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Breakfast and weight loss
Eating breakfast is sometimes promulgated as a component of an effective weight loss strategy. Correlational studies have suggested that breakfast consumption is associated with lower body weight. As the thinking goes, breakfast promotes morning satiety, thus suppressing caloric intake later in the day. Skipping breakfast, however, results in increased caloric intake later in the day.
But most people are breakfast eaters. Data exist suggesting that the adverse effects of skipping breakfast may occur only in habitual breakfast eaters. In other words, it may be harmful only if you suddenly change your habits.
So, what should we be telling our “breakfast-skippers” about breakfast and weight loss?
Gabrielle LeCheminant and her colleagues conducted a randomized trial of habitual breakfast skippers to evaluate the effects of eating breakfast versus not on energy, macronutrient consumption, and physical activity over 1 month (Appetite. 2017 May 1. doi: 10.1016/j.appet.2016.12.041).
Subjects were required to eat within 90 minutes of waking up and finish eating by 8:30 a.m. No eating or snack restrictions were imposed after breakfast. Subjects were 18-55 years of age, ate breakfast (at least 2 days/week), slept at least 6 hours per night, and woke up consistently before 8:00 am. Biometric and food diaries were completed.
Breakfast-skippers randomized to eat breakfast consumed more calories (266) per day and weighed more (0.7 kg) at 1 month. No changes were observed in caloric compensation with subsequent meals nor in self-reported hunger or satiety. No additional physical activity was observed with the addition of breakfast.
Weight gain was minimal, and the time frame of the study was short. Even so, I think the take-home message from this is: Don’t tell habitual breakfast skippers to start eating breakfast with the goal of losing weight. It appears that the opposite may be true.
Dr. Ebbert is a professor of medicine and general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article.
Eating breakfast is sometimes promulgated as a component of an effective weight loss strategy. Correlational studies have suggested that breakfast consumption is associated with lower body weight. As the thinking goes, breakfast promotes morning satiety, thus suppressing caloric intake later in the day. Skipping breakfast, however, results in increased caloric intake later in the day.
But most people are breakfast eaters. Data exist suggesting that the adverse effects of skipping breakfast may occur only in habitual breakfast eaters. In other words, it may be harmful only if you suddenly change your habits.
So, what should we be telling our “breakfast-skippers” about breakfast and weight loss?
Gabrielle LeCheminant and her colleagues conducted a randomized trial of habitual breakfast skippers to evaluate the effects of eating breakfast versus not on energy, macronutrient consumption, and physical activity over 1 month (Appetite. 2017 May 1. doi: 10.1016/j.appet.2016.12.041).
Subjects were required to eat within 90 minutes of waking up and finish eating by 8:30 a.m. No eating or snack restrictions were imposed after breakfast. Subjects were 18-55 years of age, ate breakfast (at least 2 days/week), slept at least 6 hours per night, and woke up consistently before 8:00 am. Biometric and food diaries were completed.
Breakfast-skippers randomized to eat breakfast consumed more calories (266) per day and weighed more (0.7 kg) at 1 month. No changes were observed in caloric compensation with subsequent meals nor in self-reported hunger or satiety. No additional physical activity was observed with the addition of breakfast.
Weight gain was minimal, and the time frame of the study was short. Even so, I think the take-home message from this is: Don’t tell habitual breakfast skippers to start eating breakfast with the goal of losing weight. It appears that the opposite may be true.
Dr. Ebbert is a professor of medicine and general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article.
Eating breakfast is sometimes promulgated as a component of an effective weight loss strategy. Correlational studies have suggested that breakfast consumption is associated with lower body weight. As the thinking goes, breakfast promotes morning satiety, thus suppressing caloric intake later in the day. Skipping breakfast, however, results in increased caloric intake later in the day.
But most people are breakfast eaters. Data exist suggesting that the adverse effects of skipping breakfast may occur only in habitual breakfast eaters. In other words, it may be harmful only if you suddenly change your habits.
So, what should we be telling our “breakfast-skippers” about breakfast and weight loss?
Gabrielle LeCheminant and her colleagues conducted a randomized trial of habitual breakfast skippers to evaluate the effects of eating breakfast versus not on energy, macronutrient consumption, and physical activity over 1 month (Appetite. 2017 May 1. doi: 10.1016/j.appet.2016.12.041).
Subjects were required to eat within 90 minutes of waking up and finish eating by 8:30 a.m. No eating or snack restrictions were imposed after breakfast. Subjects were 18-55 years of age, ate breakfast (at least 2 days/week), slept at least 6 hours per night, and woke up consistently before 8:00 am. Biometric and food diaries were completed.
Breakfast-skippers randomized to eat breakfast consumed more calories (266) per day and weighed more (0.7 kg) at 1 month. No changes were observed in caloric compensation with subsequent meals nor in self-reported hunger or satiety. No additional physical activity was observed with the addition of breakfast.
Weight gain was minimal, and the time frame of the study was short. Even so, I think the take-home message from this is: Don’t tell habitual breakfast skippers to start eating breakfast with the goal of losing weight. It appears that the opposite may be true.
Dr. Ebbert is a professor of medicine and general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article.
Doctors, drug reps, and free speech
Question: The First Amendment guarantees the right of free speech, but the U.S. Supreme Court has held that under a strict scrutiny standard, the government may regulate:
A. Obscenity.
B. Fighting words.
C. Professional speech.
D. A and B.
E. A, B, and C.
Answer: D. The First Amendment forbids the government from “abridging the freedom of speech,” which extends to certain nonverbal conduct, such as flag burning. At the same time, the U.S. Supreme Court has also ruled that certain categories of speech such as obscenity and fighting words can be regulated under a strict scrutiny standard. However, it remains unsettled whether and to what extent professional speech – such as in the context of the doctor-patient relationship – may be curtailed.
Two recent cases grapple with this issue of free speech – with rather unexpected results.
The first, overturning a decades-old prohibition of the off-label detailing of drugs, surprisingly was decided against the government. The second challenges a Florida statute censoring the discussion of firearms safety between a doctor and a patient. An early decision, under reconsideration, in fact supported the state’s regulation of physicians’ freedom of speech under the circumstances.
Because the FDA has no jurisdiction over physician conduct, it has no power to regulate the off-label use of an otherwise approved drug, which explains why such off-label prescriptions are widespread, especially in the oncology field.
In U.S. v. Caronia, the defendant, a pharmaceutical sales representative, was criminally prosecuted and found guilty of conspiracy in a New York court for introducing a misbranded drug into interstate commerce.1 Specifically, Alfred Caronia promoted the drug Xyrem for use in a manner not approved by the FDA.
Orphan Medical, now known as Jazz Pharmaceuticals, is the manufacturer of Xyrem, a powerful central nervous system depressant. Xyrem’s active ingredient is gamma-hydroxybutyrate, which has been federally classified as the “date rape drug” for its use in the commission of sexual assaults. The FDA had approved Xyrem for two conditions: to treat narcolepsy patients who experience cataplexy, a condition associated with weak or paralyzed muscles; and to treat those with excessive daytime sleepiness.
Caronia was found to provide off-label detailing of the drug to doctors for unapproved indications such as chronic fatigue, fibromyalgia, restless leg syndrome, and Parkinson’s disease.
Caronia argued that in promoting an FDA-approved drug, albeit for off-label use, he was within his right of free speech under the First Amendment. In overturning his conviction, a three-judge panel of the U.S. Second Circuit Court of Appeals agreed, noting the overly broad FDA regulations and specifically that nothing Caronia did constituted conspiracy to put a false or misleading or deficient label on a drug product.
The court concluded: “The government cannot prosecute pharmaceutical manufacturers and their representatives under the FDCA [Federal Food, Drug, and Cosmetic Act] for speech promoting the lawful, off-label use of an FDA-approved drug.”
In 2011, the U.S. Supreme Court had used a First Amendment argument to invalidate a Vermont law that prohibited the practice of pharmaceutical data mining – purchasing information about prescribers from pharmacies and others.2
Taken together, the FDA now appears resigned to the free speech argument.3 For example, it has decided not to appeal a judge’s ruling that the First Amendment protects Amarin from promoting its fish-oil capsules for unapproved uses. Just recently, the FDA published a draft proposal in tacit acceptance of this new policy position, merely recommending the disclosure of relevant information including limitations and unfavorable or inconsistent findings surrounding the off-label use of a drug.
The next issue concerns professional speech. It is well documented that the presence of a gun in the home increases the risk of death especially by suicide, and this serves as the impetus for the long-established recommendation that physicians discuss firearm safety with their patients.
The medical profession was therefore aghast when Florida enacted its law on “Privacy of Firearm Owners.”4 Codified on June 2, 2011, it provides that a licensed practitioner or facility may not record firearm ownership information in a patient’s medical record, and that unless information is relevant to the patient’s medical care or safety or safety of others, inquiries regarding firearm ownership or possession should not be made. A practitioner is also forbidden from unnecessarily harassing a patient about firearm ownership during an examination.
Violation can result in disciplinary action; the original intent was to make this a third-degree felony with penalties of up to $5 million in fines and 5 years of imprisonment, but the final bill was stripped of criminal penalties.
In July 2015, a panel of three judges of the U.S. 11th Circuit Court of Appeals, in a split 2-1 decision, found that the inquiry, record-keeping, and harassment provisions of the act specifically regulate professional speech, which is subject to an intermediate level of scrutiny. Under this level of scrutiny, the court found that the act was precisely tailored to directly advance the state’s substantial interests in protecting the public and patient privacy rights.
Holding that the act was not so overly broad as to violate the First Amendment, the court ruled that laws regulating speech that occurs in the course of the physician-patient relationship are constitutional if they directly advance a substantial state interest.5
Predictably, several medical societies, including the AMA, have filed briefs arguing that the law is unconstitutional and intrudes on the practice of medicine. Effective medical care is believed to require “unfettered communications” between physicians and their patients. Besides, the law is at odds with the AMA’s longstanding policy that encourages members to inquire into the presence of firearms in households and to promote the use of safety locks on guns in an effort to reduce injuries to children.
On June 21, 2016, the full 11th Circuit Court of Appeals (sitting “en banc”) heard arguments, and the profession eagerly awaits its final opinion.
Meanwhile, commentators have expressed concerns that such laws threaten the sanctity of the physician-patient relationship, which relies on truthful communication to freely counsel patients.
This infringement may be gathering force. Missouri and Montana already have similar gun privacy laws, while other states have required physicians to keep confidential any information regarding chemicals used in fracking, or mandate the provision of various birth-related information prior to a woman’s decision to have an abortion.6
References
1. U.S. v. Caronia, 703 F.3d 149 (2d Cir. 2012).
2. Sorrell v. IMS Health, 131 S. Ct. 2653 (2011).
3. N Engl J Med. 2013 Jan 10;368(2):103-5.
4. Fla. St. 381.026, 456.072, 790.338.
5. Wollschlaeger v. Governor of Florida, 797 F.3d 859 (11th Cir. 2015).
6. N Engl J Med. 2016 Jun 16;374(24):2304-7.
Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, and currently directs the St. Francis International Center for Healthcare Ethics in Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. Some of the articles in this series are adapted from the author’s 2006 book, “Medical Malpractice: Understanding the Law, Managing the Risk,” and his 2012 Halsbury treatise, “Medical Negligence and Professional Misconduct.” For additional information, readers may contact the author at [email protected].
Question: The First Amendment guarantees the right of free speech, but the U.S. Supreme Court has held that under a strict scrutiny standard, the government may regulate:
A. Obscenity.
B. Fighting words.
C. Professional speech.
D. A and B.
E. A, B, and C.
Answer: D. The First Amendment forbids the government from “abridging the freedom of speech,” which extends to certain nonverbal conduct, such as flag burning. At the same time, the U.S. Supreme Court has also ruled that certain categories of speech such as obscenity and fighting words can be regulated under a strict scrutiny standard. However, it remains unsettled whether and to what extent professional speech – such as in the context of the doctor-patient relationship – may be curtailed.
Two recent cases grapple with this issue of free speech – with rather unexpected results.
The first, overturning a decades-old prohibition of the off-label detailing of drugs, surprisingly was decided against the government. The second challenges a Florida statute censoring the discussion of firearms safety between a doctor and a patient. An early decision, under reconsideration, in fact supported the state’s regulation of physicians’ freedom of speech under the circumstances.
Because the FDA has no jurisdiction over physician conduct, it has no power to regulate the off-label use of an otherwise approved drug, which explains why such off-label prescriptions are widespread, especially in the oncology field.
In U.S. v. Caronia, the defendant, a pharmaceutical sales representative, was criminally prosecuted and found guilty of conspiracy in a New York court for introducing a misbranded drug into interstate commerce.1 Specifically, Alfred Caronia promoted the drug Xyrem for use in a manner not approved by the FDA.
Orphan Medical, now known as Jazz Pharmaceuticals, is the manufacturer of Xyrem, a powerful central nervous system depressant. Xyrem’s active ingredient is gamma-hydroxybutyrate, which has been federally classified as the “date rape drug” for its use in the commission of sexual assaults. The FDA had approved Xyrem for two conditions: to treat narcolepsy patients who experience cataplexy, a condition associated with weak or paralyzed muscles; and to treat those with excessive daytime sleepiness.
Caronia was found to provide off-label detailing of the drug to doctors for unapproved indications such as chronic fatigue, fibromyalgia, restless leg syndrome, and Parkinson’s disease.
Caronia argued that in promoting an FDA-approved drug, albeit for off-label use, he was within his right of free speech under the First Amendment. In overturning his conviction, a three-judge panel of the U.S. Second Circuit Court of Appeals agreed, noting the overly broad FDA regulations and specifically that nothing Caronia did constituted conspiracy to put a false or misleading or deficient label on a drug product.
The court concluded: “The government cannot prosecute pharmaceutical manufacturers and their representatives under the FDCA [Federal Food, Drug, and Cosmetic Act] for speech promoting the lawful, off-label use of an FDA-approved drug.”
In 2011, the U.S. Supreme Court had used a First Amendment argument to invalidate a Vermont law that prohibited the practice of pharmaceutical data mining – purchasing information about prescribers from pharmacies and others.2
Taken together, the FDA now appears resigned to the free speech argument.3 For example, it has decided not to appeal a judge’s ruling that the First Amendment protects Amarin from promoting its fish-oil capsules for unapproved uses. Just recently, the FDA published a draft proposal in tacit acceptance of this new policy position, merely recommending the disclosure of relevant information including limitations and unfavorable or inconsistent findings surrounding the off-label use of a drug.
The next issue concerns professional speech. It is well documented that the presence of a gun in the home increases the risk of death especially by suicide, and this serves as the impetus for the long-established recommendation that physicians discuss firearm safety with their patients.
The medical profession was therefore aghast when Florida enacted its law on “Privacy of Firearm Owners.”4 Codified on June 2, 2011, it provides that a licensed practitioner or facility may not record firearm ownership information in a patient’s medical record, and that unless information is relevant to the patient’s medical care or safety or safety of others, inquiries regarding firearm ownership or possession should not be made. A practitioner is also forbidden from unnecessarily harassing a patient about firearm ownership during an examination.
Violation can result in disciplinary action; the original intent was to make this a third-degree felony with penalties of up to $5 million in fines and 5 years of imprisonment, but the final bill was stripped of criminal penalties.
In July 2015, a panel of three judges of the U.S. 11th Circuit Court of Appeals, in a split 2-1 decision, found that the inquiry, record-keeping, and harassment provisions of the act specifically regulate professional speech, which is subject to an intermediate level of scrutiny. Under this level of scrutiny, the court found that the act was precisely tailored to directly advance the state’s substantial interests in protecting the public and patient privacy rights.
Holding that the act was not so overly broad as to violate the First Amendment, the court ruled that laws regulating speech that occurs in the course of the physician-patient relationship are constitutional if they directly advance a substantial state interest.5
Predictably, several medical societies, including the AMA, have filed briefs arguing that the law is unconstitutional and intrudes on the practice of medicine. Effective medical care is believed to require “unfettered communications” between physicians and their patients. Besides, the law is at odds with the AMA’s longstanding policy that encourages members to inquire into the presence of firearms in households and to promote the use of safety locks on guns in an effort to reduce injuries to children.
On June 21, 2016, the full 11th Circuit Court of Appeals (sitting “en banc”) heard arguments, and the profession eagerly awaits its final opinion.
Meanwhile, commentators have expressed concerns that such laws threaten the sanctity of the physician-patient relationship, which relies on truthful communication to freely counsel patients.
This infringement may be gathering force. Missouri and Montana already have similar gun privacy laws, while other states have required physicians to keep confidential any information regarding chemicals used in fracking, or mandate the provision of various birth-related information prior to a woman’s decision to have an abortion.6
References
1. U.S. v. Caronia, 703 F.3d 149 (2d Cir. 2012).
2. Sorrell v. IMS Health, 131 S. Ct. 2653 (2011).
3. N Engl J Med. 2013 Jan 10;368(2):103-5.
4. Fla. St. 381.026, 456.072, 790.338.
5. Wollschlaeger v. Governor of Florida, 797 F.3d 859 (11th Cir. 2015).
6. N Engl J Med. 2016 Jun 16;374(24):2304-7.
Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, and currently directs the St. Francis International Center for Healthcare Ethics in Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. Some of the articles in this series are adapted from the author’s 2006 book, “Medical Malpractice: Understanding the Law, Managing the Risk,” and his 2012 Halsbury treatise, “Medical Negligence and Professional Misconduct.” For additional information, readers may contact the author at [email protected].
Question: The First Amendment guarantees the right of free speech, but the U.S. Supreme Court has held that under a strict scrutiny standard, the government may regulate:
A. Obscenity.
B. Fighting words.
C. Professional speech.
D. A and B.
E. A, B, and C.
Answer: D. The First Amendment forbids the government from “abridging the freedom of speech,” which extends to certain nonverbal conduct, such as flag burning. At the same time, the U.S. Supreme Court has also ruled that certain categories of speech such as obscenity and fighting words can be regulated under a strict scrutiny standard. However, it remains unsettled whether and to what extent professional speech – such as in the context of the doctor-patient relationship – may be curtailed.
Two recent cases grapple with this issue of free speech – with rather unexpected results.
The first, overturning a decades-old prohibition of the off-label detailing of drugs, surprisingly was decided against the government. The second challenges a Florida statute censoring the discussion of firearms safety between a doctor and a patient. An early decision, under reconsideration, in fact supported the state’s regulation of physicians’ freedom of speech under the circumstances.
Because the FDA has no jurisdiction over physician conduct, it has no power to regulate the off-label use of an otherwise approved drug, which explains why such off-label prescriptions are widespread, especially in the oncology field.
In U.S. v. Caronia, the defendant, a pharmaceutical sales representative, was criminally prosecuted and found guilty of conspiracy in a New York court for introducing a misbranded drug into interstate commerce.1 Specifically, Alfred Caronia promoted the drug Xyrem for use in a manner not approved by the FDA.
Orphan Medical, now known as Jazz Pharmaceuticals, is the manufacturer of Xyrem, a powerful central nervous system depressant. Xyrem’s active ingredient is gamma-hydroxybutyrate, which has been federally classified as the “date rape drug” for its use in the commission of sexual assaults. The FDA had approved Xyrem for two conditions: to treat narcolepsy patients who experience cataplexy, a condition associated with weak or paralyzed muscles; and to treat those with excessive daytime sleepiness.
Caronia was found to provide off-label detailing of the drug to doctors for unapproved indications such as chronic fatigue, fibromyalgia, restless leg syndrome, and Parkinson’s disease.
Caronia argued that in promoting an FDA-approved drug, albeit for off-label use, he was within his right of free speech under the First Amendment. In overturning his conviction, a three-judge panel of the U.S. Second Circuit Court of Appeals agreed, noting the overly broad FDA regulations and specifically that nothing Caronia did constituted conspiracy to put a false or misleading or deficient label on a drug product.
The court concluded: “The government cannot prosecute pharmaceutical manufacturers and their representatives under the FDCA [Federal Food, Drug, and Cosmetic Act] for speech promoting the lawful, off-label use of an FDA-approved drug.”
In 2011, the U.S. Supreme Court had used a First Amendment argument to invalidate a Vermont law that prohibited the practice of pharmaceutical data mining – purchasing information about prescribers from pharmacies and others.2
Taken together, the FDA now appears resigned to the free speech argument.3 For example, it has decided not to appeal a judge’s ruling that the First Amendment protects Amarin from promoting its fish-oil capsules for unapproved uses. Just recently, the FDA published a draft proposal in tacit acceptance of this new policy position, merely recommending the disclosure of relevant information including limitations and unfavorable or inconsistent findings surrounding the off-label use of a drug.
The next issue concerns professional speech. It is well documented that the presence of a gun in the home increases the risk of death especially by suicide, and this serves as the impetus for the long-established recommendation that physicians discuss firearm safety with their patients.
The medical profession was therefore aghast when Florida enacted its law on “Privacy of Firearm Owners.”4 Codified on June 2, 2011, it provides that a licensed practitioner or facility may not record firearm ownership information in a patient’s medical record, and that unless information is relevant to the patient’s medical care or safety or safety of others, inquiries regarding firearm ownership or possession should not be made. A practitioner is also forbidden from unnecessarily harassing a patient about firearm ownership during an examination.
Violation can result in disciplinary action; the original intent was to make this a third-degree felony with penalties of up to $5 million in fines and 5 years of imprisonment, but the final bill was stripped of criminal penalties.
In July 2015, a panel of three judges of the U.S. 11th Circuit Court of Appeals, in a split 2-1 decision, found that the inquiry, record-keeping, and harassment provisions of the act specifically regulate professional speech, which is subject to an intermediate level of scrutiny. Under this level of scrutiny, the court found that the act was precisely tailored to directly advance the state’s substantial interests in protecting the public and patient privacy rights.
Holding that the act was not so overly broad as to violate the First Amendment, the court ruled that laws regulating speech that occurs in the course of the physician-patient relationship are constitutional if they directly advance a substantial state interest.5
Predictably, several medical societies, including the AMA, have filed briefs arguing that the law is unconstitutional and intrudes on the practice of medicine. Effective medical care is believed to require “unfettered communications” between physicians and their patients. Besides, the law is at odds with the AMA’s longstanding policy that encourages members to inquire into the presence of firearms in households and to promote the use of safety locks on guns in an effort to reduce injuries to children.
On June 21, 2016, the full 11th Circuit Court of Appeals (sitting “en banc”) heard arguments, and the profession eagerly awaits its final opinion.
Meanwhile, commentators have expressed concerns that such laws threaten the sanctity of the physician-patient relationship, which relies on truthful communication to freely counsel patients.
This infringement may be gathering force. Missouri and Montana already have similar gun privacy laws, while other states have required physicians to keep confidential any information regarding chemicals used in fracking, or mandate the provision of various birth-related information prior to a woman’s decision to have an abortion.6
References
1. U.S. v. Caronia, 703 F.3d 149 (2d Cir. 2012).
2. Sorrell v. IMS Health, 131 S. Ct. 2653 (2011).
3. N Engl J Med. 2013 Jan 10;368(2):103-5.
4. Fla. St. 381.026, 456.072, 790.338.
5. Wollschlaeger v. Governor of Florida, 797 F.3d 859 (11th Cir. 2015).
6. N Engl J Med. 2016 Jun 16;374(24):2304-7.
Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, and currently directs the St. Francis International Center for Healthcare Ethics in Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. Some of the articles in this series are adapted from the author’s 2006 book, “Medical Malpractice: Understanding the Law, Managing the Risk,” and his 2012 Halsbury treatise, “Medical Negligence and Professional Misconduct.” For additional information, readers may contact the author at [email protected].
Nurse Jackie and Patrick Kennedy
Nurse Jackie is an amazing woman: She’s a fantastically competent and compassionate ER nurse who will do anything for her patients, and she is far better than the caricature ER docs she works with who all care more about their designer shoes and designer egos then about their jobs. She’s a wife – at least in the early episodes – and mother to two adorable girls with a life that includes Mommy and Me tap dancing classes. She somehow juggles it all.
In her fictional life as the star of a Showtime series, “Jackie Peyton” – played by actress Edie Falco, formerly known for her role as Tony Soprano’s wife, Carmela – manages even more: She does it all while popping pain pills by the handful throughout the work day and snorting whatever there is to snort. The interesting thing about Jackie is that her drug habit never interferes with her ability to function. There are no episodes where she makes mistakes or falls asleep. She doesn’t get too wired and is rarely irritable, and she certainly doesn’t pass out from overdoses. She shows up at work on time and never falls off her tightrope of responsibilities in the busy All Saints Hospital ER of New York City.
Without the drugs, she gets ill, but with them, she just functions. And she doesn’t just hold her own with a busy life; she also juggles the secret life of what it takes to get her daily fix, including daily lunchtime sex with the hospital pharmacist, who provides her with pain medicines for her aching back and doesn’t initially know that she’s married with children.
By Season 6, her personal life has broken down, and her daughter Grace, now an angry teenager with her own difficulties and secret life, notes that mom Jackie is incredibly good at hiding her drug use, and that no one can tell when she’s using.
With each season, Jackie’s personal life unwinds a little more, but it’s not because of the effects constant pill-popping has on her behavior; it’s because of the difficulties she has obtaining the drugs. If she could go to the store and buy large amounts of oxycontin and whatever else she takes, she’d have no problem. Her cauldron, however, is filled with constant lies and deception and the secret lives she lives to obtain drugs and to avoid boiling in her own self-made addictive mess.
You wouldn’t expect a review of a dark comedy TV series together with a review of a very serious memoir written by former Rep. Patrick J. Kennedy, but somehow, the two fit together for me.
In “A Common Struggle,” Patrick Kennedy and author Stephen Fried march through Kennedy’s long history of mental illness and substance abuse. Kennedy talks about his life in psychotherapy starting in childhood, related to his parents’ separation. He talks about the treatment he received in college and during his time as a state legislator in Providence, R.I., and how he parked far from his psychiatrist’s office so no one would learn he was in treatment.
Unfortunately, while he found treatment to be very helpful, he stopped when his doctor, Peter Kramer, became a celebrity in his own right after the publication of “Listening to Prozac” (New York: Penguin Books, 1997), and Kennedy became “spooked.” He goes on to talk about the many treatments – including lists of medications – he received over the years and his diagnosis of bipolar disorder, type II. But he doesn’t document what symptoms or episodes led to this diagnosis, and I couldn’t help but wonder how much of his mood disorder was part and parcel of his substance abuse problem. I imagine his doctors may have had the same problem.
So while Kennedy is vague about his psychiatric illness, he is much more forthcoming with his substance abuse problem. Like Nurse Jackie, he has the constant flow of pills – prescribed opiates starting with the diagnosis of a spinal tumor, a handful of Adderall here, some benzodiazepines there, and an enormous issue with alcohol on top of all that. Unlike Nurse Jackie, Kennedy wears the results of his addictions openly. He sleeps through mornings, and his schedulers know to accommodate this. He says things he otherwise wouldn’t while intoxicated, and he embarrasses himself and has others on edge. His mentor in the House of Representatives was Dick Gephardt, and Gephardt’s chief of staff summoned Kennedy to ask him to become chairman of the Democratic Congressional Campaign Committee – a tremendous honor for a 31-year-old congressman.
“There was, however, one catch,” the authors wrote. “ ‘If you do this,’ he said, ‘you can’t drink.’ ” Kennedy notes that he didn’t have the insight to realize how odd this was, and in reflection calls it his first intervention.
While most of his difficulties remained relatively private, one night he mixed Ambien and Phenergan, and in a state of confusion, he went for a drive and crashed into a Capitol Hill concrete barrier – an event that led to media coverage, scandal, and, as his chief of staff put it, “ ‘Patrick,’ he said, ‘we have a problem.’ ” While his father, Sen. Ted Kennedy, dismissed this as “a little fendah bendah,” the son made a public statement and checked himself into a rehab unit at the Mayo Clinic. It was to be the second of many attempts at rehab, his first having been in high school.
What makes “A Common Struggle” (New York: Blue Rider Press, 2015) so special is not just that it is a strikingly candid memoir of addiction and illness in a successful congressman, nor that the congressman happens to be a Kennedy with all the glamour and tragedy that come with being born into that family. What makes it special is the way that Kennedy and Fried weave so much more into this riveting book. It’s the story of one man’s life, taken in the full context of a family bound by tragedies: the assassinations of two of his uncles before his birth, an aunt who’d had a lobotomy and inspired a whole advocacy organization for developmental disabilities, two siblings who struggled with cancer, and two parents with their own addictions and scandalous behaviors. His mother’s psychiatric illness was severe enough that her children obtained guardianship, and that’s just a smattering of all the Kennedy family events that are reported here.
The story unfolds against the backdrop of major news events in America, and combines itself with the complex story of parity legislation and the struggle to legitimize brain diseases as worthy of funding, awareness, and destigmatization. And if that’s not enough for one book to do, it all takes place within Patrick Kennedy’s poignant and powerful desire to gain his father’s approval. Ultimately, the son achieves an extended period of sobriety in the context of falling in love and starting a family, well into his 40s.
Nurse Jackie, despite her drug use and personal woes, is fictional and entertaining. “A Common Struggle” is a serious book and heartfelt look at how addiction and mental illness destroy lives; there is little doubt here that without the Kennedy machine for support and privilege, a 20-year-old compromised college student would not have been able to start or maintain a successful political career. Kudos to Mr. Kennedy for sharing his pain and for helping to break the stereotype that those with mental illness and substance abuse can only be found in jails or under bridges.
Dr. Miller is coauthor of “Committed: The Battle Over Involuntary Care,” which was released last fall (Baltimore: Johns Hopkins University Press).
Nurse Jackie is an amazing woman: She’s a fantastically competent and compassionate ER nurse who will do anything for her patients, and she is far better than the caricature ER docs she works with who all care more about their designer shoes and designer egos then about their jobs. She’s a wife – at least in the early episodes – and mother to two adorable girls with a life that includes Mommy and Me tap dancing classes. She somehow juggles it all.
In her fictional life as the star of a Showtime series, “Jackie Peyton” – played by actress Edie Falco, formerly known for her role as Tony Soprano’s wife, Carmela – manages even more: She does it all while popping pain pills by the handful throughout the work day and snorting whatever there is to snort. The interesting thing about Jackie is that her drug habit never interferes with her ability to function. There are no episodes where she makes mistakes or falls asleep. She doesn’t get too wired and is rarely irritable, and she certainly doesn’t pass out from overdoses. She shows up at work on time and never falls off her tightrope of responsibilities in the busy All Saints Hospital ER of New York City.
Without the drugs, she gets ill, but with them, she just functions. And she doesn’t just hold her own with a busy life; she also juggles the secret life of what it takes to get her daily fix, including daily lunchtime sex with the hospital pharmacist, who provides her with pain medicines for her aching back and doesn’t initially know that she’s married with children.
By Season 6, her personal life has broken down, and her daughter Grace, now an angry teenager with her own difficulties and secret life, notes that mom Jackie is incredibly good at hiding her drug use, and that no one can tell when she’s using.
With each season, Jackie’s personal life unwinds a little more, but it’s not because of the effects constant pill-popping has on her behavior; it’s because of the difficulties she has obtaining the drugs. If she could go to the store and buy large amounts of oxycontin and whatever else she takes, she’d have no problem. Her cauldron, however, is filled with constant lies and deception and the secret lives she lives to obtain drugs and to avoid boiling in her own self-made addictive mess.
You wouldn’t expect a review of a dark comedy TV series together with a review of a very serious memoir written by former Rep. Patrick J. Kennedy, but somehow, the two fit together for me.
In “A Common Struggle,” Patrick Kennedy and author Stephen Fried march through Kennedy’s long history of mental illness and substance abuse. Kennedy talks about his life in psychotherapy starting in childhood, related to his parents’ separation. He talks about the treatment he received in college and during his time as a state legislator in Providence, R.I., and how he parked far from his psychiatrist’s office so no one would learn he was in treatment.
Unfortunately, while he found treatment to be very helpful, he stopped when his doctor, Peter Kramer, became a celebrity in his own right after the publication of “Listening to Prozac” (New York: Penguin Books, 1997), and Kennedy became “spooked.” He goes on to talk about the many treatments – including lists of medications – he received over the years and his diagnosis of bipolar disorder, type II. But he doesn’t document what symptoms or episodes led to this diagnosis, and I couldn’t help but wonder how much of his mood disorder was part and parcel of his substance abuse problem. I imagine his doctors may have had the same problem.
So while Kennedy is vague about his psychiatric illness, he is much more forthcoming with his substance abuse problem. Like Nurse Jackie, he has the constant flow of pills – prescribed opiates starting with the diagnosis of a spinal tumor, a handful of Adderall here, some benzodiazepines there, and an enormous issue with alcohol on top of all that. Unlike Nurse Jackie, Kennedy wears the results of his addictions openly. He sleeps through mornings, and his schedulers know to accommodate this. He says things he otherwise wouldn’t while intoxicated, and he embarrasses himself and has others on edge. His mentor in the House of Representatives was Dick Gephardt, and Gephardt’s chief of staff summoned Kennedy to ask him to become chairman of the Democratic Congressional Campaign Committee – a tremendous honor for a 31-year-old congressman.
“There was, however, one catch,” the authors wrote. “ ‘If you do this,’ he said, ‘you can’t drink.’ ” Kennedy notes that he didn’t have the insight to realize how odd this was, and in reflection calls it his first intervention.
While most of his difficulties remained relatively private, one night he mixed Ambien and Phenergan, and in a state of confusion, he went for a drive and crashed into a Capitol Hill concrete barrier – an event that led to media coverage, scandal, and, as his chief of staff put it, “ ‘Patrick,’ he said, ‘we have a problem.’ ” While his father, Sen. Ted Kennedy, dismissed this as “a little fendah bendah,” the son made a public statement and checked himself into a rehab unit at the Mayo Clinic. It was to be the second of many attempts at rehab, his first having been in high school.
What makes “A Common Struggle” (New York: Blue Rider Press, 2015) so special is not just that it is a strikingly candid memoir of addiction and illness in a successful congressman, nor that the congressman happens to be a Kennedy with all the glamour and tragedy that come with being born into that family. What makes it special is the way that Kennedy and Fried weave so much more into this riveting book. It’s the story of one man’s life, taken in the full context of a family bound by tragedies: the assassinations of two of his uncles before his birth, an aunt who’d had a lobotomy and inspired a whole advocacy organization for developmental disabilities, two siblings who struggled with cancer, and two parents with their own addictions and scandalous behaviors. His mother’s psychiatric illness was severe enough that her children obtained guardianship, and that’s just a smattering of all the Kennedy family events that are reported here.
The story unfolds against the backdrop of major news events in America, and combines itself with the complex story of parity legislation and the struggle to legitimize brain diseases as worthy of funding, awareness, and destigmatization. And if that’s not enough for one book to do, it all takes place within Patrick Kennedy’s poignant and powerful desire to gain his father’s approval. Ultimately, the son achieves an extended period of sobriety in the context of falling in love and starting a family, well into his 40s.
Nurse Jackie, despite her drug use and personal woes, is fictional and entertaining. “A Common Struggle” is a serious book and heartfelt look at how addiction and mental illness destroy lives; there is little doubt here that without the Kennedy machine for support and privilege, a 20-year-old compromised college student would not have been able to start or maintain a successful political career. Kudos to Mr. Kennedy for sharing his pain and for helping to break the stereotype that those with mental illness and substance abuse can only be found in jails or under bridges.
Dr. Miller is coauthor of “Committed: The Battle Over Involuntary Care,” which was released last fall (Baltimore: Johns Hopkins University Press).
Nurse Jackie is an amazing woman: She’s a fantastically competent and compassionate ER nurse who will do anything for her patients, and she is far better than the caricature ER docs she works with who all care more about their designer shoes and designer egos then about their jobs. She’s a wife – at least in the early episodes – and mother to two adorable girls with a life that includes Mommy and Me tap dancing classes. She somehow juggles it all.
In her fictional life as the star of a Showtime series, “Jackie Peyton” – played by actress Edie Falco, formerly known for her role as Tony Soprano’s wife, Carmela – manages even more: She does it all while popping pain pills by the handful throughout the work day and snorting whatever there is to snort. The interesting thing about Jackie is that her drug habit never interferes with her ability to function. There are no episodes where she makes mistakes or falls asleep. She doesn’t get too wired and is rarely irritable, and she certainly doesn’t pass out from overdoses. She shows up at work on time and never falls off her tightrope of responsibilities in the busy All Saints Hospital ER of New York City.
Without the drugs, she gets ill, but with them, she just functions. And she doesn’t just hold her own with a busy life; she also juggles the secret life of what it takes to get her daily fix, including daily lunchtime sex with the hospital pharmacist, who provides her with pain medicines for her aching back and doesn’t initially know that she’s married with children.
By Season 6, her personal life has broken down, and her daughter Grace, now an angry teenager with her own difficulties and secret life, notes that mom Jackie is incredibly good at hiding her drug use, and that no one can tell when she’s using.
With each season, Jackie’s personal life unwinds a little more, but it’s not because of the effects constant pill-popping has on her behavior; it’s because of the difficulties she has obtaining the drugs. If she could go to the store and buy large amounts of oxycontin and whatever else she takes, she’d have no problem. Her cauldron, however, is filled with constant lies and deception and the secret lives she lives to obtain drugs and to avoid boiling in her own self-made addictive mess.
You wouldn’t expect a review of a dark comedy TV series together with a review of a very serious memoir written by former Rep. Patrick J. Kennedy, but somehow, the two fit together for me.
In “A Common Struggle,” Patrick Kennedy and author Stephen Fried march through Kennedy’s long history of mental illness and substance abuse. Kennedy talks about his life in psychotherapy starting in childhood, related to his parents’ separation. He talks about the treatment he received in college and during his time as a state legislator in Providence, R.I., and how he parked far from his psychiatrist’s office so no one would learn he was in treatment.
Unfortunately, while he found treatment to be very helpful, he stopped when his doctor, Peter Kramer, became a celebrity in his own right after the publication of “Listening to Prozac” (New York: Penguin Books, 1997), and Kennedy became “spooked.” He goes on to talk about the many treatments – including lists of medications – he received over the years and his diagnosis of bipolar disorder, type II. But he doesn’t document what symptoms or episodes led to this diagnosis, and I couldn’t help but wonder how much of his mood disorder was part and parcel of his substance abuse problem. I imagine his doctors may have had the same problem.
So while Kennedy is vague about his psychiatric illness, he is much more forthcoming with his substance abuse problem. Like Nurse Jackie, he has the constant flow of pills – prescribed opiates starting with the diagnosis of a spinal tumor, a handful of Adderall here, some benzodiazepines there, and an enormous issue with alcohol on top of all that. Unlike Nurse Jackie, Kennedy wears the results of his addictions openly. He sleeps through mornings, and his schedulers know to accommodate this. He says things he otherwise wouldn’t while intoxicated, and he embarrasses himself and has others on edge. His mentor in the House of Representatives was Dick Gephardt, and Gephardt’s chief of staff summoned Kennedy to ask him to become chairman of the Democratic Congressional Campaign Committee – a tremendous honor for a 31-year-old congressman.
“There was, however, one catch,” the authors wrote. “ ‘If you do this,’ he said, ‘you can’t drink.’ ” Kennedy notes that he didn’t have the insight to realize how odd this was, and in reflection calls it his first intervention.
While most of his difficulties remained relatively private, one night he mixed Ambien and Phenergan, and in a state of confusion, he went for a drive and crashed into a Capitol Hill concrete barrier – an event that led to media coverage, scandal, and, as his chief of staff put it, “ ‘Patrick,’ he said, ‘we have a problem.’ ” While his father, Sen. Ted Kennedy, dismissed this as “a little fendah bendah,” the son made a public statement and checked himself into a rehab unit at the Mayo Clinic. It was to be the second of many attempts at rehab, his first having been in high school.
What makes “A Common Struggle” (New York: Blue Rider Press, 2015) so special is not just that it is a strikingly candid memoir of addiction and illness in a successful congressman, nor that the congressman happens to be a Kennedy with all the glamour and tragedy that come with being born into that family. What makes it special is the way that Kennedy and Fried weave so much more into this riveting book. It’s the story of one man’s life, taken in the full context of a family bound by tragedies: the assassinations of two of his uncles before his birth, an aunt who’d had a lobotomy and inspired a whole advocacy organization for developmental disabilities, two siblings who struggled with cancer, and two parents with their own addictions and scandalous behaviors. His mother’s psychiatric illness was severe enough that her children obtained guardianship, and that’s just a smattering of all the Kennedy family events that are reported here.
The story unfolds against the backdrop of major news events in America, and combines itself with the complex story of parity legislation and the struggle to legitimize brain diseases as worthy of funding, awareness, and destigmatization. And if that’s not enough for one book to do, it all takes place within Patrick Kennedy’s poignant and powerful desire to gain his father’s approval. Ultimately, the son achieves an extended period of sobriety in the context of falling in love and starting a family, well into his 40s.
Nurse Jackie, despite her drug use and personal woes, is fictional and entertaining. “A Common Struggle” is a serious book and heartfelt look at how addiction and mental illness destroy lives; there is little doubt here that without the Kennedy machine for support and privilege, a 20-year-old compromised college student would not have been able to start or maintain a successful political career. Kudos to Mr. Kennedy for sharing his pain and for helping to break the stereotype that those with mental illness and substance abuse can only be found in jails or under bridges.
Dr. Miller is coauthor of “Committed: The Battle Over Involuntary Care,” which was released last fall (Baltimore: Johns Hopkins University Press).
The last call
It’s 7:30 on a Tuesday evening, and you will be on call until 8 o’clock the next morning. You have already been in the office 9 hours. Usual start time is 8 a.m., but that extra hour at home is a perk you have earned by being on call tonight.
A quick glance at the schedule screen suggests that if nothing ugly crops up, you will finish seeing your last patient and be out the door and on your way home by 8:15 p.m. The phone has been quiet for the last half hour, but as you are making your quickstep transition between exam rooms, the nurse tells you that the receptionist has received a call from a very anxious mother who has just discovered that her 6-year-old has a fever of 103° F. The child didn’t eat any dinner and is now complaining that he has a sore throat. The mother is worried because the child had a couple of febrile seizures when he was a toddler, and she has heard of several cases of strep in his class at school.
On the other hand, you could ask the nurse to reassure the mother that a febrile seizure at age 6 is very unlikely and encourage the mother to call you if she continues to be concerned. The problem here hinges on the experience and skills of the nurse. Even if your office has a well-vetted portfolio of clinical algorithms, you may be relying on a nurse with whom you aren’t familiar. Or maybe your past experience makes you uncomfortable with this particular nurse. She or he may have missed some obvious red flags in the past or may be so unskillful at reassurance that it is very likely that you will be getting a 2 a.m. call from this worried parent.
Another option could be to suggest that after reassuring the mother, the nurse offer her a first of the morning appointment tomorrow. There are several problems with this strategy, and I have always discouraged our office staff from making these next morning appointments for sick children. The offer of the appointment seldom reassures the very anxious parents nor does it prevent the middle of the night calls. More importantly, our experience, and I suspect yours, is that half of those newly sick children with fevers will be better by the next morning or their parents ended up going to the emergency room. This will leave you with a wasted appointment slot that you would really like to have available when the phones heat up in the morning. A more efficient strategy is to promise parents that if the child is still sick in the morning, you can guarantee them a timely appointment.
Finally, there are two responses that worked best for me. The first is to have the nurse ask the parents how long it will take them to get to the office. Add 15 minutes to their estimate, and if you can accept that estimated time of arrival, have the nurse tell that family to hustle on in. Send the staff home unless they want the overtime, and see the patient yourself.
The second response is to get on the phone yourself and talk directly to the mother. You were probably going to end up speaking with her in the middle of the night anyway, so you might as well invest the time now in taking your own history. Even if your own version of reassurance fails to prevent a 2 a.m. call, at least you will have some frame of reference when you need to make one of those dangerous middle of the night clinical decisions. A quiet night may depend on how you manage that last call of the day.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
It’s 7:30 on a Tuesday evening, and you will be on call until 8 o’clock the next morning. You have already been in the office 9 hours. Usual start time is 8 a.m., but that extra hour at home is a perk you have earned by being on call tonight.
A quick glance at the schedule screen suggests that if nothing ugly crops up, you will finish seeing your last patient and be out the door and on your way home by 8:15 p.m. The phone has been quiet for the last half hour, but as you are making your quickstep transition between exam rooms, the nurse tells you that the receptionist has received a call from a very anxious mother who has just discovered that her 6-year-old has a fever of 103° F. The child didn’t eat any dinner and is now complaining that he has a sore throat. The mother is worried because the child had a couple of febrile seizures when he was a toddler, and she has heard of several cases of strep in his class at school.
On the other hand, you could ask the nurse to reassure the mother that a febrile seizure at age 6 is very unlikely and encourage the mother to call you if she continues to be concerned. The problem here hinges on the experience and skills of the nurse. Even if your office has a well-vetted portfolio of clinical algorithms, you may be relying on a nurse with whom you aren’t familiar. Or maybe your past experience makes you uncomfortable with this particular nurse. She or he may have missed some obvious red flags in the past or may be so unskillful at reassurance that it is very likely that you will be getting a 2 a.m. call from this worried parent.
Another option could be to suggest that after reassuring the mother, the nurse offer her a first of the morning appointment tomorrow. There are several problems with this strategy, and I have always discouraged our office staff from making these next morning appointments for sick children. The offer of the appointment seldom reassures the very anxious parents nor does it prevent the middle of the night calls. More importantly, our experience, and I suspect yours, is that half of those newly sick children with fevers will be better by the next morning or their parents ended up going to the emergency room. This will leave you with a wasted appointment slot that you would really like to have available when the phones heat up in the morning. A more efficient strategy is to promise parents that if the child is still sick in the morning, you can guarantee them a timely appointment.
Finally, there are two responses that worked best for me. The first is to have the nurse ask the parents how long it will take them to get to the office. Add 15 minutes to their estimate, and if you can accept that estimated time of arrival, have the nurse tell that family to hustle on in. Send the staff home unless they want the overtime, and see the patient yourself.
The second response is to get on the phone yourself and talk directly to the mother. You were probably going to end up speaking with her in the middle of the night anyway, so you might as well invest the time now in taking your own history. Even if your own version of reassurance fails to prevent a 2 a.m. call, at least you will have some frame of reference when you need to make one of those dangerous middle of the night clinical decisions. A quiet night may depend on how you manage that last call of the day.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
It’s 7:30 on a Tuesday evening, and you will be on call until 8 o’clock the next morning. You have already been in the office 9 hours. Usual start time is 8 a.m., but that extra hour at home is a perk you have earned by being on call tonight.
A quick glance at the schedule screen suggests that if nothing ugly crops up, you will finish seeing your last patient and be out the door and on your way home by 8:15 p.m. The phone has been quiet for the last half hour, but as you are making your quickstep transition between exam rooms, the nurse tells you that the receptionist has received a call from a very anxious mother who has just discovered that her 6-year-old has a fever of 103° F. The child didn’t eat any dinner and is now complaining that he has a sore throat. The mother is worried because the child had a couple of febrile seizures when he was a toddler, and she has heard of several cases of strep in his class at school.
On the other hand, you could ask the nurse to reassure the mother that a febrile seizure at age 6 is very unlikely and encourage the mother to call you if she continues to be concerned. The problem here hinges on the experience and skills of the nurse. Even if your office has a well-vetted portfolio of clinical algorithms, you may be relying on a nurse with whom you aren’t familiar. Or maybe your past experience makes you uncomfortable with this particular nurse. She or he may have missed some obvious red flags in the past or may be so unskillful at reassurance that it is very likely that you will be getting a 2 a.m. call from this worried parent.
Another option could be to suggest that after reassuring the mother, the nurse offer her a first of the morning appointment tomorrow. There are several problems with this strategy, and I have always discouraged our office staff from making these next morning appointments for sick children. The offer of the appointment seldom reassures the very anxious parents nor does it prevent the middle of the night calls. More importantly, our experience, and I suspect yours, is that half of those newly sick children with fevers will be better by the next morning or their parents ended up going to the emergency room. This will leave you with a wasted appointment slot that you would really like to have available when the phones heat up in the morning. A more efficient strategy is to promise parents that if the child is still sick in the morning, you can guarantee them a timely appointment.
Finally, there are two responses that worked best for me. The first is to have the nurse ask the parents how long it will take them to get to the office. Add 15 minutes to their estimate, and if you can accept that estimated time of arrival, have the nurse tell that family to hustle on in. Send the staff home unless they want the overtime, and see the patient yourself.
The second response is to get on the phone yourself and talk directly to the mother. You were probably going to end up speaking with her in the middle of the night anyway, so you might as well invest the time now in taking your own history. Even if your own version of reassurance fails to prevent a 2 a.m. call, at least you will have some frame of reference when you need to make one of those dangerous middle of the night clinical decisions. A quiet night may depend on how you manage that last call of the day.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
Dropping the A-bomb
Your first patient of the day is a 2½-year-old who has a runny nose and a cough. His mother has brought him in because his cough is more frequent and persistent than she is accustomed to hearing. He is happy and playful, and has a low-grade fever. You notice that he is slightly tachypneic, and you hear fine wheezes scattered throughout his lung fields. You also recall that at age 6 months, he was diagnosed with bronchiolitis but was never hospitalized.
Will you give him antibiotics and send him home with a nebulizer? Just the nebulizer? Just the antibiotics? Neither? We can debate those answers for hours, and you can plead for more information before you commit to an answer. But let’s skip over the question about what you are going to do and focus on what you are going to say. I want to know what diagnosis you are going to share with this mother.
Or are you going to try a pseudoscientific smoke screen and tell her that her that her son has “reactive airway disease”? You could soften it even further by reassuring her that his diagnosis is so common that it has an abbreviation: “We usually just call it RAD.”
You may not have trouble telling a parent that her child has asthma, but most clinicians struggle with dropping the A-bomb. Why? It may be that we don’t want the family to freak out. You could end up spending the rest of the morning coaxing them back off the ledge because you have diagnosed their child with a chronic illness that could kill him. This kind of exaggerated reaction is far less of a problem now than it was 30 or 40 years ago. Almost every parent knows at least one family with an asthmatic child who seems to be doing just fine. In my opinion, this apparent increase in prevalence of asthma is primarily the result of an improved awareness and a relabeling phenomenon.
Your own experience probably reflects the national statistics that less than a third of preschoolers with recurrent wheezing still have asthma by the time they finish kindergarten. And you may be hesitant to use the asthma diagnosis because you don’t want to be labeled as a clinician who cries wolf.
It may be that subconsciously you are afraid that by raising the asthma red flag you will be committing yourself to the time gobbling task of managing another patient with a chronic disease. You could gamble that he will only have one or two more episodes of wheezing, and you will be able to treat his illnesses simply as a short series of unconnected events.
Is there any harm in dancing around the asthma diagnosis? The authors of a Perspectives article in the January 2017 issue of Pediatrics argue persuasively that vague descriptive and nondiagnostic terms such as “reactive airways disease” are confusing and should be abandoned (“RAD: Reactive Airway Disease or Really Asthma Disease?” Pediatrics. 2017 Jan. doi: 10.1542/peds.2016-0625). They question why we would treat a condition with asthma medications and not call it asthma just because a child will probably out grow it later.
It’s more than just about sloppy language. Jose A. Castro-Rodriguez, MD, a physician who has pioneered one of the tools than can be used to predict persistent asthma in young children, observes that by failing to signal to parents that the child has a chronic condition, we run the risk that the child will be less adherent to the medication and management program we recommend. (“The Asthma Predictive Index,” Curr Opin Allergy Clin Immunol. 2011;11[3]:157-61).
If we are going to tighten up our language and drop the vague substitute terms like RAD, and if we are hesitant to drop the A-bomb because it sounds too much like a lifelong disease when the truth is that most young children will outgrow asthma, what should we tell all those parents of wheezing preschoolers? The authors of the article in Pediatrics have several suggestions. Their favorite and the one that appeals most to me is toddler asthma. As they observe, the term “toddler asthma” implies an endpoint and the need for reevaluation to determine if the child is one of the minority who has “real” asthma.
Although it’s almost always about the money. When it's not about the money, it's usually about the labels we use.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
Your first patient of the day is a 2½-year-old who has a runny nose and a cough. His mother has brought him in because his cough is more frequent and persistent than she is accustomed to hearing. He is happy and playful, and has a low-grade fever. You notice that he is slightly tachypneic, and you hear fine wheezes scattered throughout his lung fields. You also recall that at age 6 months, he was diagnosed with bronchiolitis but was never hospitalized.
Will you give him antibiotics and send him home with a nebulizer? Just the nebulizer? Just the antibiotics? Neither? We can debate those answers for hours, and you can plead for more information before you commit to an answer. But let’s skip over the question about what you are going to do and focus on what you are going to say. I want to know what diagnosis you are going to share with this mother.
Or are you going to try a pseudoscientific smoke screen and tell her that her that her son has “reactive airway disease”? You could soften it even further by reassuring her that his diagnosis is so common that it has an abbreviation: “We usually just call it RAD.”
You may not have trouble telling a parent that her child has asthma, but most clinicians struggle with dropping the A-bomb. Why? It may be that we don’t want the family to freak out. You could end up spending the rest of the morning coaxing them back off the ledge because you have diagnosed their child with a chronic illness that could kill him. This kind of exaggerated reaction is far less of a problem now than it was 30 or 40 years ago. Almost every parent knows at least one family with an asthmatic child who seems to be doing just fine. In my opinion, this apparent increase in prevalence of asthma is primarily the result of an improved awareness and a relabeling phenomenon.
Your own experience probably reflects the national statistics that less than a third of preschoolers with recurrent wheezing still have asthma by the time they finish kindergarten. And you may be hesitant to use the asthma diagnosis because you don’t want to be labeled as a clinician who cries wolf.
It may be that subconsciously you are afraid that by raising the asthma red flag you will be committing yourself to the time gobbling task of managing another patient with a chronic disease. You could gamble that he will only have one or two more episodes of wheezing, and you will be able to treat his illnesses simply as a short series of unconnected events.
Is there any harm in dancing around the asthma diagnosis? The authors of a Perspectives article in the January 2017 issue of Pediatrics argue persuasively that vague descriptive and nondiagnostic terms such as “reactive airways disease” are confusing and should be abandoned (“RAD: Reactive Airway Disease or Really Asthma Disease?” Pediatrics. 2017 Jan. doi: 10.1542/peds.2016-0625). They question why we would treat a condition with asthma medications and not call it asthma just because a child will probably out grow it later.
It’s more than just about sloppy language. Jose A. Castro-Rodriguez, MD, a physician who has pioneered one of the tools than can be used to predict persistent asthma in young children, observes that by failing to signal to parents that the child has a chronic condition, we run the risk that the child will be less adherent to the medication and management program we recommend. (“The Asthma Predictive Index,” Curr Opin Allergy Clin Immunol. 2011;11[3]:157-61).
If we are going to tighten up our language and drop the vague substitute terms like RAD, and if we are hesitant to drop the A-bomb because it sounds too much like a lifelong disease when the truth is that most young children will outgrow asthma, what should we tell all those parents of wheezing preschoolers? The authors of the article in Pediatrics have several suggestions. Their favorite and the one that appeals most to me is toddler asthma. As they observe, the term “toddler asthma” implies an endpoint and the need for reevaluation to determine if the child is one of the minority who has “real” asthma.
Although it’s almost always about the money. When it's not about the money, it's usually about the labels we use.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
Your first patient of the day is a 2½-year-old who has a runny nose and a cough. His mother has brought him in because his cough is more frequent and persistent than she is accustomed to hearing. He is happy and playful, and has a low-grade fever. You notice that he is slightly tachypneic, and you hear fine wheezes scattered throughout his lung fields. You also recall that at age 6 months, he was diagnosed with bronchiolitis but was never hospitalized.
Will you give him antibiotics and send him home with a nebulizer? Just the nebulizer? Just the antibiotics? Neither? We can debate those answers for hours, and you can plead for more information before you commit to an answer. But let’s skip over the question about what you are going to do and focus on what you are going to say. I want to know what diagnosis you are going to share with this mother.
Or are you going to try a pseudoscientific smoke screen and tell her that her that her son has “reactive airway disease”? You could soften it even further by reassuring her that his diagnosis is so common that it has an abbreviation: “We usually just call it RAD.”
You may not have trouble telling a parent that her child has asthma, but most clinicians struggle with dropping the A-bomb. Why? It may be that we don’t want the family to freak out. You could end up spending the rest of the morning coaxing them back off the ledge because you have diagnosed their child with a chronic illness that could kill him. This kind of exaggerated reaction is far less of a problem now than it was 30 or 40 years ago. Almost every parent knows at least one family with an asthmatic child who seems to be doing just fine. In my opinion, this apparent increase in prevalence of asthma is primarily the result of an improved awareness and a relabeling phenomenon.
Your own experience probably reflects the national statistics that less than a third of preschoolers with recurrent wheezing still have asthma by the time they finish kindergarten. And you may be hesitant to use the asthma diagnosis because you don’t want to be labeled as a clinician who cries wolf.
It may be that subconsciously you are afraid that by raising the asthma red flag you will be committing yourself to the time gobbling task of managing another patient with a chronic disease. You could gamble that he will only have one or two more episodes of wheezing, and you will be able to treat his illnesses simply as a short series of unconnected events.
Is there any harm in dancing around the asthma diagnosis? The authors of a Perspectives article in the January 2017 issue of Pediatrics argue persuasively that vague descriptive and nondiagnostic terms such as “reactive airways disease” are confusing and should be abandoned (“RAD: Reactive Airway Disease or Really Asthma Disease?” Pediatrics. 2017 Jan. doi: 10.1542/peds.2016-0625). They question why we would treat a condition with asthma medications and not call it asthma just because a child will probably out grow it later.
It’s more than just about sloppy language. Jose A. Castro-Rodriguez, MD, a physician who has pioneered one of the tools than can be used to predict persistent asthma in young children, observes that by failing to signal to parents that the child has a chronic condition, we run the risk that the child will be less adherent to the medication and management program we recommend. (“The Asthma Predictive Index,” Curr Opin Allergy Clin Immunol. 2011;11[3]:157-61).
If we are going to tighten up our language and drop the vague substitute terms like RAD, and if we are hesitant to drop the A-bomb because it sounds too much like a lifelong disease when the truth is that most young children will outgrow asthma, what should we tell all those parents of wheezing preschoolers? The authors of the article in Pediatrics have several suggestions. Their favorite and the one that appeals most to me is toddler asthma. As they observe, the term “toddler asthma” implies an endpoint and the need for reevaluation to determine if the child is one of the minority who has “real” asthma.
Although it’s almost always about the money. When it's not about the money, it's usually about the labels we use.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
Out to lunch
I’m sure there are folks here in town who wondered how I could keep up a professional pace that often included being on call 2 nights a week and working every third weekend. Even when I was in my early 50s, people asked me if I was getting ready to retire. I hope it wasn’t because I appeared unhappy or looked 15 years older than I was. I suspect that some parents who didn’t know me well predicted that my career would have ended far short of 40 years.
One of the secrets of what appeared to be my superhuman stamina was that almost every day at noon I was out to lunch. That doesn’t mean that I always took time to eat lunch. In fact, I must admit that more often than not my midday diet consisted of several handfuls of cashews or an energy bar eaten on the fly.
The feeling of invigoration and renewal that came in its wake fueled my commitment to my habit of lunchtime outdoor activity. Although to some people it may be counterintuitive, the physical activity energized me. The second half of my workday was no more fatiguing than the morning. However, if some thoughtless hospital or practice administrator scheduled a noon meeting, the rest of my day was a grump fest.
A recent study has demonstrated just how powerful lunchtime exercise can be in improving worker attitude and mood, even if the activity is just going for a walk. (“Changes in work affect in response to lunchtime walking in previously physically inactive employees: A randomized trial” (Scand J Med Sci Sports. 2015 Dec;25[6]:778-87). There have been other studies that have pointed to the value of an activity break, but these investigators collected real-time reports from subjects using their cell phones. “Lunchtime walks improved enthusiasm, relaxation, and nervousness at work,” the researchers noted.
The problem comes in getting employees to take that first step toward developing a lunchtime activity habit. A few, usually women, have discovered the value for themselves and enjoy the social interaction as much as they do the affect-improving aspects of the activity and change of scene. I have tried to encourage lunchtime walking in the workplace with several strategies, including small monetary rewards, prizes, and contests between groups of workers. One year we even bought umbrellas to encourage employees to walk even if it was raining. But without a vigorous and persistent support system, inertia wins, and only those who have discovered the benefits of lunchtime activity for themselves persist.
You may be asking yourself how I managed to find time in my schedule for that hour of lunchtime activity; actually it was usually an hour and half to include a shower. The answer is that I built my schedule around it, and that meant getting to the office earlier and working later. But in my mind that was a small price to pay for the benefits I received. The other secret to my apparent stamina was that I lived a 5-minute bike ride from both hospitals and my office. Don’t underestimate the toll your commute is taking on your life and happiness.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”
I’m sure there are folks here in town who wondered how I could keep up a professional pace that often included being on call 2 nights a week and working every third weekend. Even when I was in my early 50s, people asked me if I was getting ready to retire. I hope it wasn’t because I appeared unhappy or looked 15 years older than I was. I suspect that some parents who didn’t know me well predicted that my career would have ended far short of 40 years.
One of the secrets of what appeared to be my superhuman stamina was that almost every day at noon I was out to lunch. That doesn’t mean that I always took time to eat lunch. In fact, I must admit that more often than not my midday diet consisted of several handfuls of cashews or an energy bar eaten on the fly.
The feeling of invigoration and renewal that came in its wake fueled my commitment to my habit of lunchtime outdoor activity. Although to some people it may be counterintuitive, the physical activity energized me. The second half of my workday was no more fatiguing than the morning. However, if some thoughtless hospital or practice administrator scheduled a noon meeting, the rest of my day was a grump fest.
A recent study has demonstrated just how powerful lunchtime exercise can be in improving worker attitude and mood, even if the activity is just going for a walk. (“Changes in work affect in response to lunchtime walking in previously physically inactive employees: A randomized trial” (Scand J Med Sci Sports. 2015 Dec;25[6]:778-87). There have been other studies that have pointed to the value of an activity break, but these investigators collected real-time reports from subjects using their cell phones. “Lunchtime walks improved enthusiasm, relaxation, and nervousness at work,” the researchers noted.
The problem comes in getting employees to take that first step toward developing a lunchtime activity habit. A few, usually women, have discovered the value for themselves and enjoy the social interaction as much as they do the affect-improving aspects of the activity and change of scene. I have tried to encourage lunchtime walking in the workplace with several strategies, including small monetary rewards, prizes, and contests between groups of workers. One year we even bought umbrellas to encourage employees to walk even if it was raining. But without a vigorous and persistent support system, inertia wins, and only those who have discovered the benefits of lunchtime activity for themselves persist.
You may be asking yourself how I managed to find time in my schedule for that hour of lunchtime activity; actually it was usually an hour and half to include a shower. The answer is that I built my schedule around it, and that meant getting to the office earlier and working later. But in my mind that was a small price to pay for the benefits I received. The other secret to my apparent stamina was that I lived a 5-minute bike ride from both hospitals and my office. Don’t underestimate the toll your commute is taking on your life and happiness.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”
I’m sure there are folks here in town who wondered how I could keep up a professional pace that often included being on call 2 nights a week and working every third weekend. Even when I was in my early 50s, people asked me if I was getting ready to retire. I hope it wasn’t because I appeared unhappy or looked 15 years older than I was. I suspect that some parents who didn’t know me well predicted that my career would have ended far short of 40 years.
One of the secrets of what appeared to be my superhuman stamina was that almost every day at noon I was out to lunch. That doesn’t mean that I always took time to eat lunch. In fact, I must admit that more often than not my midday diet consisted of several handfuls of cashews or an energy bar eaten on the fly.
The feeling of invigoration and renewal that came in its wake fueled my commitment to my habit of lunchtime outdoor activity. Although to some people it may be counterintuitive, the physical activity energized me. The second half of my workday was no more fatiguing than the morning. However, if some thoughtless hospital or practice administrator scheduled a noon meeting, the rest of my day was a grump fest.
A recent study has demonstrated just how powerful lunchtime exercise can be in improving worker attitude and mood, even if the activity is just going for a walk. (“Changes in work affect in response to lunchtime walking in previously physically inactive employees: A randomized trial” (Scand J Med Sci Sports. 2015 Dec;25[6]:778-87). There have been other studies that have pointed to the value of an activity break, but these investigators collected real-time reports from subjects using their cell phones. “Lunchtime walks improved enthusiasm, relaxation, and nervousness at work,” the researchers noted.
The problem comes in getting employees to take that first step toward developing a lunchtime activity habit. A few, usually women, have discovered the value for themselves and enjoy the social interaction as much as they do the affect-improving aspects of the activity and change of scene. I have tried to encourage lunchtime walking in the workplace with several strategies, including small monetary rewards, prizes, and contests between groups of workers. One year we even bought umbrellas to encourage employees to walk even if it was raining. But without a vigorous and persistent support system, inertia wins, and only those who have discovered the benefits of lunchtime activity for themselves persist.
You may be asking yourself how I managed to find time in my schedule for that hour of lunchtime activity; actually it was usually an hour and half to include a shower. The answer is that I built my schedule around it, and that meant getting to the office earlier and working later. But in my mind that was a small price to pay for the benefits I received. The other secret to my apparent stamina was that I lived a 5-minute bike ride from both hospitals and my office. Don’t underestimate the toll your commute is taking on your life and happiness.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”
Open vs. endovascular for chronic mesenteric ischemia
Chronic mesenteric ischemia is best treated in an open operation.
Chronic mesenteric ischemia is a rare disorder accounting for about 1 out of 100,000 admissions.1 Because of the rarity of this disease, diagnosis is often delayed. Patients are often evaluated for other gastrointestinal diseases and/or malignancies, which in turn contributes to significant delays in diagnosis. Additionally, there are no prospective, randomized trials on which to base decisions regarding treatment; and it is unlikely that such studies will ever be undertaken.
Chronic mesenteric ischemia develops when two or more of the mesenteric vessels (celiac, superior mesenteric [SMA], or inferior mesenteric [IMA]) become occluded or develop severe stenosis. In my experience, patients most often develop occlusion (as opposed to stenosis) of their mesenteric vessels. The atherosclerotic plaque responsible for the disease originates within the aorta and the stenosis/occlusion develops at the vessel origin.
As a whole, these comorbidities would suggest that a more minimally invasive approach would be preferred. Yet, an open operation for chronic mesenteric ischemia should not be discarded as an initial operation.
Endovascular treatment of mesenteric ischemia is not without risk. As in all endovascular procedures there are complications associated with the access vessels. The orientation of the mesenteric vessels as they arise from the aorta often favors an approach from the left arm. The brachial artery is smaller than the femoral artery, and it is more difficult to apply pressure to the brachial artery to control the puncture site. This leads to a higher rate of access site complications including hemorrhage, pseudoaneurysm and thrombosis of the vessel. Bleeding or hematoma formation within the brachial neurovascular sheath can result in significant neurologic dysfunction of the arm and hand. There is risk of stroke, especially when the access vessel is the brachial artery. There are also complications directly related to the endovascular procedure.
Atheroembolism of plaque can result in occlusion of small mesenteric vessels and focal areas of bowel necrosis. Dissection of the mesenteric vessel can occur. Oderich has advocated for the use of a covered stent.2 A covered stent could cover proximal branches, and thus, in theory, the treatment itself could cause bowel ischemia or infarction. Many series that have compared open and endovascular surgery show no difference in early outcomes, but demonstrate early restenosis, decreased primary patency, and decreased assisted primary patency with endovascular treatment as compared with open operations.3-5
Another concern regarding the treatment of mesenteric ischemia is the status of the end organ, the bowel. Successful treatment of mesenteric ischemia cannot only assess the atherosclerotic lesion, but requires the surgeon to be cognizant of the condition of the bowel.
This concern is especially true for acute mesenteric ischemia,6 but the status of the bowel must also be kept in mind for chronic mesenteric ischemia. Unlike the lower extremity where the results of treatment are easily observed by inspection (color, evidence of atheroembolization), palpation (temperature, pulse), and physiologic testing (ABI), the bowel is not accessible. There are no highly accurate tests to determine if the patient has on-going bowel ischemia or has developed infarction. Should a complication occur, physical examination findings and laboratory changes often become apparent late in the course of the disease. As previously noted, these patients are often physiologically compromised and have little reserve and may not survive such complications. An open operation allows visualization of the bowel, before and after revascularization.
Traditional teaching for the surgical treatment of chronic mesenteric ischemia has emphasized that two mesenteric vessels, usually the celiac and SMA, should be revascularized.7,8 Various approaches to revascularization have been suggested including transaortic endarterectomy and an antegrade bifurcated bypass originating from the supraceliac aorta. These operations are effective in restoring flow to the mesenteric circulation, but both of these approaches involve aortic cross-clamping and are physiologically challenging for patients.
There are alternatives for open revascularization of the mesenteric vessels. The infrarenal aorta, iliac vessels, and even renal arteries can be, and have been used as the inflow source. It has been my experience that a bypass graft using an iliac artery (common or external) as the inflow source is well tolerated by patients. I have preferentially used either great saphenous vein or femoral-popliteal vein as the conduit. In many cases, the distal anastomosis is simply the SMA. However, both the celiac and SMA can be revascularized by creating a side-side anastomosis to the SMA and an end-side anastomosis to the common or proper hepatic artery. Such procedures have been durable, providing relief of symptoms and allowing patients to regain weight.9
In reality, I believe that an endovascular approach for the treatment of chronic mesenteric ischemia has a role. Vascular surgeons are uniquely positioned to carefully evaluate each patient and recommend what they feel is most appropriate. I tend to feel that an endovascular approach is less likely to be successful for patients with occluded vessels, especially those with a flush occlusion, and so will preferentially recommend an open operation for these patients. On the other hand, in my practice, I have used an endovascular approach for patients with severe stenosis, and as Dr. Harris states, know that a bypass is always an option should this be unsuccessful or ultimately fail.
References
1. Ann Vasc Surg. 1991;5:403-6
2. J Vasc Surg. 2013;58:1316-23
3. Ann Vasc Surg. 2015:29;934-40
4. World J Gastroenerol. 2013;19:1333-7
5. J Vasc Surg. 2007;45:1162-71
6. J Vasc Surg. 2015;62:767-72
7. J Vasc Surg. 2002:35:853-9
8. Surgery. 1981;90:940-6
9. J Vasc Surg. 2000;32:37-47
Eric Endean, MD, is the director of the aortic center, Gordon L. Hyde Endowed Professor and Chair, and vascular surgery section head, vascular and endovascular surgery at UK HealthCare, University of Kentucky, Lexington. He had no relevant disclosures.
Presenting the case for endovascular intervention
Chronic mesenteric ischemia (CMI) is an uncommon, but lethal, problem when left untreated. Before the endovascular era, the only option was open revascularization, which is challenging in this chronically ill, malnourished population with diffuse, systemic, atherosclerotic disease. Morbidity and mortality was relatively high because of the comorbid conditions and chronically ill status of the patients. The first mesenteric bypass was performed in 1958 by Maynard and Shaw.1
Options for open repair include transaortic endarterectomy, antegrade bypass from the supraceliac aorta or distal thoracic aorta, or retrograde bypass from the iliac artery, all of which are major abdominal procedures. Endovascular interventions are now the most commonly performed procedures for CMI in the United States based on national studies.2
Technical success with endovascular interventions can be achieved in well over 90% of patients, and multiple vessels can be treated simultaneously from either a femoral or brachial approach. The primary concern with endovascular interventions has been long-term patency, with restenosis from intimal hyperplasia or thrombosis causing recurrent symptoms in up to 30%-50% at 3-5 years.5-7 However, these rates are based on use of bare metal stents, rather than covered stents. Recent studies8 suggest that stent grafts have markedly improved outcomes over bare metal stents for ostial lesions, decreasing recurrence. Oderich found that freedom from recurrence was 92% with stent grafts as compared with 53% for bare metal stents, with primary patency rates of 92%, at 3 years8, comparable to even the best open bypass results. Schoch first reported the use of covered stents in the mesenteric circulation, and found that no patients developed recurrent stenosis at 2 years.9 Other concerns with endovascular intervention include embolization and dissection, which have not been frequently reported.
Mortality from open surgery ranges from 5% to 15%, with morbidity of 30%-40%.4 Mortality from endovascular intervention is markedly lower, in the range of 3.56% vs. 7.23%.5 Long-term survival is not different between endovascular vs. open repair (69% vs. 65%),4 with the majority of deaths related to cardiac, pulmonary, or malignancy issues. Moghadamyeghaneh, in a review of the Nationwide Inpatient Sample database, found that open surgery was one of the major predictors for higher morbidity (odds ratio, 5.07) and mortality (OR, 5.13), despite the fact that endovascular patients were older (another risk factor for adverse outcomes) and had more comorbidities in this nonrandomized, real-world study.2
Further, if one considers cost as a metric for decision making, a Markov clinical decision model by Hogendoorn et al suggests an endovascular first approach is preferred, despite the presumed higher rate of recurrence expected with use of bare metal stents, rather than covered stents, utilized for this analysis.10 Clearly, the financial advantage would be even greater for endovascular with the lower rates of recurrence with covered stents more recently reported.
If a patient develops recurrent stenosis after endovascular intervention, open bypass may be considered as an alternate to repeat endovascular intervention, dependent on the nutritional status, life expectancy, and initial intervention undertaken. Alternately, patients who undergo open repair are not immune to restenosis, with a recurrence rate of 10%-20%.11,12 Oderich found that there was a 22% mortality in those treated with repeat open interventions, with a 47% complication rate. Endovascular interventions, however, had a significantly lower rate of complications, 16%, and mortality. For patients with recurrent disease after open revascularization for CMI, the endovascular approach should also be the preferred approach.
Any lesion which is anatomically suitable for endovascular repair should first have an attempt made via this approach, utilizing covered stents. While there is a role for open revascularization, endovascular interventions can be safely performed, with minimal morbidity and mortality, and good long-term patency, even in the sickest patients. Endovascular intervention should be the procedure of choice for chronic mesenteric ischemia and recurrent chronic mesenteric ischemia.
References
1. NEJM. 1958;258:874-8
2. Am Surg. 2015;81:1149-56
3. Cardiovasc Intervent Radiol. 1980;3:43-4
4. Ann Vasc Surg. 2009;23:700-12
5. Ann Vasc Surg. 2013;27:113-22
6. J Vasc Surg. 2011;54:1422-29
7. J Vasc Surg. 2010;51:140-7
8. J Vasc Surg. 2013;58:1316-24
9. JACS. 2001;212:668-75
10. J Vasc Surg. 2014;60;715-25
11. J Vasc Surg. 200;49:1472-9
12. J Vasc Surg. 2007;45:1162-71
Linda Harris, MD, is professor of surgery; chief, division of vascular surgery; program director, vascular surgery residency & fellowship at the State University of New York at Buffalo; and an associate medical editor for Vascular Specialist. She had no relevant disclosures.
Chronic mesenteric ischemia is best treated in an open operation.
Chronic mesenteric ischemia is a rare disorder accounting for about 1 out of 100,000 admissions.1 Because of the rarity of this disease, diagnosis is often delayed. Patients are often evaluated for other gastrointestinal diseases and/or malignancies, which in turn contributes to significant delays in diagnosis. Additionally, there are no prospective, randomized trials on which to base decisions regarding treatment; and it is unlikely that such studies will ever be undertaken.
Chronic mesenteric ischemia develops when two or more of the mesenteric vessels (celiac, superior mesenteric [SMA], or inferior mesenteric [IMA]) become occluded or develop severe stenosis. In my experience, patients most often develop occlusion (as opposed to stenosis) of their mesenteric vessels. The atherosclerotic plaque responsible for the disease originates within the aorta and the stenosis/occlusion develops at the vessel origin.
As a whole, these comorbidities would suggest that a more minimally invasive approach would be preferred. Yet, an open operation for chronic mesenteric ischemia should not be discarded as an initial operation.
Endovascular treatment of mesenteric ischemia is not without risk. As in all endovascular procedures there are complications associated with the access vessels. The orientation of the mesenteric vessels as they arise from the aorta often favors an approach from the left arm. The brachial artery is smaller than the femoral artery, and it is more difficult to apply pressure to the brachial artery to control the puncture site. This leads to a higher rate of access site complications including hemorrhage, pseudoaneurysm and thrombosis of the vessel. Bleeding or hematoma formation within the brachial neurovascular sheath can result in significant neurologic dysfunction of the arm and hand. There is risk of stroke, especially when the access vessel is the brachial artery. There are also complications directly related to the endovascular procedure.
Atheroembolism of plaque can result in occlusion of small mesenteric vessels and focal areas of bowel necrosis. Dissection of the mesenteric vessel can occur. Oderich has advocated for the use of a covered stent.2 A covered stent could cover proximal branches, and thus, in theory, the treatment itself could cause bowel ischemia or infarction. Many series that have compared open and endovascular surgery show no difference in early outcomes, but demonstrate early restenosis, decreased primary patency, and decreased assisted primary patency with endovascular treatment as compared with open operations.3-5
Another concern regarding the treatment of mesenteric ischemia is the status of the end organ, the bowel. Successful treatment of mesenteric ischemia cannot only assess the atherosclerotic lesion, but requires the surgeon to be cognizant of the condition of the bowel.
This concern is especially true for acute mesenteric ischemia,6 but the status of the bowel must also be kept in mind for chronic mesenteric ischemia. Unlike the lower extremity where the results of treatment are easily observed by inspection (color, evidence of atheroembolization), palpation (temperature, pulse), and physiologic testing (ABI), the bowel is not accessible. There are no highly accurate tests to determine if the patient has on-going bowel ischemia or has developed infarction. Should a complication occur, physical examination findings and laboratory changes often become apparent late in the course of the disease. As previously noted, these patients are often physiologically compromised and have little reserve and may not survive such complications. An open operation allows visualization of the bowel, before and after revascularization.
Traditional teaching for the surgical treatment of chronic mesenteric ischemia has emphasized that two mesenteric vessels, usually the celiac and SMA, should be revascularized.7,8 Various approaches to revascularization have been suggested including transaortic endarterectomy and an antegrade bifurcated bypass originating from the supraceliac aorta. These operations are effective in restoring flow to the mesenteric circulation, but both of these approaches involve aortic cross-clamping and are physiologically challenging for patients.
There are alternatives for open revascularization of the mesenteric vessels. The infrarenal aorta, iliac vessels, and even renal arteries can be, and have been used as the inflow source. It has been my experience that a bypass graft using an iliac artery (common or external) as the inflow source is well tolerated by patients. I have preferentially used either great saphenous vein or femoral-popliteal vein as the conduit. In many cases, the distal anastomosis is simply the SMA. However, both the celiac and SMA can be revascularized by creating a side-side anastomosis to the SMA and an end-side anastomosis to the common or proper hepatic artery. Such procedures have been durable, providing relief of symptoms and allowing patients to regain weight.9
In reality, I believe that an endovascular approach for the treatment of chronic mesenteric ischemia has a role. Vascular surgeons are uniquely positioned to carefully evaluate each patient and recommend what they feel is most appropriate. I tend to feel that an endovascular approach is less likely to be successful for patients with occluded vessels, especially those with a flush occlusion, and so will preferentially recommend an open operation for these patients. On the other hand, in my practice, I have used an endovascular approach for patients with severe stenosis, and as Dr. Harris states, know that a bypass is always an option should this be unsuccessful or ultimately fail.
References
1. Ann Vasc Surg. 1991;5:403-6
2. J Vasc Surg. 2013;58:1316-23
3. Ann Vasc Surg. 2015:29;934-40
4. World J Gastroenerol. 2013;19:1333-7
5. J Vasc Surg. 2007;45:1162-71
6. J Vasc Surg. 2015;62:767-72
7. J Vasc Surg. 2002:35:853-9
8. Surgery. 1981;90:940-6
9. J Vasc Surg. 2000;32:37-47
Eric Endean, MD, is the director of the aortic center, Gordon L. Hyde Endowed Professor and Chair, and vascular surgery section head, vascular and endovascular surgery at UK HealthCare, University of Kentucky, Lexington. He had no relevant disclosures.
Presenting the case for endovascular intervention
Chronic mesenteric ischemia (CMI) is an uncommon, but lethal, problem when left untreated. Before the endovascular era, the only option was open revascularization, which is challenging in this chronically ill, malnourished population with diffuse, systemic, atherosclerotic disease. Morbidity and mortality was relatively high because of the comorbid conditions and chronically ill status of the patients. The first mesenteric bypass was performed in 1958 by Maynard and Shaw.1
Options for open repair include transaortic endarterectomy, antegrade bypass from the supraceliac aorta or distal thoracic aorta, or retrograde bypass from the iliac artery, all of which are major abdominal procedures. Endovascular interventions are now the most commonly performed procedures for CMI in the United States based on national studies.2
Technical success with endovascular interventions can be achieved in well over 90% of patients, and multiple vessels can be treated simultaneously from either a femoral or brachial approach. The primary concern with endovascular interventions has been long-term patency, with restenosis from intimal hyperplasia or thrombosis causing recurrent symptoms in up to 30%-50% at 3-5 years.5-7 However, these rates are based on use of bare metal stents, rather than covered stents. Recent studies8 suggest that stent grafts have markedly improved outcomes over bare metal stents for ostial lesions, decreasing recurrence. Oderich found that freedom from recurrence was 92% with stent grafts as compared with 53% for bare metal stents, with primary patency rates of 92%, at 3 years8, comparable to even the best open bypass results. Schoch first reported the use of covered stents in the mesenteric circulation, and found that no patients developed recurrent stenosis at 2 years.9 Other concerns with endovascular intervention include embolization and dissection, which have not been frequently reported.
Mortality from open surgery ranges from 5% to 15%, with morbidity of 30%-40%.4 Mortality from endovascular intervention is markedly lower, in the range of 3.56% vs. 7.23%.5 Long-term survival is not different between endovascular vs. open repair (69% vs. 65%),4 with the majority of deaths related to cardiac, pulmonary, or malignancy issues. Moghadamyeghaneh, in a review of the Nationwide Inpatient Sample database, found that open surgery was one of the major predictors for higher morbidity (odds ratio, 5.07) and mortality (OR, 5.13), despite the fact that endovascular patients were older (another risk factor for adverse outcomes) and had more comorbidities in this nonrandomized, real-world study.2
Further, if one considers cost as a metric for decision making, a Markov clinical decision model by Hogendoorn et al suggests an endovascular first approach is preferred, despite the presumed higher rate of recurrence expected with use of bare metal stents, rather than covered stents, utilized for this analysis.10 Clearly, the financial advantage would be even greater for endovascular with the lower rates of recurrence with covered stents more recently reported.
If a patient develops recurrent stenosis after endovascular intervention, open bypass may be considered as an alternate to repeat endovascular intervention, dependent on the nutritional status, life expectancy, and initial intervention undertaken. Alternately, patients who undergo open repair are not immune to restenosis, with a recurrence rate of 10%-20%.11,12 Oderich found that there was a 22% mortality in those treated with repeat open interventions, with a 47% complication rate. Endovascular interventions, however, had a significantly lower rate of complications, 16%, and mortality. For patients with recurrent disease after open revascularization for CMI, the endovascular approach should also be the preferred approach.
Any lesion which is anatomically suitable for endovascular repair should first have an attempt made via this approach, utilizing covered stents. While there is a role for open revascularization, endovascular interventions can be safely performed, with minimal morbidity and mortality, and good long-term patency, even in the sickest patients. Endovascular intervention should be the procedure of choice for chronic mesenteric ischemia and recurrent chronic mesenteric ischemia.
References
1. NEJM. 1958;258:874-8
2. Am Surg. 2015;81:1149-56
3. Cardiovasc Intervent Radiol. 1980;3:43-4
4. Ann Vasc Surg. 2009;23:700-12
5. Ann Vasc Surg. 2013;27:113-22
6. J Vasc Surg. 2011;54:1422-29
7. J Vasc Surg. 2010;51:140-7
8. J Vasc Surg. 2013;58:1316-24
9. JACS. 2001;212:668-75
10. J Vasc Surg. 2014;60;715-25
11. J Vasc Surg. 200;49:1472-9
12. J Vasc Surg. 2007;45:1162-71
Linda Harris, MD, is professor of surgery; chief, division of vascular surgery; program director, vascular surgery residency & fellowship at the State University of New York at Buffalo; and an associate medical editor for Vascular Specialist. She had no relevant disclosures.
Chronic mesenteric ischemia is best treated in an open operation.
Chronic mesenteric ischemia is a rare disorder accounting for about 1 out of 100,000 admissions.1 Because of the rarity of this disease, diagnosis is often delayed. Patients are often evaluated for other gastrointestinal diseases and/or malignancies, which in turn contributes to significant delays in diagnosis. Additionally, there are no prospective, randomized trials on which to base decisions regarding treatment; and it is unlikely that such studies will ever be undertaken.
Chronic mesenteric ischemia develops when two or more of the mesenteric vessels (celiac, superior mesenteric [SMA], or inferior mesenteric [IMA]) become occluded or develop severe stenosis. In my experience, patients most often develop occlusion (as opposed to stenosis) of their mesenteric vessels. The atherosclerotic plaque responsible for the disease originates within the aorta and the stenosis/occlusion develops at the vessel origin.
As a whole, these comorbidities would suggest that a more minimally invasive approach would be preferred. Yet, an open operation for chronic mesenteric ischemia should not be discarded as an initial operation.
Endovascular treatment of mesenteric ischemia is not without risk. As in all endovascular procedures there are complications associated with the access vessels. The orientation of the mesenteric vessels as they arise from the aorta often favors an approach from the left arm. The brachial artery is smaller than the femoral artery, and it is more difficult to apply pressure to the brachial artery to control the puncture site. This leads to a higher rate of access site complications including hemorrhage, pseudoaneurysm and thrombosis of the vessel. Bleeding or hematoma formation within the brachial neurovascular sheath can result in significant neurologic dysfunction of the arm and hand. There is risk of stroke, especially when the access vessel is the brachial artery. There are also complications directly related to the endovascular procedure.
Atheroembolism of plaque can result in occlusion of small mesenteric vessels and focal areas of bowel necrosis. Dissection of the mesenteric vessel can occur. Oderich has advocated for the use of a covered stent.2 A covered stent could cover proximal branches, and thus, in theory, the treatment itself could cause bowel ischemia or infarction. Many series that have compared open and endovascular surgery show no difference in early outcomes, but demonstrate early restenosis, decreased primary patency, and decreased assisted primary patency with endovascular treatment as compared with open operations.3-5
Another concern regarding the treatment of mesenteric ischemia is the status of the end organ, the bowel. Successful treatment of mesenteric ischemia cannot only assess the atherosclerotic lesion, but requires the surgeon to be cognizant of the condition of the bowel.
This concern is especially true for acute mesenteric ischemia,6 but the status of the bowel must also be kept in mind for chronic mesenteric ischemia. Unlike the lower extremity where the results of treatment are easily observed by inspection (color, evidence of atheroembolization), palpation (temperature, pulse), and physiologic testing (ABI), the bowel is not accessible. There are no highly accurate tests to determine if the patient has on-going bowel ischemia or has developed infarction. Should a complication occur, physical examination findings and laboratory changes often become apparent late in the course of the disease. As previously noted, these patients are often physiologically compromised and have little reserve and may not survive such complications. An open operation allows visualization of the bowel, before and after revascularization.
Traditional teaching for the surgical treatment of chronic mesenteric ischemia has emphasized that two mesenteric vessels, usually the celiac and SMA, should be revascularized.7,8 Various approaches to revascularization have been suggested including transaortic endarterectomy and an antegrade bifurcated bypass originating from the supraceliac aorta. These operations are effective in restoring flow to the mesenteric circulation, but both of these approaches involve aortic cross-clamping and are physiologically challenging for patients.
There are alternatives for open revascularization of the mesenteric vessels. The infrarenal aorta, iliac vessels, and even renal arteries can be, and have been used as the inflow source. It has been my experience that a bypass graft using an iliac artery (common or external) as the inflow source is well tolerated by patients. I have preferentially used either great saphenous vein or femoral-popliteal vein as the conduit. In many cases, the distal anastomosis is simply the SMA. However, both the celiac and SMA can be revascularized by creating a side-side anastomosis to the SMA and an end-side anastomosis to the common or proper hepatic artery. Such procedures have been durable, providing relief of symptoms and allowing patients to regain weight.9
In reality, I believe that an endovascular approach for the treatment of chronic mesenteric ischemia has a role. Vascular surgeons are uniquely positioned to carefully evaluate each patient and recommend what they feel is most appropriate. I tend to feel that an endovascular approach is less likely to be successful for patients with occluded vessels, especially those with a flush occlusion, and so will preferentially recommend an open operation for these patients. On the other hand, in my practice, I have used an endovascular approach for patients with severe stenosis, and as Dr. Harris states, know that a bypass is always an option should this be unsuccessful or ultimately fail.
References
1. Ann Vasc Surg. 1991;5:403-6
2. J Vasc Surg. 2013;58:1316-23
3. Ann Vasc Surg. 2015:29;934-40
4. World J Gastroenerol. 2013;19:1333-7
5. J Vasc Surg. 2007;45:1162-71
6. J Vasc Surg. 2015;62:767-72
7. J Vasc Surg. 2002:35:853-9
8. Surgery. 1981;90:940-6
9. J Vasc Surg. 2000;32:37-47
Eric Endean, MD, is the director of the aortic center, Gordon L. Hyde Endowed Professor and Chair, and vascular surgery section head, vascular and endovascular surgery at UK HealthCare, University of Kentucky, Lexington. He had no relevant disclosures.
Presenting the case for endovascular intervention
Chronic mesenteric ischemia (CMI) is an uncommon, but lethal, problem when left untreated. Before the endovascular era, the only option was open revascularization, which is challenging in this chronically ill, malnourished population with diffuse, systemic, atherosclerotic disease. Morbidity and mortality was relatively high because of the comorbid conditions and chronically ill status of the patients. The first mesenteric bypass was performed in 1958 by Maynard and Shaw.1
Options for open repair include transaortic endarterectomy, antegrade bypass from the supraceliac aorta or distal thoracic aorta, or retrograde bypass from the iliac artery, all of which are major abdominal procedures. Endovascular interventions are now the most commonly performed procedures for CMI in the United States based on national studies.2
Technical success with endovascular interventions can be achieved in well over 90% of patients, and multiple vessels can be treated simultaneously from either a femoral or brachial approach. The primary concern with endovascular interventions has been long-term patency, with restenosis from intimal hyperplasia or thrombosis causing recurrent symptoms in up to 30%-50% at 3-5 years.5-7 However, these rates are based on use of bare metal stents, rather than covered stents. Recent studies8 suggest that stent grafts have markedly improved outcomes over bare metal stents for ostial lesions, decreasing recurrence. Oderich found that freedom from recurrence was 92% with stent grafts as compared with 53% for bare metal stents, with primary patency rates of 92%, at 3 years8, comparable to even the best open bypass results. Schoch first reported the use of covered stents in the mesenteric circulation, and found that no patients developed recurrent stenosis at 2 years.9 Other concerns with endovascular intervention include embolization and dissection, which have not been frequently reported.
Mortality from open surgery ranges from 5% to 15%, with morbidity of 30%-40%.4 Mortality from endovascular intervention is markedly lower, in the range of 3.56% vs. 7.23%.5 Long-term survival is not different between endovascular vs. open repair (69% vs. 65%),4 with the majority of deaths related to cardiac, pulmonary, or malignancy issues. Moghadamyeghaneh, in a review of the Nationwide Inpatient Sample database, found that open surgery was one of the major predictors for higher morbidity (odds ratio, 5.07) and mortality (OR, 5.13), despite the fact that endovascular patients were older (another risk factor for adverse outcomes) and had more comorbidities in this nonrandomized, real-world study.2
Further, if one considers cost as a metric for decision making, a Markov clinical decision model by Hogendoorn et al suggests an endovascular first approach is preferred, despite the presumed higher rate of recurrence expected with use of bare metal stents, rather than covered stents, utilized for this analysis.10 Clearly, the financial advantage would be even greater for endovascular with the lower rates of recurrence with covered stents more recently reported.
If a patient develops recurrent stenosis after endovascular intervention, open bypass may be considered as an alternate to repeat endovascular intervention, dependent on the nutritional status, life expectancy, and initial intervention undertaken. Alternately, patients who undergo open repair are not immune to restenosis, with a recurrence rate of 10%-20%.11,12 Oderich found that there was a 22% mortality in those treated with repeat open interventions, with a 47% complication rate. Endovascular interventions, however, had a significantly lower rate of complications, 16%, and mortality. For patients with recurrent disease after open revascularization for CMI, the endovascular approach should also be the preferred approach.
Any lesion which is anatomically suitable for endovascular repair should first have an attempt made via this approach, utilizing covered stents. While there is a role for open revascularization, endovascular interventions can be safely performed, with minimal morbidity and mortality, and good long-term patency, even in the sickest patients. Endovascular intervention should be the procedure of choice for chronic mesenteric ischemia and recurrent chronic mesenteric ischemia.
References
1. NEJM. 1958;258:874-8
2. Am Surg. 2015;81:1149-56
3. Cardiovasc Intervent Radiol. 1980;3:43-4
4. Ann Vasc Surg. 2009;23:700-12
5. Ann Vasc Surg. 2013;27:113-22
6. J Vasc Surg. 2011;54:1422-29
7. J Vasc Surg. 2010;51:140-7
8. J Vasc Surg. 2013;58:1316-24
9. JACS. 2001;212:668-75
10. J Vasc Surg. 2014;60;715-25
11. J Vasc Surg. 200;49:1472-9
12. J Vasc Surg. 2007;45:1162-71
Linda Harris, MD, is professor of surgery; chief, division of vascular surgery; program director, vascular surgery residency & fellowship at the State University of New York at Buffalo; and an associate medical editor for Vascular Specialist. She had no relevant disclosures.
Our new year’s resolutions
Be at war with your vices, at peace with your neighbors, and let every new year find you a better person.
– Benjamin Franklin
Traditionally, the new year is a time for reflection, looking back to review what could have been done better, and looking forward to the opportunity to rectify those inadequacies over the coming year. We thought we would take this opportunity to look at our use of the electronic health record and think about the things we might do over the next year to make our lives easier and our charting better.
Top of our list is a renewed commitment to finish our notes by the end of each session. Too many physicians we know rush through patient hours and then are left with 10-20 notes to finish at the end of the day. Realistically, this is when we least feel like completing notes. Such work encroaches on personal and family time, likely contributes to the burnout that has been increasing among physicians, and is much less likely to accurately represent the encounter than notes completed in real time.
As we have spoken with many of our colleagues, it has become clear to us that many clinicians have learned how to be “just proficient enough” in their use of their EHR; they are not pulling out their hair every 5 minutes in frustration, but they have not taken the extra time and effort that are needed to optimize their productivity. To efficiently use an EHR requires some time spent designing templates and macros to make it easy to repetitively carry out common tasks.
A lot of physicians – particularly physicians over 40 years of age – are still typing their notes with the ol’ two-finger hunt-and-peck technique. This is incredibly time consuming, inefficient, and frustrating.
While many solutions have been proposed, including having a scribe walk around with the doctor, the simplest and easiest to implement is voice transcription. Even though medical transcription software is expensive, the return on investment is large for those who do not type well. After a short period of training on the software, notes are generally of higher quality and are finished considerably faster than when typing. The technology also has the ability to learn the names of frequently used consultants, medications, and procedures, so users don’t even have to type uncommon names or words.
Another area in which we hope to advance over the next year is working more effectively as a team to share the documentation burden. Nurses and medical assistants – within the boundaries of their licensing – can be empowered to document in predefined areas of the chart as much as possible.
For example, given the fact that the prevalence of depression is about twice as high in patients with diabetes as it is in the general population, our medical assistants now screen our diabetes patients with a PHQ-2 depression screen and record the results in the chart. This has been good for our patients, satisfying for our medical assistants, and has offloaded this task from the doctors.
We need to think of more areas where we can facilitate team care and really make everyone – physicians, nurses, front staff, and patients – more satisfied with the care that is being given.
Most EHRs have a reminder function – the ability to prompt a user to follow up on an abnormal x-ray or lab results in case a patient does not come back into the office as recommended. Our sense is that most of us are not using this function. It is worth finding out how to use it and giving it a try.
Patient portals have gained a lot of traction over the past few years. For a little while, we were really making an effort to have patients register, so that currently many (but by far not most) of our patients have signed up. We want to make better use of this fantastic resource.
We say “fantastic” because when we talk to patients (or friends or family) who use the portal, they have shared that it really makes their lives easier. They are able to see their labs, ponder the meaning of their results (perhaps of a slightly high glucose or an LDL cholesterol level), and if they have questions, they can correspond electronically with their care providers. It enhances care and allows us to spend less time on the phone, while giving patients better access to information.
New year’s resolutions are an opportunity for reflection and optimism. As we look back on the past year, we should learn from our experience and approach the year in front of us with greater enthusiasm, in the hope that through that enthusiasm we can continue to grow, be better and healthier, and simply be more like the people we want to be.
The electronic health record affects all of our interactions with patients and colleagues, and, when not used optimally, encroaches into our personal and family lives. It is a perfect place to focus during the new year to enable us to have more productive, effective, and happier times both in the office and at home.
Dr. Notte is a family physician and clinical informaticist for Abington (Pa.) Memorial Hospital. He is a partner in EHR Practice Consultants, a firm that aids physicians in adopting electronic health records. Dr. Skolnik is associate director of the family medicine residency program at Abington Memorial Hospital and professor of family and community medicine at Temple University in Philadelphia.
Be at war with your vices, at peace with your neighbors, and let every new year find you a better person.
– Benjamin Franklin
Traditionally, the new year is a time for reflection, looking back to review what could have been done better, and looking forward to the opportunity to rectify those inadequacies over the coming year. We thought we would take this opportunity to look at our use of the electronic health record and think about the things we might do over the next year to make our lives easier and our charting better.
Top of our list is a renewed commitment to finish our notes by the end of each session. Too many physicians we know rush through patient hours and then are left with 10-20 notes to finish at the end of the day. Realistically, this is when we least feel like completing notes. Such work encroaches on personal and family time, likely contributes to the burnout that has been increasing among physicians, and is much less likely to accurately represent the encounter than notes completed in real time.
As we have spoken with many of our colleagues, it has become clear to us that many clinicians have learned how to be “just proficient enough” in their use of their EHR; they are not pulling out their hair every 5 minutes in frustration, but they have not taken the extra time and effort that are needed to optimize their productivity. To efficiently use an EHR requires some time spent designing templates and macros to make it easy to repetitively carry out common tasks.
A lot of physicians – particularly physicians over 40 years of age – are still typing their notes with the ol’ two-finger hunt-and-peck technique. This is incredibly time consuming, inefficient, and frustrating.
While many solutions have been proposed, including having a scribe walk around with the doctor, the simplest and easiest to implement is voice transcription. Even though medical transcription software is expensive, the return on investment is large for those who do not type well. After a short period of training on the software, notes are generally of higher quality and are finished considerably faster than when typing. The technology also has the ability to learn the names of frequently used consultants, medications, and procedures, so users don’t even have to type uncommon names or words.
Another area in which we hope to advance over the next year is working more effectively as a team to share the documentation burden. Nurses and medical assistants – within the boundaries of their licensing – can be empowered to document in predefined areas of the chart as much as possible.
For example, given the fact that the prevalence of depression is about twice as high in patients with diabetes as it is in the general population, our medical assistants now screen our diabetes patients with a PHQ-2 depression screen and record the results in the chart. This has been good for our patients, satisfying for our medical assistants, and has offloaded this task from the doctors.
We need to think of more areas where we can facilitate team care and really make everyone – physicians, nurses, front staff, and patients – more satisfied with the care that is being given.
Most EHRs have a reminder function – the ability to prompt a user to follow up on an abnormal x-ray or lab results in case a patient does not come back into the office as recommended. Our sense is that most of us are not using this function. It is worth finding out how to use it and giving it a try.
Patient portals have gained a lot of traction over the past few years. For a little while, we were really making an effort to have patients register, so that currently many (but by far not most) of our patients have signed up. We want to make better use of this fantastic resource.
We say “fantastic” because when we talk to patients (or friends or family) who use the portal, they have shared that it really makes their lives easier. They are able to see their labs, ponder the meaning of their results (perhaps of a slightly high glucose or an LDL cholesterol level), and if they have questions, they can correspond electronically with their care providers. It enhances care and allows us to spend less time on the phone, while giving patients better access to information.
New year’s resolutions are an opportunity for reflection and optimism. As we look back on the past year, we should learn from our experience and approach the year in front of us with greater enthusiasm, in the hope that through that enthusiasm we can continue to grow, be better and healthier, and simply be more like the people we want to be.
The electronic health record affects all of our interactions with patients and colleagues, and, when not used optimally, encroaches into our personal and family lives. It is a perfect place to focus during the new year to enable us to have more productive, effective, and happier times both in the office and at home.
Dr. Notte is a family physician and clinical informaticist for Abington (Pa.) Memorial Hospital. He is a partner in EHR Practice Consultants, a firm that aids physicians in adopting electronic health records. Dr. Skolnik is associate director of the family medicine residency program at Abington Memorial Hospital and professor of family and community medicine at Temple University in Philadelphia.
Be at war with your vices, at peace with your neighbors, and let every new year find you a better person.
– Benjamin Franklin
Traditionally, the new year is a time for reflection, looking back to review what could have been done better, and looking forward to the opportunity to rectify those inadequacies over the coming year. We thought we would take this opportunity to look at our use of the electronic health record and think about the things we might do over the next year to make our lives easier and our charting better.
Top of our list is a renewed commitment to finish our notes by the end of each session. Too many physicians we know rush through patient hours and then are left with 10-20 notes to finish at the end of the day. Realistically, this is when we least feel like completing notes. Such work encroaches on personal and family time, likely contributes to the burnout that has been increasing among physicians, and is much less likely to accurately represent the encounter than notes completed in real time.
As we have spoken with many of our colleagues, it has become clear to us that many clinicians have learned how to be “just proficient enough” in their use of their EHR; they are not pulling out their hair every 5 minutes in frustration, but they have not taken the extra time and effort that are needed to optimize their productivity. To efficiently use an EHR requires some time spent designing templates and macros to make it easy to repetitively carry out common tasks.
A lot of physicians – particularly physicians over 40 years of age – are still typing their notes with the ol’ two-finger hunt-and-peck technique. This is incredibly time consuming, inefficient, and frustrating.
While many solutions have been proposed, including having a scribe walk around with the doctor, the simplest and easiest to implement is voice transcription. Even though medical transcription software is expensive, the return on investment is large for those who do not type well. After a short period of training on the software, notes are generally of higher quality and are finished considerably faster than when typing. The technology also has the ability to learn the names of frequently used consultants, medications, and procedures, so users don’t even have to type uncommon names or words.
Another area in which we hope to advance over the next year is working more effectively as a team to share the documentation burden. Nurses and medical assistants – within the boundaries of their licensing – can be empowered to document in predefined areas of the chart as much as possible.
For example, given the fact that the prevalence of depression is about twice as high in patients with diabetes as it is in the general population, our medical assistants now screen our diabetes patients with a PHQ-2 depression screen and record the results in the chart. This has been good for our patients, satisfying for our medical assistants, and has offloaded this task from the doctors.
We need to think of more areas where we can facilitate team care and really make everyone – physicians, nurses, front staff, and patients – more satisfied with the care that is being given.
Most EHRs have a reminder function – the ability to prompt a user to follow up on an abnormal x-ray or lab results in case a patient does not come back into the office as recommended. Our sense is that most of us are not using this function. It is worth finding out how to use it and giving it a try.
Patient portals have gained a lot of traction over the past few years. For a little while, we were really making an effort to have patients register, so that currently many (but by far not most) of our patients have signed up. We want to make better use of this fantastic resource.
We say “fantastic” because when we talk to patients (or friends or family) who use the portal, they have shared that it really makes their lives easier. They are able to see their labs, ponder the meaning of their results (perhaps of a slightly high glucose or an LDL cholesterol level), and if they have questions, they can correspond electronically with their care providers. It enhances care and allows us to spend less time on the phone, while giving patients better access to information.
New year’s resolutions are an opportunity for reflection and optimism. As we look back on the past year, we should learn from our experience and approach the year in front of us with greater enthusiasm, in the hope that through that enthusiasm we can continue to grow, be better and healthier, and simply be more like the people we want to be.
The electronic health record affects all of our interactions with patients and colleagues, and, when not used optimally, encroaches into our personal and family lives. It is a perfect place to focus during the new year to enable us to have more productive, effective, and happier times both in the office and at home.
Dr. Notte is a family physician and clinical informaticist for Abington (Pa.) Memorial Hospital. He is a partner in EHR Practice Consultants, a firm that aids physicians in adopting electronic health records. Dr. Skolnik is associate director of the family medicine residency program at Abington Memorial Hospital and professor of family and community medicine at Temple University in Philadelphia.
The Role of Biologic Therapy for Psoriasis in Cardiovascular Risk Reduction
The cardiovascular comorbidities associated with psoriasis have been well documented; however, the mechanism by which psoriasis increases the risk for cardiovascular disease (CVD) remains unclear. Elevated systemic inflammatory cytokines and mediators may play a key role in their association, which prompts the questions: Do systemic medications have a protective effect? Do patients on systemic antipsoriatic treatment have a decreased risk for major adverse cardiovascular events (MACEs) compared with untreated patients?
We believe the shared inflammatory processes involved in psoriasis and atherosclerosis formation are potential targets for therapy in reducing the incidence of CVD and its associated complications. A growing amount of evidence suggests cardioprotective effects associated with antipsoriatic treatments such as tumor necrosis factor (TNF) inhibitors and methotrexate. Gkalpakiotis et al1 demonstrated a reduction in serum E-selectin (mean [standard deviation], 53.04 [23.54] ng/mL vs 35.32 [8.70] ng/mL; P<.001) and IL-22 (25.11 [19.9] pg/mL vs 12.83 [8.42] pg/mL; P<.001) after 3 months of adalimumab administration in patients with moderate to severe psoriasis. Both E-selectin and IL-22 are associated with the development of atherosclerosis, endothelial dysfunction, and an increased incidence of CVD. Similarly, Wu et al2 demonstrated a statistically significant reduction (–5.04 mg/dL [95% confidence interval [CI], –8.24 to –2.12; P<.01) in C-reactive protein in patients with psoriasis, psoriatic arthritis, and rheumatoid arthritis after concurrent use of methotrexate and TNF inhibitors.
Solomon et al3 compared the rate of newly diagnosed diabetes mellitus among psoriasis and rheumatoid arthritis patients treated with TNF inhibitors, methotrexate, hydroxychloroquine, and other nonbiologic disease-modifying antirheumatic drugs. The authors’ findings suggest that those who take a TNF inhibitor (hazard ratio [HR], 0.62; 95% CI, 0.42-0.91) and hydroxychloroquine (HR, 0.54; 95% CI, 0.36-0.80) are at lower risk for diabetes mellitus compared to those treated with nonbiologic disease-modifying antirheumatic drugs. Conversely, the methotrexate (HR, 0.77; 95% CI, 0.53-1.13) cohort did not show a statistically significant reduction in diabetes risk.3
Pina et al4 revealed improvement in endothelial function after 6 months of adalimumab use in patients with moderate to severe psoriasis. To evaluate the presence of subclinical endothelial dysfunction, the authors assessed brachial artery reactivity by measuring flow-mediated dilation and carotid artery stiffness by pulse wave velocity. Patients showed an increase in flow-mediated dilation (mean [SD], 6.19% [2.44%] vs 7.46% [2.43%]; P=.008) and reduction in pulse wave velocity (6.28 [1.04] m/s vs 5.69 [1.31] m/s; P=.03) compared to baseline measurements, indicating an improvement of endothelial function.4
Ahlehoff et al5 observed for improvements in subclinical left ventricular dysfunction in psoriasis patients after treatment with biologics. Using echocardiography, they assessed for changes in diastolic function and left ventricular systolic deformation (defined by global longitudinal strain). Of patients who received 3 months of biologic therapy (TNF inhibitor orIL-12/23 inhibitor) and maintained at minimum a psoriasis area and severity index 50 response, all demonstrated an improvement in diastolic function (mean [SD], 8.1 [2.1] vs 6.7 [1.9]; P<.001) and global longitudinal strain (mean [SD], –16.8% [2.1%] vs –18.3% [2.3%]; P<.001). Of note, patients who did not achieve a psoriasis area and severity index 50 response at follow-up did not exhibit an improvement in subclinical myocardial function.5
Moreover, a Danish nationwide study with up to 5-year follow-up evaluated the risk for MACE (ie, cardiovascular death, myocardial infarction, stroke) in patients with severe psoriasis receiving systemic anti-inflammatory medications and nonsystemic therapies including topical treatments, phototherapy, and climate therapy.6 Compared to nonsystemic therapies, methotrexate use (HR, 0.53; 95% CI, 0.34-0.83) was associated with a decreased risk for cardiovascular events. However, a protective decreased risk was not found among patients who used systemic cyclosporine (HR, 1.06; 95% CI, 0.26-4.27) or retinoids (HR, 1.80; 95% CI, 1.03-2.96). Any biological drug use had a comparable but nonsignificant reduction of cardiovascular events (HR, 0.58; 95% CI, 0.30-1.10). After multivariable adjustment, TNF inhibitors were associated with a statistically significant decreased risk for cardiovascular events (HR, 0.46; 95% CI, 0.22-0.98; P=.04) compared to nonsystemic therapies. The IL-12/23 inhibitor did not demonstrate this relationship (HR, 1.52; 95% CI, 0.47-4.94).6
Lastly, Wu et al7 compared the risk for MACE (ie, myocardial infarction, stroke, unstable angina, transient ischemic attack) between patients with psoriasis who received TNF inhibitors or methotrexate. The TNF inhibitor and methotrexate cohorts were observed for a median of 12 months and 9 months, respectively. After adjusting for potential confounding factors, they found a 45% reduction (HR, 0.55; 95% CI, 0.45-0.67) in cardiovascular event risk in the TNF inhibitor cohort compared with the methotrexate cohort. Notably, analyses also showed comparatively fewer cardiovascular events in the TNF inhibitor cohort throughout all time points—6, 12, 18, 24, 60 months—in the observation period. Regression analysis revealed an 11% reduction in cardiovascular events (HR, 0.89; 95% CI, 0.80-0.98) with each additional 6 months of cumulative TNF inhibitor exposure.
The current sum of evidence suggests cardioprotective effects of TNF inhibitor and methotrexate use. However, given the cumulative systemic toxicity and inferior cutaneous efficacy of methotrexate, TNF inhibitors will likely play a more significant role going forward. The role of methotrexate may be for its simultaneous use with biologic therapies to limit immunogenicity. Newer biologic agents such as IL-12/23 and IL-17 inhibitors have not yet been as extensively studied for their effects on cardiovascular risk as their TNF inhibitor counterparts. However, because of their shared ability to target specific immunological pathways, it is plausible that IL-12/23 and IL-17 agents may exhibit cardioprotective effects.8
Patients with psoriasis should be counseled and educated about the increased risk for CVD and its associated morbidity and mortality risk. Screening for modifiable risk factors and recommending therapeutic lifestyle changes also is appropriate. Future studies should help define the role of specific systemic drugs in reducing the risk for CVD in patients with psoriasis.
- Gkalpakiotis S, Arenbergerova M, Gkalpakioti P, et al. Impact of adalimumab treatment on cardiovascular risk biomarkers in psoriasis: results of a pilot study [published online October 24, 2016]. J Dermatol. doi:10.1111/1346-8138.13661.
- Wu JJ, Rowan CG, Bebchuk JD, et al. Association between tumor necrosis factor inhibitor (TNFi) therapy and changes in C-reactive protein (CRP), blood pressure, and alanine aminotransferase (ALT) among patients with psoriasis, psoriatic arthritis, or rheumatoid arthritis [published online March 5, 2015]. J Am Acad Dermatol. 2015;72:917-919.
- Solomon DH, Massarotti E, Garg R, et al. Association between disease-modifying antirheumatic drugs and diabetes risk in patients with rheumatoid arthritis and psoriasis. JAMA. 2011;305:2525-2531.
- Pina T, Corrales A, Lopez-Mejias R, et al. Anti-tumor necrosis factor-alpha therapy improves endothelial function and arterial stiffness in patients with moderate to severe psoriasis: a 6-month prospective study. J Dermatol. 2016;43:1267-1272.
- Ahlehoff O, Hansen PR, Gislason GH, et al. Myocardial function and effects of biologic therapy in patients with severe psoriasis: a prospective echocardiographic study [published online April 6, 2015]. J Eur Acad Dermatol Venereol. 2016;30:819-823.
- Ahlehoff O, Skov L, Gislason G, et al. Cardiovascular outcomes and systemic anti-inflammatory drugs in patients with severe psoriasis: 5-year follow-up of a Danish nationwide cohort [published online October 10, 2014]. J Eur Acad Dermatol Venereol. 2015;29:1128-1134.
- Wu JJ, Guérin A, Sundaram M, et al. Cardiovascular event risk assessment in psoriasis patients treated with tumor necrosis factor-α inhibitors versus methotrexate [published online October 26, 2016]. J Am Acad Dermatol. 2017;76:81-90.
- Egeberg A, Skov L. Management of cardiovascular disease in patients with psoriasis. Expert Opin Pharmacother. 2016;17:1509-1516.
The cardiovascular comorbidities associated with psoriasis have been well documented; however, the mechanism by which psoriasis increases the risk for cardiovascular disease (CVD) remains unclear. Elevated systemic inflammatory cytokines and mediators may play a key role in their association, which prompts the questions: Do systemic medications have a protective effect? Do patients on systemic antipsoriatic treatment have a decreased risk for major adverse cardiovascular events (MACEs) compared with untreated patients?
We believe the shared inflammatory processes involved in psoriasis and atherosclerosis formation are potential targets for therapy in reducing the incidence of CVD and its associated complications. A growing amount of evidence suggests cardioprotective effects associated with antipsoriatic treatments such as tumor necrosis factor (TNF) inhibitors and methotrexate. Gkalpakiotis et al1 demonstrated a reduction in serum E-selectin (mean [standard deviation], 53.04 [23.54] ng/mL vs 35.32 [8.70] ng/mL; P<.001) and IL-22 (25.11 [19.9] pg/mL vs 12.83 [8.42] pg/mL; P<.001) after 3 months of adalimumab administration in patients with moderate to severe psoriasis. Both E-selectin and IL-22 are associated with the development of atherosclerosis, endothelial dysfunction, and an increased incidence of CVD. Similarly, Wu et al2 demonstrated a statistically significant reduction (–5.04 mg/dL [95% confidence interval [CI], –8.24 to –2.12; P<.01) in C-reactive protein in patients with psoriasis, psoriatic arthritis, and rheumatoid arthritis after concurrent use of methotrexate and TNF inhibitors.
Solomon et al3 compared the rate of newly diagnosed diabetes mellitus among psoriasis and rheumatoid arthritis patients treated with TNF inhibitors, methotrexate, hydroxychloroquine, and other nonbiologic disease-modifying antirheumatic drugs. The authors’ findings suggest that those who take a TNF inhibitor (hazard ratio [HR], 0.62; 95% CI, 0.42-0.91) and hydroxychloroquine (HR, 0.54; 95% CI, 0.36-0.80) are at lower risk for diabetes mellitus compared to those treated with nonbiologic disease-modifying antirheumatic drugs. Conversely, the methotrexate (HR, 0.77; 95% CI, 0.53-1.13) cohort did not show a statistically significant reduction in diabetes risk.3
Pina et al4 revealed improvement in endothelial function after 6 months of adalimumab use in patients with moderate to severe psoriasis. To evaluate the presence of subclinical endothelial dysfunction, the authors assessed brachial artery reactivity by measuring flow-mediated dilation and carotid artery stiffness by pulse wave velocity. Patients showed an increase in flow-mediated dilation (mean [SD], 6.19% [2.44%] vs 7.46% [2.43%]; P=.008) and reduction in pulse wave velocity (6.28 [1.04] m/s vs 5.69 [1.31] m/s; P=.03) compared to baseline measurements, indicating an improvement of endothelial function.4
Ahlehoff et al5 observed for improvements in subclinical left ventricular dysfunction in psoriasis patients after treatment with biologics. Using echocardiography, they assessed for changes in diastolic function and left ventricular systolic deformation (defined by global longitudinal strain). Of patients who received 3 months of biologic therapy (TNF inhibitor orIL-12/23 inhibitor) and maintained at minimum a psoriasis area and severity index 50 response, all demonstrated an improvement in diastolic function (mean [SD], 8.1 [2.1] vs 6.7 [1.9]; P<.001) and global longitudinal strain (mean [SD], –16.8% [2.1%] vs –18.3% [2.3%]; P<.001). Of note, patients who did not achieve a psoriasis area and severity index 50 response at follow-up did not exhibit an improvement in subclinical myocardial function.5
Moreover, a Danish nationwide study with up to 5-year follow-up evaluated the risk for MACE (ie, cardiovascular death, myocardial infarction, stroke) in patients with severe psoriasis receiving systemic anti-inflammatory medications and nonsystemic therapies including topical treatments, phototherapy, and climate therapy.6 Compared to nonsystemic therapies, methotrexate use (HR, 0.53; 95% CI, 0.34-0.83) was associated with a decreased risk for cardiovascular events. However, a protective decreased risk was not found among patients who used systemic cyclosporine (HR, 1.06; 95% CI, 0.26-4.27) or retinoids (HR, 1.80; 95% CI, 1.03-2.96). Any biological drug use had a comparable but nonsignificant reduction of cardiovascular events (HR, 0.58; 95% CI, 0.30-1.10). After multivariable adjustment, TNF inhibitors were associated with a statistically significant decreased risk for cardiovascular events (HR, 0.46; 95% CI, 0.22-0.98; P=.04) compared to nonsystemic therapies. The IL-12/23 inhibitor did not demonstrate this relationship (HR, 1.52; 95% CI, 0.47-4.94).6
Lastly, Wu et al7 compared the risk for MACE (ie, myocardial infarction, stroke, unstable angina, transient ischemic attack) between patients with psoriasis who received TNF inhibitors or methotrexate. The TNF inhibitor and methotrexate cohorts were observed for a median of 12 months and 9 months, respectively. After adjusting for potential confounding factors, they found a 45% reduction (HR, 0.55; 95% CI, 0.45-0.67) in cardiovascular event risk in the TNF inhibitor cohort compared with the methotrexate cohort. Notably, analyses also showed comparatively fewer cardiovascular events in the TNF inhibitor cohort throughout all time points—6, 12, 18, 24, 60 months—in the observation period. Regression analysis revealed an 11% reduction in cardiovascular events (HR, 0.89; 95% CI, 0.80-0.98) with each additional 6 months of cumulative TNF inhibitor exposure.
The current sum of evidence suggests cardioprotective effects of TNF inhibitor and methotrexate use. However, given the cumulative systemic toxicity and inferior cutaneous efficacy of methotrexate, TNF inhibitors will likely play a more significant role going forward. The role of methotrexate may be for its simultaneous use with biologic therapies to limit immunogenicity. Newer biologic agents such as IL-12/23 and IL-17 inhibitors have not yet been as extensively studied for their effects on cardiovascular risk as their TNF inhibitor counterparts. However, because of their shared ability to target specific immunological pathways, it is plausible that IL-12/23 and IL-17 agents may exhibit cardioprotective effects.8
Patients with psoriasis should be counseled and educated about the increased risk for CVD and its associated morbidity and mortality risk. Screening for modifiable risk factors and recommending therapeutic lifestyle changes also is appropriate. Future studies should help define the role of specific systemic drugs in reducing the risk for CVD in patients with psoriasis.
The cardiovascular comorbidities associated with psoriasis have been well documented; however, the mechanism by which psoriasis increases the risk for cardiovascular disease (CVD) remains unclear. Elevated systemic inflammatory cytokines and mediators may play a key role in their association, which prompts the questions: Do systemic medications have a protective effect? Do patients on systemic antipsoriatic treatment have a decreased risk for major adverse cardiovascular events (MACEs) compared with untreated patients?
We believe the shared inflammatory processes involved in psoriasis and atherosclerosis formation are potential targets for therapy in reducing the incidence of CVD and its associated complications. A growing amount of evidence suggests cardioprotective effects associated with antipsoriatic treatments such as tumor necrosis factor (TNF) inhibitors and methotrexate. Gkalpakiotis et al1 demonstrated a reduction in serum E-selectin (mean [standard deviation], 53.04 [23.54] ng/mL vs 35.32 [8.70] ng/mL; P<.001) and IL-22 (25.11 [19.9] pg/mL vs 12.83 [8.42] pg/mL; P<.001) after 3 months of adalimumab administration in patients with moderate to severe psoriasis. Both E-selectin and IL-22 are associated with the development of atherosclerosis, endothelial dysfunction, and an increased incidence of CVD. Similarly, Wu et al2 demonstrated a statistically significant reduction (–5.04 mg/dL [95% confidence interval [CI], –8.24 to –2.12; P<.01) in C-reactive protein in patients with psoriasis, psoriatic arthritis, and rheumatoid arthritis after concurrent use of methotrexate and TNF inhibitors.
Solomon et al3 compared the rate of newly diagnosed diabetes mellitus among psoriasis and rheumatoid arthritis patients treated with TNF inhibitors, methotrexate, hydroxychloroquine, and other nonbiologic disease-modifying antirheumatic drugs. The authors’ findings suggest that those who take a TNF inhibitor (hazard ratio [HR], 0.62; 95% CI, 0.42-0.91) and hydroxychloroquine (HR, 0.54; 95% CI, 0.36-0.80) are at lower risk for diabetes mellitus compared to those treated with nonbiologic disease-modifying antirheumatic drugs. Conversely, the methotrexate (HR, 0.77; 95% CI, 0.53-1.13) cohort did not show a statistically significant reduction in diabetes risk.3
Pina et al4 revealed improvement in endothelial function after 6 months of adalimumab use in patients with moderate to severe psoriasis. To evaluate the presence of subclinical endothelial dysfunction, the authors assessed brachial artery reactivity by measuring flow-mediated dilation and carotid artery stiffness by pulse wave velocity. Patients showed an increase in flow-mediated dilation (mean [SD], 6.19% [2.44%] vs 7.46% [2.43%]; P=.008) and reduction in pulse wave velocity (6.28 [1.04] m/s vs 5.69 [1.31] m/s; P=.03) compared to baseline measurements, indicating an improvement of endothelial function.4
Ahlehoff et al5 observed for improvements in subclinical left ventricular dysfunction in psoriasis patients after treatment with biologics. Using echocardiography, they assessed for changes in diastolic function and left ventricular systolic deformation (defined by global longitudinal strain). Of patients who received 3 months of biologic therapy (TNF inhibitor orIL-12/23 inhibitor) and maintained at minimum a psoriasis area and severity index 50 response, all demonstrated an improvement in diastolic function (mean [SD], 8.1 [2.1] vs 6.7 [1.9]; P<.001) and global longitudinal strain (mean [SD], –16.8% [2.1%] vs –18.3% [2.3%]; P<.001). Of note, patients who did not achieve a psoriasis area and severity index 50 response at follow-up did not exhibit an improvement in subclinical myocardial function.5
Moreover, a Danish nationwide study with up to 5-year follow-up evaluated the risk for MACE (ie, cardiovascular death, myocardial infarction, stroke) in patients with severe psoriasis receiving systemic anti-inflammatory medications and nonsystemic therapies including topical treatments, phototherapy, and climate therapy.6 Compared to nonsystemic therapies, methotrexate use (HR, 0.53; 95% CI, 0.34-0.83) was associated with a decreased risk for cardiovascular events. However, a protective decreased risk was not found among patients who used systemic cyclosporine (HR, 1.06; 95% CI, 0.26-4.27) or retinoids (HR, 1.80; 95% CI, 1.03-2.96). Any biological drug use had a comparable but nonsignificant reduction of cardiovascular events (HR, 0.58; 95% CI, 0.30-1.10). After multivariable adjustment, TNF inhibitors were associated with a statistically significant decreased risk for cardiovascular events (HR, 0.46; 95% CI, 0.22-0.98; P=.04) compared to nonsystemic therapies. The IL-12/23 inhibitor did not demonstrate this relationship (HR, 1.52; 95% CI, 0.47-4.94).6
Lastly, Wu et al7 compared the risk for MACE (ie, myocardial infarction, stroke, unstable angina, transient ischemic attack) between patients with psoriasis who received TNF inhibitors or methotrexate. The TNF inhibitor and methotrexate cohorts were observed for a median of 12 months and 9 months, respectively. After adjusting for potential confounding factors, they found a 45% reduction (HR, 0.55; 95% CI, 0.45-0.67) in cardiovascular event risk in the TNF inhibitor cohort compared with the methotrexate cohort. Notably, analyses also showed comparatively fewer cardiovascular events in the TNF inhibitor cohort throughout all time points—6, 12, 18, 24, 60 months—in the observation period. Regression analysis revealed an 11% reduction in cardiovascular events (HR, 0.89; 95% CI, 0.80-0.98) with each additional 6 months of cumulative TNF inhibitor exposure.
The current sum of evidence suggests cardioprotective effects of TNF inhibitor and methotrexate use. However, given the cumulative systemic toxicity and inferior cutaneous efficacy of methotrexate, TNF inhibitors will likely play a more significant role going forward. The role of methotrexate may be for its simultaneous use with biologic therapies to limit immunogenicity. Newer biologic agents such as IL-12/23 and IL-17 inhibitors have not yet been as extensively studied for their effects on cardiovascular risk as their TNF inhibitor counterparts. However, because of their shared ability to target specific immunological pathways, it is plausible that IL-12/23 and IL-17 agents may exhibit cardioprotective effects.8
Patients with psoriasis should be counseled and educated about the increased risk for CVD and its associated morbidity and mortality risk. Screening for modifiable risk factors and recommending therapeutic lifestyle changes also is appropriate. Future studies should help define the role of specific systemic drugs in reducing the risk for CVD in patients with psoriasis.
- Gkalpakiotis S, Arenbergerova M, Gkalpakioti P, et al. Impact of adalimumab treatment on cardiovascular risk biomarkers in psoriasis: results of a pilot study [published online October 24, 2016]. J Dermatol. doi:10.1111/1346-8138.13661.
- Wu JJ, Rowan CG, Bebchuk JD, et al. Association between tumor necrosis factor inhibitor (TNFi) therapy and changes in C-reactive protein (CRP), blood pressure, and alanine aminotransferase (ALT) among patients with psoriasis, psoriatic arthritis, or rheumatoid arthritis [published online March 5, 2015]. J Am Acad Dermatol. 2015;72:917-919.
- Solomon DH, Massarotti E, Garg R, et al. Association between disease-modifying antirheumatic drugs and diabetes risk in patients with rheumatoid arthritis and psoriasis. JAMA. 2011;305:2525-2531.
- Pina T, Corrales A, Lopez-Mejias R, et al. Anti-tumor necrosis factor-alpha therapy improves endothelial function and arterial stiffness in patients with moderate to severe psoriasis: a 6-month prospective study. J Dermatol. 2016;43:1267-1272.
- Ahlehoff O, Hansen PR, Gislason GH, et al. Myocardial function and effects of biologic therapy in patients with severe psoriasis: a prospective echocardiographic study [published online April 6, 2015]. J Eur Acad Dermatol Venereol. 2016;30:819-823.
- Ahlehoff O, Skov L, Gislason G, et al. Cardiovascular outcomes and systemic anti-inflammatory drugs in patients with severe psoriasis: 5-year follow-up of a Danish nationwide cohort [published online October 10, 2014]. J Eur Acad Dermatol Venereol. 2015;29:1128-1134.
- Wu JJ, Guérin A, Sundaram M, et al. Cardiovascular event risk assessment in psoriasis patients treated with tumor necrosis factor-α inhibitors versus methotrexate [published online October 26, 2016]. J Am Acad Dermatol. 2017;76:81-90.
- Egeberg A, Skov L. Management of cardiovascular disease in patients with psoriasis. Expert Opin Pharmacother. 2016;17:1509-1516.
- Gkalpakiotis S, Arenbergerova M, Gkalpakioti P, et al. Impact of adalimumab treatment on cardiovascular risk biomarkers in psoriasis: results of a pilot study [published online October 24, 2016]. J Dermatol. doi:10.1111/1346-8138.13661.
- Wu JJ, Rowan CG, Bebchuk JD, et al. Association between tumor necrosis factor inhibitor (TNFi) therapy and changes in C-reactive protein (CRP), blood pressure, and alanine aminotransferase (ALT) among patients with psoriasis, psoriatic arthritis, or rheumatoid arthritis [published online March 5, 2015]. J Am Acad Dermatol. 2015;72:917-919.
- Solomon DH, Massarotti E, Garg R, et al. Association between disease-modifying antirheumatic drugs and diabetes risk in patients with rheumatoid arthritis and psoriasis. JAMA. 2011;305:2525-2531.
- Pina T, Corrales A, Lopez-Mejias R, et al. Anti-tumor necrosis factor-alpha therapy improves endothelial function and arterial stiffness in patients with moderate to severe psoriasis: a 6-month prospective study. J Dermatol. 2016;43:1267-1272.
- Ahlehoff O, Hansen PR, Gislason GH, et al. Myocardial function and effects of biologic therapy in patients with severe psoriasis: a prospective echocardiographic study [published online April 6, 2015]. J Eur Acad Dermatol Venereol. 2016;30:819-823.
- Ahlehoff O, Skov L, Gislason G, et al. Cardiovascular outcomes and systemic anti-inflammatory drugs in patients with severe psoriasis: 5-year follow-up of a Danish nationwide cohort [published online October 10, 2014]. J Eur Acad Dermatol Venereol. 2015;29:1128-1134.
- Wu JJ, Guérin A, Sundaram M, et al. Cardiovascular event risk assessment in psoriasis patients treated with tumor necrosis factor-α inhibitors versus methotrexate [published online October 26, 2016]. J Am Acad Dermatol. 2017;76:81-90.
- Egeberg A, Skov L. Management of cardiovascular disease in patients with psoriasis. Expert Opin Pharmacother. 2016;17:1509-1516.
Ovarian cancer screening update
Ovarian cancer remains the most deadly gynecologic malignancy in the United States with more than 14,000 deaths in 2016. Yet, the prevalence remains low with approximately 22,000 cases in 2016. Stage at diagnosis is one of the strongest predictors of overall survival. The 5-year overall survival is more than 90% with stage I disease; this drops to 25% for those with distant metastases. Unfortunately, three-quarters of patients have disease spread beyond the ovary at the time ovarian cancer is clinically identified.
In this update, we will review:
• The fundamentals of ovarian cancer screening.
• How to identify patients who would benefit from surveillance.
• The usefulness of tumor markers.
• The results from recent large ovarian cancer screening trials.
Screening is a critical part of secondary prevention through early disease detection, when patients are asymptomatic and treatment can stop progression. Core principles of a good screening test are that the test is noninvasive, tolerable to the patient, and not costly. The disease should pose a major health threat and be detected at a stage at which intervention can impart a survival advantage. Most critically, the test should be sensitive and specific (i.e., detect disease when it is truly present and rarely be positive in the absence of disease).
Screening vs. case finding
A significant distinction should be made between average-risk patients and high-risk patients. Ob.gyns. frequently encounter high-risk patients who would benefit from regular surveillance or case finding (for example, patients with BRCA deleterious mutations or with Lynch syndrome). There are multiple risk factors for ovarian cancer, but the strongest known is family history, which is present in 15% of ovarian cancer patients. Having one relative with ovarian cancer increases the lifetime risk of ovarian cancer up to 5%. When a patient reports having one or more family members with ovarian cancer, it is important to differentiate between a common sporadic presentation and a rare familial cancer syndrome. ACOG Practice Bulletin 103 provides excellent guidance on which patients warrant formal genetic risk assessments by a genetic counselor.2
Tumor markers
During the last 25 years, screening for ovarian cancer in an average-risk population has been evaluated in multiple large prospective studies using serum tumor markers (i.e., CA 125) and ultrasound results.
CA 125 and HE4 tumor markers are frequently elevated in ovarian cancer and have been studied in ovarian cancer screening. However, while having a high sensitivity for detecting disease, they are nonspecific because they are also elevated in numerous benign conditions and therefore have not proven to be a useful screening tool in the average-risk population. There are clinically available tumor marker panels that are not intended for screening. Rather, they clarify the uncertainty of the presurgical adnexal mass evaluation by providing a risk score. High risk scores are generally managed in conjunction with a gynecologic oncology referral.
Multimodal screening
Combined assessment of both ultrasound findings and tumor marker levels shows more promise with respect to prediction of ovarian cancer. However, a systematic review of 25 ovarian cancer screening studies concluded that screening low-risk populations should not be included in clinical practice until randomized trials assessed the effect on mortality and the risk of adverse events. Three large randomized controlled trials have been completed to date.3,4,5
The U.K. Collaborative Trial of Ovarian Cancer Screening (UKCTOCS) results appear promising. However, the revealing analysis was post hoc since the original study design did not take into account the inherent delayed effect in screening studies. While these results may provide a basis for future successful screening for ovarian cancer, confirmatory further analysis is pending, using additional data over a period of the next 3 years.
Ultimately, we are all excited about the possibility of effective screening protocols for ovarian cancer and await completed analyses of UKCTOCS. Until their benefits are confirmed, screening and preventive measures should be limited to those at high risk for ovarian cancer.
References
1. Hippokratia. 2007 Apr;11(2):63-6.
2. Obstet Gynecol. 2009 Apr;113(4):957-66.
3. Am J Obstet Gynecol. 2005 Nov;193(5):1630-9.
4. Int J Gynecol Cancer. 2008 May-Jun;18(3):414-20.
5. Lancet. 2016 Mar 5;387(10022):945-56.
Dr. Pierce is a gynecologic oncology fellow in the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill. Dr. Rossi is an assistant professor in the division of gynecologic oncology at UNC–Chapel Hill. They reported having no relevant financial disclosures.
Ovarian cancer remains the most deadly gynecologic malignancy in the United States with more than 14,000 deaths in 2016. Yet, the prevalence remains low with approximately 22,000 cases in 2016. Stage at diagnosis is one of the strongest predictors of overall survival. The 5-year overall survival is more than 90% with stage I disease; this drops to 25% for those with distant metastases. Unfortunately, three-quarters of patients have disease spread beyond the ovary at the time ovarian cancer is clinically identified.
In this update, we will review:
• The fundamentals of ovarian cancer screening.
• How to identify patients who would benefit from surveillance.
• The usefulness of tumor markers.
• The results from recent large ovarian cancer screening trials.
Screening is a critical part of secondary prevention through early disease detection, when patients are asymptomatic and treatment can stop progression. Core principles of a good screening test are that the test is noninvasive, tolerable to the patient, and not costly. The disease should pose a major health threat and be detected at a stage at which intervention can impart a survival advantage. Most critically, the test should be sensitive and specific (i.e., detect disease when it is truly present and rarely be positive in the absence of disease).
Screening vs. case finding
A significant distinction should be made between average-risk patients and high-risk patients. Ob.gyns. frequently encounter high-risk patients who would benefit from regular surveillance or case finding (for example, patients with BRCA deleterious mutations or with Lynch syndrome). There are multiple risk factors for ovarian cancer, but the strongest known is family history, which is present in 15% of ovarian cancer patients. Having one relative with ovarian cancer increases the lifetime risk of ovarian cancer up to 5%. When a patient reports having one or more family members with ovarian cancer, it is important to differentiate between a common sporadic presentation and a rare familial cancer syndrome. ACOG Practice Bulletin 103 provides excellent guidance on which patients warrant formal genetic risk assessments by a genetic counselor.2
Tumor markers
During the last 25 years, screening for ovarian cancer in an average-risk population has been evaluated in multiple large prospective studies using serum tumor markers (i.e., CA 125) and ultrasound results.
CA 125 and HE4 tumor markers are frequently elevated in ovarian cancer and have been studied in ovarian cancer screening. However, while having a high sensitivity for detecting disease, they are nonspecific because they are also elevated in numerous benign conditions and therefore have not proven to be a useful screening tool in the average-risk population. There are clinically available tumor marker panels that are not intended for screening. Rather, they clarify the uncertainty of the presurgical adnexal mass evaluation by providing a risk score. High risk scores are generally managed in conjunction with a gynecologic oncology referral.
Multimodal screening
Combined assessment of both ultrasound findings and tumor marker levels shows more promise with respect to prediction of ovarian cancer. However, a systematic review of 25 ovarian cancer screening studies concluded that screening low-risk populations should not be included in clinical practice until randomized trials assessed the effect on mortality and the risk of adverse events. Three large randomized controlled trials have been completed to date.3,4,5
The U.K. Collaborative Trial of Ovarian Cancer Screening (UKCTOCS) results appear promising. However, the revealing analysis was post hoc since the original study design did not take into account the inherent delayed effect in screening studies. While these results may provide a basis for future successful screening for ovarian cancer, confirmatory further analysis is pending, using additional data over a period of the next 3 years.
Ultimately, we are all excited about the possibility of effective screening protocols for ovarian cancer and await completed analyses of UKCTOCS. Until their benefits are confirmed, screening and preventive measures should be limited to those at high risk for ovarian cancer.
References
1. Hippokratia. 2007 Apr;11(2):63-6.
2. Obstet Gynecol. 2009 Apr;113(4):957-66.
3. Am J Obstet Gynecol. 2005 Nov;193(5):1630-9.
4. Int J Gynecol Cancer. 2008 May-Jun;18(3):414-20.
5. Lancet. 2016 Mar 5;387(10022):945-56.
Dr. Pierce is a gynecologic oncology fellow in the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill. Dr. Rossi is an assistant professor in the division of gynecologic oncology at UNC–Chapel Hill. They reported having no relevant financial disclosures.
Ovarian cancer remains the most deadly gynecologic malignancy in the United States with more than 14,000 deaths in 2016. Yet, the prevalence remains low with approximately 22,000 cases in 2016. Stage at diagnosis is one of the strongest predictors of overall survival. The 5-year overall survival is more than 90% with stage I disease; this drops to 25% for those with distant metastases. Unfortunately, three-quarters of patients have disease spread beyond the ovary at the time ovarian cancer is clinically identified.
In this update, we will review:
• The fundamentals of ovarian cancer screening.
• How to identify patients who would benefit from surveillance.
• The usefulness of tumor markers.
• The results from recent large ovarian cancer screening trials.
Screening is a critical part of secondary prevention through early disease detection, when patients are asymptomatic and treatment can stop progression. Core principles of a good screening test are that the test is noninvasive, tolerable to the patient, and not costly. The disease should pose a major health threat and be detected at a stage at which intervention can impart a survival advantage. Most critically, the test should be sensitive and specific (i.e., detect disease when it is truly present and rarely be positive in the absence of disease).
Screening vs. case finding
A significant distinction should be made between average-risk patients and high-risk patients. Ob.gyns. frequently encounter high-risk patients who would benefit from regular surveillance or case finding (for example, patients with BRCA deleterious mutations or with Lynch syndrome). There are multiple risk factors for ovarian cancer, but the strongest known is family history, which is present in 15% of ovarian cancer patients. Having one relative with ovarian cancer increases the lifetime risk of ovarian cancer up to 5%. When a patient reports having one or more family members with ovarian cancer, it is important to differentiate between a common sporadic presentation and a rare familial cancer syndrome. ACOG Practice Bulletin 103 provides excellent guidance on which patients warrant formal genetic risk assessments by a genetic counselor.2
Tumor markers
During the last 25 years, screening for ovarian cancer in an average-risk population has been evaluated in multiple large prospective studies using serum tumor markers (i.e., CA 125) and ultrasound results.
CA 125 and HE4 tumor markers are frequently elevated in ovarian cancer and have been studied in ovarian cancer screening. However, while having a high sensitivity for detecting disease, they are nonspecific because they are also elevated in numerous benign conditions and therefore have not proven to be a useful screening tool in the average-risk population. There are clinically available tumor marker panels that are not intended for screening. Rather, they clarify the uncertainty of the presurgical adnexal mass evaluation by providing a risk score. High risk scores are generally managed in conjunction with a gynecologic oncology referral.
Multimodal screening
Combined assessment of both ultrasound findings and tumor marker levels shows more promise with respect to prediction of ovarian cancer. However, a systematic review of 25 ovarian cancer screening studies concluded that screening low-risk populations should not be included in clinical practice until randomized trials assessed the effect on mortality and the risk of adverse events. Three large randomized controlled trials have been completed to date.3,4,5
The U.K. Collaborative Trial of Ovarian Cancer Screening (UKCTOCS) results appear promising. However, the revealing analysis was post hoc since the original study design did not take into account the inherent delayed effect in screening studies. While these results may provide a basis for future successful screening for ovarian cancer, confirmatory further analysis is pending, using additional data over a period of the next 3 years.
Ultimately, we are all excited about the possibility of effective screening protocols for ovarian cancer and await completed analyses of UKCTOCS. Until their benefits are confirmed, screening and preventive measures should be limited to those at high risk for ovarian cancer.
References
1. Hippokratia. 2007 Apr;11(2):63-6.
2. Obstet Gynecol. 2009 Apr;113(4):957-66.
3. Am J Obstet Gynecol. 2005 Nov;193(5):1630-9.
4. Int J Gynecol Cancer. 2008 May-Jun;18(3):414-20.
5. Lancet. 2016 Mar 5;387(10022):945-56.
Dr. Pierce is a gynecologic oncology fellow in the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill. Dr. Rossi is an assistant professor in the division of gynecologic oncology at UNC–Chapel Hill. They reported having no relevant financial disclosures.