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IV ketamine, intranasal esketamine likely to ‘happily coexist’
Dr. Steven Levine offers perspective on how the FDA approval will affect patients, practice
Q: Why is this a “banner day” for psychiatry?
A: This is truly the first new option for depression in 60 years. The selective serotonin reuptake inhibitors (SSRIs) developed in the mid-’80s were not truly new, not much different from the monoamine oxidase inhibitors (MAOI) and tricyclic antidepressants. In fact, they work much like watered-down MAOIs. Esketamine works by a truly novel mechanism.
Even though it constitutes a relatively new treatment, ketamine is a very old medicine, and we probably know more about the pharmacology and mechanisms in depression than for the SSRIs.
The idea of SSRIs working by increasing levels of neurotransmitters like serotonin has never held water. We never really believed that, but for people who respond to them – and many are helped – what is really happening weeks to months down the line is that these drugs increase the plasticity of the brain. Depression, like other mental health conditions, disrupts connections between important brain regions, reducing the number, function, and quality of the connections, and we believe SSRIs improve these.
Ketamine does these same things by a different route and much, much more quickly.
Q: What is esketamine’s method of action, and how long will a dose last?
A: Ketamine and esketamine bind to and block glutamate N-methyl-D-aspartate (NMDA) receptors. This leads to the release of several chemical messengers, the result of which increases the production of neurotrophic factors, in particular brain-derived neurotrophic factor (BDNF), that play a key role in healing damaged connections in the brain. A single dose of esketamine would only be expected to relieve depression symptoms for days, up to a week or 2. Multiple doses over the first few weeks can extend the durability of response to several weeks and sometimes months.
It is not true for every patient, but some do have improvement within 2-4 hours that correlates with physiologic changes. Others can be later responders and require up to 6 exposures.
Q: The FDA approval requires those who administer the drug to complete special training and meet licensure requirements. Is this realistic for small practices?
A: Initially, not every psychiatrist will be able to offer esketamine, and I think it might be beyond the reach of small practices, and that’s probably okay. Enough people and enough centers will be able to offer it to meet the initial demand.
Q: Is esketamine “better” than ketamine infusions? With the approved drug available, will ketamine infusion clinics still have a place?
A: There are major pros with this. The FDA approval takes out of the gray area of off-label administration. It will most likely be covered by insurance now – a huge advantage that will put this in the reach of so many patients who haven’t been able to access this treatment.
I think that, because there are advantages and disadvantages for both IV ketamine and nasal esketamine, they will happily coexist for years to come. However, because nasal esketamine will likely be restricted to prescription by psychiatrists, it may have more impact on non-psychiatrist-led practices. In this way,
Dr. Steven Levine is the founder of Actify Neurotherapies, which operates nine clinics providing ketamine treatment for depression.
Dr. Steven Levine offers perspective on how the FDA approval will affect patients, practice
Dr. Steven Levine offers perspective on how the FDA approval will affect patients, practice
Q: Why is this a “banner day” for psychiatry?
A: This is truly the first new option for depression in 60 years. The selective serotonin reuptake inhibitors (SSRIs) developed in the mid-’80s were not truly new, not much different from the monoamine oxidase inhibitors (MAOI) and tricyclic antidepressants. In fact, they work much like watered-down MAOIs. Esketamine works by a truly novel mechanism.
Even though it constitutes a relatively new treatment, ketamine is a very old medicine, and we probably know more about the pharmacology and mechanisms in depression than for the SSRIs.
The idea of SSRIs working by increasing levels of neurotransmitters like serotonin has never held water. We never really believed that, but for people who respond to them – and many are helped – what is really happening weeks to months down the line is that these drugs increase the plasticity of the brain. Depression, like other mental health conditions, disrupts connections between important brain regions, reducing the number, function, and quality of the connections, and we believe SSRIs improve these.
Ketamine does these same things by a different route and much, much more quickly.
Q: What is esketamine’s method of action, and how long will a dose last?
A: Ketamine and esketamine bind to and block glutamate N-methyl-D-aspartate (NMDA) receptors. This leads to the release of several chemical messengers, the result of which increases the production of neurotrophic factors, in particular brain-derived neurotrophic factor (BDNF), that play a key role in healing damaged connections in the brain. A single dose of esketamine would only be expected to relieve depression symptoms for days, up to a week or 2. Multiple doses over the first few weeks can extend the durability of response to several weeks and sometimes months.
It is not true for every patient, but some do have improvement within 2-4 hours that correlates with physiologic changes. Others can be later responders and require up to 6 exposures.
Q: The FDA approval requires those who administer the drug to complete special training and meet licensure requirements. Is this realistic for small practices?
A: Initially, not every psychiatrist will be able to offer esketamine, and I think it might be beyond the reach of small practices, and that’s probably okay. Enough people and enough centers will be able to offer it to meet the initial demand.
Q: Is esketamine “better” than ketamine infusions? With the approved drug available, will ketamine infusion clinics still have a place?
A: There are major pros with this. The FDA approval takes out of the gray area of off-label administration. It will most likely be covered by insurance now – a huge advantage that will put this in the reach of so many patients who haven’t been able to access this treatment.
I think that, because there are advantages and disadvantages for both IV ketamine and nasal esketamine, they will happily coexist for years to come. However, because nasal esketamine will likely be restricted to prescription by psychiatrists, it may have more impact on non-psychiatrist-led practices. In this way,
Dr. Steven Levine is the founder of Actify Neurotherapies, which operates nine clinics providing ketamine treatment for depression.
Q: Why is this a “banner day” for psychiatry?
A: This is truly the first new option for depression in 60 years. The selective serotonin reuptake inhibitors (SSRIs) developed in the mid-’80s were not truly new, not much different from the monoamine oxidase inhibitors (MAOI) and tricyclic antidepressants. In fact, they work much like watered-down MAOIs. Esketamine works by a truly novel mechanism.
Even though it constitutes a relatively new treatment, ketamine is a very old medicine, and we probably know more about the pharmacology and mechanisms in depression than for the SSRIs.
The idea of SSRIs working by increasing levels of neurotransmitters like serotonin has never held water. We never really believed that, but for people who respond to them – and many are helped – what is really happening weeks to months down the line is that these drugs increase the plasticity of the brain. Depression, like other mental health conditions, disrupts connections between important brain regions, reducing the number, function, and quality of the connections, and we believe SSRIs improve these.
Ketamine does these same things by a different route and much, much more quickly.
Q: What is esketamine’s method of action, and how long will a dose last?
A: Ketamine and esketamine bind to and block glutamate N-methyl-D-aspartate (NMDA) receptors. This leads to the release of several chemical messengers, the result of which increases the production of neurotrophic factors, in particular brain-derived neurotrophic factor (BDNF), that play a key role in healing damaged connections in the brain. A single dose of esketamine would only be expected to relieve depression symptoms for days, up to a week or 2. Multiple doses over the first few weeks can extend the durability of response to several weeks and sometimes months.
It is not true for every patient, but some do have improvement within 2-4 hours that correlates with physiologic changes. Others can be later responders and require up to 6 exposures.
Q: The FDA approval requires those who administer the drug to complete special training and meet licensure requirements. Is this realistic for small practices?
A: Initially, not every psychiatrist will be able to offer esketamine, and I think it might be beyond the reach of small practices, and that’s probably okay. Enough people and enough centers will be able to offer it to meet the initial demand.
Q: Is esketamine “better” than ketamine infusions? With the approved drug available, will ketamine infusion clinics still have a place?
A: There are major pros with this. The FDA approval takes out of the gray area of off-label administration. It will most likely be covered by insurance now – a huge advantage that will put this in the reach of so many patients who haven’t been able to access this treatment.
I think that, because there are advantages and disadvantages for both IV ketamine and nasal esketamine, they will happily coexist for years to come. However, because nasal esketamine will likely be restricted to prescription by psychiatrists, it may have more impact on non-psychiatrist-led practices. In this way,
Dr. Steven Levine is the founder of Actify Neurotherapies, which operates nine clinics providing ketamine treatment for depression.
Try behavioral interventions for chronic insomnia
“The greatest medicine of all is teaching people how not to need it.” – Hippocrates
For many years, over-the-counter and prescription medications indicated for sleep problems/disorders have been available to patients. But the side effects associated with some of these medications are many. In light of the numerous nonpharmacologic interventions that are available to patients, they should be offered first when appropriate.
One of the top nonpharmacologic interventions is cognitive-behavioral therapy for insomnia, or CBT-I, which the American Academy of Sleep Medicine’s clinical guidelines say should be used as initial treatment if possible.1 Elements of CBT-I include cognitive therapy, which is aimed at reducing dysfunctional beliefs about sleep. Common distortions expressed by patients include: “I cannot sleep without medications” and “I must get 8 hours of sleep to feel refreshed and function well the next day.” It helps in dealing with anxiety and catastrophic thinking to establish realistic expectations and treatment related to insomnia.
CBT-I can be delivered in the form of monotherapy or in a combined manner. The individual components include psychoeducation, behavioral strategies, cognitive therapy, and relaxation training. CBT-I combines cognitive therapy with behavioral interventions. Behavioral elements include stimulus control therapy and sleep restriction therapy. Relaxation therapy might or might not be included. Sleep hygiene education usually is a part of it.2
Two other kinds of CBT that can be effective options are telephone-based CBT-I and Internet-based CBT-I.3,4 Meanwhile, among the disadvantages of CBT for insomnia are longer duration of therapy and lack of skilled clinicians.5
Many other kinds of behavioral interventions are available to patients with problems related to sleep, including stimulus control therapy, relaxation therapy, exercise therapy, and sleep restriction therapy.
Stimulus control therapy
This is a strategy aimed at strengthening the association of bed and bedroom to sleep, establishing a consistent sleep-wake rhythm, and reducing the activities that might interfere with sleep. This behavioral therapy is based on the idea that arousal occurs as a conditioned response to the stimulus of sleep environment, and it is among the most effective behavioral treatments.6,7 Strategies include the following:
1. Lie down with the intention of sleeping when sleepy.
2. Do not watch television, read, eat or worry while in bed. Use bed only for sleep and sex.
3. Get out of bed if unable to fall asleep within 10-15 minutes and go to another room. Return to bed only when sleepy. Do not watch the clock. Repeat this step as many times as necessary throughout the night.
4. Set an alarm clock to wake up at a fixed time each morning, including weekends, regardless of how much sleep you got during the night.
5. Do not take a nap during the day.
The goal of these strategies is to extinguish negative associations between bed and undesirable outcomes, such as wakefulness and frustration. One study showed that stimulus control participants, unlike control group participants, experienced significant improvement at follow-up for total sleep time, sleep efficiency, and sleep quality.8
Relaxation therapy
This encompasses different techniques that produce a relaxation response and reduce somatic arousal. It can be implemented before each sleep period. Progressive muscle relaxation, autogenic training, and biofeedback help reduce somatic arousal. Attention-focused procedures, such as imagery training and meditation, tend to lower presleep cognitive arousal (for example, intrusive thoughts, racing minds).9 Slow paced breathing prior to onset of sleep enhances vagal activity, which results in improved sleep parameters.10 One study showed improved quality of sleep and cognitive functions in the elderly by self-relaxation training.11
Exercise training
Participating in physical exercise can be useful in the treatment of insomnia.12 One randomized, controlled trial found that exercising regularly for at least 150 minutes per week was optimal.13 Another study found that, among overweight and obese men with insomnia, aerobic exercise over a 6-month period reduced difficulty in initiating and improving sleep.14
Sleep restriction therapy
The goal of this therapy is to increase the homeostatic drive to sleep. This is carried out by limiting the amount of time spent in bed to the same amount of time that the person reports sleeping. Naps are not allowed. Patients improve with increased drive to sleep in successive nights. In patients with bipolar disorder, however, sleep restriction should be used with caution as it can trigger manic episodes.15
Always ask about sleep
Clinicians should always ask patients about sleep during visits. Sleep duration and sleep quality should be assessed. Insomnia, which is an independent condition, may or may not coexist with other conditions. It is important to determine whether another sleep disorder, or a physical (such as pain, heart, or lung disease), neurological (such as Parkinson’s disease or cerebrovascular disease), or psychiatric disorder (such as depressive illness, anxiety disorder, or substance misuse) is the primary diagnosis. Treatment of insomnia can improve comorbidities.16
In addition, it is important to teach patients about basic sleep hygiene, which includes abiding by a consistent bedtime, and avoiding coffee, alcohol, and nicotine. Eliminating a bedroom clock, not exercising in the late afternoon/early evening, and consuming light bedtime snacks are other measures that can be taken. Avoiding the prolonged use of light-emitting screens before bedtime is another positive step.17
In conclusion, cognitive and behavioral methods are just as effective as prescription medications for short-term treatment of chronic insomnia and should be considered as first line before considering medications. The beneficial effects of CBT-I, in contrast to those produced by medication, might last well beyond the termination of active treatment.
References
1. J Clin Sleep Med. 2008 Oct 15;4(5):487-504.
2. J Clin Psychol. 2010;66(11):1148-60.
3. Sleep. 2013 Mar 1;36(3):353-62.
4. Sleep Med Rev. 2016 Dec;30:1-10.
5. BMC Family Prac. 2012;13:40.
6. Sleep. 2006 Nov;29(11):1398-414.
7. Behavioral Treatments for Sleep Disorders. 1991. doi: 10.1016/13978-0-12-381522-4.00002-X.
8. Behav Modif 1998 Jan;22(1):3-28.
9. Am Fam Physician. 1999 Jun;59(11):3029-38.
10. Psychophysiology. 2015 Mar;52(3):388-96.
11. J Clin Nursing. 2013 April 10. doi: 10.1111/jocn.12096.
12. J Physiother. 2012;58(3):157-63.
13. J Sleep Res. 2015 Oct;24(5):526-34.
14 Sleep Med. 2016 Sep;25:113-121.
15. Am J Psychiatry. 2013 Jul;170(7):716-20.
16. JAMA Intern Med. 2015 Sep;175(9):1461-72.
17. Proc Natl Acad Sci USA. 2015;112(4):1232-7.
Dr. Lamba is a psychiatrist and medical director at Bayridge Hospital in Lynn, Mass. Dr. Rana is assistant professor of pediatrics at Boston University.
“The greatest medicine of all is teaching people how not to need it.” – Hippocrates
For many years, over-the-counter and prescription medications indicated for sleep problems/disorders have been available to patients. But the side effects associated with some of these medications are many. In light of the numerous nonpharmacologic interventions that are available to patients, they should be offered first when appropriate.
One of the top nonpharmacologic interventions is cognitive-behavioral therapy for insomnia, or CBT-I, which the American Academy of Sleep Medicine’s clinical guidelines say should be used as initial treatment if possible.1 Elements of CBT-I include cognitive therapy, which is aimed at reducing dysfunctional beliefs about sleep. Common distortions expressed by patients include: “I cannot sleep without medications” and “I must get 8 hours of sleep to feel refreshed and function well the next day.” It helps in dealing with anxiety and catastrophic thinking to establish realistic expectations and treatment related to insomnia.
CBT-I can be delivered in the form of monotherapy or in a combined manner. The individual components include psychoeducation, behavioral strategies, cognitive therapy, and relaxation training. CBT-I combines cognitive therapy with behavioral interventions. Behavioral elements include stimulus control therapy and sleep restriction therapy. Relaxation therapy might or might not be included. Sleep hygiene education usually is a part of it.2
Two other kinds of CBT that can be effective options are telephone-based CBT-I and Internet-based CBT-I.3,4 Meanwhile, among the disadvantages of CBT for insomnia are longer duration of therapy and lack of skilled clinicians.5
Many other kinds of behavioral interventions are available to patients with problems related to sleep, including stimulus control therapy, relaxation therapy, exercise therapy, and sleep restriction therapy.
Stimulus control therapy
This is a strategy aimed at strengthening the association of bed and bedroom to sleep, establishing a consistent sleep-wake rhythm, and reducing the activities that might interfere with sleep. This behavioral therapy is based on the idea that arousal occurs as a conditioned response to the stimulus of sleep environment, and it is among the most effective behavioral treatments.6,7 Strategies include the following:
1. Lie down with the intention of sleeping when sleepy.
2. Do not watch television, read, eat or worry while in bed. Use bed only for sleep and sex.
3. Get out of bed if unable to fall asleep within 10-15 minutes and go to another room. Return to bed only when sleepy. Do not watch the clock. Repeat this step as many times as necessary throughout the night.
4. Set an alarm clock to wake up at a fixed time each morning, including weekends, regardless of how much sleep you got during the night.
5. Do not take a nap during the day.
The goal of these strategies is to extinguish negative associations between bed and undesirable outcomes, such as wakefulness and frustration. One study showed that stimulus control participants, unlike control group participants, experienced significant improvement at follow-up for total sleep time, sleep efficiency, and sleep quality.8
Relaxation therapy
This encompasses different techniques that produce a relaxation response and reduce somatic arousal. It can be implemented before each sleep period. Progressive muscle relaxation, autogenic training, and biofeedback help reduce somatic arousal. Attention-focused procedures, such as imagery training and meditation, tend to lower presleep cognitive arousal (for example, intrusive thoughts, racing minds).9 Slow paced breathing prior to onset of sleep enhances vagal activity, which results in improved sleep parameters.10 One study showed improved quality of sleep and cognitive functions in the elderly by self-relaxation training.11
Exercise training
Participating in physical exercise can be useful in the treatment of insomnia.12 One randomized, controlled trial found that exercising regularly for at least 150 minutes per week was optimal.13 Another study found that, among overweight and obese men with insomnia, aerobic exercise over a 6-month period reduced difficulty in initiating and improving sleep.14
Sleep restriction therapy
The goal of this therapy is to increase the homeostatic drive to sleep. This is carried out by limiting the amount of time spent in bed to the same amount of time that the person reports sleeping. Naps are not allowed. Patients improve with increased drive to sleep in successive nights. In patients with bipolar disorder, however, sleep restriction should be used with caution as it can trigger manic episodes.15
Always ask about sleep
Clinicians should always ask patients about sleep during visits. Sleep duration and sleep quality should be assessed. Insomnia, which is an independent condition, may or may not coexist with other conditions. It is important to determine whether another sleep disorder, or a physical (such as pain, heart, or lung disease), neurological (such as Parkinson’s disease or cerebrovascular disease), or psychiatric disorder (such as depressive illness, anxiety disorder, or substance misuse) is the primary diagnosis. Treatment of insomnia can improve comorbidities.16
In addition, it is important to teach patients about basic sleep hygiene, which includes abiding by a consistent bedtime, and avoiding coffee, alcohol, and nicotine. Eliminating a bedroom clock, not exercising in the late afternoon/early evening, and consuming light bedtime snacks are other measures that can be taken. Avoiding the prolonged use of light-emitting screens before bedtime is another positive step.17
In conclusion, cognitive and behavioral methods are just as effective as prescription medications for short-term treatment of chronic insomnia and should be considered as first line before considering medications. The beneficial effects of CBT-I, in contrast to those produced by medication, might last well beyond the termination of active treatment.
References
1. J Clin Sleep Med. 2008 Oct 15;4(5):487-504.
2. J Clin Psychol. 2010;66(11):1148-60.
3. Sleep. 2013 Mar 1;36(3):353-62.
4. Sleep Med Rev. 2016 Dec;30:1-10.
5. BMC Family Prac. 2012;13:40.
6. Sleep. 2006 Nov;29(11):1398-414.
7. Behavioral Treatments for Sleep Disorders. 1991. doi: 10.1016/13978-0-12-381522-4.00002-X.
8. Behav Modif 1998 Jan;22(1):3-28.
9. Am Fam Physician. 1999 Jun;59(11):3029-38.
10. Psychophysiology. 2015 Mar;52(3):388-96.
11. J Clin Nursing. 2013 April 10. doi: 10.1111/jocn.12096.
12. J Physiother. 2012;58(3):157-63.
13. J Sleep Res. 2015 Oct;24(5):526-34.
14 Sleep Med. 2016 Sep;25:113-121.
15. Am J Psychiatry. 2013 Jul;170(7):716-20.
16. JAMA Intern Med. 2015 Sep;175(9):1461-72.
17. Proc Natl Acad Sci USA. 2015;112(4):1232-7.
Dr. Lamba is a psychiatrist and medical director at Bayridge Hospital in Lynn, Mass. Dr. Rana is assistant professor of pediatrics at Boston University.
“The greatest medicine of all is teaching people how not to need it.” – Hippocrates
For many years, over-the-counter and prescription medications indicated for sleep problems/disorders have been available to patients. But the side effects associated with some of these medications are many. In light of the numerous nonpharmacologic interventions that are available to patients, they should be offered first when appropriate.
One of the top nonpharmacologic interventions is cognitive-behavioral therapy for insomnia, or CBT-I, which the American Academy of Sleep Medicine’s clinical guidelines say should be used as initial treatment if possible.1 Elements of CBT-I include cognitive therapy, which is aimed at reducing dysfunctional beliefs about sleep. Common distortions expressed by patients include: “I cannot sleep without medications” and “I must get 8 hours of sleep to feel refreshed and function well the next day.” It helps in dealing with anxiety and catastrophic thinking to establish realistic expectations and treatment related to insomnia.
CBT-I can be delivered in the form of monotherapy or in a combined manner. The individual components include psychoeducation, behavioral strategies, cognitive therapy, and relaxation training. CBT-I combines cognitive therapy with behavioral interventions. Behavioral elements include stimulus control therapy and sleep restriction therapy. Relaxation therapy might or might not be included. Sleep hygiene education usually is a part of it.2
Two other kinds of CBT that can be effective options are telephone-based CBT-I and Internet-based CBT-I.3,4 Meanwhile, among the disadvantages of CBT for insomnia are longer duration of therapy and lack of skilled clinicians.5
Many other kinds of behavioral interventions are available to patients with problems related to sleep, including stimulus control therapy, relaxation therapy, exercise therapy, and sleep restriction therapy.
Stimulus control therapy
This is a strategy aimed at strengthening the association of bed and bedroom to sleep, establishing a consistent sleep-wake rhythm, and reducing the activities that might interfere with sleep. This behavioral therapy is based on the idea that arousal occurs as a conditioned response to the stimulus of sleep environment, and it is among the most effective behavioral treatments.6,7 Strategies include the following:
1. Lie down with the intention of sleeping when sleepy.
2. Do not watch television, read, eat or worry while in bed. Use bed only for sleep and sex.
3. Get out of bed if unable to fall asleep within 10-15 minutes and go to another room. Return to bed only when sleepy. Do not watch the clock. Repeat this step as many times as necessary throughout the night.
4. Set an alarm clock to wake up at a fixed time each morning, including weekends, regardless of how much sleep you got during the night.
5. Do not take a nap during the day.
The goal of these strategies is to extinguish negative associations between bed and undesirable outcomes, such as wakefulness and frustration. One study showed that stimulus control participants, unlike control group participants, experienced significant improvement at follow-up for total sleep time, sleep efficiency, and sleep quality.8
Relaxation therapy
This encompasses different techniques that produce a relaxation response and reduce somatic arousal. It can be implemented before each sleep period. Progressive muscle relaxation, autogenic training, and biofeedback help reduce somatic arousal. Attention-focused procedures, such as imagery training and meditation, tend to lower presleep cognitive arousal (for example, intrusive thoughts, racing minds).9 Slow paced breathing prior to onset of sleep enhances vagal activity, which results in improved sleep parameters.10 One study showed improved quality of sleep and cognitive functions in the elderly by self-relaxation training.11
Exercise training
Participating in physical exercise can be useful in the treatment of insomnia.12 One randomized, controlled trial found that exercising regularly for at least 150 minutes per week was optimal.13 Another study found that, among overweight and obese men with insomnia, aerobic exercise over a 6-month period reduced difficulty in initiating and improving sleep.14
Sleep restriction therapy
The goal of this therapy is to increase the homeostatic drive to sleep. This is carried out by limiting the amount of time spent in bed to the same amount of time that the person reports sleeping. Naps are not allowed. Patients improve with increased drive to sleep in successive nights. In patients with bipolar disorder, however, sleep restriction should be used with caution as it can trigger manic episodes.15
Always ask about sleep
Clinicians should always ask patients about sleep during visits. Sleep duration and sleep quality should be assessed. Insomnia, which is an independent condition, may or may not coexist with other conditions. It is important to determine whether another sleep disorder, or a physical (such as pain, heart, or lung disease), neurological (such as Parkinson’s disease or cerebrovascular disease), or psychiatric disorder (such as depressive illness, anxiety disorder, or substance misuse) is the primary diagnosis. Treatment of insomnia can improve comorbidities.16
In addition, it is important to teach patients about basic sleep hygiene, which includes abiding by a consistent bedtime, and avoiding coffee, alcohol, and nicotine. Eliminating a bedroom clock, not exercising in the late afternoon/early evening, and consuming light bedtime snacks are other measures that can be taken. Avoiding the prolonged use of light-emitting screens before bedtime is another positive step.17
In conclusion, cognitive and behavioral methods are just as effective as prescription medications for short-term treatment of chronic insomnia and should be considered as first line before considering medications. The beneficial effects of CBT-I, in contrast to those produced by medication, might last well beyond the termination of active treatment.
References
1. J Clin Sleep Med. 2008 Oct 15;4(5):487-504.
2. J Clin Psychol. 2010;66(11):1148-60.
3. Sleep. 2013 Mar 1;36(3):353-62.
4. Sleep Med Rev. 2016 Dec;30:1-10.
5. BMC Family Prac. 2012;13:40.
6. Sleep. 2006 Nov;29(11):1398-414.
7. Behavioral Treatments for Sleep Disorders. 1991. doi: 10.1016/13978-0-12-381522-4.00002-X.
8. Behav Modif 1998 Jan;22(1):3-28.
9. Am Fam Physician. 1999 Jun;59(11):3029-38.
10. Psychophysiology. 2015 Mar;52(3):388-96.
11. J Clin Nursing. 2013 April 10. doi: 10.1111/jocn.12096.
12. J Physiother. 2012;58(3):157-63.
13. J Sleep Res. 2015 Oct;24(5):526-34.
14 Sleep Med. 2016 Sep;25:113-121.
15. Am J Psychiatry. 2013 Jul;170(7):716-20.
16. JAMA Intern Med. 2015 Sep;175(9):1461-72.
17. Proc Natl Acad Sci USA. 2015;112(4):1232-7.
Dr. Lamba is a psychiatrist and medical director at Bayridge Hospital in Lynn, Mass. Dr. Rana is assistant professor of pediatrics at Boston University.
A couple of little known side effects of medications
A 46-year-old woman with diabetes and seizure disorder presents with nausea and fatigue. Her physical exam is unremarkable.
Meds: Glyburide 5 mg daily, metformin 850 mg b.i.d., phenytoin 300 mg daily, topiramate 400 mg daily, pantoprazole 40 mg daily.
Labs: Na 133, K 3.9, Cl 112, HCO3 13, Glu 158, Bun 18, Cr 1.0.
What is the most likely cause of this patient’s acidosis?
A. Phenytoin
B. Topiramate
C. Metformin
D. Pantoprazole
The correct answer to this question is topiramate.
Metformin has had warnings about risk of lactic acidosis occurring in patients with kidney disease, but there is no evidence that metformin is associated with lactic acidosis or raised serum lactate levels in patients with diabetes with normal renal function.1 and its use may decrease CV risk in patients with stage 3 CKD.2 This patient has a non–anion gap acidosis (anion gap is 8).
Topiramate acts as a carbonic anhydrase inhibitor, which causes impairment of both the normal reabsorption of filtered HCO3 by the proximal renal tubule and the excretion of hydrogen ion by the distal tubule.3 Acidosis occurs in most patients who are treated with topiramate. Dr. Ture and colleagues did a cross-sectional study to assess the frequency of metabolic acidosis in patients who were taking topiramate.4 Eighty patients who were on topiramate for seizure prevention prior to elective craniotomy were studied. Metabolic acidosis was present in 71% of the patients. Patients treated with topiramate also have a higher risk for kidney stones and uric acid elevation.
A 60-year-old patient presents with right great toe pain. On exam he has warmth and erythema of the 1st MTP joint. Aspiration of the joint shows uric acid crystals. He has had BP’s of 150-160 mm Hg systolic on his home BP monitoring over the past 6 months. In clinic today BP is 156/90 mm Hg. Labs: Bun 10, Cr 1.0, K 3.8, Uric acid 7.4.
Which blood pressure medication would you recommend?
A. Hydrochlorothiazide
B. Chlorthalidone
C. Lisinopril
D. Losartan
E. Irbesartan
In a patient with gout, diuretics should be avoided if possible, as they increase uric acid levels. Of the other three options, losartan offers the added benefit of lowering uric acid levels. Losartan has uricosuric effects and lowers uric acid levels, a property that is unique to losartan of the angiotensin receptor blockers (ARBs) that have been studied.5-6 The uric acid lowering appears to be a probenecid-like effect. Losartan has also been evaluated to see whether using it in combination with a thiazide diuretic can reduce the rise in uric acid that occurs with thiazides. Dr. Matsumura et al. looked at data from the COMFORT trial, focusing on the effect of combining losartan with hydrochlorothiazide on uric acid levels.7 They looked at a group of 118 patients on an ARB other than losartan plus a diuretic, who were then randomly assigned to losartan 50 mg/hydrochlorothiazide 12.5 mg or continuation of another ARB plus a diuretic. Blood pressure control was the same between groups, but the patients who received the losartan combination had lower uric acid levels (P = .01).
Pearls: Topiramate acts as a cerbonic anhydrase inhibitor and can cause a non–anion gap acidosis. Losartan has a modest uricosuric effect and can modestly lower uric acid levels. This is a unique property of losartan and is not shared by other ARBs.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].
References
1. Salpeter SR et al. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. 2010;4:CD002967.
2. Charytan DM et al. Metformin use and cardiovascular events in patients with type 2 diabetes and chronic kidney disease. Diabetes Obes Metab. 2019 Jan 22. doi: 10.1111/dom.13642.
3. Mirza N et al. Effect of topiramate on acid-base balance: extent, mechanism and effects. Br J Clin Pharmacol. 2009 Nov;68(5):655-61.
4. Ture H et al. The frequency and severity of metabolic acidosis related to topiramate. J Int Med Res. 2016;44(6):1376-80.
5. Würzner G et al. Comparative effects of losartan and irbesartan on serum uric acid in hypertensive patients with hyperuricaemia and gout. J Hypertens. 2001 Oct;19(10):1855-60.
6. Puig JG et al. Effect of eprosartan and losartan on uric acid metabolism in patients with essential hypertension. J Hypertens. 1999 Jul;17(7):1033-9.
7. Matsumura K et al. Effect of losartan on serum uric acid in hypertension treated with a diuretic: the COMFORT study. Clin Exp Hypertens. 2015;37(3):192-6.
A 46-year-old woman with diabetes and seizure disorder presents with nausea and fatigue. Her physical exam is unremarkable.
Meds: Glyburide 5 mg daily, metformin 850 mg b.i.d., phenytoin 300 mg daily, topiramate 400 mg daily, pantoprazole 40 mg daily.
Labs: Na 133, K 3.9, Cl 112, HCO3 13, Glu 158, Bun 18, Cr 1.0.
What is the most likely cause of this patient’s acidosis?
A. Phenytoin
B. Topiramate
C. Metformin
D. Pantoprazole
The correct answer to this question is topiramate.
Metformin has had warnings about risk of lactic acidosis occurring in patients with kidney disease, but there is no evidence that metformin is associated with lactic acidosis or raised serum lactate levels in patients with diabetes with normal renal function.1 and its use may decrease CV risk in patients with stage 3 CKD.2 This patient has a non–anion gap acidosis (anion gap is 8).
Topiramate acts as a carbonic anhydrase inhibitor, which causes impairment of both the normal reabsorption of filtered HCO3 by the proximal renal tubule and the excretion of hydrogen ion by the distal tubule.3 Acidosis occurs in most patients who are treated with topiramate. Dr. Ture and colleagues did a cross-sectional study to assess the frequency of metabolic acidosis in patients who were taking topiramate.4 Eighty patients who were on topiramate for seizure prevention prior to elective craniotomy were studied. Metabolic acidosis was present in 71% of the patients. Patients treated with topiramate also have a higher risk for kidney stones and uric acid elevation.
A 60-year-old patient presents with right great toe pain. On exam he has warmth and erythema of the 1st MTP joint. Aspiration of the joint shows uric acid crystals. He has had BP’s of 150-160 mm Hg systolic on his home BP monitoring over the past 6 months. In clinic today BP is 156/90 mm Hg. Labs: Bun 10, Cr 1.0, K 3.8, Uric acid 7.4.
Which blood pressure medication would you recommend?
A. Hydrochlorothiazide
B. Chlorthalidone
C. Lisinopril
D. Losartan
E. Irbesartan
In a patient with gout, diuretics should be avoided if possible, as they increase uric acid levels. Of the other three options, losartan offers the added benefit of lowering uric acid levels. Losartan has uricosuric effects and lowers uric acid levels, a property that is unique to losartan of the angiotensin receptor blockers (ARBs) that have been studied.5-6 The uric acid lowering appears to be a probenecid-like effect. Losartan has also been evaluated to see whether using it in combination with a thiazide diuretic can reduce the rise in uric acid that occurs with thiazides. Dr. Matsumura et al. looked at data from the COMFORT trial, focusing on the effect of combining losartan with hydrochlorothiazide on uric acid levels.7 They looked at a group of 118 patients on an ARB other than losartan plus a diuretic, who were then randomly assigned to losartan 50 mg/hydrochlorothiazide 12.5 mg or continuation of another ARB plus a diuretic. Blood pressure control was the same between groups, but the patients who received the losartan combination had lower uric acid levels (P = .01).
Pearls: Topiramate acts as a cerbonic anhydrase inhibitor and can cause a non–anion gap acidosis. Losartan has a modest uricosuric effect and can modestly lower uric acid levels. This is a unique property of losartan and is not shared by other ARBs.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].
References
1. Salpeter SR et al. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. 2010;4:CD002967.
2. Charytan DM et al. Metformin use and cardiovascular events in patients with type 2 diabetes and chronic kidney disease. Diabetes Obes Metab. 2019 Jan 22. doi: 10.1111/dom.13642.
3. Mirza N et al. Effect of topiramate on acid-base balance: extent, mechanism and effects. Br J Clin Pharmacol. 2009 Nov;68(5):655-61.
4. Ture H et al. The frequency and severity of metabolic acidosis related to topiramate. J Int Med Res. 2016;44(6):1376-80.
5. Würzner G et al. Comparative effects of losartan and irbesartan on serum uric acid in hypertensive patients with hyperuricaemia and gout. J Hypertens. 2001 Oct;19(10):1855-60.
6. Puig JG et al. Effect of eprosartan and losartan on uric acid metabolism in patients with essential hypertension. J Hypertens. 1999 Jul;17(7):1033-9.
7. Matsumura K et al. Effect of losartan on serum uric acid in hypertension treated with a diuretic: the COMFORT study. Clin Exp Hypertens. 2015;37(3):192-6.
A 46-year-old woman with diabetes and seizure disorder presents with nausea and fatigue. Her physical exam is unremarkable.
Meds: Glyburide 5 mg daily, metformin 850 mg b.i.d., phenytoin 300 mg daily, topiramate 400 mg daily, pantoprazole 40 mg daily.
Labs: Na 133, K 3.9, Cl 112, HCO3 13, Glu 158, Bun 18, Cr 1.0.
What is the most likely cause of this patient’s acidosis?
A. Phenytoin
B. Topiramate
C. Metformin
D. Pantoprazole
The correct answer to this question is topiramate.
Metformin has had warnings about risk of lactic acidosis occurring in patients with kidney disease, but there is no evidence that metformin is associated with lactic acidosis or raised serum lactate levels in patients with diabetes with normal renal function.1 and its use may decrease CV risk in patients with stage 3 CKD.2 This patient has a non–anion gap acidosis (anion gap is 8).
Topiramate acts as a carbonic anhydrase inhibitor, which causes impairment of both the normal reabsorption of filtered HCO3 by the proximal renal tubule and the excretion of hydrogen ion by the distal tubule.3 Acidosis occurs in most patients who are treated with topiramate. Dr. Ture and colleagues did a cross-sectional study to assess the frequency of metabolic acidosis in patients who were taking topiramate.4 Eighty patients who were on topiramate for seizure prevention prior to elective craniotomy were studied. Metabolic acidosis was present in 71% of the patients. Patients treated with topiramate also have a higher risk for kidney stones and uric acid elevation.
A 60-year-old patient presents with right great toe pain. On exam he has warmth and erythema of the 1st MTP joint. Aspiration of the joint shows uric acid crystals. He has had BP’s of 150-160 mm Hg systolic on his home BP monitoring over the past 6 months. In clinic today BP is 156/90 mm Hg. Labs: Bun 10, Cr 1.0, K 3.8, Uric acid 7.4.
Which blood pressure medication would you recommend?
A. Hydrochlorothiazide
B. Chlorthalidone
C. Lisinopril
D. Losartan
E. Irbesartan
In a patient with gout, diuretics should be avoided if possible, as they increase uric acid levels. Of the other three options, losartan offers the added benefit of lowering uric acid levels. Losartan has uricosuric effects and lowers uric acid levels, a property that is unique to losartan of the angiotensin receptor blockers (ARBs) that have been studied.5-6 The uric acid lowering appears to be a probenecid-like effect. Losartan has also been evaluated to see whether using it in combination with a thiazide diuretic can reduce the rise in uric acid that occurs with thiazides. Dr. Matsumura et al. looked at data from the COMFORT trial, focusing on the effect of combining losartan with hydrochlorothiazide on uric acid levels.7 They looked at a group of 118 patients on an ARB other than losartan plus a diuretic, who were then randomly assigned to losartan 50 mg/hydrochlorothiazide 12.5 mg or continuation of another ARB plus a diuretic. Blood pressure control was the same between groups, but the patients who received the losartan combination had lower uric acid levels (P = .01).
Pearls: Topiramate acts as a cerbonic anhydrase inhibitor and can cause a non–anion gap acidosis. Losartan has a modest uricosuric effect and can modestly lower uric acid levels. This is a unique property of losartan and is not shared by other ARBs.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].
References
1. Salpeter SR et al. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. 2010;4:CD002967.
2. Charytan DM et al. Metformin use and cardiovascular events in patients with type 2 diabetes and chronic kidney disease. Diabetes Obes Metab. 2019 Jan 22. doi: 10.1111/dom.13642.
3. Mirza N et al. Effect of topiramate on acid-base balance: extent, mechanism and effects. Br J Clin Pharmacol. 2009 Nov;68(5):655-61.
4. Ture H et al. The frequency and severity of metabolic acidosis related to topiramate. J Int Med Res. 2016;44(6):1376-80.
5. Würzner G et al. Comparative effects of losartan and irbesartan on serum uric acid in hypertensive patients with hyperuricaemia and gout. J Hypertens. 2001 Oct;19(10):1855-60.
6. Puig JG et al. Effect of eprosartan and losartan on uric acid metabolism in patients with essential hypertension. J Hypertens. 1999 Jul;17(7):1033-9.
7. Matsumura K et al. Effect of losartan on serum uric acid in hypertension treated with a diuretic: the COMFORT study. Clin Exp Hypertens. 2015;37(3):192-6.
Who is in charge here?
My first patient of the afternoon was a simple hypertension follow-up, or so I thought as I was walking into the room. She was a healthy 50-year-old woman with no medical problems other than her blood pressure, which was measured at 130/76 in the office. Her heart and lungs were normal, she had no chest pain or shortness of breath, and she was taking her medications without any problem. All simple enough. I complimented her on how she was doing, told her to continue her medications, and return in 6 months.
She put up her hand and said, “Wait a minute.”
Then she pulled out her smartphone. She tapped open an app, and handed it to me so I could look at a graph of her home blood pressures. The graph had all of her readings from the last 4 months, taken 2-3 times a day. It had automatically labeled each blood pressure in green, yellow, or red to indicate whether they were normal, higher than normal, or elevated, respectively.
Of course, the app creators had determined that a ‘green’ (normal) systolic pressure was less than 120 mm Hg. Values above that were yellow (higher than normal), until a systolic pressure of 130, at which point they became red (elevated). This is consistent with the most recent American Heart Association guidelines, but these guidelines have been the subject of a lot of controversy. There are many, including myself, who believe that the correct systolic pressure to define hypertension should be 140 for many patients, rather than 130. The app disagrees, and patients using the app see the app’s definition of hypertension every time they enter a blood pressure. In the case of my patient, since normal was indicated only by a systolic of less than 120 (which is a relatively rare event), I had to explain the difference between normal blood pressure and her blood pressure goal, and why the two were not the same.
Later that afternoon I was seeing a 60-year-old male who had electrical cardioversion of his atrial fibrillation 2 weeks prior to the visit. He had been sent home, as is usually the case, on an antiarrhythmic and an oral anticoagulant. He was feeling fine and had not noticed any palpitations, chest discomfort, or shortness of breath. I listened to his heart and lungs, which sounded normal, and I told him it sounded like he was doing well. Then he said, “I have an Apple watch.” I had a feeling I knew what was coming next.
He handed me his iPhone and asked me if I could review his rhythm strips. For those unacquainted with the new Apple watch, all he had to do to obtain those strips was open an EKG app and touch the crown of his watch with a finger from his other hand. This essentially made an electrical connection from his left to right arm, allowing the watch to generate a one-lead EKG tracing. The device then provides a computer-generated rhythm strip and sends that image and an interpretation of it to an iPhone, which is connected to the watch via Bluetooth. These results can then be shared or printed out as a pdf document.
The patient wanted to know if the smartphone’s interpretation of those rhythm strips was correct, and if he was really having frequent asymptomatic recurrence of his atrial fibrillation. Unsurprising to me or anyone who has used one of these (or other) phone-based EKG devices, the watch-generated rhythm strips looked clean and clear and the interpretation was spot on. It correctly identified his frequent asymptomatic episodes of atrial fibrillation. This was important information, which markedly affected his medical care.
These two very different examples are early indications that the way that we will be collecting information will rapidly and radically change over the next few years. It has always been clear that making long-term decisions about the treatment of hypertension based on a single reading in the office setting is not optimal. It has been equally clear that a single office EKG provides a limited snapshot into the frequency of intermittent atrial fibrillation. Deciding how to treat patients has never been easy and many decisions are plagued with ambiguity. Having limited information is a blessing and a curse; it’s quick and easy to review a small amount of data, but there is a nagging recognition that those data are only a distant representation of a patient’s real health outside of the office.
As we move forward we will increasingly have the ability to see a patient’s physiologic parameters where and when those values are most important: during the countless hours when they are not in our offices. The new American Heart Association hypertension guideline, issued in late 2017, has placed increased emphasis on ambulatory blood pressure monitoring. Determining how to use all this new information will be a challenge. It will take time to become comfortable with interpreting and making sense of an incredible number of data points. For example, if a patient checks his blood pressure twice a day for 3 months, his efforts will generate 180 separate blood pressure readings! You can bet there is going to be a good deal of inconsistency in those readings, making interpretation challenging. There will also probably be a few high readings, such as the occasional 190/110, which are likely to cause concern and anxiety in patients. There is little question that the availability of such detailed information holds the potential to allow us to make better decisions. The challenge will be in deciding how to use it to actually improve – not just complicate – patient care.
What are your thoughts on this? Feel free to email us at [email protected].
Dr. Skolnik is a professor of family and community medicine at Jefferson Medical College, Philadelphia, and an associate director of the family medicine residency program at Abington (Pa.) Jefferson Health. Dr. Notte is a family physician and associate chief medical information officer for Abington (Pa.) Jefferson Health. Follow him on twitter (@doctornotte).
My first patient of the afternoon was a simple hypertension follow-up, or so I thought as I was walking into the room. She was a healthy 50-year-old woman with no medical problems other than her blood pressure, which was measured at 130/76 in the office. Her heart and lungs were normal, she had no chest pain or shortness of breath, and she was taking her medications without any problem. All simple enough. I complimented her on how she was doing, told her to continue her medications, and return in 6 months.
She put up her hand and said, “Wait a minute.”
Then she pulled out her smartphone. She tapped open an app, and handed it to me so I could look at a graph of her home blood pressures. The graph had all of her readings from the last 4 months, taken 2-3 times a day. It had automatically labeled each blood pressure in green, yellow, or red to indicate whether they were normal, higher than normal, or elevated, respectively.
Of course, the app creators had determined that a ‘green’ (normal) systolic pressure was less than 120 mm Hg. Values above that were yellow (higher than normal), until a systolic pressure of 130, at which point they became red (elevated). This is consistent with the most recent American Heart Association guidelines, but these guidelines have been the subject of a lot of controversy. There are many, including myself, who believe that the correct systolic pressure to define hypertension should be 140 for many patients, rather than 130. The app disagrees, and patients using the app see the app’s definition of hypertension every time they enter a blood pressure. In the case of my patient, since normal was indicated only by a systolic of less than 120 (which is a relatively rare event), I had to explain the difference between normal blood pressure and her blood pressure goal, and why the two were not the same.
Later that afternoon I was seeing a 60-year-old male who had electrical cardioversion of his atrial fibrillation 2 weeks prior to the visit. He had been sent home, as is usually the case, on an antiarrhythmic and an oral anticoagulant. He was feeling fine and had not noticed any palpitations, chest discomfort, or shortness of breath. I listened to his heart and lungs, which sounded normal, and I told him it sounded like he was doing well. Then he said, “I have an Apple watch.” I had a feeling I knew what was coming next.
He handed me his iPhone and asked me if I could review his rhythm strips. For those unacquainted with the new Apple watch, all he had to do to obtain those strips was open an EKG app and touch the crown of his watch with a finger from his other hand. This essentially made an electrical connection from his left to right arm, allowing the watch to generate a one-lead EKG tracing. The device then provides a computer-generated rhythm strip and sends that image and an interpretation of it to an iPhone, which is connected to the watch via Bluetooth. These results can then be shared or printed out as a pdf document.
The patient wanted to know if the smartphone’s interpretation of those rhythm strips was correct, and if he was really having frequent asymptomatic recurrence of his atrial fibrillation. Unsurprising to me or anyone who has used one of these (or other) phone-based EKG devices, the watch-generated rhythm strips looked clean and clear and the interpretation was spot on. It correctly identified his frequent asymptomatic episodes of atrial fibrillation. This was important information, which markedly affected his medical care.
These two very different examples are early indications that the way that we will be collecting information will rapidly and radically change over the next few years. It has always been clear that making long-term decisions about the treatment of hypertension based on a single reading in the office setting is not optimal. It has been equally clear that a single office EKG provides a limited snapshot into the frequency of intermittent atrial fibrillation. Deciding how to treat patients has never been easy and many decisions are plagued with ambiguity. Having limited information is a blessing and a curse; it’s quick and easy to review a small amount of data, but there is a nagging recognition that those data are only a distant representation of a patient’s real health outside of the office.
As we move forward we will increasingly have the ability to see a patient’s physiologic parameters where and when those values are most important: during the countless hours when they are not in our offices. The new American Heart Association hypertension guideline, issued in late 2017, has placed increased emphasis on ambulatory blood pressure monitoring. Determining how to use all this new information will be a challenge. It will take time to become comfortable with interpreting and making sense of an incredible number of data points. For example, if a patient checks his blood pressure twice a day for 3 months, his efforts will generate 180 separate blood pressure readings! You can bet there is going to be a good deal of inconsistency in those readings, making interpretation challenging. There will also probably be a few high readings, such as the occasional 190/110, which are likely to cause concern and anxiety in patients. There is little question that the availability of such detailed information holds the potential to allow us to make better decisions. The challenge will be in deciding how to use it to actually improve – not just complicate – patient care.
What are your thoughts on this? Feel free to email us at [email protected].
Dr. Skolnik is a professor of family and community medicine at Jefferson Medical College, Philadelphia, and an associate director of the family medicine residency program at Abington (Pa.) Jefferson Health. Dr. Notte is a family physician and associate chief medical information officer for Abington (Pa.) Jefferson Health. Follow him on twitter (@doctornotte).
My first patient of the afternoon was a simple hypertension follow-up, or so I thought as I was walking into the room. She was a healthy 50-year-old woman with no medical problems other than her blood pressure, which was measured at 130/76 in the office. Her heart and lungs were normal, she had no chest pain or shortness of breath, and she was taking her medications without any problem. All simple enough. I complimented her on how she was doing, told her to continue her medications, and return in 6 months.
She put up her hand and said, “Wait a minute.”
Then she pulled out her smartphone. She tapped open an app, and handed it to me so I could look at a graph of her home blood pressures. The graph had all of her readings from the last 4 months, taken 2-3 times a day. It had automatically labeled each blood pressure in green, yellow, or red to indicate whether they were normal, higher than normal, or elevated, respectively.
Of course, the app creators had determined that a ‘green’ (normal) systolic pressure was less than 120 mm Hg. Values above that were yellow (higher than normal), until a systolic pressure of 130, at which point they became red (elevated). This is consistent with the most recent American Heart Association guidelines, but these guidelines have been the subject of a lot of controversy. There are many, including myself, who believe that the correct systolic pressure to define hypertension should be 140 for many patients, rather than 130. The app disagrees, and patients using the app see the app’s definition of hypertension every time they enter a blood pressure. In the case of my patient, since normal was indicated only by a systolic of less than 120 (which is a relatively rare event), I had to explain the difference between normal blood pressure and her blood pressure goal, and why the two were not the same.
Later that afternoon I was seeing a 60-year-old male who had electrical cardioversion of his atrial fibrillation 2 weeks prior to the visit. He had been sent home, as is usually the case, on an antiarrhythmic and an oral anticoagulant. He was feeling fine and had not noticed any palpitations, chest discomfort, or shortness of breath. I listened to his heart and lungs, which sounded normal, and I told him it sounded like he was doing well. Then he said, “I have an Apple watch.” I had a feeling I knew what was coming next.
He handed me his iPhone and asked me if I could review his rhythm strips. For those unacquainted with the new Apple watch, all he had to do to obtain those strips was open an EKG app and touch the crown of his watch with a finger from his other hand. This essentially made an electrical connection from his left to right arm, allowing the watch to generate a one-lead EKG tracing. The device then provides a computer-generated rhythm strip and sends that image and an interpretation of it to an iPhone, which is connected to the watch via Bluetooth. These results can then be shared or printed out as a pdf document.
The patient wanted to know if the smartphone’s interpretation of those rhythm strips was correct, and if he was really having frequent asymptomatic recurrence of his atrial fibrillation. Unsurprising to me or anyone who has used one of these (or other) phone-based EKG devices, the watch-generated rhythm strips looked clean and clear and the interpretation was spot on. It correctly identified his frequent asymptomatic episodes of atrial fibrillation. This was important information, which markedly affected his medical care.
These two very different examples are early indications that the way that we will be collecting information will rapidly and radically change over the next few years. It has always been clear that making long-term decisions about the treatment of hypertension based on a single reading in the office setting is not optimal. It has been equally clear that a single office EKG provides a limited snapshot into the frequency of intermittent atrial fibrillation. Deciding how to treat patients has never been easy and many decisions are plagued with ambiguity. Having limited information is a blessing and a curse; it’s quick and easy to review a small amount of data, but there is a nagging recognition that those data are only a distant representation of a patient’s real health outside of the office.
As we move forward we will increasingly have the ability to see a patient’s physiologic parameters where and when those values are most important: during the countless hours when they are not in our offices. The new American Heart Association hypertension guideline, issued in late 2017, has placed increased emphasis on ambulatory blood pressure monitoring. Determining how to use all this new information will be a challenge. It will take time to become comfortable with interpreting and making sense of an incredible number of data points. For example, if a patient checks his blood pressure twice a day for 3 months, his efforts will generate 180 separate blood pressure readings! You can bet there is going to be a good deal of inconsistency in those readings, making interpretation challenging. There will also probably be a few high readings, such as the occasional 190/110, which are likely to cause concern and anxiety in patients. There is little question that the availability of such detailed information holds the potential to allow us to make better decisions. The challenge will be in deciding how to use it to actually improve – not just complicate – patient care.
What are your thoughts on this? Feel free to email us at [email protected].
Dr. Skolnik is a professor of family and community medicine at Jefferson Medical College, Philadelphia, and an associate director of the family medicine residency program at Abington (Pa.) Jefferson Health. Dr. Notte is a family physician and associate chief medical information officer for Abington (Pa.) Jefferson Health. Follow him on twitter (@doctornotte).
Patients who want to make you retire, and how to cope
I was at a meeting in Orlando, sitting in the front row. The speaker was a former Disney executive who was telling us how to improve our offices. He kept walking very close to the edge of the stage – so close I was worried he might step off with the Klieg lights in his eyes. Then he got to the heart of his message, telling us that we need to make each patient encounter a marvelous experience, and how he and his staff had done so for millions of mouseketeers. “You need to make each customer feel special,” he said. He went on with saccharine examples of staff going above and beyond – for example, replacing toddlers’ dropped ice creams before they could cry.
That hit my trigger. From that point on, I was almost hoping he would fall off the stage.
Of course, there is a story behind my reaction.
One sunny day, while I was sitting at the most cluttered desk in the world, one of my staff came into my office to tell me a patient had called. The patient was very unhappy, I was told, and she planned to stink bomb me on social media. Concerned, I pulled the patient’s before-and-after photos. It looked as though she had a great result from her treatment, so I was perplexed. I phoned the patient, but she refused to tell me why she was unhappy. “I’m very unhappy, and I’m going to punish you,” she said. I urged her to come to the office and see me, at her convenience.
When we spoke face-to-face, I examined her nose and took a picture. I explained that her cancer was cured; her result was beautiful, the site was almost imperceptible. I added that I thought the appearance would continue to improve with time.
My patient refused to look at me, and refused to look at the site in the mirror. She shoved the preop defect photo away without giving it a glance. Instead, she told me how inconvenient it was for her to have had a skin cancer at all. Traffic had been terrible coming into the office on the morning of the procedure. There had been a 45-minute backup on the bridge on her way home. Her ex-husband had refused to help with her wound care. She continued in a similar vein for 15 minutes as I waited for her to accuse me of my transgressions. She concluded with a scowl and a whimper, “You just didn’t make me feel special.”
Everyone has difficult patients, and everyone has bad days, but I can’t recall ever being ambushed quite so adroitly in my 30 years of practice. I recognized my patient was being passive-aggressive and was playing a social media–augmented game of “Now I’ve got you, you S.O.B,” right out of Eric Berne’s book “Games People Play.” I’d say that this book should still be required reading for dealing with difficult patients.
There are ways to defuse such patients. One of the best is to slow things down and spread them around. The wider the array of interactions with people (the medical assistant, the nurse, the fellow, the Mohs surgeon, maybe the plastic surgeon), the more times the patient has to vent and the anger is defused across many targets. This also speaks to the value of requiring a preoperative consultation days before the procedure As I thought about this patient, I recalled that, because of the distance she was traveling, I had not done so.
I looked my patient in the eye and told her I was sorry she was unhappy. I told her I would be glad to see her again. I told her I realized how far she was driving and thought the traffic would not be a problem this early in the afternoon. I thanked her and showed her to the door. She stalked out of the office.
Technically and emotionally difficult patients are sometimes referred to you. They are patients who you might prefer not to take on but you do because, as a specialist, you may be at the end of the referral pipeline. Sometimes you can win the day, striking up a friendship or jollying them past their resentment at the world.
And The third law of surviving internship from Samuel Shem’s book “The House of God” is germane here. Remember, “the patient is the one with the disease.” And sometimes the disease is complicated by the patient’s emotional baggage. This is one of the reasons social media ratings can be so unfair. We have to realize that we are all going to be trashed unfairly at some point, and probably sued unfairly as well. As a malpractice attorney told me once, “You doctors shouldn’t take this so personally; it’s just business.”
And my patient? Despite my admonishments to you not to take things personally, I did feel bad for a week or so after our encounter. I did mail her a copy of her pre- and postoperative photographs. I have not seen her again. I did not look to see whether she burned me online.
But, by gosh, I’d really like to lock that Disney executive in a room with her for five minutes.
Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at [email protected].
I was at a meeting in Orlando, sitting in the front row. The speaker was a former Disney executive who was telling us how to improve our offices. He kept walking very close to the edge of the stage – so close I was worried he might step off with the Klieg lights in his eyes. Then he got to the heart of his message, telling us that we need to make each patient encounter a marvelous experience, and how he and his staff had done so for millions of mouseketeers. “You need to make each customer feel special,” he said. He went on with saccharine examples of staff going above and beyond – for example, replacing toddlers’ dropped ice creams before they could cry.
That hit my trigger. From that point on, I was almost hoping he would fall off the stage.
Of course, there is a story behind my reaction.
One sunny day, while I was sitting at the most cluttered desk in the world, one of my staff came into my office to tell me a patient had called. The patient was very unhappy, I was told, and she planned to stink bomb me on social media. Concerned, I pulled the patient’s before-and-after photos. It looked as though she had a great result from her treatment, so I was perplexed. I phoned the patient, but she refused to tell me why she was unhappy. “I’m very unhappy, and I’m going to punish you,” she said. I urged her to come to the office and see me, at her convenience.
When we spoke face-to-face, I examined her nose and took a picture. I explained that her cancer was cured; her result was beautiful, the site was almost imperceptible. I added that I thought the appearance would continue to improve with time.
My patient refused to look at me, and refused to look at the site in the mirror. She shoved the preop defect photo away without giving it a glance. Instead, she told me how inconvenient it was for her to have had a skin cancer at all. Traffic had been terrible coming into the office on the morning of the procedure. There had been a 45-minute backup on the bridge on her way home. Her ex-husband had refused to help with her wound care. She continued in a similar vein for 15 minutes as I waited for her to accuse me of my transgressions. She concluded with a scowl and a whimper, “You just didn’t make me feel special.”
Everyone has difficult patients, and everyone has bad days, but I can’t recall ever being ambushed quite so adroitly in my 30 years of practice. I recognized my patient was being passive-aggressive and was playing a social media–augmented game of “Now I’ve got you, you S.O.B,” right out of Eric Berne’s book “Games People Play.” I’d say that this book should still be required reading for dealing with difficult patients.
There are ways to defuse such patients. One of the best is to slow things down and spread them around. The wider the array of interactions with people (the medical assistant, the nurse, the fellow, the Mohs surgeon, maybe the plastic surgeon), the more times the patient has to vent and the anger is defused across many targets. This also speaks to the value of requiring a preoperative consultation days before the procedure As I thought about this patient, I recalled that, because of the distance she was traveling, I had not done so.
I looked my patient in the eye and told her I was sorry she was unhappy. I told her I would be glad to see her again. I told her I realized how far she was driving and thought the traffic would not be a problem this early in the afternoon. I thanked her and showed her to the door. She stalked out of the office.
Technically and emotionally difficult patients are sometimes referred to you. They are patients who you might prefer not to take on but you do because, as a specialist, you may be at the end of the referral pipeline. Sometimes you can win the day, striking up a friendship or jollying them past their resentment at the world.
And The third law of surviving internship from Samuel Shem’s book “The House of God” is germane here. Remember, “the patient is the one with the disease.” And sometimes the disease is complicated by the patient’s emotional baggage. This is one of the reasons social media ratings can be so unfair. We have to realize that we are all going to be trashed unfairly at some point, and probably sued unfairly as well. As a malpractice attorney told me once, “You doctors shouldn’t take this so personally; it’s just business.”
And my patient? Despite my admonishments to you not to take things personally, I did feel bad for a week or so after our encounter. I did mail her a copy of her pre- and postoperative photographs. I have not seen her again. I did not look to see whether she burned me online.
But, by gosh, I’d really like to lock that Disney executive in a room with her for five minutes.
Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at [email protected].
I was at a meeting in Orlando, sitting in the front row. The speaker was a former Disney executive who was telling us how to improve our offices. He kept walking very close to the edge of the stage – so close I was worried he might step off with the Klieg lights in his eyes. Then he got to the heart of his message, telling us that we need to make each patient encounter a marvelous experience, and how he and his staff had done so for millions of mouseketeers. “You need to make each customer feel special,” he said. He went on with saccharine examples of staff going above and beyond – for example, replacing toddlers’ dropped ice creams before they could cry.
That hit my trigger. From that point on, I was almost hoping he would fall off the stage.
Of course, there is a story behind my reaction.
One sunny day, while I was sitting at the most cluttered desk in the world, one of my staff came into my office to tell me a patient had called. The patient was very unhappy, I was told, and she planned to stink bomb me on social media. Concerned, I pulled the patient’s before-and-after photos. It looked as though she had a great result from her treatment, so I was perplexed. I phoned the patient, but she refused to tell me why she was unhappy. “I’m very unhappy, and I’m going to punish you,” she said. I urged her to come to the office and see me, at her convenience.
When we spoke face-to-face, I examined her nose and took a picture. I explained that her cancer was cured; her result was beautiful, the site was almost imperceptible. I added that I thought the appearance would continue to improve with time.
My patient refused to look at me, and refused to look at the site in the mirror. She shoved the preop defect photo away without giving it a glance. Instead, she told me how inconvenient it was for her to have had a skin cancer at all. Traffic had been terrible coming into the office on the morning of the procedure. There had been a 45-minute backup on the bridge on her way home. Her ex-husband had refused to help with her wound care. She continued in a similar vein for 15 minutes as I waited for her to accuse me of my transgressions. She concluded with a scowl and a whimper, “You just didn’t make me feel special.”
Everyone has difficult patients, and everyone has bad days, but I can’t recall ever being ambushed quite so adroitly in my 30 years of practice. I recognized my patient was being passive-aggressive and was playing a social media–augmented game of “Now I’ve got you, you S.O.B,” right out of Eric Berne’s book “Games People Play.” I’d say that this book should still be required reading for dealing with difficult patients.
There are ways to defuse such patients. One of the best is to slow things down and spread them around. The wider the array of interactions with people (the medical assistant, the nurse, the fellow, the Mohs surgeon, maybe the plastic surgeon), the more times the patient has to vent and the anger is defused across many targets. This also speaks to the value of requiring a preoperative consultation days before the procedure As I thought about this patient, I recalled that, because of the distance she was traveling, I had not done so.
I looked my patient in the eye and told her I was sorry she was unhappy. I told her I would be glad to see her again. I told her I realized how far she was driving and thought the traffic would not be a problem this early in the afternoon. I thanked her and showed her to the door. She stalked out of the office.
Technically and emotionally difficult patients are sometimes referred to you. They are patients who you might prefer not to take on but you do because, as a specialist, you may be at the end of the referral pipeline. Sometimes you can win the day, striking up a friendship or jollying them past their resentment at the world.
And The third law of surviving internship from Samuel Shem’s book “The House of God” is germane here. Remember, “the patient is the one with the disease.” And sometimes the disease is complicated by the patient’s emotional baggage. This is one of the reasons social media ratings can be so unfair. We have to realize that we are all going to be trashed unfairly at some point, and probably sued unfairly as well. As a malpractice attorney told me once, “You doctors shouldn’t take this so personally; it’s just business.”
And my patient? Despite my admonishments to you not to take things personally, I did feel bad for a week or so after our encounter. I did mail her a copy of her pre- and postoperative photographs. I have not seen her again. I did not look to see whether she burned me online.
But, by gosh, I’d really like to lock that Disney executive in a room with her for five minutes.
Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at [email protected].
Workers’ compensation law
Question: Employee, a poorly controlled diabetic, accidentally stepped on a nail at work. Surrounding cellulitis and abscess formation set in, but because he was slow in getting to a doctor, the infection invaded the underlying bone, causing osteomyelitis. He ended up with a partial foot amputation. In a claim for workers’ compensation (WC) benefits, which of the following is best?
A. Employee has a claim under WC, a quasi no-fault system that requires an employer to compensate its employees only for accidents occurring in the workplace.
B. Employer may offer employee’s preexisting diabetic condition and his failure to promptly seek medical attention as substantial rebuttable evidence against compensability.
C. A similar no-fault system has been proposed as an alternative to medical tort litigation, but it has yet to be established in the developed world.
D. All are incorrect.
E. All are correct.
Answer: D. Fashioned after Europe’s Workers’ Accident Insurance system that was put into place by Germany’s Otto von Bismarck, workers’ compensation (WC) laws found their way into the United States by 1908. Today, all states have enacted such laws to effectuate the policy that work injuries are among the costs of production, which industry is required to bear. Such laws purport to do away with vexatious issues like contributory negligence, agency principles that negate an employment relationship, and assumption of risk defenses, all of which had previously been used to deny an injured worker compensatory benefits.
WC laws differ somewhat from state to state, both in statutory provisions and judicial interpretations. However, an illness or disease condition that is related to work conditions will suffice. The employer bears the burden of proof and is required to affirmatively rebut the presumption of compensability. This is usually a high bar to scale, and preexisting conditions and poor patient compliance are insufficient to negate a WC claim, although they are used in apportioning payments to the injured worker.
Take Hawaii, widely viewed as a proworker jurisdiction, as an example. Its key WC statutory language covers any employee who “suffers a personal injury either by accident arising out of and in the course of employment or by disease proximately caused by or resulting from the nature of the employment.”1 In Chung v. Animal Clinic Inc.,2 Dr. Chung suffered a heart attack after office hours while jogging around the Kalani High School track in Honolulu. One of the issues was whether his heart attack arose out of and in the course of his employment and, if so, whether the employer substantially rebutted the presumption that the heart attack was work connected.
The Supreme Court of Hawaii used the work-connection approach in interpreting the phrase “arising out of and in the course of employment,” thereby rejecting the necessity of establishing temporal, spatial, and circumstantial proximity between the injury and employment. It held that the work-connection approach simply requires the finding of a causal connection between the injury and any incidents or conditions of employment. The only relevant inquiry was whether Dr. Chung’s heart attack in fact was aggravated or accelerated by his work activity and whether there was substantial evidence to the contrary.
The employer provided expert testimony from a cardiologist attributing the heart attack to preexisting arteriosclerosis and physical exertion from jogging. On the other hand, another physician believed that Dr. Chung’s employment activities as principal veterinarian, administrator, and president of Animal Clinic, which engaged Dr. Chung for long hours, as well as his other business-related activities, generated a substantial amount of mental and emotional stress which was strongly linked to the production of heart disease. This was sufficient to establish a work connection. The Court also had this to say about legal versus medical causation: “... a medical man may give a generalized opinion that there was no connection between an incident at work and a heart attack, and, in his own mind, may mean thereby that a preexisting pathological condition was the overwhelming factor in bringing about the attack and that the part played by the work was insignificant. But, while it may be sound medically to say that the work did not ‘cause’ the attack, it may well be bad law, because, in general, existing law treats the slightest factor of aggravation as an adequate ‘cause.’ ”
In a recent seminal case,3 the same Court reiterated that, in order to be exonerated, the employer must adduce specific evidence to indicate why the work event did not or could not have caused, aggravated, or accelerated the injury. It ruled that the claim in question was compensable because all three experts had failed to explain why the industrial accident could not have caused the slightest aggravation or acceleration of an existing injury. The patient, previously asymptomatic, had sustained shoulder injuries at work. Notwithstanding X-ray evidence of preexisting degenerative changes, the Court found for the worker because the medical reports of the employer’s physicians did not provide a sufficient degree of specificity to constitute substantial rebuttable evidence since “under our workers’ compensation statute, the slightest aggravation or acceleration of an injury by the employment activity mandates compensation.”
WC’s quasi no-fault approach has been proposed as a model for adjudicating medical malpractice claims, which are currently decided by a fault-finding, adversarial system.4 The injured patient is randomly and unjustly compensated, and the combative nature of the proceedings traumatizes the doctor-patient relationship and promotes the wasteful practice of defensive medicine. In many instances, fault simply cannot be ascertained. Some of these same criticisms led to the introduction of the no-fault system for auto injuries and for workers’ compensation. However, injuries arising out of medical care differ in one essential aspect from all other injuries: They may be a natural and unavoidable consequence of the underlying illness or treatment. If all complications were deemed compensable, including those that are unavoidable, then a true comprehensive no-fault system would exist. However, it would prove prohibitively expensive.
No-fault medical injury systems are presently in place in countries like Sweden and New Zealand. The latter’s no-fault compensation scheme came into effect in 1974 under its Accident Compensation Act, which removed all accidental injuries including medical injuries from the tort system. Under the initial scheme, which has since undergone numerous major revisions, injured patients did not have to prove fault. All the claimant had to establish was “medical, surgical, dental, or first aid misadventure.” However, the revised Act of 1992 required the claimant to show “medical error,” which was defined (like negligence) as “the failure of a registered health professional to observe a standard of care and skill reasonably to be expected in the circumstances.” Now renamed the Accident Compensation Act 2001, it covers medical injuries that are “not a necessary part, or ordinary consequence, of the treatment.” The fact that the treatment did not achieve a desired result does not, of itself, constitute treatment injury.
Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. For additional information, readers may contact the author at [email protected].
References
1. Hawaii Revised Statutes (HRS) Section 386-3.
2. Chung v. Animal Clinic Inc., 636 P.2d 721 (1981).
3. Panoke v. Reef Development of Hawaii Inc., Supreme Court of Hawaii. No. SCWC–11–0000556. Decided: December 14, 2015.
4. Tan, SY. In Medical Malpractice: Understanding the Law, Managing the Risks. World Scientific Publishing Co. Pte Ltd., Singapore, 2006.
Question: Employee, a poorly controlled diabetic, accidentally stepped on a nail at work. Surrounding cellulitis and abscess formation set in, but because he was slow in getting to a doctor, the infection invaded the underlying bone, causing osteomyelitis. He ended up with a partial foot amputation. In a claim for workers’ compensation (WC) benefits, which of the following is best?
A. Employee has a claim under WC, a quasi no-fault system that requires an employer to compensate its employees only for accidents occurring in the workplace.
B. Employer may offer employee’s preexisting diabetic condition and his failure to promptly seek medical attention as substantial rebuttable evidence against compensability.
C. A similar no-fault system has been proposed as an alternative to medical tort litigation, but it has yet to be established in the developed world.
D. All are incorrect.
E. All are correct.
Answer: D. Fashioned after Europe’s Workers’ Accident Insurance system that was put into place by Germany’s Otto von Bismarck, workers’ compensation (WC) laws found their way into the United States by 1908. Today, all states have enacted such laws to effectuate the policy that work injuries are among the costs of production, which industry is required to bear. Such laws purport to do away with vexatious issues like contributory negligence, agency principles that negate an employment relationship, and assumption of risk defenses, all of which had previously been used to deny an injured worker compensatory benefits.
WC laws differ somewhat from state to state, both in statutory provisions and judicial interpretations. However, an illness or disease condition that is related to work conditions will suffice. The employer bears the burden of proof and is required to affirmatively rebut the presumption of compensability. This is usually a high bar to scale, and preexisting conditions and poor patient compliance are insufficient to negate a WC claim, although they are used in apportioning payments to the injured worker.
Take Hawaii, widely viewed as a proworker jurisdiction, as an example. Its key WC statutory language covers any employee who “suffers a personal injury either by accident arising out of and in the course of employment or by disease proximately caused by or resulting from the nature of the employment.”1 In Chung v. Animal Clinic Inc.,2 Dr. Chung suffered a heart attack after office hours while jogging around the Kalani High School track in Honolulu. One of the issues was whether his heart attack arose out of and in the course of his employment and, if so, whether the employer substantially rebutted the presumption that the heart attack was work connected.
The Supreme Court of Hawaii used the work-connection approach in interpreting the phrase “arising out of and in the course of employment,” thereby rejecting the necessity of establishing temporal, spatial, and circumstantial proximity between the injury and employment. It held that the work-connection approach simply requires the finding of a causal connection between the injury and any incidents or conditions of employment. The only relevant inquiry was whether Dr. Chung’s heart attack in fact was aggravated or accelerated by his work activity and whether there was substantial evidence to the contrary.
The employer provided expert testimony from a cardiologist attributing the heart attack to preexisting arteriosclerosis and physical exertion from jogging. On the other hand, another physician believed that Dr. Chung’s employment activities as principal veterinarian, administrator, and president of Animal Clinic, which engaged Dr. Chung for long hours, as well as his other business-related activities, generated a substantial amount of mental and emotional stress which was strongly linked to the production of heart disease. This was sufficient to establish a work connection. The Court also had this to say about legal versus medical causation: “... a medical man may give a generalized opinion that there was no connection between an incident at work and a heart attack, and, in his own mind, may mean thereby that a preexisting pathological condition was the overwhelming factor in bringing about the attack and that the part played by the work was insignificant. But, while it may be sound medically to say that the work did not ‘cause’ the attack, it may well be bad law, because, in general, existing law treats the slightest factor of aggravation as an adequate ‘cause.’ ”
In a recent seminal case,3 the same Court reiterated that, in order to be exonerated, the employer must adduce specific evidence to indicate why the work event did not or could not have caused, aggravated, or accelerated the injury. It ruled that the claim in question was compensable because all three experts had failed to explain why the industrial accident could not have caused the slightest aggravation or acceleration of an existing injury. The patient, previously asymptomatic, had sustained shoulder injuries at work. Notwithstanding X-ray evidence of preexisting degenerative changes, the Court found for the worker because the medical reports of the employer’s physicians did not provide a sufficient degree of specificity to constitute substantial rebuttable evidence since “under our workers’ compensation statute, the slightest aggravation or acceleration of an injury by the employment activity mandates compensation.”
WC’s quasi no-fault approach has been proposed as a model for adjudicating medical malpractice claims, which are currently decided by a fault-finding, adversarial system.4 The injured patient is randomly and unjustly compensated, and the combative nature of the proceedings traumatizes the doctor-patient relationship and promotes the wasteful practice of defensive medicine. In many instances, fault simply cannot be ascertained. Some of these same criticisms led to the introduction of the no-fault system for auto injuries and for workers’ compensation. However, injuries arising out of medical care differ in one essential aspect from all other injuries: They may be a natural and unavoidable consequence of the underlying illness or treatment. If all complications were deemed compensable, including those that are unavoidable, then a true comprehensive no-fault system would exist. However, it would prove prohibitively expensive.
No-fault medical injury systems are presently in place in countries like Sweden and New Zealand. The latter’s no-fault compensation scheme came into effect in 1974 under its Accident Compensation Act, which removed all accidental injuries including medical injuries from the tort system. Under the initial scheme, which has since undergone numerous major revisions, injured patients did not have to prove fault. All the claimant had to establish was “medical, surgical, dental, or first aid misadventure.” However, the revised Act of 1992 required the claimant to show “medical error,” which was defined (like negligence) as “the failure of a registered health professional to observe a standard of care and skill reasonably to be expected in the circumstances.” Now renamed the Accident Compensation Act 2001, it covers medical injuries that are “not a necessary part, or ordinary consequence, of the treatment.” The fact that the treatment did not achieve a desired result does not, of itself, constitute treatment injury.
Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. For additional information, readers may contact the author at [email protected].
References
1. Hawaii Revised Statutes (HRS) Section 386-3.
2. Chung v. Animal Clinic Inc., 636 P.2d 721 (1981).
3. Panoke v. Reef Development of Hawaii Inc., Supreme Court of Hawaii. No. SCWC–11–0000556. Decided: December 14, 2015.
4. Tan, SY. In Medical Malpractice: Understanding the Law, Managing the Risks. World Scientific Publishing Co. Pte Ltd., Singapore, 2006.
Question: Employee, a poorly controlled diabetic, accidentally stepped on a nail at work. Surrounding cellulitis and abscess formation set in, but because he was slow in getting to a doctor, the infection invaded the underlying bone, causing osteomyelitis. He ended up with a partial foot amputation. In a claim for workers’ compensation (WC) benefits, which of the following is best?
A. Employee has a claim under WC, a quasi no-fault system that requires an employer to compensate its employees only for accidents occurring in the workplace.
B. Employer may offer employee’s preexisting diabetic condition and his failure to promptly seek medical attention as substantial rebuttable evidence against compensability.
C. A similar no-fault system has been proposed as an alternative to medical tort litigation, but it has yet to be established in the developed world.
D. All are incorrect.
E. All are correct.
Answer: D. Fashioned after Europe’s Workers’ Accident Insurance system that was put into place by Germany’s Otto von Bismarck, workers’ compensation (WC) laws found their way into the United States by 1908. Today, all states have enacted such laws to effectuate the policy that work injuries are among the costs of production, which industry is required to bear. Such laws purport to do away with vexatious issues like contributory negligence, agency principles that negate an employment relationship, and assumption of risk defenses, all of which had previously been used to deny an injured worker compensatory benefits.
WC laws differ somewhat from state to state, both in statutory provisions and judicial interpretations. However, an illness or disease condition that is related to work conditions will suffice. The employer bears the burden of proof and is required to affirmatively rebut the presumption of compensability. This is usually a high bar to scale, and preexisting conditions and poor patient compliance are insufficient to negate a WC claim, although they are used in apportioning payments to the injured worker.
Take Hawaii, widely viewed as a proworker jurisdiction, as an example. Its key WC statutory language covers any employee who “suffers a personal injury either by accident arising out of and in the course of employment or by disease proximately caused by or resulting from the nature of the employment.”1 In Chung v. Animal Clinic Inc.,2 Dr. Chung suffered a heart attack after office hours while jogging around the Kalani High School track in Honolulu. One of the issues was whether his heart attack arose out of and in the course of his employment and, if so, whether the employer substantially rebutted the presumption that the heart attack was work connected.
The Supreme Court of Hawaii used the work-connection approach in interpreting the phrase “arising out of and in the course of employment,” thereby rejecting the necessity of establishing temporal, spatial, and circumstantial proximity between the injury and employment. It held that the work-connection approach simply requires the finding of a causal connection between the injury and any incidents or conditions of employment. The only relevant inquiry was whether Dr. Chung’s heart attack in fact was aggravated or accelerated by his work activity and whether there was substantial evidence to the contrary.
The employer provided expert testimony from a cardiologist attributing the heart attack to preexisting arteriosclerosis and physical exertion from jogging. On the other hand, another physician believed that Dr. Chung’s employment activities as principal veterinarian, administrator, and president of Animal Clinic, which engaged Dr. Chung for long hours, as well as his other business-related activities, generated a substantial amount of mental and emotional stress which was strongly linked to the production of heart disease. This was sufficient to establish a work connection. The Court also had this to say about legal versus medical causation: “... a medical man may give a generalized opinion that there was no connection between an incident at work and a heart attack, and, in his own mind, may mean thereby that a preexisting pathological condition was the overwhelming factor in bringing about the attack and that the part played by the work was insignificant. But, while it may be sound medically to say that the work did not ‘cause’ the attack, it may well be bad law, because, in general, existing law treats the slightest factor of aggravation as an adequate ‘cause.’ ”
In a recent seminal case,3 the same Court reiterated that, in order to be exonerated, the employer must adduce specific evidence to indicate why the work event did not or could not have caused, aggravated, or accelerated the injury. It ruled that the claim in question was compensable because all three experts had failed to explain why the industrial accident could not have caused the slightest aggravation or acceleration of an existing injury. The patient, previously asymptomatic, had sustained shoulder injuries at work. Notwithstanding X-ray evidence of preexisting degenerative changes, the Court found for the worker because the medical reports of the employer’s physicians did not provide a sufficient degree of specificity to constitute substantial rebuttable evidence since “under our workers’ compensation statute, the slightest aggravation or acceleration of an injury by the employment activity mandates compensation.”
WC’s quasi no-fault approach has been proposed as a model for adjudicating medical malpractice claims, which are currently decided by a fault-finding, adversarial system.4 The injured patient is randomly and unjustly compensated, and the combative nature of the proceedings traumatizes the doctor-patient relationship and promotes the wasteful practice of defensive medicine. In many instances, fault simply cannot be ascertained. Some of these same criticisms led to the introduction of the no-fault system for auto injuries and for workers’ compensation. However, injuries arising out of medical care differ in one essential aspect from all other injuries: They may be a natural and unavoidable consequence of the underlying illness or treatment. If all complications were deemed compensable, including those that are unavoidable, then a true comprehensive no-fault system would exist. However, it would prove prohibitively expensive.
No-fault medical injury systems are presently in place in countries like Sweden and New Zealand. The latter’s no-fault compensation scheme came into effect in 1974 under its Accident Compensation Act, which removed all accidental injuries including medical injuries from the tort system. Under the initial scheme, which has since undergone numerous major revisions, injured patients did not have to prove fault. All the claimant had to establish was “medical, surgical, dental, or first aid misadventure.” However, the revised Act of 1992 required the claimant to show “medical error,” which was defined (like negligence) as “the failure of a registered health professional to observe a standard of care and skill reasonably to be expected in the circumstances.” Now renamed the Accident Compensation Act 2001, it covers medical injuries that are “not a necessary part, or ordinary consequence, of the treatment.” The fact that the treatment did not achieve a desired result does not, of itself, constitute treatment injury.
Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. For additional information, readers may contact the author at [email protected].
References
1. Hawaii Revised Statutes (HRS) Section 386-3.
2. Chung v. Animal Clinic Inc., 636 P.2d 721 (1981).
3. Panoke v. Reef Development of Hawaii Inc., Supreme Court of Hawaii. No. SCWC–11–0000556. Decided: December 14, 2015.
4. Tan, SY. In Medical Malpractice: Understanding the Law, Managing the Risks. World Scientific Publishing Co. Pte Ltd., Singapore, 2006.
Achieving recovery not a one-size-fits-all proposition
The experience of recovering from addiction can look different in different people, according to a Washington Post article. Some patients hit “rock bottom” and are able to climb back after connecting with a therapist. Others maintain sobriety by working with sponsors through 12-step programs. Still others are able to attain sobriety and maintain it by carefully vetting social invitations and bypassing situations in which drugs or lots of alcohol are involved. Medications that manage cravings are another intervention used by some of the 22 million Americans reportedly in recovery from drugs and alcohol. A major milestone for those seeking recovery is reaching the 3- to 5-year mark, said Robert D. Ashford, MSW, of the Substance Use Disorders Institute at the University of Pennsylvania, Philadelphia. “That benchmark can signal a reduced risk of returning to substance use because The Washington Post.
University life can be rewarding, but stress is a reality – and for some, that stress can either exacerbate or trigger mental health challenges. More universities have recognized the mental toll that campus life can exact and have put supports in place. At the University of California, Los Angeles, Internet-based screenings and online mental health treatment are offered with one-on-one personal contact with “resilience peers.” The latter are not licensed counselors, but they are trained to listen and provide an outlet for stressed students. The online help teaches skills that are useful in combating anxiety and depression. The goal is to help as many students as fast as possible. “This program fundamentally changed who I am and how I approach my life,” said UCLA student Nivi Ahlawat. “I may not remember the structures of all the intermediates of the glycolysis pathway I learned in biochemistry class. But I’ll remember what I’ve learned about active listening, motivational interviewing, and mindfulness intervention for the rest of my life.” Meanwhile, Kent (Ohio) State University has provided mental health training to more than 700 students, faculty, and staff. And at Jefferson Community College in Watertown, N.Y., mental health help includes a “wraparound” model that provides aid to economically disadvantaged students whose stress includes putting food on the table for their children. The New York Times.
Sen. Richard Briggs, MD, has proposed a resolution that seeks to loosen the purses of insurance companies in Tennessee, with the aim of better coverage for those with mental health or substance use issues who are seeking treatment. In introducing the resolution, Dr. Briggs noted that, despite the opioid crisis in his state, there is an “undeniable difference in coverage for mental health and substance abuse services for Tennesseans suffering from substance use disorder or opioid use disorder,” compared with the way other traditional diseases are covered and insured. “Mental illness is an illness just like any other medical illness, and should be treated and reimbursed to physicians in the same manner,” said Dr. Briggs, a heart and lung surgeon who served combat tours in Iraq and Afghanistan. NewsChannel 5 in Nashville.
“When I tell you I moved down to Miami for the weather, I really mean I moved to South Florida to escape my depression,” wrote Minhae Shim Roth. But for some, other factors get in the way. “The problem is that the heat and humidity can be so oppressive that people are forced indoors, negating the positive benefits of the sunshine,” said Daniel E. Jimenez, PhD, an assistant professor of psychiatry and behavioral sciences at the University of Miami. Last year, more than 560,000 Floridians – or 3.5% of the state’s adults – reportedly contemplated suicide, statistics show. Those stats are comparable with those of New York state. One difference, however, is that people in Miami are less willing to talk about mental health challenges, Ms. Roth suggested. “It’s easy to believe living in the Magic City is like a booze-, drug-, and fun-filled party that never stops. This pervasive hedonistic reputation makes it unpopular and shameful to admit you’re depressed. Everyone’s having fun, so why aren’t you?” Ms. Roth wrote. Those who seek help face an understaffed and underfunded system where an appointment with a psychiatrist can take months to secure. Help needs to come in other forms, according to Ms. Roth, and include “compassion and empathy, public initiatives aimed at combating the stigma of mental illness, greater accessibility to mental health services, and readily available intervention tools.” Miami New Times.
Seven in 10 U.S. teens see anxiety and depression as major problems among their peers. The concerns cut across gender, racial and socioeconomic lines, according to a survey of 920 teens aged 13-17 years. The major reason for the anxiety and depression is school, with 61% of the respondents feeling pressure to excel academically. Girls were far more likely than boys to say they planned to attend a 4-year college (68% vs. 51%). About half of the teens surveyed viewed drug addiction and alcohol consumption as major problems among people their age. Pew Research Center.
The experience of recovering from addiction can look different in different people, according to a Washington Post article. Some patients hit “rock bottom” and are able to climb back after connecting with a therapist. Others maintain sobriety by working with sponsors through 12-step programs. Still others are able to attain sobriety and maintain it by carefully vetting social invitations and bypassing situations in which drugs or lots of alcohol are involved. Medications that manage cravings are another intervention used by some of the 22 million Americans reportedly in recovery from drugs and alcohol. A major milestone for those seeking recovery is reaching the 3- to 5-year mark, said Robert D. Ashford, MSW, of the Substance Use Disorders Institute at the University of Pennsylvania, Philadelphia. “That benchmark can signal a reduced risk of returning to substance use because The Washington Post.
University life can be rewarding, but stress is a reality – and for some, that stress can either exacerbate or trigger mental health challenges. More universities have recognized the mental toll that campus life can exact and have put supports in place. At the University of California, Los Angeles, Internet-based screenings and online mental health treatment are offered with one-on-one personal contact with “resilience peers.” The latter are not licensed counselors, but they are trained to listen and provide an outlet for stressed students. The online help teaches skills that are useful in combating anxiety and depression. The goal is to help as many students as fast as possible. “This program fundamentally changed who I am and how I approach my life,” said UCLA student Nivi Ahlawat. “I may not remember the structures of all the intermediates of the glycolysis pathway I learned in biochemistry class. But I’ll remember what I’ve learned about active listening, motivational interviewing, and mindfulness intervention for the rest of my life.” Meanwhile, Kent (Ohio) State University has provided mental health training to more than 700 students, faculty, and staff. And at Jefferson Community College in Watertown, N.Y., mental health help includes a “wraparound” model that provides aid to economically disadvantaged students whose stress includes putting food on the table for their children. The New York Times.
Sen. Richard Briggs, MD, has proposed a resolution that seeks to loosen the purses of insurance companies in Tennessee, with the aim of better coverage for those with mental health or substance use issues who are seeking treatment. In introducing the resolution, Dr. Briggs noted that, despite the opioid crisis in his state, there is an “undeniable difference in coverage for mental health and substance abuse services for Tennesseans suffering from substance use disorder or opioid use disorder,” compared with the way other traditional diseases are covered and insured. “Mental illness is an illness just like any other medical illness, and should be treated and reimbursed to physicians in the same manner,” said Dr. Briggs, a heart and lung surgeon who served combat tours in Iraq and Afghanistan. NewsChannel 5 in Nashville.
“When I tell you I moved down to Miami for the weather, I really mean I moved to South Florida to escape my depression,” wrote Minhae Shim Roth. But for some, other factors get in the way. “The problem is that the heat and humidity can be so oppressive that people are forced indoors, negating the positive benefits of the sunshine,” said Daniel E. Jimenez, PhD, an assistant professor of psychiatry and behavioral sciences at the University of Miami. Last year, more than 560,000 Floridians – or 3.5% of the state’s adults – reportedly contemplated suicide, statistics show. Those stats are comparable with those of New York state. One difference, however, is that people in Miami are less willing to talk about mental health challenges, Ms. Roth suggested. “It’s easy to believe living in the Magic City is like a booze-, drug-, and fun-filled party that never stops. This pervasive hedonistic reputation makes it unpopular and shameful to admit you’re depressed. Everyone’s having fun, so why aren’t you?” Ms. Roth wrote. Those who seek help face an understaffed and underfunded system where an appointment with a psychiatrist can take months to secure. Help needs to come in other forms, according to Ms. Roth, and include “compassion and empathy, public initiatives aimed at combating the stigma of mental illness, greater accessibility to mental health services, and readily available intervention tools.” Miami New Times.
Seven in 10 U.S. teens see anxiety and depression as major problems among their peers. The concerns cut across gender, racial and socioeconomic lines, according to a survey of 920 teens aged 13-17 years. The major reason for the anxiety and depression is school, with 61% of the respondents feeling pressure to excel academically. Girls were far more likely than boys to say they planned to attend a 4-year college (68% vs. 51%). About half of the teens surveyed viewed drug addiction and alcohol consumption as major problems among people their age. Pew Research Center.
The experience of recovering from addiction can look different in different people, according to a Washington Post article. Some patients hit “rock bottom” and are able to climb back after connecting with a therapist. Others maintain sobriety by working with sponsors through 12-step programs. Still others are able to attain sobriety and maintain it by carefully vetting social invitations and bypassing situations in which drugs or lots of alcohol are involved. Medications that manage cravings are another intervention used by some of the 22 million Americans reportedly in recovery from drugs and alcohol. A major milestone for those seeking recovery is reaching the 3- to 5-year mark, said Robert D. Ashford, MSW, of the Substance Use Disorders Institute at the University of Pennsylvania, Philadelphia. “That benchmark can signal a reduced risk of returning to substance use because The Washington Post.
University life can be rewarding, but stress is a reality – and for some, that stress can either exacerbate or trigger mental health challenges. More universities have recognized the mental toll that campus life can exact and have put supports in place. At the University of California, Los Angeles, Internet-based screenings and online mental health treatment are offered with one-on-one personal contact with “resilience peers.” The latter are not licensed counselors, but they are trained to listen and provide an outlet for stressed students. The online help teaches skills that are useful in combating anxiety and depression. The goal is to help as many students as fast as possible. “This program fundamentally changed who I am and how I approach my life,” said UCLA student Nivi Ahlawat. “I may not remember the structures of all the intermediates of the glycolysis pathway I learned in biochemistry class. But I’ll remember what I’ve learned about active listening, motivational interviewing, and mindfulness intervention for the rest of my life.” Meanwhile, Kent (Ohio) State University has provided mental health training to more than 700 students, faculty, and staff. And at Jefferson Community College in Watertown, N.Y., mental health help includes a “wraparound” model that provides aid to economically disadvantaged students whose stress includes putting food on the table for their children. The New York Times.
Sen. Richard Briggs, MD, has proposed a resolution that seeks to loosen the purses of insurance companies in Tennessee, with the aim of better coverage for those with mental health or substance use issues who are seeking treatment. In introducing the resolution, Dr. Briggs noted that, despite the opioid crisis in his state, there is an “undeniable difference in coverage for mental health and substance abuse services for Tennesseans suffering from substance use disorder or opioid use disorder,” compared with the way other traditional diseases are covered and insured. “Mental illness is an illness just like any other medical illness, and should be treated and reimbursed to physicians in the same manner,” said Dr. Briggs, a heart and lung surgeon who served combat tours in Iraq and Afghanistan. NewsChannel 5 in Nashville.
“When I tell you I moved down to Miami for the weather, I really mean I moved to South Florida to escape my depression,” wrote Minhae Shim Roth. But for some, other factors get in the way. “The problem is that the heat and humidity can be so oppressive that people are forced indoors, negating the positive benefits of the sunshine,” said Daniel E. Jimenez, PhD, an assistant professor of psychiatry and behavioral sciences at the University of Miami. Last year, more than 560,000 Floridians – or 3.5% of the state’s adults – reportedly contemplated suicide, statistics show. Those stats are comparable with those of New York state. One difference, however, is that people in Miami are less willing to talk about mental health challenges, Ms. Roth suggested. “It’s easy to believe living in the Magic City is like a booze-, drug-, and fun-filled party that never stops. This pervasive hedonistic reputation makes it unpopular and shameful to admit you’re depressed. Everyone’s having fun, so why aren’t you?” Ms. Roth wrote. Those who seek help face an understaffed and underfunded system where an appointment with a psychiatrist can take months to secure. Help needs to come in other forms, according to Ms. Roth, and include “compassion and empathy, public initiatives aimed at combating the stigma of mental illness, greater accessibility to mental health services, and readily available intervention tools.” Miami New Times.
Seven in 10 U.S. teens see anxiety and depression as major problems among their peers. The concerns cut across gender, racial and socioeconomic lines, according to a survey of 920 teens aged 13-17 years. The major reason for the anxiety and depression is school, with 61% of the respondents feeling pressure to excel academically. Girls were far more likely than boys to say they planned to attend a 4-year college (68% vs. 51%). About half of the teens surveyed viewed drug addiction and alcohol consumption as major problems among people their age. Pew Research Center.
Charity case
A 45-year-old comes to the emergency department because of abdominal pain for the last few months. She has been belching and hiccuping, and she has lost 20 pounds.
A 45-year-old comes to the emergency department, where a CT scan shows a large mass in her stomach. There also are enlarged lymph nodes nearby and far away, and the wall of her abdomen is studded with smaller tumors.
A 45-year-old comes to the emergency department and is told she needs to be admitted to the hospital to work this up. It’s likely cancer, she is told, but the only way to confirm the diagnosis is with a biopsy. They do a procedure in which they insert a camera through her mouth and down her esophagus, and they take a sample of the large mass in her stomach. It is cancer – and it’s widely metastatic.
The resident on her team sends me a text. She wants to know: “What do you do in cases like this?”
Except she is not asking for my advice on medical management. The same day the patient is told it’s cancer, she has a confession. She has no insurance.
I read the text, then turn to the oncology case manager sitting next to me. We talk it through and the answer is as I suspected.
“She can be seen in the county clinic,” I text back, and give the name of an oncologist there. “Or, she can apply for emergency Medi-Cal to follow up at our hospital. But that process can take over a month to get approval.”
Except the case manager looks into it further. Actually, she does not qualify for emergency Medi-Cal because she invoked it earlier that year when she had an infection.
When it’s an emergency, hospitals tend to handle this kind of situation well. I’ve seen hospitals absorb the costs of major medical interventions when a person is acutely ill. They call it a charity case, and they cover all the costs of acute illness and treatment when the patient cannot.
But what this person needs is different. The treatment she needs is not emergent. What she needs is a regular oncologist who can give chemotherapy, monitor for side effects, check her blood counts, get regular scans to monitor the disease, and have conversations with her to navigate the bigger questions. What she needs is an ongoing relationship.
That is harder for a hospital to absorb.
I think back to a year ago, when I was volunteering at the free clinic. A 77-year-old man came in complaining of increased urinary frequency. I did a rectal exam, and I felt it: a large, irregular prostate mass. I thought of all I would normally do, down the algorithm of treatment – I’d order a PSA blood test, arrange for him to have a biopsy, likely get a CT scan, then get him back in the clinic to start treatment. But there, I could not do any of that. There, I was lucky when I could get someone a $4 medication. There, all I could do was hand him the truth. “I am concerned you have prostate cancer,” I said.
I remember how he began crying tears of joy. “God bless you,” he said, grabbing my hand. God bless me? For what? For handing him a problem but no solution? For sharing a suspicion of a diagnosis that could kill him but being unable to intervene? Is it really better knowing?
I deliver a lot of bad news in oncology, but I usually get to blame the disease. The cancer is aggressive. The cancer is causing your pain.
What I hate perhaps even more is the other type of bad news: having our hands tied by a system I disagree with – and yet am somehow part of. We can offer X, but not Y. You can be seen in this clinic, but not in that one. This treatment is covered, but that part would be out of pocket. Negotiating what is absolutely necessary and what is preferred.
A 45-year-old comes to the emergency department with abdominal pain. She is told she has metastatic cancer that will take her life in less than 6 months without treatment. She has many questions for me, the inpatient oncology fellow. But they are not about the disease, the prognosis, or the treatment. They are all about insurance options, reimbursement, and cost.
Like everyone with a new devastating diagnosis, she is weighing her options. Except her decisions are weighted with the fear of bankruptcy; her calculus trying to compute the cost of her life.
“I wish things were different,” I say.
Minor details of this story were altered to protect privacy.
Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.
A 45-year-old comes to the emergency department because of abdominal pain for the last few months. She has been belching and hiccuping, and she has lost 20 pounds.
A 45-year-old comes to the emergency department, where a CT scan shows a large mass in her stomach. There also are enlarged lymph nodes nearby and far away, and the wall of her abdomen is studded with smaller tumors.
A 45-year-old comes to the emergency department and is told she needs to be admitted to the hospital to work this up. It’s likely cancer, she is told, but the only way to confirm the diagnosis is with a biopsy. They do a procedure in which they insert a camera through her mouth and down her esophagus, and they take a sample of the large mass in her stomach. It is cancer – and it’s widely metastatic.
The resident on her team sends me a text. She wants to know: “What do you do in cases like this?”
Except she is not asking for my advice on medical management. The same day the patient is told it’s cancer, she has a confession. She has no insurance.
I read the text, then turn to the oncology case manager sitting next to me. We talk it through and the answer is as I suspected.
“She can be seen in the county clinic,” I text back, and give the name of an oncologist there. “Or, she can apply for emergency Medi-Cal to follow up at our hospital. But that process can take over a month to get approval.”
Except the case manager looks into it further. Actually, she does not qualify for emergency Medi-Cal because she invoked it earlier that year when she had an infection.
When it’s an emergency, hospitals tend to handle this kind of situation well. I’ve seen hospitals absorb the costs of major medical interventions when a person is acutely ill. They call it a charity case, and they cover all the costs of acute illness and treatment when the patient cannot.
But what this person needs is different. The treatment she needs is not emergent. What she needs is a regular oncologist who can give chemotherapy, monitor for side effects, check her blood counts, get regular scans to monitor the disease, and have conversations with her to navigate the bigger questions. What she needs is an ongoing relationship.
That is harder for a hospital to absorb.
I think back to a year ago, when I was volunteering at the free clinic. A 77-year-old man came in complaining of increased urinary frequency. I did a rectal exam, and I felt it: a large, irregular prostate mass. I thought of all I would normally do, down the algorithm of treatment – I’d order a PSA blood test, arrange for him to have a biopsy, likely get a CT scan, then get him back in the clinic to start treatment. But there, I could not do any of that. There, I was lucky when I could get someone a $4 medication. There, all I could do was hand him the truth. “I am concerned you have prostate cancer,” I said.
I remember how he began crying tears of joy. “God bless you,” he said, grabbing my hand. God bless me? For what? For handing him a problem but no solution? For sharing a suspicion of a diagnosis that could kill him but being unable to intervene? Is it really better knowing?
I deliver a lot of bad news in oncology, but I usually get to blame the disease. The cancer is aggressive. The cancer is causing your pain.
What I hate perhaps even more is the other type of bad news: having our hands tied by a system I disagree with – and yet am somehow part of. We can offer X, but not Y. You can be seen in this clinic, but not in that one. This treatment is covered, but that part would be out of pocket. Negotiating what is absolutely necessary and what is preferred.
A 45-year-old comes to the emergency department with abdominal pain. She is told she has metastatic cancer that will take her life in less than 6 months without treatment. She has many questions for me, the inpatient oncology fellow. But they are not about the disease, the prognosis, or the treatment. They are all about insurance options, reimbursement, and cost.
Like everyone with a new devastating diagnosis, she is weighing her options. Except her decisions are weighted with the fear of bankruptcy; her calculus trying to compute the cost of her life.
“I wish things were different,” I say.
Minor details of this story were altered to protect privacy.
Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.
A 45-year-old comes to the emergency department because of abdominal pain for the last few months. She has been belching and hiccuping, and she has lost 20 pounds.
A 45-year-old comes to the emergency department, where a CT scan shows a large mass in her stomach. There also are enlarged lymph nodes nearby and far away, and the wall of her abdomen is studded with smaller tumors.
A 45-year-old comes to the emergency department and is told she needs to be admitted to the hospital to work this up. It’s likely cancer, she is told, but the only way to confirm the diagnosis is with a biopsy. They do a procedure in which they insert a camera through her mouth and down her esophagus, and they take a sample of the large mass in her stomach. It is cancer – and it’s widely metastatic.
The resident on her team sends me a text. She wants to know: “What do you do in cases like this?”
Except she is not asking for my advice on medical management. The same day the patient is told it’s cancer, she has a confession. She has no insurance.
I read the text, then turn to the oncology case manager sitting next to me. We talk it through and the answer is as I suspected.
“She can be seen in the county clinic,” I text back, and give the name of an oncologist there. “Or, she can apply for emergency Medi-Cal to follow up at our hospital. But that process can take over a month to get approval.”
Except the case manager looks into it further. Actually, she does not qualify for emergency Medi-Cal because she invoked it earlier that year when she had an infection.
When it’s an emergency, hospitals tend to handle this kind of situation well. I’ve seen hospitals absorb the costs of major medical interventions when a person is acutely ill. They call it a charity case, and they cover all the costs of acute illness and treatment when the patient cannot.
But what this person needs is different. The treatment she needs is not emergent. What she needs is a regular oncologist who can give chemotherapy, monitor for side effects, check her blood counts, get regular scans to monitor the disease, and have conversations with her to navigate the bigger questions. What she needs is an ongoing relationship.
That is harder for a hospital to absorb.
I think back to a year ago, when I was volunteering at the free clinic. A 77-year-old man came in complaining of increased urinary frequency. I did a rectal exam, and I felt it: a large, irregular prostate mass. I thought of all I would normally do, down the algorithm of treatment – I’d order a PSA blood test, arrange for him to have a biopsy, likely get a CT scan, then get him back in the clinic to start treatment. But there, I could not do any of that. There, I was lucky when I could get someone a $4 medication. There, all I could do was hand him the truth. “I am concerned you have prostate cancer,” I said.
I remember how he began crying tears of joy. “God bless you,” he said, grabbing my hand. God bless me? For what? For handing him a problem but no solution? For sharing a suspicion of a diagnosis that could kill him but being unable to intervene? Is it really better knowing?
I deliver a lot of bad news in oncology, but I usually get to blame the disease. The cancer is aggressive. The cancer is causing your pain.
What I hate perhaps even more is the other type of bad news: having our hands tied by a system I disagree with – and yet am somehow part of. We can offer X, but not Y. You can be seen in this clinic, but not in that one. This treatment is covered, but that part would be out of pocket. Negotiating what is absolutely necessary and what is preferred.
A 45-year-old comes to the emergency department with abdominal pain. She is told she has metastatic cancer that will take her life in less than 6 months without treatment. She has many questions for me, the inpatient oncology fellow. But they are not about the disease, the prognosis, or the treatment. They are all about insurance options, reimbursement, and cost.
Like everyone with a new devastating diagnosis, she is weighing her options. Except her decisions are weighted with the fear of bankruptcy; her calculus trying to compute the cost of her life.
“I wish things were different,” I say.
Minor details of this story were altered to protect privacy.
Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.
Melatonin update, Part 2
Recall that melatonin displays multiple biological functions, acting as an antioxidant, cytokine, neurotransmitter, and global regulator of the circadian clock, the latter for which it is best known.1-3 At the cutaneous level, melatonin exhibits antioxidant (direct, as a radical scavenger; indirect, through upregulating antioxidant enzymes), anti-inflammatory, photoprotective, tissue regenerative, and cytoprotective activity, particularly in its capacity to preserve mitochondrial function.4-8
Melatonin also protects skin homeostasis,6 and, consequently, is believed to act against carcinogenesis and potentially other deleterious dysfunctions such as hyperproliferative/inflammatory conditions.5 Notably, , further buttressing the critical role that melatonin plays in skin health.5 Melatonin also displays immunomodulatory, thermoregulatory, and antitumor functions.9 The topical application of melatonin has been demonstrated to diminish markers of reactive oxygen species as well as reverse manifestations of cutaneous aging.5
Melatonin is both produced by and metabolized in the skin. The hormone and its metabolites (6-hydroxymelatonin, N1-acetyl-N2-formyl-5-methoxykynuramine [AFMK], N-acetyl-serotonin, and 5-methoxytryptamine) reduce UVB-induced oxidative cell damage in human keratinocytes and melanocytes, and also act as radioprotectors.6
Melatonin has been shown to protect human dermal fibroblasts from UVA- and UVB-induced damage.9 In addition, melatonin and its metabolites have been demonstrated to suppress the growth of cultured human melanomas, and high doses of melatonin used in clinical trials in late metastatic melanoma stages have enhanced the efficacy of or diminished the side effects of chemotherapy/chemo-immunotherapy.9
UVB and melatonin in the lab
In a 2018 hairless mouse study in which animals were irradiated by UVB for 8 weeks, Park et al. showed that melatonin displays anti-wrinkle activity by suppressing reactive oxygen species- and sonic hedgehog-mediated inflammatory proteins. Melatonin also protected against transepidermal water loss and prevented epidermal thickness as well as dermal collagen degradation.10
Also that year, Skobowiat et al. found that the topical application of melatonin and its active derivatives (N1-acetyl-N2-formyl-5-methoxykynurenine and N-acetylserotonin) yielded photoprotective effects pre- and post-UVB treatment in human and porcine skin ex vivo. They concluded that their results justify additional investigation of the clinical applications of melatonin and its metabolites for its potential to exert protective effects against UVB in human subjects.8
Although the preponderance of previous work identifies melatonin as a strong antioxidant, Kocyigit et al. reported in 2018 on new in vitro studies suggesting that melatonin dose-dependently exerts cytotoxic and apoptotic activity on several cell types, including both human epidermoid carcinoma and normal skin fibroblasts. Their findings showed that melatonin exhibited proliferative effects on cancerous and normal cells at low doses and cytotoxic effects at high doses.11
Melatonin as a sunscreen ingredient
Further supporting its use in the topical armamentarium for skin health, melatonin is a key ingredient in a sunscreen formulation, the creation of which was driven by the need to protect the skin of military personnel facing lengthy UV exposure. Specifically, the formulation containing avobenzone, octinoxate, oxybenzone, and titanium dioxide along with melatonin and pumpkin seed oil underwent a preclinical safety evaluation in 2017, as reported by Bora et al. The formulation was found to be nonmutagenic, nontoxic, and safe in animal models and is deemed ready to test for its efficacy in humans.12 Melatonin is also among a host of systemic treatment options for skin lightening.13
Oral and topical melatonin in human studies
In a 2017 study on the impact of melatonin treatment on the skin of former smokers, Sagan et al. assessed oxidative damage to membrane lipids in blood serum and in epidermis exfoliated during microdermabrasion (at baseline, 2 weeks after, and 4 weeks after treatment) in postmenopausal women. Never smokers (n = 44) and former smokers (n = 46) were divided into control, melatonin topical, antioxidant topical, and melatonin oral treatment groups. The investigators found that after only 2 weeks, melatonin oral treatment significantly reversed the elevated serum lipid peroxidation in former smokers. Oral melatonin increased elasticity, moisture, and sebum levels after 4 weeks of treatment and topical melatonin increased sebum level. They concluded that the use of exogenous melatonin reverses the effects of oxidative damage to membrane lipids and ameliorates cutaneous biophysical traits in postmenopausal women who once smoked. The researchers added that melatonin use for all former smokers is warranted and that topically applied melatonin merits consideration for improving the effects of facial microdermabrasion.14
In a systematic literature review in 2017, Scheuer identified 20 studies (4 human and 16 experimental) indicating that melatonin exerts a protective effect against artificial UV-induced erythema when applied pre-exposure.7 Also that year, Scheuer and colleagues conducted randomized, double-blind, placebo-controlled work demonstrating that topical melatonin (12.5%) significantly reduced erythema resulting from natural sunlight, and in a separate randomized, double-blind, placebo-controlled crossover study that the same concentration of a full body application of melatonin exhibited no significant impact on cognition and should be considered safe for dermal application.7 Scheuer added that additional longitudinal research is needed to ascertain effects of topical melatonin usage over time.
Early in 2018, Milani and Sparavigna reported on a randomized, split-face, assessor-blinded, prospective 3-month study of 22 women (mean age 55 years) with moderate to severe facial skin aging; the study was designed to test the efficacy of melatonin-based day and night creams. All of the women completed the proof-of-concept trial in which crow’s feet were found to be significantly diminished on the sides of the face treated with the creams compared with the nontreated skin.
Both well-tolerated melatonin formulations were associated with significant improvements in surface microrelief, skin profilometry, tonicity, and dryness. With marked enhancement of skin hydration and reduction of roughness noted, the investigators concluded that their results supported the notion that the tested melatonin topical formulations yielded antiaging effects.4
Conclusion
The majority of research on the potent hormone melatonin over nearly the last quarter century indicates that this dynamic substance provides multifaceted benefits in performing several biological functions. Topical melatonin is available over the counter. Its expanded use in skin care warrants greater attention as we learn more about this versatile endogenous substance.
Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote two textbooks: “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and “Cosmeceuticals and Cosmetic Ingredients,” (New York: McGraw-Hill, 2014), and a New York Times Best Sellers book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Evolus, Galderma, and Revance. She is the founder and CEO of Skin Type Solutions Franchise Systems LLC. Write to her at [email protected].
References
1. Zmijewski MA et al. Dermatoendocrinol. 2011 Jan;3(1):3-10.
2. Slominski A et al. Trends Endocrinol Metab. 2008 Jan;19(1):17-24.
3. Slominski A et al. J Cell Physiol. 2003 Jul;196(1):144-53.
4. Milani M et al. Clin Cosmet Investig Dermatol. 2018 Jan 24;11:51-7.
5. Day D et al. J Drugs Dermatol. 2018 Sep 1;17(9):966-9.
6. Slominski AT et al. Cell Mol Life Sci. 2017 Nov;74(21):3913-25.
7. Scheuer C. Dan Med J. 2017 Jun;64(6). pii:B5358.
8. Skobowiat C et al. J Pineal Res. 2018 Sep;65(2):e12501.
9. Slominski AT et al. J Invest Dermatol. 2018 Mar;138(3):490-9.
10. Park EK et al. Int J Mol Sci. 2018 Jul 8;19(7). pii: E1995.
11. Kocyigit A et al. Mutat Res. 2018 May-Jun;829-30:50-60.
12. Bora NS et al. Regul Toxicol Pharmacol. 2017 Oct;89:1-12.
13. Juhasz MLW et al. J Cosmet Dermatol. 2018 Dec;17(6):1144-57.
14. Sagan D et al. Ann Agric Environ Med. 2017 Dec 23;24(4):659-66.
Recall that melatonin displays multiple biological functions, acting as an antioxidant, cytokine, neurotransmitter, and global regulator of the circadian clock, the latter for which it is best known.1-3 At the cutaneous level, melatonin exhibits antioxidant (direct, as a radical scavenger; indirect, through upregulating antioxidant enzymes), anti-inflammatory, photoprotective, tissue regenerative, and cytoprotective activity, particularly in its capacity to preserve mitochondrial function.4-8
Melatonin also protects skin homeostasis,6 and, consequently, is believed to act against carcinogenesis and potentially other deleterious dysfunctions such as hyperproliferative/inflammatory conditions.5 Notably, , further buttressing the critical role that melatonin plays in skin health.5 Melatonin also displays immunomodulatory, thermoregulatory, and antitumor functions.9 The topical application of melatonin has been demonstrated to diminish markers of reactive oxygen species as well as reverse manifestations of cutaneous aging.5
Melatonin is both produced by and metabolized in the skin. The hormone and its metabolites (6-hydroxymelatonin, N1-acetyl-N2-formyl-5-methoxykynuramine [AFMK], N-acetyl-serotonin, and 5-methoxytryptamine) reduce UVB-induced oxidative cell damage in human keratinocytes and melanocytes, and also act as radioprotectors.6
Melatonin has been shown to protect human dermal fibroblasts from UVA- and UVB-induced damage.9 In addition, melatonin and its metabolites have been demonstrated to suppress the growth of cultured human melanomas, and high doses of melatonin used in clinical trials in late metastatic melanoma stages have enhanced the efficacy of or diminished the side effects of chemotherapy/chemo-immunotherapy.9
UVB and melatonin in the lab
In a 2018 hairless mouse study in which animals were irradiated by UVB for 8 weeks, Park et al. showed that melatonin displays anti-wrinkle activity by suppressing reactive oxygen species- and sonic hedgehog-mediated inflammatory proteins. Melatonin also protected against transepidermal water loss and prevented epidermal thickness as well as dermal collagen degradation.10
Also that year, Skobowiat et al. found that the topical application of melatonin and its active derivatives (N1-acetyl-N2-formyl-5-methoxykynurenine and N-acetylserotonin) yielded photoprotective effects pre- and post-UVB treatment in human and porcine skin ex vivo. They concluded that their results justify additional investigation of the clinical applications of melatonin and its metabolites for its potential to exert protective effects against UVB in human subjects.8
Although the preponderance of previous work identifies melatonin as a strong antioxidant, Kocyigit et al. reported in 2018 on new in vitro studies suggesting that melatonin dose-dependently exerts cytotoxic and apoptotic activity on several cell types, including both human epidermoid carcinoma and normal skin fibroblasts. Their findings showed that melatonin exhibited proliferative effects on cancerous and normal cells at low doses and cytotoxic effects at high doses.11
Melatonin as a sunscreen ingredient
Further supporting its use in the topical armamentarium for skin health, melatonin is a key ingredient in a sunscreen formulation, the creation of which was driven by the need to protect the skin of military personnel facing lengthy UV exposure. Specifically, the formulation containing avobenzone, octinoxate, oxybenzone, and titanium dioxide along with melatonin and pumpkin seed oil underwent a preclinical safety evaluation in 2017, as reported by Bora et al. The formulation was found to be nonmutagenic, nontoxic, and safe in animal models and is deemed ready to test for its efficacy in humans.12 Melatonin is also among a host of systemic treatment options for skin lightening.13
Oral and topical melatonin in human studies
In a 2017 study on the impact of melatonin treatment on the skin of former smokers, Sagan et al. assessed oxidative damage to membrane lipids in blood serum and in epidermis exfoliated during microdermabrasion (at baseline, 2 weeks after, and 4 weeks after treatment) in postmenopausal women. Never smokers (n = 44) and former smokers (n = 46) were divided into control, melatonin topical, antioxidant topical, and melatonin oral treatment groups. The investigators found that after only 2 weeks, melatonin oral treatment significantly reversed the elevated serum lipid peroxidation in former smokers. Oral melatonin increased elasticity, moisture, and sebum levels after 4 weeks of treatment and topical melatonin increased sebum level. They concluded that the use of exogenous melatonin reverses the effects of oxidative damage to membrane lipids and ameliorates cutaneous biophysical traits in postmenopausal women who once smoked. The researchers added that melatonin use for all former smokers is warranted and that topically applied melatonin merits consideration for improving the effects of facial microdermabrasion.14
In a systematic literature review in 2017, Scheuer identified 20 studies (4 human and 16 experimental) indicating that melatonin exerts a protective effect against artificial UV-induced erythema when applied pre-exposure.7 Also that year, Scheuer and colleagues conducted randomized, double-blind, placebo-controlled work demonstrating that topical melatonin (12.5%) significantly reduced erythema resulting from natural sunlight, and in a separate randomized, double-blind, placebo-controlled crossover study that the same concentration of a full body application of melatonin exhibited no significant impact on cognition and should be considered safe for dermal application.7 Scheuer added that additional longitudinal research is needed to ascertain effects of topical melatonin usage over time.
Early in 2018, Milani and Sparavigna reported on a randomized, split-face, assessor-blinded, prospective 3-month study of 22 women (mean age 55 years) with moderate to severe facial skin aging; the study was designed to test the efficacy of melatonin-based day and night creams. All of the women completed the proof-of-concept trial in which crow’s feet were found to be significantly diminished on the sides of the face treated with the creams compared with the nontreated skin.
Both well-tolerated melatonin formulations were associated with significant improvements in surface microrelief, skin profilometry, tonicity, and dryness. With marked enhancement of skin hydration and reduction of roughness noted, the investigators concluded that their results supported the notion that the tested melatonin topical formulations yielded antiaging effects.4
Conclusion
The majority of research on the potent hormone melatonin over nearly the last quarter century indicates that this dynamic substance provides multifaceted benefits in performing several biological functions. Topical melatonin is available over the counter. Its expanded use in skin care warrants greater attention as we learn more about this versatile endogenous substance.
Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote two textbooks: “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and “Cosmeceuticals and Cosmetic Ingredients,” (New York: McGraw-Hill, 2014), and a New York Times Best Sellers book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Evolus, Galderma, and Revance. She is the founder and CEO of Skin Type Solutions Franchise Systems LLC. Write to her at [email protected].
References
1. Zmijewski MA et al. Dermatoendocrinol. 2011 Jan;3(1):3-10.
2. Slominski A et al. Trends Endocrinol Metab. 2008 Jan;19(1):17-24.
3. Slominski A et al. J Cell Physiol. 2003 Jul;196(1):144-53.
4. Milani M et al. Clin Cosmet Investig Dermatol. 2018 Jan 24;11:51-7.
5. Day D et al. J Drugs Dermatol. 2018 Sep 1;17(9):966-9.
6. Slominski AT et al. Cell Mol Life Sci. 2017 Nov;74(21):3913-25.
7. Scheuer C. Dan Med J. 2017 Jun;64(6). pii:B5358.
8. Skobowiat C et al. J Pineal Res. 2018 Sep;65(2):e12501.
9. Slominski AT et al. J Invest Dermatol. 2018 Mar;138(3):490-9.
10. Park EK et al. Int J Mol Sci. 2018 Jul 8;19(7). pii: E1995.
11. Kocyigit A et al. Mutat Res. 2018 May-Jun;829-30:50-60.
12. Bora NS et al. Regul Toxicol Pharmacol. 2017 Oct;89:1-12.
13. Juhasz MLW et al. J Cosmet Dermatol. 2018 Dec;17(6):1144-57.
14. Sagan D et al. Ann Agric Environ Med. 2017 Dec 23;24(4):659-66.
Recall that melatonin displays multiple biological functions, acting as an antioxidant, cytokine, neurotransmitter, and global regulator of the circadian clock, the latter for which it is best known.1-3 At the cutaneous level, melatonin exhibits antioxidant (direct, as a radical scavenger; indirect, through upregulating antioxidant enzymes), anti-inflammatory, photoprotective, tissue regenerative, and cytoprotective activity, particularly in its capacity to preserve mitochondrial function.4-8
Melatonin also protects skin homeostasis,6 and, consequently, is believed to act against carcinogenesis and potentially other deleterious dysfunctions such as hyperproliferative/inflammatory conditions.5 Notably, , further buttressing the critical role that melatonin plays in skin health.5 Melatonin also displays immunomodulatory, thermoregulatory, and antitumor functions.9 The topical application of melatonin has been demonstrated to diminish markers of reactive oxygen species as well as reverse manifestations of cutaneous aging.5
Melatonin is both produced by and metabolized in the skin. The hormone and its metabolites (6-hydroxymelatonin, N1-acetyl-N2-formyl-5-methoxykynuramine [AFMK], N-acetyl-serotonin, and 5-methoxytryptamine) reduce UVB-induced oxidative cell damage in human keratinocytes and melanocytes, and also act as radioprotectors.6
Melatonin has been shown to protect human dermal fibroblasts from UVA- and UVB-induced damage.9 In addition, melatonin and its metabolites have been demonstrated to suppress the growth of cultured human melanomas, and high doses of melatonin used in clinical trials in late metastatic melanoma stages have enhanced the efficacy of or diminished the side effects of chemotherapy/chemo-immunotherapy.9
UVB and melatonin in the lab
In a 2018 hairless mouse study in which animals were irradiated by UVB for 8 weeks, Park et al. showed that melatonin displays anti-wrinkle activity by suppressing reactive oxygen species- and sonic hedgehog-mediated inflammatory proteins. Melatonin also protected against transepidermal water loss and prevented epidermal thickness as well as dermal collagen degradation.10
Also that year, Skobowiat et al. found that the topical application of melatonin and its active derivatives (N1-acetyl-N2-formyl-5-methoxykynurenine and N-acetylserotonin) yielded photoprotective effects pre- and post-UVB treatment in human and porcine skin ex vivo. They concluded that their results justify additional investigation of the clinical applications of melatonin and its metabolites for its potential to exert protective effects against UVB in human subjects.8
Although the preponderance of previous work identifies melatonin as a strong antioxidant, Kocyigit et al. reported in 2018 on new in vitro studies suggesting that melatonin dose-dependently exerts cytotoxic and apoptotic activity on several cell types, including both human epidermoid carcinoma and normal skin fibroblasts. Their findings showed that melatonin exhibited proliferative effects on cancerous and normal cells at low doses and cytotoxic effects at high doses.11
Melatonin as a sunscreen ingredient
Further supporting its use in the topical armamentarium for skin health, melatonin is a key ingredient in a sunscreen formulation, the creation of which was driven by the need to protect the skin of military personnel facing lengthy UV exposure. Specifically, the formulation containing avobenzone, octinoxate, oxybenzone, and titanium dioxide along with melatonin and pumpkin seed oil underwent a preclinical safety evaluation in 2017, as reported by Bora et al. The formulation was found to be nonmutagenic, nontoxic, and safe in animal models and is deemed ready to test for its efficacy in humans.12 Melatonin is also among a host of systemic treatment options for skin lightening.13
Oral and topical melatonin in human studies
In a 2017 study on the impact of melatonin treatment on the skin of former smokers, Sagan et al. assessed oxidative damage to membrane lipids in blood serum and in epidermis exfoliated during microdermabrasion (at baseline, 2 weeks after, and 4 weeks after treatment) in postmenopausal women. Never smokers (n = 44) and former smokers (n = 46) were divided into control, melatonin topical, antioxidant topical, and melatonin oral treatment groups. The investigators found that after only 2 weeks, melatonin oral treatment significantly reversed the elevated serum lipid peroxidation in former smokers. Oral melatonin increased elasticity, moisture, and sebum levels after 4 weeks of treatment and topical melatonin increased sebum level. They concluded that the use of exogenous melatonin reverses the effects of oxidative damage to membrane lipids and ameliorates cutaneous biophysical traits in postmenopausal women who once smoked. The researchers added that melatonin use for all former smokers is warranted and that topically applied melatonin merits consideration for improving the effects of facial microdermabrasion.14
In a systematic literature review in 2017, Scheuer identified 20 studies (4 human and 16 experimental) indicating that melatonin exerts a protective effect against artificial UV-induced erythema when applied pre-exposure.7 Also that year, Scheuer and colleagues conducted randomized, double-blind, placebo-controlled work demonstrating that topical melatonin (12.5%) significantly reduced erythema resulting from natural sunlight, and in a separate randomized, double-blind, placebo-controlled crossover study that the same concentration of a full body application of melatonin exhibited no significant impact on cognition and should be considered safe for dermal application.7 Scheuer added that additional longitudinal research is needed to ascertain effects of topical melatonin usage over time.
Early in 2018, Milani and Sparavigna reported on a randomized, split-face, assessor-blinded, prospective 3-month study of 22 women (mean age 55 years) with moderate to severe facial skin aging; the study was designed to test the efficacy of melatonin-based day and night creams. All of the women completed the proof-of-concept trial in which crow’s feet were found to be significantly diminished on the sides of the face treated with the creams compared with the nontreated skin.
Both well-tolerated melatonin formulations were associated with significant improvements in surface microrelief, skin profilometry, tonicity, and dryness. With marked enhancement of skin hydration and reduction of roughness noted, the investigators concluded that their results supported the notion that the tested melatonin topical formulations yielded antiaging effects.4
Conclusion
The majority of research on the potent hormone melatonin over nearly the last quarter century indicates that this dynamic substance provides multifaceted benefits in performing several biological functions. Topical melatonin is available over the counter. Its expanded use in skin care warrants greater attention as we learn more about this versatile endogenous substance.
Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote two textbooks: “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and “Cosmeceuticals and Cosmetic Ingredients,” (New York: McGraw-Hill, 2014), and a New York Times Best Sellers book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Evolus, Galderma, and Revance. She is the founder and CEO of Skin Type Solutions Franchise Systems LLC. Write to her at [email protected].
References
1. Zmijewski MA et al. Dermatoendocrinol. 2011 Jan;3(1):3-10.
2. Slominski A et al. Trends Endocrinol Metab. 2008 Jan;19(1):17-24.
3. Slominski A et al. J Cell Physiol. 2003 Jul;196(1):144-53.
4. Milani M et al. Clin Cosmet Investig Dermatol. 2018 Jan 24;11:51-7.
5. Day D et al. J Drugs Dermatol. 2018 Sep 1;17(9):966-9.
6. Slominski AT et al. Cell Mol Life Sci. 2017 Nov;74(21):3913-25.
7. Scheuer C. Dan Med J. 2017 Jun;64(6). pii:B5358.
8. Skobowiat C et al. J Pineal Res. 2018 Sep;65(2):e12501.
9. Slominski AT et al. J Invest Dermatol. 2018 Mar;138(3):490-9.
10. Park EK et al. Int J Mol Sci. 2018 Jul 8;19(7). pii: E1995.
11. Kocyigit A et al. Mutat Res. 2018 May-Jun;829-30:50-60.
12. Bora NS et al. Regul Toxicol Pharmacol. 2017 Oct;89:1-12.
13. Juhasz MLW et al. J Cosmet Dermatol. 2018 Dec;17(6):1144-57.
14. Sagan D et al. Ann Agric Environ Med. 2017 Dec 23;24(4):659-66.
Online vitriol’s expansion into doctor discussion sites
The web is full of doctor discussion sites. Sermo, Doximity, and many others. Each is slightly different, but the idea is similar. Give docs a place to joke, discuss cases, etc. A virtual doctors’ lounge.
Roughly 10 years ago I was active on Sermo. It was fun to check in a few days a week after work, ask questions about my own cases, and see if anyone had ideas on them, make a few suggestions on others, occasionally gripe about administrative issues at my hospital and commiserate about such online.
I don’t do that anymore.
This morning I logged in to see if anyone had previously encountered an unusual case, but was quickly pushed off by venom.
Yes, they do have a political discussion board, but staying away from politics is easier said than done online. Like mud, it tends to ooze into places it doesn’t belong. Even a routine post asking about new treatments for multiple sclerosis quickly degenerates. In a demonstration of Godwin’s Law, any comment about the pros and cons of a new agent devolves into a fight over government vs. private insurance, the United States’ vs. other countries’ health systems, and, inevitably, Trump, Obama, and name calling.
Makes it hard to actually kick around thoughts on Ocrevus (or whatever).
Generally, this won’t happen in a real doctors’ lounge because you know each other. Even if you’re not friends, people generally (not always) tend to be civil in person. Even differences are usually handled with a polite agreement to disagree.
I suspect the majority of people on Sermo and similar sites are reasonable and joined the sites for the same reasons I did. Unfortunately, we’ve been drowned out by a handful of angry voices who hijack these sites by posting intentionally inflammatory statements just to pick a fight or derail a thoughtful discussion on epilepsy management with nasty jabs relating medical issues directly to politics.
So my time using these sites has dropped. Occasionally, if I was bored, I’d log in to see if there were any interesting cases in my field, but even those often get dragged down by the angry as you try to contribute thoughts and answer questions in the comments.
Sadly, this has became the norm rather then the exception. For me, at least, it’s easier to just walk away entirely.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
The web is full of doctor discussion sites. Sermo, Doximity, and many others. Each is slightly different, but the idea is similar. Give docs a place to joke, discuss cases, etc. A virtual doctors’ lounge.
Roughly 10 years ago I was active on Sermo. It was fun to check in a few days a week after work, ask questions about my own cases, and see if anyone had ideas on them, make a few suggestions on others, occasionally gripe about administrative issues at my hospital and commiserate about such online.
I don’t do that anymore.
This morning I logged in to see if anyone had previously encountered an unusual case, but was quickly pushed off by venom.
Yes, they do have a political discussion board, but staying away from politics is easier said than done online. Like mud, it tends to ooze into places it doesn’t belong. Even a routine post asking about new treatments for multiple sclerosis quickly degenerates. In a demonstration of Godwin’s Law, any comment about the pros and cons of a new agent devolves into a fight over government vs. private insurance, the United States’ vs. other countries’ health systems, and, inevitably, Trump, Obama, and name calling.
Makes it hard to actually kick around thoughts on Ocrevus (or whatever).
Generally, this won’t happen in a real doctors’ lounge because you know each other. Even if you’re not friends, people generally (not always) tend to be civil in person. Even differences are usually handled with a polite agreement to disagree.
I suspect the majority of people on Sermo and similar sites are reasonable and joined the sites for the same reasons I did. Unfortunately, we’ve been drowned out by a handful of angry voices who hijack these sites by posting intentionally inflammatory statements just to pick a fight or derail a thoughtful discussion on epilepsy management with nasty jabs relating medical issues directly to politics.
So my time using these sites has dropped. Occasionally, if I was bored, I’d log in to see if there were any interesting cases in my field, but even those often get dragged down by the angry as you try to contribute thoughts and answer questions in the comments.
Sadly, this has became the norm rather then the exception. For me, at least, it’s easier to just walk away entirely.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
The web is full of doctor discussion sites. Sermo, Doximity, and many others. Each is slightly different, but the idea is similar. Give docs a place to joke, discuss cases, etc. A virtual doctors’ lounge.
Roughly 10 years ago I was active on Sermo. It was fun to check in a few days a week after work, ask questions about my own cases, and see if anyone had ideas on them, make a few suggestions on others, occasionally gripe about administrative issues at my hospital and commiserate about such online.
I don’t do that anymore.
This morning I logged in to see if anyone had previously encountered an unusual case, but was quickly pushed off by venom.
Yes, they do have a political discussion board, but staying away from politics is easier said than done online. Like mud, it tends to ooze into places it doesn’t belong. Even a routine post asking about new treatments for multiple sclerosis quickly degenerates. In a demonstration of Godwin’s Law, any comment about the pros and cons of a new agent devolves into a fight over government vs. private insurance, the United States’ vs. other countries’ health systems, and, inevitably, Trump, Obama, and name calling.
Makes it hard to actually kick around thoughts on Ocrevus (or whatever).
Generally, this won’t happen in a real doctors’ lounge because you know each other. Even if you’re not friends, people generally (not always) tend to be civil in person. Even differences are usually handled with a polite agreement to disagree.
I suspect the majority of people on Sermo and similar sites are reasonable and joined the sites for the same reasons I did. Unfortunately, we’ve been drowned out by a handful of angry voices who hijack these sites by posting intentionally inflammatory statements just to pick a fight or derail a thoughtful discussion on epilepsy management with nasty jabs relating medical issues directly to politics.
So my time using these sites has dropped. Occasionally, if I was bored, I’d log in to see if there were any interesting cases in my field, but even those often get dragged down by the angry as you try to contribute thoughts and answer questions in the comments.
Sadly, this has became the norm rather then the exception. For me, at least, it’s easier to just walk away entirely.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.