy can be crucial. Gels and creams can help with lubrication. Communication with providers and between partners and families is the most important ingredient.
Asking About Sexual Health
I encourage all medical personnel who treat active-duty service members or veterans to (1) discuss sexual health with their patients; (2) learn the basics of how to evaluate, treat, or refer ED, including SSRI AEs; and (3) understand how to discuss the effects of physical injury, pain, and disability on sexual functioning.
The conversation should touch on sexual activity, satisfaction with intimacy, exposure to sexually transmitted diseases, and if appropriate, previous sexual abuse. The appropriate time and place for a conversation about sexual health depends on the setting. In the outpatient setting, I bring up the subject after I ask about sleep and appetite and before I ask about suicidal and homicidal thoughts; others may choose elsewhere in the patient history. However, asking about sexual issues may or may not be appropriate in an emergency department situation.
Providers often are uncomfortable with asking about sexual issues, perhaps more so if they are young and female and the patient is older and male. Therefore, I encourage expanded training in medical school and throughout residency.
Sexual Difficulties and Suicide
In the military, the suicide rate has been rising from about 10 per 100,000 per year in 2004 to about 20 per 20,000 in this decade.4,5 According to the VA Office of Suicide Prevention, about 20 veterans die by suicide daily.6 One question that has received little attention is the relationship between sexual difficulties and suicide. Although there has been an important focus on causes of suicide in the military and veterans, little is known about the important issue of how many service members die by suicide because of impotence.
We do know a lot about the big picture as to why service members die by suicide. In about two-thirds of the completed suicides, there were relationship issues. In addition, there are often legal, occupational, and financial difficulties. About two-thirds of service members die by suicide using firearms. Jumping and strangulation are other common methods.4,5
But there is much we do not know. What percentage of relationship difficulties are related to sexual dysfunction? Is ED the straw that breaks the camel’s back and leads to the shot to the chest? Other subjects outside the scope of this column (but included in Intimacy Post Injury) include sexual therapy, fertility, adaptations for those with disabilities, reproductive AEs of toxin exposure, and surgeries that include penile transplantation.
My hypothesis is that sexual problems, specifically ED or impotence, contribute to feelings of failure and inadequacy and thus to suicidal or homicidal thoughts.
Conclusion
Health care providers do not always talk to patients about their sexual health and may barely mention the sexual AEs of psychiatric or other medications. In whatever setting you practice, you should not neglect asking questions about sexual health, as it is a critical issue for many of our patients and should be for us.
1. Committee on the Assessment of Ongoing Efforts in the Treatment of Posttraumatic Stress Disorder, Board of Health of Selected Populations. Treatment of Posttraumatic Stress Disorder in Military and Veteran Populations: Final Assessment. Washington, DC: National Academies Press; 2014.
2. Ritchie EC, ed. Intimacy Post-Injury: Combat Trauma and Sexual Health. New York: Oxford University Press; 2016.
3. Higgins A, Nash M, Lynch AM. Antidepressant-associated sexual dysfunction: impact, effects and treatment. Drug Healthc Patient Saf. 2010;2:141-150.
4. Black SA, Gallaway S, Bell MR, Ritchie EC. Prevalence and risk factors associated with suicides of army soldiers 2001-2009. Mil Psychol. 2011;23:433-451.
5. Ritchie EC. Suicides and the United States army: perspectives from the former psychiatry consultant to the army surgeon general. Cerebrum. 2012;2012:1.
6. U.S. Department of Veterans Affairs. Suicide among veterans and other Americans 2001-2014. http://www.mentalhealth.va.gov/docs/2016suicidedatareport.pdf. Published August 3, 2016. Accessed December 27, 2016.
1. Committee on the Assessment of Ongoing Efforts in the Treatment of Posttraumatic Stress Disorder, Board of Health of Selected Populations. Treatment of Posttraumatic Stress Disorder in Military and Veteran Populations: Final Assessment. Washington, DC: National Academies Press; 2014.
2. Ritchie EC, ed. Intimacy Post-Injury: Combat Trauma and Sexual Health. New York: Oxford University Press; 2016.
3. Higgins A, Nash M, Lynch AM. Antidepressant-associated sexual dysfunction: impact, effects and treatment. Drug Healthc Patient Saf. 2010;2:141-150.
4. Black SA, Gallaway S, Bell MR, Ritchie EC. Prevalence and risk factors associated with suicides of army soldiers 2001-2009. Mil Psychol. 2011;23:433-451.
5. Ritchie EC. Suicides and the United States army: perspectives from the former psychiatry consultant to the army surgeon general. Cerebrum. 2012;2012:1.
6. U.S. Department of Veterans Affairs. Suicide among veterans and other Americans 2001-2014. http://www.mentalhealth.va.gov/docs/2016suicidedatareport.pdf. Published August 3, 2016. Accessed December 27, 2016.
Yoga may improve QOL in kids with cancer
Photo by Bill Branson
A yoga program for children with cancer can be carried out during cancer treatment and has quality of life (QOL) benefits for the children as well as their caregivers, according to research published in Rehabilitation Oncology.
However, the program was not feasible for all patients. More than half of those initially enrolled could not complete the study due to treatment toxicity or scheduling conflicts.
Andrea Orsey, MD, of Connecticut Children’s Medical Center in Hartford, and her colleagues conducted this research to evaluate the feasibility and effectiveness of a yoga intervention for children with cancer and their families.
The team began by conducting a survey of 20 children and adolescents with cancer and their parents/guardians.
Survey respondents expressed interest in a yoga program. But they also perceived several barriers to such a program, including concerns about side effects, pain/discomfort, and physical limitations.
With these barriers in mind, Dr Orsey and her colleagues developed a yoga intervention for pediatric cancer patients, delivered by certified yoga instructors.
The program was designed to be performed in a variety of settings and tailored to the children’s physical condition or mobility issues.
A pilot evaluation included 10 children with cancer and their caregivers. Twenty-two patient/caregiver pairs were actually enrolled, but 6 pairs withdrew because of treatment toxicity, and 6 had the study window lapse due to scheduling conflicts.
Although limited by its small size, the study suggested that yoga improved health-related QOL for both caregivers and children.
The children had significant improvements in both social and emotional QOL. They had an overall improvement in fatigue, but this was not statistically significant.
Caregivers had a significant improvement in mental health but not physical health or caregiver burden.
Both caregivers and children said they were satisfied with the yoga program and would recommend it to others.
Dr Orsey and her colleagues hope this pilot study will help guide future efforts to provide yoga to children with cancer and their families.
The researchers noted that a key issue will be coordinating yoga sessions with the medical demands of chemotherapy. 
Photo by Bill Branson
A yoga program for children with cancer can be carried out during cancer treatment and has quality of life (QOL) benefits for the children as well as their caregivers, according to research published in Rehabilitation Oncology.
However, the program was not feasible for all patients. More than half of those initially enrolled could not complete the study due to treatment toxicity or scheduling conflicts.
Andrea Orsey, MD, of Connecticut Children’s Medical Center in Hartford, and her colleagues conducted this research to evaluate the feasibility and effectiveness of a yoga intervention for children with cancer and their families.
The team began by conducting a survey of 20 children and adolescents with cancer and their parents/guardians.
Survey respondents expressed interest in a yoga program. But they also perceived several barriers to such a program, including concerns about side effects, pain/discomfort, and physical limitations.
With these barriers in mind, Dr Orsey and her colleagues developed a yoga intervention for pediatric cancer patients, delivered by certified yoga instructors.
The program was designed to be performed in a variety of settings and tailored to the children’s physical condition or mobility issues.
A pilot evaluation included 10 children with cancer and their caregivers. Twenty-two patient/caregiver pairs were actually enrolled, but 6 pairs withdrew because of treatment toxicity, and 6 had the study window lapse due to scheduling conflicts.
Although limited by its small size, the study suggested that yoga improved health-related QOL for both caregivers and children.
The children had significant improvements in both social and emotional QOL. They had an overall improvement in fatigue, but this was not statistically significant.
Caregivers had a significant improvement in mental health but not physical health or caregiver burden.
Both caregivers and children said they were satisfied with the yoga program and would recommend it to others.
Dr Orsey and her colleagues hope this pilot study will help guide future efforts to provide yoga to children with cancer and their families.
The researchers noted that a key issue will be coordinating yoga sessions with the medical demands of chemotherapy.
Photo by Bill Branson
A yoga program for children with cancer can be carried out during cancer treatment and has quality of life (QOL) benefits for the children as well as their caregivers, according to research published in Rehabilitation Oncology.
However, the program was not feasible for all patients. More than half of those initially enrolled could not complete the study due to treatment toxicity or scheduling conflicts.
Andrea Orsey, MD, of Connecticut Children’s Medical Center in Hartford, and her colleagues conducted this research to evaluate the feasibility and effectiveness of a yoga intervention for children with cancer and their families.
The team began by conducting a survey of 20 children and adolescents with cancer and their parents/guardians.
Survey respondents expressed interest in a yoga program. But they also perceived several barriers to such a program, including concerns about side effects, pain/discomfort, and physical limitations.
With these barriers in mind, Dr Orsey and her colleagues developed a yoga intervention for pediatric cancer patients, delivered by certified yoga instructors.
The program was designed to be performed in a variety of settings and tailored to the children’s physical condition or mobility issues.
A pilot evaluation included 10 children with cancer and their caregivers. Twenty-two patient/caregiver pairs were actually enrolled, but 6 pairs withdrew because of treatment toxicity, and 6 had the study window lapse due to scheduling conflicts.
Although limited by its small size, the study suggested that yoga improved health-related QOL for both caregivers and children.
The children had significant improvements in both social and emotional QOL. They had an overall improvement in fatigue, but this was not statistically significant.
Caregivers had a significant improvement in mental health but not physical health or caregiver burden.
Both caregivers and children said they were satisfied with the yoga program and would recommend it to others.
Dr Orsey and her colleagues hope this pilot study will help guide future efforts to provide yoga to children with cancer and their families.
The researchers noted that a key issue will be coordinating yoga sessions with the medical demands of chemotherapy.
US cancer cases may near 1.7 million in 2017
patient and her father
Photo by Rhoda Baer
The US may see nearly 1.7 million new cancer cases in 2017 and more than 600,000 cancer-related deaths, according to a report from the American Cancer Society (ACS).
In addition to estimates for 2017, the report, “Cancer Statistics 2017,” includes the most recent data on cancer incidence, mortality, and survival in the US.
The report was published in CA: A Cancer Journal for Clinicians.
The report projects there will be 1,688,780 new cancer cases and 600,920 cancer deaths in the US this year.
This includes:
- 80,500 new cases of lymphoma and 21,210 lymphoma deaths
- 62,130 new cases of leukemia and 24,500 leukemia deaths
- 30,280 new cases of myeloma and 12,590 myeloma deaths.
The report also shows that, from 2004 to 2013, the overall cancer incidence rate was stable in women and declined by about 2% per year in men. From 2005 to 2014, the cancer death rate declined by about 1.5% annually in both men and women.
Overall, the cancer death rate dropped 25% from its peak of 215.1 (per 100,000 population) in 1991 to 161.2 (per 100,000 population) in 2014, the latest year for which data was available. This translates to about 2,143,200 fewer cancer deaths.
“The continuing drops in the cancer death rate are a powerful sign of the potential we have to reduce cancer’s deadly toll,” said Otis W. Brawley, MD, chief medical officer of the ACS.
He said the decrease in cancer death rates is the result of steady reductions in smoking and advances in early detection and treatment. The decrease is driven by decreasing death rates for the 4 major cancer sites—lung, breast, colorectal, and prostate.
The report also shows that racial disparities in cancer death rates continue to decline. The excess risk of cancer death in black men has dropped from 47% in 1990 to 21% in 2014. The black/white disparity declined similarly in women, from a peak of 20% in 1998 to 13% in 2014.
On the other hand, significant gender disparities persist for both cancer incidence and death in the US. For all cancer sites combined, the incidence rate is 20% higher in men than in women, and the cancer death rate is 40% higher in men.
Dr Brawley said the gender gap in cancer mortality largely reflects variation in the distribution of cancers that occur in men and women, much of which is due to differences in the prevalence of cancer risk factors.
The yearly “Cancer Statistics” reports have been published by ACS researchers since 1967 to inform and guide clinicians, investigators, and others in public health in prioritizing efforts to reduce the burden of cancer.
Cancer incidence data for the current report were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data were collected by the National Center for Health Statistics.
patient and her father
Photo by Rhoda Baer
The US may see nearly 1.7 million new cancer cases in 2017 and more than 600,000 cancer-related deaths, according to a report from the American Cancer Society (ACS).
In addition to estimates for 2017, the report, “Cancer Statistics 2017,” includes the most recent data on cancer incidence, mortality, and survival in the US.
The report was published in CA: A Cancer Journal for Clinicians.
The report projects there will be 1,688,780 new cancer cases and 600,920 cancer deaths in the US this year.
This includes:
- 80,500 new cases of lymphoma and 21,210 lymphoma deaths
- 62,130 new cases of leukemia and 24,500 leukemia deaths
- 30,280 new cases of myeloma and 12,590 myeloma deaths.
The report also shows that, from 2004 to 2013, the overall cancer incidence rate was stable in women and declined by about 2% per year in men. From 2005 to 2014, the cancer death rate declined by about 1.5% annually in both men and women.
Overall, the cancer death rate dropped 25% from its peak of 215.1 (per 100,000 population) in 1991 to 161.2 (per 100,000 population) in 2014, the latest year for which data was available. This translates to about 2,143,200 fewer cancer deaths.
“The continuing drops in the cancer death rate are a powerful sign of the potential we have to reduce cancer’s deadly toll,” said Otis W. Brawley, MD, chief medical officer of the ACS.
He said the decrease in cancer death rates is the result of steady reductions in smoking and advances in early detection and treatment. The decrease is driven by decreasing death rates for the 4 major cancer sites—lung, breast, colorectal, and prostate.
The report also shows that racial disparities in cancer death rates continue to decline. The excess risk of cancer death in black men has dropped from 47% in 1990 to 21% in 2014. The black/white disparity declined similarly in women, from a peak of 20% in 1998 to 13% in 2014.
On the other hand, significant gender disparities persist for both cancer incidence and death in the US. For all cancer sites combined, the incidence rate is 20% higher in men than in women, and the cancer death rate is 40% higher in men.
Dr Brawley said the gender gap in cancer mortality largely reflects variation in the distribution of cancers that occur in men and women, much of which is due to differences in the prevalence of cancer risk factors.
The yearly “Cancer Statistics” reports have been published by ACS researchers since 1967 to inform and guide clinicians, investigators, and others in public health in prioritizing efforts to reduce the burden of cancer.
Cancer incidence data for the current report were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data were collected by the National Center for Health Statistics.
patient and her father
Photo by Rhoda Baer
The US may see nearly 1.7 million new cancer cases in 2017 and more than 600,000 cancer-related deaths, according to a report from the American Cancer Society (ACS).
In addition to estimates for 2017, the report, “Cancer Statistics 2017,” includes the most recent data on cancer incidence, mortality, and survival in the US.
The report was published in CA: A Cancer Journal for Clinicians.
The report projects there will be 1,688,780 new cancer cases and 600,920 cancer deaths in the US this year.
This includes:
- 80,500 new cases of lymphoma and 21,210 lymphoma deaths
- 62,130 new cases of leukemia and 24,500 leukemia deaths
- 30,280 new cases of myeloma and 12,590 myeloma deaths.
The report also shows that, from 2004 to 2013, the overall cancer incidence rate was stable in women and declined by about 2% per year in men. From 2005 to 2014, the cancer death rate declined by about 1.5% annually in both men and women.
Overall, the cancer death rate dropped 25% from its peak of 215.1 (per 100,000 population) in 1991 to 161.2 (per 100,000 population) in 2014, the latest year for which data was available. This translates to about 2,143,200 fewer cancer deaths.
“The continuing drops in the cancer death rate are a powerful sign of the potential we have to reduce cancer’s deadly toll,” said Otis W. Brawley, MD, chief medical officer of the ACS.
He said the decrease in cancer death rates is the result of steady reductions in smoking and advances in early detection and treatment. The decrease is driven by decreasing death rates for the 4 major cancer sites—lung, breast, colorectal, and prostate.
The report also shows that racial disparities in cancer death rates continue to decline. The excess risk of cancer death in black men has dropped from 47% in 1990 to 21% in 2014. The black/white disparity declined similarly in women, from a peak of 20% in 1998 to 13% in 2014.
On the other hand, significant gender disparities persist for both cancer incidence and death in the US. For all cancer sites combined, the incidence rate is 20% higher in men than in women, and the cancer death rate is 40% higher in men.
Dr Brawley said the gender gap in cancer mortality largely reflects variation in the distribution of cancers that occur in men and women, much of which is due to differences in the prevalence of cancer risk factors.
The yearly “Cancer Statistics” reports have been published by ACS researchers since 1967 to inform and guide clinicians, investigators, and others in public health in prioritizing efforts to reduce the burden of cancer.
Cancer incidence data for the current report were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data were collected by the National Center for Health Statistics.
Cancer genomic data released to public
Photo courtesy of the
National Institute of
General Medical Sciences
The American Association for Cancer Research (AACR) has announced the first public release of cancer genomic data aggregated through the AACR Project Genomics Evidence Neoplasia Information Exchange (GENIE).
The data set includes nearly 19,000 de-identified genomic records collected from patients who were treated at 8 international institutions, making it one of the largest public cancer genomic data sets released to date.
The release includes data for 59 major cancer types, including leukemias, lymphomas, and multiple myeloma.
The genomic data and a limited amount of linked clinical data for each patient can be accessed via the AACR Project GENIE cBioPortal or from Sage Bionetworks. (Users must create an account for either site to access the data.)
“We are excited to make publicly available this very large set of clinical-grade, next-generation sequencing data obtained during routine patient care,” said Charles L. Sawyers, MD, AACR Project GENIE Steering Committee chairperson.
“These data were generated as part of routine patient care and, without AACR Project GENIE, they would likely never have been shared with the global cancer research community.”
AACR Project GENIE is a multi-phase, international data-sharing project aimed at catalyzing precision oncology through the development of a registry that aggregates and links clinical-grade cancer genomic data with clinical outcomes from tens of thousands of cancer patients treated at multiple institutions.
The newly released data are fully de-identified in compliance with the Health Insurance Portability and Accountability Act (HIPAA).
The data are derived from patients whose tumors were genetically sequenced as part of their care at any of the 8 institutions that participated in the first phase of AACR Project GENIE.
The goal of releasing these data to the cancer research community is to aid new research that will accelerate the pace of progress against cancer.
According to AACR, the data can be used to validate gene signatures of drug response or prognosis, identify new patient populations for drugs that are currently available, and uncover new drug targets and biomarkers.
“I am extremely proud that the American Association for Cancer Research, as the coordinating center for AACR Project GENIE, is delivering on its promise to make these important data publicly available just over a year after unveiling the initiative,” said Margaret Foti, PhD, MD, chief executive officer of the AACR.
To expand the AACR Project GENIE registry, the consortium is accepting applications for new participating centers. Any nonprofit institution that meets certain criteria can submit an application to become a project participant.
For more information on AACR Project GENIE, visit the project website or send an email to [email protected].
Photo courtesy of the
National Institute of
General Medical Sciences
The American Association for Cancer Research (AACR) has announced the first public release of cancer genomic data aggregated through the AACR Project Genomics Evidence Neoplasia Information Exchange (GENIE).
The data set includes nearly 19,000 de-identified genomic records collected from patients who were treated at 8 international institutions, making it one of the largest public cancer genomic data sets released to date.
The release includes data for 59 major cancer types, including leukemias, lymphomas, and multiple myeloma.
The genomic data and a limited amount of linked clinical data for each patient can be accessed via the AACR Project GENIE cBioPortal or from Sage Bionetworks. (Users must create an account for either site to access the data.)
“We are excited to make publicly available this very large set of clinical-grade, next-generation sequencing data obtained during routine patient care,” said Charles L. Sawyers, MD, AACR Project GENIE Steering Committee chairperson.
“These data were generated as part of routine patient care and, without AACR Project GENIE, they would likely never have been shared with the global cancer research community.”
AACR Project GENIE is a multi-phase, international data-sharing project aimed at catalyzing precision oncology through the development of a registry that aggregates and links clinical-grade cancer genomic data with clinical outcomes from tens of thousands of cancer patients treated at multiple institutions.
The newly released data are fully de-identified in compliance with the Health Insurance Portability and Accountability Act (HIPAA).
The data are derived from patients whose tumors were genetically sequenced as part of their care at any of the 8 institutions that participated in the first phase of AACR Project GENIE.
The goal of releasing these data to the cancer research community is to aid new research that will accelerate the pace of progress against cancer.
According to AACR, the data can be used to validate gene signatures of drug response or prognosis, identify new patient populations for drugs that are currently available, and uncover new drug targets and biomarkers.
“I am extremely proud that the American Association for Cancer Research, as the coordinating center for AACR Project GENIE, is delivering on its promise to make these important data publicly available just over a year after unveiling the initiative,” said Margaret Foti, PhD, MD, chief executive officer of the AACR.
To expand the AACR Project GENIE registry, the consortium is accepting applications for new participating centers. Any nonprofit institution that meets certain criteria can submit an application to become a project participant.
For more information on AACR Project GENIE, visit the project website or send an email to [email protected].
Photo courtesy of the
National Institute of
General Medical Sciences
The American Association for Cancer Research (AACR) has announced the first public release of cancer genomic data aggregated through the AACR Project Genomics Evidence Neoplasia Information Exchange (GENIE).
The data set includes nearly 19,000 de-identified genomic records collected from patients who were treated at 8 international institutions, making it one of the largest public cancer genomic data sets released to date.
The release includes data for 59 major cancer types, including leukemias, lymphomas, and multiple myeloma.
The genomic data and a limited amount of linked clinical data for each patient can be accessed via the AACR Project GENIE cBioPortal or from Sage Bionetworks. (Users must create an account for either site to access the data.)
“We are excited to make publicly available this very large set of clinical-grade, next-generation sequencing data obtained during routine patient care,” said Charles L. Sawyers, MD, AACR Project GENIE Steering Committee chairperson.
“These data were generated as part of routine patient care and, without AACR Project GENIE, they would likely never have been shared with the global cancer research community.”
AACR Project GENIE is a multi-phase, international data-sharing project aimed at catalyzing precision oncology through the development of a registry that aggregates and links clinical-grade cancer genomic data with clinical outcomes from tens of thousands of cancer patients treated at multiple institutions.
The newly released data are fully de-identified in compliance with the Health Insurance Portability and Accountability Act (HIPAA).
The data are derived from patients whose tumors were genetically sequenced as part of their care at any of the 8 institutions that participated in the first phase of AACR Project GENIE.
The goal of releasing these data to the cancer research community is to aid new research that will accelerate the pace of progress against cancer.
According to AACR, the data can be used to validate gene signatures of drug response or prognosis, identify new patient populations for drugs that are currently available, and uncover new drug targets and biomarkers.
“I am extremely proud that the American Association for Cancer Research, as the coordinating center for AACR Project GENIE, is delivering on its promise to make these important data publicly available just over a year after unveiling the initiative,” said Margaret Foti, PhD, MD, chief executive officer of the AACR.
To expand the AACR Project GENIE registry, the consortium is accepting applications for new participating centers. Any nonprofit institution that meets certain criteria can submit an application to become a project participant.
For more information on AACR Project GENIE, visit the project website or send an email to [email protected].
FDA lifts full clinical hold on pacritinib
The US Food and Drug Administration (FDA) has lifted the full clinical hold placed on all clinical trials conducted under the investigational new drug application for pacritinib, an oral kinase inhibitor being developed as a treatment for myelofibrosis (MF).
The FDA placed the hold on pacritinib trials in February 2016 after results from 2 phase 3 trials, PERSIST-1 and PERSIST-2, showed excess mortality in patients who received pacritinib.
Both trials suggested pacritinib can be more effective than the best available therapy for MF.
However, interim overall survival results from PERSIST-2 indicated that pacritinib had a detrimental effect on survival, which was consistent with the results from PERSIST-1.
Due to the full clinical hold, CTI BioPharma withdrew the new drug application for pacritinib while reviewing data from PERSIST-2.
When the FDA enacted the hold, the agency recommended that CTI BioPharma conduct dose-exploration studies for pacritinib, submit final study reports and data sets for PERSIST-1 and PERSIST-2, make certain modifications to protocols and study-related documents, and request a meeting with the FDA prior to submitting a response to the full clinical hold.
CTI BioPharma followed the FDA’s recommendations and submitted a response to the hold that included final clinical study reports for PERSIST-1 and PERSIST-2 and a protocol for a dose-exploration trial.
The trial, PAC203, should enroll up to approximately 105 patients with primary MF who have failed prior ruxolitinib therapy. The goal is to evaluate the safety and the dose-response relationship for efficacy (spleen volume reduction at 24 weeks) of pacritinib at 3 doses: 100 mg once daily, 100 mg twice daily (BID), and 200 mg BID. The 200 mg BID dose regimen was used in PERSIST-2.
CTI BioPharma said it expects to start the trial in the second quarter of 2017.
“We are pleased to resolve the full clinical hold through working diligently with the FDA to provide a comprehensive response to their requests,” said Richard Love, interim president and chief executive officer of CTI BioPharma.
“We look forward to discussing with the FDA the future development of pacritinib. We believe pacritinib can ultimately address the unmet need of patients with myelofibrosis who are ineligible to receive or are not benefitting from the approved JAK1/JAK2 inhibitor, ruxolitinib, as these patients have limited treatment options.”
The US Food and Drug Administration (FDA) has lifted the full clinical hold placed on all clinical trials conducted under the investigational new drug application for pacritinib, an oral kinase inhibitor being developed as a treatment for myelofibrosis (MF).
The FDA placed the hold on pacritinib trials in February 2016 after results from 2 phase 3 trials, PERSIST-1 and PERSIST-2, showed excess mortality in patients who received pacritinib.
Both trials suggested pacritinib can be more effective than the best available therapy for MF.
However, interim overall survival results from PERSIST-2 indicated that pacritinib had a detrimental effect on survival, which was consistent with the results from PERSIST-1.
Due to the full clinical hold, CTI BioPharma withdrew the new drug application for pacritinib while reviewing data from PERSIST-2.
When the FDA enacted the hold, the agency recommended that CTI BioPharma conduct dose-exploration studies for pacritinib, submit final study reports and data sets for PERSIST-1 and PERSIST-2, make certain modifications to protocols and study-related documents, and request a meeting with the FDA prior to submitting a response to the full clinical hold.
CTI BioPharma followed the FDA’s recommendations and submitted a response to the hold that included final clinical study reports for PERSIST-1 and PERSIST-2 and a protocol for a dose-exploration trial.
The trial, PAC203, should enroll up to approximately 105 patients with primary MF who have failed prior ruxolitinib therapy. The goal is to evaluate the safety and the dose-response relationship for efficacy (spleen volume reduction at 24 weeks) of pacritinib at 3 doses: 100 mg once daily, 100 mg twice daily (BID), and 200 mg BID. The 200 mg BID dose regimen was used in PERSIST-2.
CTI BioPharma said it expects to start the trial in the second quarter of 2017.
“We are pleased to resolve the full clinical hold through working diligently with the FDA to provide a comprehensive response to their requests,” said Richard Love, interim president and chief executive officer of CTI BioPharma.
“We look forward to discussing with the FDA the future development of pacritinib. We believe pacritinib can ultimately address the unmet need of patients with myelofibrosis who are ineligible to receive or are not benefitting from the approved JAK1/JAK2 inhibitor, ruxolitinib, as these patients have limited treatment options.”
The US Food and Drug Administration (FDA) has lifted the full clinical hold placed on all clinical trials conducted under the investigational new drug application for pacritinib, an oral kinase inhibitor being developed as a treatment for myelofibrosis (MF).
The FDA placed the hold on pacritinib trials in February 2016 after results from 2 phase 3 trials, PERSIST-1 and PERSIST-2, showed excess mortality in patients who received pacritinib.
Both trials suggested pacritinib can be more effective than the best available therapy for MF.
However, interim overall survival results from PERSIST-2 indicated that pacritinib had a detrimental effect on survival, which was consistent with the results from PERSIST-1.
Due to the full clinical hold, CTI BioPharma withdrew the new drug application for pacritinib while reviewing data from PERSIST-2.
When the FDA enacted the hold, the agency recommended that CTI BioPharma conduct dose-exploration studies for pacritinib, submit final study reports and data sets for PERSIST-1 and PERSIST-2, make certain modifications to protocols and study-related documents, and request a meeting with the FDA prior to submitting a response to the full clinical hold.
CTI BioPharma followed the FDA’s recommendations and submitted a response to the hold that included final clinical study reports for PERSIST-1 and PERSIST-2 and a protocol for a dose-exploration trial.
The trial, PAC203, should enroll up to approximately 105 patients with primary MF who have failed prior ruxolitinib therapy. The goal is to evaluate the safety and the dose-response relationship for efficacy (spleen volume reduction at 24 weeks) of pacritinib at 3 doses: 100 mg once daily, 100 mg twice daily (BID), and 200 mg BID. The 200 mg BID dose regimen was used in PERSIST-2.
CTI BioPharma said it expects to start the trial in the second quarter of 2017.
“We are pleased to resolve the full clinical hold through working diligently with the FDA to provide a comprehensive response to their requests,” said Richard Love, interim president and chief executive officer of CTI BioPharma.
“We look forward to discussing with the FDA the future development of pacritinib. We believe pacritinib can ultimately address the unmet need of patients with myelofibrosis who are ineligible to receive or are not benefitting from the approved JAK1/JAK2 inhibitor, ruxolitinib, as these patients have limited treatment options.”
Bronchoscopy sedation changes in 2017
A major change in coding for bronchoscopy occurred on January 1, 2017, as moderate (conscious) sedation is now separately identified from the work relative value units (wRVUs) for the bronchoscopy codes. While traditionally the bronchoscopist provided moderate sedation, in recent clinical practice, other individuals often provide the sedation. CMS mandated refinement of separate Current Procedural Terminology (CPT®) codes to account for the work of moderate procedural sedation. In the final rule published in November 2016, CMS removed 0.25 wRVUs from many of the bronchoscopy codes to account for the work of moderate sedation. To be reimbursed appropriately, include a moderate sedation CPT code with all bronchoscopy procedures.
Use codes 99151 and 99155 for patients younger than 5 years. For a patient 5 years or older, when the bronchoscopist provides moderate sedation, report code 99152 for the initial 15 minutes and 99153 for subsequent time in 15-minute increments. For a patient 5 years or older, when a provider other than the bronchoscopist provides moderate sedation, use code 99156 for the initial 15 minutes and 99157 for subsequent time in 15-minute increments. Utilize codes 99156 and 99157 only when a second provider (other than the bronchoscopist) performs moderate sedation in the facility setting (eg, hospital, outpatient hospital/ambulatory surgery center, skilled nursing facility). When the second provider performs these services in the nonfacility setting (eg, physician office, freestanding imaging center), do not report codes 99155, 99156, or 99157. Moderate sedation does not include minimal sedation (anxiolysis), deep sedation, or monitored anesthesia care (00100-01999).
Do not use a moderate sedation code (99151-2 or 99155-6) if providing less than 10 minutes of moderate sedation. As with other time-based codes, use the subsequent codes 99153 and 99157 when moderate sedation lasts 8 minutes or longer than the initial 15 minutes. The time for moderate sedation begins with the administration of the sedating agent and concludes when the continuous face-to-face presence of the bronchoscopist ends after completion of the procedure. Intermittent, re-evaluation of the patient afterward is postservice work and is not included in the time for moderate sedation. For example, if the bronchoscopist provides moderate sedation for 25 minutes in a 65-year-old man, report 99152 (for the initial 15 minutes) and 99153 (for the subsequent 10 minutes). If an individual other than the bronchoscopist provides moderate sedation for 41 minutes in a 57-year-old woman, use 99156 (for the initial 15 minutes) and two units of 99157 (for the subsequent 26 minutes). If a bronchoscopist provides moderate sedation and reports the appropriate codes after January 1, the 0.25 wRVU change will have no financial impact compared with 2016. If a second provider performs the moderate sedation, expect an approximately $8.72 drop in reimbursement per procedure.
A major change in coding for bronchoscopy occurred on January 1, 2017, as moderate (conscious) sedation is now separately identified from the work relative value units (wRVUs) for the bronchoscopy codes. While traditionally the bronchoscopist provided moderate sedation, in recent clinical practice, other individuals often provide the sedation. CMS mandated refinement of separate Current Procedural Terminology (CPT®) codes to account for the work of moderate procedural sedation. In the final rule published in November 2016, CMS removed 0.25 wRVUs from many of the bronchoscopy codes to account for the work of moderate sedation. To be reimbursed appropriately, include a moderate sedation CPT code with all bronchoscopy procedures.
Use codes 99151 and 99155 for patients younger than 5 years. For a patient 5 years or older, when the bronchoscopist provides moderate sedation, report code 99152 for the initial 15 minutes and 99153 for subsequent time in 15-minute increments. For a patient 5 years or older, when a provider other than the bronchoscopist provides moderate sedation, use code 99156 for the initial 15 minutes and 99157 for subsequent time in 15-minute increments. Utilize codes 99156 and 99157 only when a second provider (other than the bronchoscopist) performs moderate sedation in the facility setting (eg, hospital, outpatient hospital/ambulatory surgery center, skilled nursing facility). When the second provider performs these services in the nonfacility setting (eg, physician office, freestanding imaging center), do not report codes 99155, 99156, or 99157. Moderate sedation does not include minimal sedation (anxiolysis), deep sedation, or monitored anesthesia care (00100-01999).
Do not use a moderate sedation code (99151-2 or 99155-6) if providing less than 10 minutes of moderate sedation. As with other time-based codes, use the subsequent codes 99153 and 99157 when moderate sedation lasts 8 minutes or longer than the initial 15 minutes. The time for moderate sedation begins with the administration of the sedating agent and concludes when the continuous face-to-face presence of the bronchoscopist ends after completion of the procedure. Intermittent, re-evaluation of the patient afterward is postservice work and is not included in the time for moderate sedation. For example, if the bronchoscopist provides moderate sedation for 25 minutes in a 65-year-old man, report 99152 (for the initial 15 minutes) and 99153 (for the subsequent 10 minutes). If an individual other than the bronchoscopist provides moderate sedation for 41 minutes in a 57-year-old woman, use 99156 (for the initial 15 minutes) and two units of 99157 (for the subsequent 26 minutes). If a bronchoscopist provides moderate sedation and reports the appropriate codes after January 1, the 0.25 wRVU change will have no financial impact compared with 2016. If a second provider performs the moderate sedation, expect an approximately $8.72 drop in reimbursement per procedure.
A major change in coding for bronchoscopy occurred on January 1, 2017, as moderate (conscious) sedation is now separately identified from the work relative value units (wRVUs) for the bronchoscopy codes. While traditionally the bronchoscopist provided moderate sedation, in recent clinical practice, other individuals often provide the sedation. CMS mandated refinement of separate Current Procedural Terminology (CPT®) codes to account for the work of moderate procedural sedation. In the final rule published in November 2016, CMS removed 0.25 wRVUs from many of the bronchoscopy codes to account for the work of moderate sedation. To be reimbursed appropriately, include a moderate sedation CPT code with all bronchoscopy procedures.
Use codes 99151 and 99155 for patients younger than 5 years. For a patient 5 years or older, when the bronchoscopist provides moderate sedation, report code 99152 for the initial 15 minutes and 99153 for subsequent time in 15-minute increments. For a patient 5 years or older, when a provider other than the bronchoscopist provides moderate sedation, use code 99156 for the initial 15 minutes and 99157 for subsequent time in 15-minute increments. Utilize codes 99156 and 99157 only when a second provider (other than the bronchoscopist) performs moderate sedation in the facility setting (eg, hospital, outpatient hospital/ambulatory surgery center, skilled nursing facility). When the second provider performs these services in the nonfacility setting (eg, physician office, freestanding imaging center), do not report codes 99155, 99156, or 99157. Moderate sedation does not include minimal sedation (anxiolysis), deep sedation, or monitored anesthesia care (00100-01999).
Do not use a moderate sedation code (99151-2 or 99155-6) if providing less than 10 minutes of moderate sedation. As with other time-based codes, use the subsequent codes 99153 and 99157 when moderate sedation lasts 8 minutes or longer than the initial 15 minutes. The time for moderate sedation begins with the administration of the sedating agent and concludes when the continuous face-to-face presence of the bronchoscopist ends after completion of the procedure. Intermittent, re-evaluation of the patient afterward is postservice work and is not included in the time for moderate sedation. For example, if the bronchoscopist provides moderate sedation for 25 minutes in a 65-year-old man, report 99152 (for the initial 15 minutes) and 99153 (for the subsequent 10 minutes). If an individual other than the bronchoscopist provides moderate sedation for 41 minutes in a 57-year-old woman, use 99156 (for the initial 15 minutes) and two units of 99157 (for the subsequent 26 minutes). If a bronchoscopist provides moderate sedation and reports the appropriate codes after January 1, the 0.25 wRVU change will have no financial impact compared with 2016. If a second provider performs the moderate sedation, expect an approximately $8.72 drop in reimbursement per procedure.
Sleep strategies: Sleep-disordered breathing and pregnancy complications: Emerging data and future directions
Background
Sleep-disordered breathing (SDB) conditions are characterized by abnormal respiratory patterns and abnormal gas exchange during sleep.1-3 Obstructive sleep apnea (OSA), the most common type of SDB, is characterized by repetitive episodes of airway narrowing during sleep that lead to respiratory disruption, hypoxia, and sleep fragmentation. In reproductive-aged women, epidemiologic studies suggest a 2% to 13% prevalence of OSA.4-6 Pregnancy is associated with changes that promote OSA, such as weight gain and edema of the upper airway.7 Frequent snoring, a common symptom of OSA, is endorsed by 15% to 25% of pregnant women.8-10 Health outcomes that have been linked to SDB in the nonpregnant population, such as hypertension and insulin-resistant diabetes, have clinically relevant correlates in pregnancy (preeclampsia, gestational diabetes).11-13
While several retrospective and cross-sectional studies suggest that SDB may increase the risk of developing hypertensive disorders and gestational diabetes during pregnancy,16-18 up until recently, there were limited and conflicting data from prospective observational cohorts in which SDB exposure and pregnancy outcomes have been methodically measured and confounding variables carefully considered.19-21 Louis et al.19 reported on a cohort of 175 obese women and demonstrated that women with SDB (apnea-hypopnea index greater than or equal to 5) were more likely to develop preeclampsia (adjusted odds ratio, 3.5; 95% CI, 1.3, 9.9). However, two other small studies failed to demonstrate a positive association between SDB and pregnancy-related hypertension, but one suggested a relationship between SDB and gestational diabetes.20,21
Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be Sleep-Disordered Breathing Substudy
The Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be Sleep-Disordered Breathing Substudy (nuMoM2b-SDB) was a prospective cohort study.22,23 Level 3 home sleep tests were performed using a six-channel monitor that was self-applied by the participant twice during pregnancy, first between 60 and 150 weeks of pregnancy and then again between 220 and 310 weeks. An apnea-hypopnea index (AHI) of at least 5 was used to define SDB. The study was powered to test the primary hypothesis that SDB occurring in pregnancy is associated with an increased incidence of preeclampsia. Secondary outcomes were rates of hypertensive disorders of pregnancy, defined as preeclampsia and prenatal gestational hypertension, and gestational diabetes. Crude and adjusted odds ratios and 95% confidence intervals were calculated from univariate and multivariate logistic regression models. Adjustment covariates included maternal age (less than or equal to 21, 22-35, and over 35 years), body mass index (less than 25, 25 to less than 30, greater than or equal to 30 kg/m2), chronic hypertension (yes, no), and, for midpregnancy, rate of weight gain per week between early and midpregnancy assessments, treated as a continuous variable.
Conclusions and future directions
The nuMoM2b data are provocative because sleep apnea is a potentially modifiable risk factor for adverse pregnancy outcomes. While a majority of SDB cases identified during pregnancy were mild, the nuMoM2b data demonstrate that even modest elevations of AHI in pregnancy are associated with an increased risk of developing hypertensive disorders and an increased incidence of gestational diabetes.
Pregnancy is conceivably an ideal scenario in which to better understand the role of SDB treatment as a preventive strategy for reducing cardiometabolic morbidity as the time frame needed to measure incident outcomes after initiating therapy is significantly contracted. However, data regarding the role of OSA treatment with continuous positive airway pressure (CPAP) during pregnancy, both regarding its acceptability to patients and its therapeutic benefit, are extremely limited. Further research is needed to establish whether universal screening for and treating of SDB in pregnancy can mitigate the risks and consequences of hypertensive disorders of pregnancy and gestational diabetes. However, in the meantime, we have to recognize that as our obstetric patient population is becoming more obese, we will encounter more women with symptomatic SDB in pregnancy. It is well documented that patients with symptomatic SDB, those who report that their snoring leads to chronic sleep disruption and excessive daytime sleepiness, can benefit from CPAP in terms of sleep quality and daytime function. Therefore, in addition to encouraging women already prescribed CPAP to continue their therapy during pregnancy, obstetricians who encounter a patient reporting severe SDB symptoms should refer her to a sleep specialist for further evaluation.
Dr. Facco is assistant professor, department of obstetrics and gynecology, University of Pittsburgh, Magee-Women’s Hospital, Magee Women’s Research Institute.
References
1. Berry RB, Budhiraja R, Gottlieb DJ, et al. Rules for scoring respiratory events in sleep: Update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. Deliberations of the Sleep Apnea Definitions Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2012;8(5):597-619.
2. Park JG, Ramar K, Olson EJ. Updates on definition, consequences, and management of obstructive sleep apnea. Mayo Clin Proc. 2011;86(6):549-54; quiz, 554-5.
3. Iber C, Ancoli-Israel S, Chesson A, Quan S. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. 1st ed. Westchester, Ill.: American Academy of Sleep Medicine, 2007.
4. Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013 May 1;177(9):1006-14.
5. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328(17):1230-5.
6. Young T, Finn L, Austin D, Peterson A. Menopausal status and sleep-disordered breathing in the Wisconsin Sleep Cohort Study. Am J Respir Crit Care Med. 2003;167(9):1181-5.
7. Pien GW, Schwab RJ. Sleep disorders during pregnancy. Sleep. 2004;27(7):1405-17.
8. Hedman C, Pohjasvaara T, Tolonen U, Suhonen-Malm AS, Myllyla VV. Effects of pregnancy on mothers’ sleep. Sleep Med. 2002;3(1):37-42.
9. Pien GW, Fife D, Pack AI, Nkwuo JE, Schwab RJ. Changes in symptoms of sleep-disordered breathing during pregnancy. Sleep. 2005;28(10):1299-1305.
10. Facco FL, Kramer J, Ho KH, Zee PC, Grobman WA. Sleep disturbances in pregnancy. Obstet Gynecol. 2010;115(1):77-83.
11. Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med. 2000;342(19):1378-84.
12. Punjabi NM, Shahar E, Redline S, et al. Sleep-disordered breathing, glucose intolerance, and insulin resistance: The Sleep Heart Health Study. Am J Epidemiol. 2004;160(6):521-30.
13. Reichmuth KJ, Austin D, Skatrud JB, Young T. Association of sleep apnea and type II diabetes: A population-based study. Am J Respir Crit Care Med. 2005;172(12):1590-5.
14. Dempsey JA, Veasey SC, Morgan BJ, O’Donnell CP. Pathophysiology of sleep apnea. Physiol Rev. 2010;90(1):47-112.
15. Romero R, Badr MS. A role for sleep disorders in pregnancy complications: Challenges and opportunities. Am J Obstet Gynecol. 2014;210(1):3-11.
16. O’Brien LM, Bullough AS, Owusu JT, et al. Pregnancy-onset habitual snoring, gestational hypertension, and preeclampsia: Prospective cohort study. Am J Obstet Gynecol. 2012;207(6):487.e1-9
17. Chen YH, Kang JH, Lin CC, Wang IT, Keller JJ, Lin HC. Obstructive sleep apnea and the risk of adverse pregnancy outcomes. Am J Obstet Gynecol. 2012;206(2):136.e1-5.
18. Bourjeily G, Raker CA, Chalhoub M, Miller MA, et al. Pregnancy and fetal outcomes of symptoms of sleep-disordered breathing. Eur Respir J. 2010;36(4):849-55.
19. Louis J, Auckley D, Miladinovic B, et al. Perinatal outcomes associated with obstructive sleep apnea in obese pregnant women. Obstet Gynecol. 2012;120:1085-92.
20. Facco FL, Ouyang DW, Zee PC, et al. Implications of sleep-disordered breathing in pregnancy. Am J Obstet Gynecol. 2014 Jun;210(6):559.e1-6.
21. Pien GW, Pack AI, Jackson N, Maislin G, Macones GA, Schwab RJ. Risk factors for sleep-disordered breathing in pregnancy. Thorax. 2014;69(4):371-7.
22. Facco FL, Parker CB, Reddy UM, et al. NuMoM2b Sleep-Disordered Breathing study: Objectives and methods. Am J Obstet Gynecol. 2015 April;212(4):542.e1–542.e127.
23. Facco FL, Parker CB, Reddy UM, et al. Association between sleep-disordered breathing and hypertensive disorders of pregn ancy and gestational diabetes mellitus. Obstet Gynecol. ePub. 2016 Dec 2.
Background
Sleep-disordered breathing (SDB) conditions are characterized by abnormal respiratory patterns and abnormal gas exchange during sleep.1-3 Obstructive sleep apnea (OSA), the most common type of SDB, is characterized by repetitive episodes of airway narrowing during sleep that lead to respiratory disruption, hypoxia, and sleep fragmentation. In reproductive-aged women, epidemiologic studies suggest a 2% to 13% prevalence of OSA.4-6 Pregnancy is associated with changes that promote OSA, such as weight gain and edema of the upper airway.7 Frequent snoring, a common symptom of OSA, is endorsed by 15% to 25% of pregnant women.8-10 Health outcomes that have been linked to SDB in the nonpregnant population, such as hypertension and insulin-resistant diabetes, have clinically relevant correlates in pregnancy (preeclampsia, gestational diabetes).11-13
While several retrospective and cross-sectional studies suggest that SDB may increase the risk of developing hypertensive disorders and gestational diabetes during pregnancy,16-18 up until recently, there were limited and conflicting data from prospective observational cohorts in which SDB exposure and pregnancy outcomes have been methodically measured and confounding variables carefully considered.19-21 Louis et al.19 reported on a cohort of 175 obese women and demonstrated that women with SDB (apnea-hypopnea index greater than or equal to 5) were more likely to develop preeclampsia (adjusted odds ratio, 3.5; 95% CI, 1.3, 9.9). However, two other small studies failed to demonstrate a positive association between SDB and pregnancy-related hypertension, but one suggested a relationship between SDB and gestational diabetes.20,21
Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be Sleep-Disordered Breathing Substudy
The Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be Sleep-Disordered Breathing Substudy (nuMoM2b-SDB) was a prospective cohort study.22,23 Level 3 home sleep tests were performed using a six-channel monitor that was self-applied by the participant twice during pregnancy, first between 60 and 150 weeks of pregnancy and then again between 220 and 310 weeks. An apnea-hypopnea index (AHI) of at least 5 was used to define SDB. The study was powered to test the primary hypothesis that SDB occurring in pregnancy is associated with an increased incidence of preeclampsia. Secondary outcomes were rates of hypertensive disorders of pregnancy, defined as preeclampsia and prenatal gestational hypertension, and gestational diabetes. Crude and adjusted odds ratios and 95% confidence intervals were calculated from univariate and multivariate logistic regression models. Adjustment covariates included maternal age (less than or equal to 21, 22-35, and over 35 years), body mass index (less than 25, 25 to less than 30, greater than or equal to 30 kg/m2), chronic hypertension (yes, no), and, for midpregnancy, rate of weight gain per week between early and midpregnancy assessments, treated as a continuous variable.
Conclusions and future directions
The nuMoM2b data are provocative because sleep apnea is a potentially modifiable risk factor for adverse pregnancy outcomes. While a majority of SDB cases identified during pregnancy were mild, the nuMoM2b data demonstrate that even modest elevations of AHI in pregnancy are associated with an increased risk of developing hypertensive disorders and an increased incidence of gestational diabetes.
Pregnancy is conceivably an ideal scenario in which to better understand the role of SDB treatment as a preventive strategy for reducing cardiometabolic morbidity as the time frame needed to measure incident outcomes after initiating therapy is significantly contracted. However, data regarding the role of OSA treatment with continuous positive airway pressure (CPAP) during pregnancy, both regarding its acceptability to patients and its therapeutic benefit, are extremely limited. Further research is needed to establish whether universal screening for and treating of SDB in pregnancy can mitigate the risks and consequences of hypertensive disorders of pregnancy and gestational diabetes. However, in the meantime, we have to recognize that as our obstetric patient population is becoming more obese, we will encounter more women with symptomatic SDB in pregnancy. It is well documented that patients with symptomatic SDB, those who report that their snoring leads to chronic sleep disruption and excessive daytime sleepiness, can benefit from CPAP in terms of sleep quality and daytime function. Therefore, in addition to encouraging women already prescribed CPAP to continue their therapy during pregnancy, obstetricians who encounter a patient reporting severe SDB symptoms should refer her to a sleep specialist for further evaluation.
Dr. Facco is assistant professor, department of obstetrics and gynecology, University of Pittsburgh, Magee-Women’s Hospital, Magee Women’s Research Institute.
References
1. Berry RB, Budhiraja R, Gottlieb DJ, et al. Rules for scoring respiratory events in sleep: Update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. Deliberations of the Sleep Apnea Definitions Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2012;8(5):597-619.
2. Park JG, Ramar K, Olson EJ. Updates on definition, consequences, and management of obstructive sleep apnea. Mayo Clin Proc. 2011;86(6):549-54; quiz, 554-5.
3. Iber C, Ancoli-Israel S, Chesson A, Quan S. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. 1st ed. Westchester, Ill.: American Academy of Sleep Medicine, 2007.
4. Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013 May 1;177(9):1006-14.
5. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328(17):1230-5.
6. Young T, Finn L, Austin D, Peterson A. Menopausal status and sleep-disordered breathing in the Wisconsin Sleep Cohort Study. Am J Respir Crit Care Med. 2003;167(9):1181-5.
7. Pien GW, Schwab RJ. Sleep disorders during pregnancy. Sleep. 2004;27(7):1405-17.
8. Hedman C, Pohjasvaara T, Tolonen U, Suhonen-Malm AS, Myllyla VV. Effects of pregnancy on mothers’ sleep. Sleep Med. 2002;3(1):37-42.
9. Pien GW, Fife D, Pack AI, Nkwuo JE, Schwab RJ. Changes in symptoms of sleep-disordered breathing during pregnancy. Sleep. 2005;28(10):1299-1305.
10. Facco FL, Kramer J, Ho KH, Zee PC, Grobman WA. Sleep disturbances in pregnancy. Obstet Gynecol. 2010;115(1):77-83.
11. Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med. 2000;342(19):1378-84.
12. Punjabi NM, Shahar E, Redline S, et al. Sleep-disordered breathing, glucose intolerance, and insulin resistance: The Sleep Heart Health Study. Am J Epidemiol. 2004;160(6):521-30.
13. Reichmuth KJ, Austin D, Skatrud JB, Young T. Association of sleep apnea and type II diabetes: A population-based study. Am J Respir Crit Care Med. 2005;172(12):1590-5.
14. Dempsey JA, Veasey SC, Morgan BJ, O’Donnell CP. Pathophysiology of sleep apnea. Physiol Rev. 2010;90(1):47-112.
15. Romero R, Badr MS. A role for sleep disorders in pregnancy complications: Challenges and opportunities. Am J Obstet Gynecol. 2014;210(1):3-11.
16. O’Brien LM, Bullough AS, Owusu JT, et al. Pregnancy-onset habitual snoring, gestational hypertension, and preeclampsia: Prospective cohort study. Am J Obstet Gynecol. 2012;207(6):487.e1-9
17. Chen YH, Kang JH, Lin CC, Wang IT, Keller JJ, Lin HC. Obstructive sleep apnea and the risk of adverse pregnancy outcomes. Am J Obstet Gynecol. 2012;206(2):136.e1-5.
18. Bourjeily G, Raker CA, Chalhoub M, Miller MA, et al. Pregnancy and fetal outcomes of symptoms of sleep-disordered breathing. Eur Respir J. 2010;36(4):849-55.
19. Louis J, Auckley D, Miladinovic B, et al. Perinatal outcomes associated with obstructive sleep apnea in obese pregnant women. Obstet Gynecol. 2012;120:1085-92.
20. Facco FL, Ouyang DW, Zee PC, et al. Implications of sleep-disordered breathing in pregnancy. Am J Obstet Gynecol. 2014 Jun;210(6):559.e1-6.
21. Pien GW, Pack AI, Jackson N, Maislin G, Macones GA, Schwab RJ. Risk factors for sleep-disordered breathing in pregnancy. Thorax. 2014;69(4):371-7.
22. Facco FL, Parker CB, Reddy UM, et al. NuMoM2b Sleep-Disordered Breathing study: Objectives and methods. Am J Obstet Gynecol. 2015 April;212(4):542.e1–542.e127.
23. Facco FL, Parker CB, Reddy UM, et al. Association between sleep-disordered breathing and hypertensive disorders of pregn ancy and gestational diabetes mellitus. Obstet Gynecol. ePub. 2016 Dec 2.
Background
Sleep-disordered breathing (SDB) conditions are characterized by abnormal respiratory patterns and abnormal gas exchange during sleep.1-3 Obstructive sleep apnea (OSA), the most common type of SDB, is characterized by repetitive episodes of airway narrowing during sleep that lead to respiratory disruption, hypoxia, and sleep fragmentation. In reproductive-aged women, epidemiologic studies suggest a 2% to 13% prevalence of OSA.4-6 Pregnancy is associated with changes that promote OSA, such as weight gain and edema of the upper airway.7 Frequent snoring, a common symptom of OSA, is endorsed by 15% to 25% of pregnant women.8-10 Health outcomes that have been linked to SDB in the nonpregnant population, such as hypertension and insulin-resistant diabetes, have clinically relevant correlates in pregnancy (preeclampsia, gestational diabetes).11-13
While several retrospective and cross-sectional studies suggest that SDB may increase the risk of developing hypertensive disorders and gestational diabetes during pregnancy,16-18 up until recently, there were limited and conflicting data from prospective observational cohorts in which SDB exposure and pregnancy outcomes have been methodically measured and confounding variables carefully considered.19-21 Louis et al.19 reported on a cohort of 175 obese women and demonstrated that women with SDB (apnea-hypopnea index greater than or equal to 5) were more likely to develop preeclampsia (adjusted odds ratio, 3.5; 95% CI, 1.3, 9.9). However, two other small studies failed to demonstrate a positive association between SDB and pregnancy-related hypertension, but one suggested a relationship between SDB and gestational diabetes.20,21
Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be Sleep-Disordered Breathing Substudy
The Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be Sleep-Disordered Breathing Substudy (nuMoM2b-SDB) was a prospective cohort study.22,23 Level 3 home sleep tests were performed using a six-channel monitor that was self-applied by the participant twice during pregnancy, first between 60 and 150 weeks of pregnancy and then again between 220 and 310 weeks. An apnea-hypopnea index (AHI) of at least 5 was used to define SDB. The study was powered to test the primary hypothesis that SDB occurring in pregnancy is associated with an increased incidence of preeclampsia. Secondary outcomes were rates of hypertensive disorders of pregnancy, defined as preeclampsia and prenatal gestational hypertension, and gestational diabetes. Crude and adjusted odds ratios and 95% confidence intervals were calculated from univariate and multivariate logistic regression models. Adjustment covariates included maternal age (less than or equal to 21, 22-35, and over 35 years), body mass index (less than 25, 25 to less than 30, greater than or equal to 30 kg/m2), chronic hypertension (yes, no), and, for midpregnancy, rate of weight gain per week between early and midpregnancy assessments, treated as a continuous variable.
Conclusions and future directions
The nuMoM2b data are provocative because sleep apnea is a potentially modifiable risk factor for adverse pregnancy outcomes. While a majority of SDB cases identified during pregnancy were mild, the nuMoM2b data demonstrate that even modest elevations of AHI in pregnancy are associated with an increased risk of developing hypertensive disorders and an increased incidence of gestational diabetes.
Pregnancy is conceivably an ideal scenario in which to better understand the role of SDB treatment as a preventive strategy for reducing cardiometabolic morbidity as the time frame needed to measure incident outcomes after initiating therapy is significantly contracted. However, data regarding the role of OSA treatment with continuous positive airway pressure (CPAP) during pregnancy, both regarding its acceptability to patients and its therapeutic benefit, are extremely limited. Further research is needed to establish whether universal screening for and treating of SDB in pregnancy can mitigate the risks and consequences of hypertensive disorders of pregnancy and gestational diabetes. However, in the meantime, we have to recognize that as our obstetric patient population is becoming more obese, we will encounter more women with symptomatic SDB in pregnancy. It is well documented that patients with symptomatic SDB, those who report that their snoring leads to chronic sleep disruption and excessive daytime sleepiness, can benefit from CPAP in terms of sleep quality and daytime function. Therefore, in addition to encouraging women already prescribed CPAP to continue their therapy during pregnancy, obstetricians who encounter a patient reporting severe SDB symptoms should refer her to a sleep specialist for further evaluation.
Dr. Facco is assistant professor, department of obstetrics and gynecology, University of Pittsburgh, Magee-Women’s Hospital, Magee Women’s Research Institute.
References
1. Berry RB, Budhiraja R, Gottlieb DJ, et al. Rules for scoring respiratory events in sleep: Update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. Deliberations of the Sleep Apnea Definitions Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2012;8(5):597-619.
2. Park JG, Ramar K, Olson EJ. Updates on definition, consequences, and management of obstructive sleep apnea. Mayo Clin Proc. 2011;86(6):549-54; quiz, 554-5.
3. Iber C, Ancoli-Israel S, Chesson A, Quan S. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. 1st ed. Westchester, Ill.: American Academy of Sleep Medicine, 2007.
4. Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013 May 1;177(9):1006-14.
5. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328(17):1230-5.
6. Young T, Finn L, Austin D, Peterson A. Menopausal status and sleep-disordered breathing in the Wisconsin Sleep Cohort Study. Am J Respir Crit Care Med. 2003;167(9):1181-5.
7. Pien GW, Schwab RJ. Sleep disorders during pregnancy. Sleep. 2004;27(7):1405-17.
8. Hedman C, Pohjasvaara T, Tolonen U, Suhonen-Malm AS, Myllyla VV. Effects of pregnancy on mothers’ sleep. Sleep Med. 2002;3(1):37-42.
9. Pien GW, Fife D, Pack AI, Nkwuo JE, Schwab RJ. Changes in symptoms of sleep-disordered breathing during pregnancy. Sleep. 2005;28(10):1299-1305.
10. Facco FL, Kramer J, Ho KH, Zee PC, Grobman WA. Sleep disturbances in pregnancy. Obstet Gynecol. 2010;115(1):77-83.
11. Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med. 2000;342(19):1378-84.
12. Punjabi NM, Shahar E, Redline S, et al. Sleep-disordered breathing, glucose intolerance, and insulin resistance: The Sleep Heart Health Study. Am J Epidemiol. 2004;160(6):521-30.
13. Reichmuth KJ, Austin D, Skatrud JB, Young T. Association of sleep apnea and type II diabetes: A population-based study. Am J Respir Crit Care Med. 2005;172(12):1590-5.
14. Dempsey JA, Veasey SC, Morgan BJ, O’Donnell CP. Pathophysiology of sleep apnea. Physiol Rev. 2010;90(1):47-112.
15. Romero R, Badr MS. A role for sleep disorders in pregnancy complications: Challenges and opportunities. Am J Obstet Gynecol. 2014;210(1):3-11.
16. O’Brien LM, Bullough AS, Owusu JT, et al. Pregnancy-onset habitual snoring, gestational hypertension, and preeclampsia: Prospective cohort study. Am J Obstet Gynecol. 2012;207(6):487.e1-9
17. Chen YH, Kang JH, Lin CC, Wang IT, Keller JJ, Lin HC. Obstructive sleep apnea and the risk of adverse pregnancy outcomes. Am J Obstet Gynecol. 2012;206(2):136.e1-5.
18. Bourjeily G, Raker CA, Chalhoub M, Miller MA, et al. Pregnancy and fetal outcomes of symptoms of sleep-disordered breathing. Eur Respir J. 2010;36(4):849-55.
19. Louis J, Auckley D, Miladinovic B, et al. Perinatal outcomes associated with obstructive sleep apnea in obese pregnant women. Obstet Gynecol. 2012;120:1085-92.
20. Facco FL, Ouyang DW, Zee PC, et al. Implications of sleep-disordered breathing in pregnancy. Am J Obstet Gynecol. 2014 Jun;210(6):559.e1-6.
21. Pien GW, Pack AI, Jackson N, Maislin G, Macones GA, Schwab RJ. Risk factors for sleep-disordered breathing in pregnancy. Thorax. 2014;69(4):371-7.
22. Facco FL, Parker CB, Reddy UM, et al. NuMoM2b Sleep-Disordered Breathing study: Objectives and methods. Am J Obstet Gynecol. 2015 April;212(4):542.e1–542.e127.
23. Facco FL, Parker CB, Reddy UM, et al. Association between sleep-disordered breathing and hypertensive disorders of pregn ancy and gestational diabetes mellitus. Obstet Gynecol. ePub. 2016 Dec 2.
NETWORKS: Pneumonia Day, evaluating inhalers, tobacco taxes Chest Infections Clinical Pulmonary Medicine Interprofessional Team
Pneumonia Day: Today is the day to act!
This past November 12, we celebrated “Pneumonia Day,” named for a disease that has little connotation in the real world, because of the perception that we need only a short course of antibiotics to get better. Such is the origin of the term “walking pneumonia,” which emphasizes that we can still walk even while sick with pneumonia.
However, we recently experienced the most important moment of awareness related to this condition, when one of the U.S. presidential candidates became sick with that disease known as “pneumonia.”
Suddenly, the media devoted great interest to explore this condition, as if it were a new outbreak or a rare disease that could potentially kill someone. Even the health-care providers seem to believe that “pneumonia” is not a big deal, ignoring the fact that it is the most common infectious cause of death overall, and that it not only affects children but also the elderly and patients with poor immune systems.
One out of nine patients who are admitted to the hospital for pneumonia may die during the hospitalization, and one out of four patients who get admitted to an ICU may not survive the event.
However, it also highlights that pneumonia is more than just an acute disease, compromising the brain, heart, and kidneys. In the long run, even after surviving the hospitalization for pneumonia, it can kill and cause other well-known complications leading to death, such as myocardial infarction, arrhythmias, heart failure, and sudden cardiac death.
Please, stop for one moment and ask yourself about your role in preventing pneumonia and pneumonia-related deaths in your communities. The Chest Infections NetWork is here to help you advocate for the common goal of solving this problem.
Steering Committee Member
Delivery makes a difference: Providing inhaled medication to your patients
One might ask why CHEST (American College of Chest Physicians) and Sunovion developed a steering committee of experts in the field of obstructive lung disease to evaluate the knowledge, attitudes, beliefs, and practices of physicians and other health-care professionals related to inhalational medicines and devices. While inhalers are approved by the FDA Center for Drug Evaluation Research (CEDER) as drug and device combination, the process assesses reproducibility and shelf‐life but does not address the real‐world situation that each of us face with individual patients. How often do clinicians consider the characteristics of each delivery system, as well as the medication being delivered? One might be surprised at the answer.
Patients are frequently prescribed several types of devices with different instructions for optimal use. For example, dry powder inhalers often require high flow rates (30-90 L/min) to deaggregate powder pellets into particles less than 5 mcm, while metereddose inhalers require a slow inspiratory flow (less than 30 L/min). Patients who use both types of devices often confuse which inspiratory flow rate to use with which devices, despite proper education and training. This does not even take into consideration the variable number of steps required by various inhalational devices (which can be as few as 3 steps to as many as 12 steps). Additionally, studies demonstrate that peak inspiratory flow rates, inspiratory volumes, and drug deposition in the lungs may be influenced by gender, height, and weight; as well as by the degree of pulmonary reserve and hyperinflation.
Are there data to suggest that these questions impact the care of patients with severe asthma or COPD? I eagerly await the results of the survey.
Steering Committee Member
A California victory for tobacco control
Californians approved Proposition 56, “Cigarette Tax to Fund Healthcare, Tobacco Use Prevention, Research, and Law Enforcement.” This measure increases the excise tax on all forms of tobacco by $2.00. For the first time, it applies to electronic products that vaporize nicotine that were previously only subject to sales tax. This is in addition to federal excise taxes ($1.01) and state and local sales taxes ($0.50 to $0.60). (https://ballotpedia.org/California_Proposition_56,_Tobacco _Tax_Increase_(2016)
When Prop 56 goes into effect April 1, 2017, the average price of a package of cigarettes will increase to at least $7.89. Based on data from the Surgeon General’s report on “Preventing Tobacco Use Among Youth and Young Adults,” this tax increase should equate with a fall in smoking rates by about 12%. Youth and young adults are particularly susceptible to price increases, which helps prevent smoking initiation or continuation.
Tobacco-related health-care costs Californians $3.5 billion dollars annually (Official Voter Information Guide, 2016). Funds raised by Prop 56 will be used by state and local health programs such as Medi-Cal to defray the costs of smoking prevention pro
Prop 56 expands on tougher laws implemented in 2016 that expanded the workplace prohibition of smoking, increased fees for tobacco retailers and wholesalers, broadened the definition of smoking to include e-cigarettes, and increased the minimum age to purchase tobacco to 21 years old. Combined, these measures are expected to result in a further decline in tobacco usage in California.
Alan Roth, RRT, MS, FCCP
Steering Committee Member
Pneumonia Day: Today is the day to act!
This past November 12, we celebrated “Pneumonia Day,” named for a disease that has little connotation in the real world, because of the perception that we need only a short course of antibiotics to get better. Such is the origin of the term “walking pneumonia,” which emphasizes that we can still walk even while sick with pneumonia.
However, we recently experienced the most important moment of awareness related to this condition, when one of the U.S. presidential candidates became sick with that disease known as “pneumonia.”
Suddenly, the media devoted great interest to explore this condition, as if it were a new outbreak or a rare disease that could potentially kill someone. Even the health-care providers seem to believe that “pneumonia” is not a big deal, ignoring the fact that it is the most common infectious cause of death overall, and that it not only affects children but also the elderly and patients with poor immune systems.
One out of nine patients who are admitted to the hospital for pneumonia may die during the hospitalization, and one out of four patients who get admitted to an ICU may not survive the event.
However, it also highlights that pneumonia is more than just an acute disease, compromising the brain, heart, and kidneys. In the long run, even after surviving the hospitalization for pneumonia, it can kill and cause other well-known complications leading to death, such as myocardial infarction, arrhythmias, heart failure, and sudden cardiac death.
Please, stop for one moment and ask yourself about your role in preventing pneumonia and pneumonia-related deaths in your communities. The Chest Infections NetWork is here to help you advocate for the common goal of solving this problem.
Steering Committee Member
Delivery makes a difference: Providing inhaled medication to your patients
One might ask why CHEST (American College of Chest Physicians) and Sunovion developed a steering committee of experts in the field of obstructive lung disease to evaluate the knowledge, attitudes, beliefs, and practices of physicians and other health-care professionals related to inhalational medicines and devices. While inhalers are approved by the FDA Center for Drug Evaluation Research (CEDER) as drug and device combination, the process assesses reproducibility and shelf‐life but does not address the real‐world situation that each of us face with individual patients. How often do clinicians consider the characteristics of each delivery system, as well as the medication being delivered? One might be surprised at the answer.
Patients are frequently prescribed several types of devices with different instructions for optimal use. For example, dry powder inhalers often require high flow rates (30-90 L/min) to deaggregate powder pellets into particles less than 5 mcm, while metereddose inhalers require a slow inspiratory flow (less than 30 L/min). Patients who use both types of devices often confuse which inspiratory flow rate to use with which devices, despite proper education and training. This does not even take into consideration the variable number of steps required by various inhalational devices (which can be as few as 3 steps to as many as 12 steps). Additionally, studies demonstrate that peak inspiratory flow rates, inspiratory volumes, and drug deposition in the lungs may be influenced by gender, height, and weight; as well as by the degree of pulmonary reserve and hyperinflation.
Are there data to suggest that these questions impact the care of patients with severe asthma or COPD? I eagerly await the results of the survey.
Steering Committee Member
A California victory for tobacco control
Californians approved Proposition 56, “Cigarette Tax to Fund Healthcare, Tobacco Use Prevention, Research, and Law Enforcement.” This measure increases the excise tax on all forms of tobacco by $2.00. For the first time, it applies to electronic products that vaporize nicotine that were previously only subject to sales tax. This is in addition to federal excise taxes ($1.01) and state and local sales taxes ($0.50 to $0.60). (https://ballotpedia.org/California_Proposition_56,_Tobacco _Tax_Increase_(2016)
When Prop 56 goes into effect April 1, 2017, the average price of a package of cigarettes will increase to at least $7.89. Based on data from the Surgeon General’s report on “Preventing Tobacco Use Among Youth and Young Adults,” this tax increase should equate with a fall in smoking rates by about 12%. Youth and young adults are particularly susceptible to price increases, which helps prevent smoking initiation or continuation.
Tobacco-related health-care costs Californians $3.5 billion dollars annually (Official Voter Information Guide, 2016). Funds raised by Prop 56 will be used by state and local health programs such as Medi-Cal to defray the costs of smoking prevention pro
Prop 56 expands on tougher laws implemented in 2016 that expanded the workplace prohibition of smoking, increased fees for tobacco retailers and wholesalers, broadened the definition of smoking to include e-cigarettes, and increased the minimum age to purchase tobacco to 21 years old. Combined, these measures are expected to result in a further decline in tobacco usage in California.
Alan Roth, RRT, MS, FCCP
Steering Committee Member
Pneumonia Day: Today is the day to act!
This past November 12, we celebrated “Pneumonia Day,” named for a disease that has little connotation in the real world, because of the perception that we need only a short course of antibiotics to get better. Such is the origin of the term “walking pneumonia,” which emphasizes that we can still walk even while sick with pneumonia.
However, we recently experienced the most important moment of awareness related to this condition, when one of the U.S. presidential candidates became sick with that disease known as “pneumonia.”
Suddenly, the media devoted great interest to explore this condition, as if it were a new outbreak or a rare disease that could potentially kill someone. Even the health-care providers seem to believe that “pneumonia” is not a big deal, ignoring the fact that it is the most common infectious cause of death overall, and that it not only affects children but also the elderly and patients with poor immune systems.
One out of nine patients who are admitted to the hospital for pneumonia may die during the hospitalization, and one out of four patients who get admitted to an ICU may not survive the event.
However, it also highlights that pneumonia is more than just an acute disease, compromising the brain, heart, and kidneys. In the long run, even after surviving the hospitalization for pneumonia, it can kill and cause other well-known complications leading to death, such as myocardial infarction, arrhythmias, heart failure, and sudden cardiac death.
Please, stop for one moment and ask yourself about your role in preventing pneumonia and pneumonia-related deaths in your communities. The Chest Infections NetWork is here to help you advocate for the common goal of solving this problem.
Steering Committee Member
Delivery makes a difference: Providing inhaled medication to your patients
One might ask why CHEST (American College of Chest Physicians) and Sunovion developed a steering committee of experts in the field of obstructive lung disease to evaluate the knowledge, attitudes, beliefs, and practices of physicians and other health-care professionals related to inhalational medicines and devices. While inhalers are approved by the FDA Center for Drug Evaluation Research (CEDER) as drug and device combination, the process assesses reproducibility and shelf‐life but does not address the real‐world situation that each of us face with individual patients. How often do clinicians consider the characteristics of each delivery system, as well as the medication being delivered? One might be surprised at the answer.
Patients are frequently prescribed several types of devices with different instructions for optimal use. For example, dry powder inhalers often require high flow rates (30-90 L/min) to deaggregate powder pellets into particles less than 5 mcm, while metereddose inhalers require a slow inspiratory flow (less than 30 L/min). Patients who use both types of devices often confuse which inspiratory flow rate to use with which devices, despite proper education and training. This does not even take into consideration the variable number of steps required by various inhalational devices (which can be as few as 3 steps to as many as 12 steps). Additionally, studies demonstrate that peak inspiratory flow rates, inspiratory volumes, and drug deposition in the lungs may be influenced by gender, height, and weight; as well as by the degree of pulmonary reserve and hyperinflation.
Are there data to suggest that these questions impact the care of patients with severe asthma or COPD? I eagerly await the results of the survey.
Steering Committee Member
A California victory for tobacco control
Californians approved Proposition 56, “Cigarette Tax to Fund Healthcare, Tobacco Use Prevention, Research, and Law Enforcement.” This measure increases the excise tax on all forms of tobacco by $2.00. For the first time, it applies to electronic products that vaporize nicotine that were previously only subject to sales tax. This is in addition to federal excise taxes ($1.01) and state and local sales taxes ($0.50 to $0.60). (https://ballotpedia.org/California_Proposition_56,_Tobacco _Tax_Increase_(2016)
When Prop 56 goes into effect April 1, 2017, the average price of a package of cigarettes will increase to at least $7.89. Based on data from the Surgeon General’s report on “Preventing Tobacco Use Among Youth and Young Adults,” this tax increase should equate with a fall in smoking rates by about 12%. Youth and young adults are particularly susceptible to price increases, which helps prevent smoking initiation or continuation.
Tobacco-related health-care costs Californians $3.5 billion dollars annually (Official Voter Information Guide, 2016). Funds raised by Prop 56 will be used by state and local health programs such as Medi-Cal to defray the costs of smoking prevention pro
Prop 56 expands on tougher laws implemented in 2016 that expanded the workplace prohibition of smoking, increased fees for tobacco retailers and wholesalers, broadened the definition of smoking to include e-cigarettes, and increased the minimum age to purchase tobacco to 21 years old. Combined, these measures are expected to result in a further decline in tobacco usage in California.
Alan Roth, RRT, MS, FCCP
Steering Committee Member