The reasons are, obviously, widely variable among patients and circumstances. Some are more understandable than others, but all of them add up to an empty chair across the desk and loss of income for that time slot.
CherriesJD/Thinkstock
A recent study in Neurology: Clinical Practice looked into this question. Interestingly, it found that people with certain chronic diseases, such as medication-overuse headaches, chronic daily headaches, and seizures, were among those with the highest no-show rates.
These are all conditions that require medication fine tuning, but this can be difficult without the patient coming in. There’s only so much that can be done on the phone, and in this business a direct face-to-face conversation is often needed.
On the opposite side, they noted that people with degenerative disorders that have more limited treatments, such as Alzheimer’s and Parkinson’s diseases, had the highest rate of making it to the appointment, though this may be due more to caretakers than the patients themselves.
Financial issues come into play. Younger patients with chronic diseases may have more difficulty taking time off work, or may just simply not have the money for a copay. They could also be too depressed from their situation to come in. Granted, it would be nice if they’d call to let us know they weren’t coming (at my office we don’t ask questions), but many don’t bother.
All of us are affected by this problem. Seeing patients is what drives the economics of every medical practice. An empty exam room is a financial hit, and it denies another patient who needs help a chance to be seen.
Fifteen years ago, my billing company ran some numbers and found that patients on one specific insurance plan had two to three times the rate of no-shows of any of my other contracts. With a number like that, I couldn’t see a reason to stay with them, and I dropped that plan. I felt bad for the reliable patients affected, but the hard truth is that if I can’t keep my practice open, I can’t help anyone. Why this plan had so many no-shows could be from a number of factors, but the end result was the same. Regardless of the reason, it was having a negative impact on my bottom line.
Dr. Allan M. Block
We try all kinds of different ways to remind people of their appointments. My secretary makes reminder calls. Other offices send texts or emails, or have a robocall system. These can only help to a certain degree. At some point, this becomes the “you can lead a horse to water ...” adage.
There’s no real easy answer, either. At my office, we don’t overbook. It seems to be an unwritten rule that every time we gamble that someone won’t come in and then put someone else in the slot, they both show up.
Research like this is interesting, and maybe helpful at making a predictive model about no-shows. But I’m not convinced it will eventually have everyday use in a real-world practice.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
The reasons are, obviously, widely variable among patients and circumstances. Some are more understandable than others, but all of them add up to an empty chair across the desk and loss of income for that time slot.
CherriesJD/Thinkstock
A recent study in Neurology: Clinical Practice looked into this question. Interestingly, it found that people with certain chronic diseases, such as medication-overuse headaches, chronic daily headaches, and seizures, were among those with the highest no-show rates.
These are all conditions that require medication fine tuning, but this can be difficult without the patient coming in. There’s only so much that can be done on the phone, and in this business a direct face-to-face conversation is often needed.
On the opposite side, they noted that people with degenerative disorders that have more limited treatments, such as Alzheimer’s and Parkinson’s diseases, had the highest rate of making it to the appointment, though this may be due more to caretakers than the patients themselves.
Financial issues come into play. Younger patients with chronic diseases may have more difficulty taking time off work, or may just simply not have the money for a copay. They could also be too depressed from their situation to come in. Granted, it would be nice if they’d call to let us know they weren’t coming (at my office we don’t ask questions), but many don’t bother.
All of us are affected by this problem. Seeing patients is what drives the economics of every medical practice. An empty exam room is a financial hit, and it denies another patient who needs help a chance to be seen.
Fifteen years ago, my billing company ran some numbers and found that patients on one specific insurance plan had two to three times the rate of no-shows of any of my other contracts. With a number like that, I couldn’t see a reason to stay with them, and I dropped that plan. I felt bad for the reliable patients affected, but the hard truth is that if I can’t keep my practice open, I can’t help anyone. Why this plan had so many no-shows could be from a number of factors, but the end result was the same. Regardless of the reason, it was having a negative impact on my bottom line.
Dr. Allan M. Block
We try all kinds of different ways to remind people of their appointments. My secretary makes reminder calls. Other offices send texts or emails, or have a robocall system. These can only help to a certain degree. At some point, this becomes the “you can lead a horse to water ...” adage.
There’s no real easy answer, either. At my office, we don’t overbook. It seems to be an unwritten rule that every time we gamble that someone won’t come in and then put someone else in the slot, they both show up.
Research like this is interesting, and maybe helpful at making a predictive model about no-shows. But I’m not convinced it will eventually have everyday use in a real-world practice.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
Why do patients no-show?
The reasons are, obviously, widely variable among patients and circumstances. Some are more understandable than others, but all of them add up to an empty chair across the desk and loss of income for that time slot.
CherriesJD/Thinkstock
A recent study in Neurology: Clinical Practice looked into this question. Interestingly, it found that people with certain chronic diseases, such as medication-overuse headaches, chronic daily headaches, and seizures, were among those with the highest no-show rates.
These are all conditions that require medication fine tuning, but this can be difficult without the patient coming in. There’s only so much that can be done on the phone, and in this business a direct face-to-face conversation is often needed.
On the opposite side, they noted that people with degenerative disorders that have more limited treatments, such as Alzheimer’s and Parkinson’s diseases, had the highest rate of making it to the appointment, though this may be due more to caretakers than the patients themselves.
Financial issues come into play. Younger patients with chronic diseases may have more difficulty taking time off work, or may just simply not have the money for a copay. They could also be too depressed from their situation to come in. Granted, it would be nice if they’d call to let us know they weren’t coming (at my office we don’t ask questions), but many don’t bother.
All of us are affected by this problem. Seeing patients is what drives the economics of every medical practice. An empty exam room is a financial hit, and it denies another patient who needs help a chance to be seen.
Fifteen years ago, my billing company ran some numbers and found that patients on one specific insurance plan had two to three times the rate of no-shows of any of my other contracts. With a number like that, I couldn’t see a reason to stay with them, and I dropped that plan. I felt bad for the reliable patients affected, but the hard truth is that if I can’t keep my practice open, I can’t help anyone. Why this plan had so many no-shows could be from a number of factors, but the end result was the same. Regardless of the reason, it was having a negative impact on my bottom line.
Dr. Allan M. Block
We try all kinds of different ways to remind people of their appointments. My secretary makes reminder calls. Other offices send texts or emails, or have a robocall system. These can only help to a certain degree. At some point, this becomes the “you can lead a horse to water ...” adage.
There’s no real easy answer, either. At my office, we don’t overbook. It seems to be an unwritten rule that every time we gamble that someone won’t come in and then put someone else in the slot, they both show up.
Research like this is interesting, and maybe helpful at making a predictive model about no-shows. But I’m not convinced it will eventually have everyday use in a real-world practice.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
What is the largest endocrine organ in the human body?
Here is a clue: It is also the largest immune organ in humans!
Still scratching your head? Here is another clue: This organ also contains a “second brain,” which is connected to big brain inside the head by the vagus nerve.
Okay, enough guessing: It’s the 30-foot long gastrointestinal (GI) tract, which is generally associated only with eating and digestion. But it is far more than a digestive tract. It is home to about 100 trillion diverse bacteria, including 1,000 known species, which together are known as “microbiota.” Its combined DNA is called the “microbiome” and is 10,000% larger than the human genome. Those trillions of bacteria in our guts are a symbiotic (commensal) organ that is vital for the normal functions of the human body.1
While this vast array of microorganisms is vital to sustaining a healthy human existence, it can also be involved in multiple psychiatric disorders, including depression, psychosis, anxiety, autism, and attention-deficit/hyperactivity disorder (ADHD). Humans acquire their unique sets of microbiota as they pass through the mother’s vagina at birth and while breastfeeding, as well as from exposure to various environmental sources in the first few months of life.2
The microbiota in the GI tract are an intimate neighbor of the “enteric brain,” comprised of 100 million neurons plus glia-like support cell structures. This “second brain” produces over 30 neurotransmitters, several of which (dopamine, serotonin, γ-aminobutyric acid [GABA], acetylcholine) have been implicated in major psychiatric disorders.3
The brain and gut have a dynamic bidirectional communication system, mediated by neural, hormonal, and immunological crosstalk and influences. The GI tract secretes dozens of peptides and other signaling molecules that influence the brain. The microbiota also interact with and are regulated by gut hormones such as oxytocin, ghrelin, neuropeptide Y, cholecystokinin, corticotrophin-releasing factor, and pancreatic polypeptide.4 The microbiota modulate brain development, functions, and behavior, and maintain the intestinal barrier, which, if disrupted, would result in the gut becoming “leaky” and triggering low-grade inflammation such as that associated with depression.5
Continue to: But don't overlook the importance of...
But don’t overlook the importance of diet. It is a major factor in shaping the composition of the microbiota. What we eat can have a preventative or reparative effect on neuroimmune or neuroinflammatory disease. An emerging body of evidence suggests that the diet and its effects on the gut microbiota can modify a person’s genes by epigenetic mechanisms (altering DNA methylation and histone effects). Probiotics can exert epigenetic effects by influencing cytokines, by producing short-chain fatty acids (SCFAs), by vitamin synthesis, and by producing several well-known neurotransmitters.6
The bidirectional trafficking across the microbiome-gut-brain axis includes reciprocal effects. The brain influences the microbiome composition by regulating satiety, the hypothalamic-pituitary axis, and with neuropeptides.7 In return, the microbiome conveys information to the brain about the intestinal status via infectious agents, intestinal neurotransmitters and modulators, cytokines, sensory vagal fibers, and various metabolites. Failure of these normal interactions can lead to a variety of pathological processes, including inflammatory, autoimmune, degenerative, metabolic, cognitive, mood, and behavioral adverse effects. Therapeutic interventions for these adverse consequences can be implemented through microbiome manipulations (such as fecal transplants), nutritional strategies, and reinforcement of the enteric and brain barriers.
Alterations in the microbiota, such as by the intake of antibiotics or by intestinal inflammation, can lead to psychiatric disorders.8 The following findings link gut microbiome disruptions with several psychiatric disorders:
Schizophrenia prodrome.Fecal bacteria show an increase in SCFAs, which can activate microglia (the initial step in triggering psychosis).9 These bacteria have been shown to lead to an increase in choline levels in the anterior cingulate, a known biomarker for membrane dysfunction, which is one of the biological models of schizophrenia.
Schizophrenia—first-episode.A recent study reported abnormalities in the gut microbiota of patients with first-episode psychosis, with a lower number of certain fecal bacteria (including bifidobacterium, E. coli, and lactobacillus) and high levels of Clostridium coccoides. After 6 months of risperidone treatment, the above changes were reversed.10
Continue to: Another study of fecal microbiota...
Another study of fecal microbiota in a first-episode psychosis cohort found significant differences in several bacterial strains compared with a healthy control group, and those with the strongest difference had more severe psychotic symptoms and poorer response after 12 months of antipsychotic treatment.11
Autism has been linked to increased microbiota diversity, and an excess of bacteroides has been associated with a higher diversity of autism. Fecal samples from autistic children were reported to have an increase in SCFAs. Interestingly, a certain strain of lactobacillus can modulate oxytocin or reverse some autistic symptoms.
Depression has been associated with increased diversity of microbiota alpha. Patients with depression have been reported to have low numbers of bifidobacterium and lactobacillus. Certain strains have been reported to reduce depression and anxiety behaviors in animal studies. The microbiota-friendly Mediterranean diet, but not the Western diet, appears to mitigate the risk of depression. Certain probiotics have been reported to increase resilience to stress.12,13
ADHD.Some studies suggest that ADHD may be linked to factors that can alter gut microbiota, including birthing mode, type of infant feeding, maternal health, and early stressors. In addition, dietary influences on gut microbiota can modify ADHD symptoms.14
Alzheimer’s disease.Metabolic dysregulation, such as obesity and diabetes, can inflame the gut microbiota, and are known risk factors for Alzheimer’s disease.15
Continue to: Irritable bowel sydrome...
Irritable bowel syndrome (IBS).Fecal microbiota transplantation has been shown to improve IBS by increasing the diversity of gut microbiota.16 It also improves patients’ mood, not just their IBS symptoms.
Alcohol use.Both alcohol consumption and alcohol withdrawal have been shown to cause immune dysregulation in the brain leading to neuroinflammation. This is attributed to the alteration in the composition of the microbiome (dysbiosis), which has a negative effect on the microbe-host homeostasis.17
The discovery of microbiome-gut-brain interactions and their bidirectional immune, endocrine, and neurotransmitter effects has been a momentous paradigm shift in health, neuroscience, and psychiatry.18 It has opened wide vistas of research for potential innovations in the prevention and treatment of various psychiatric disorders. Radical medical interventions that were previously inconceivable, such as fecal transplantation,19 are an example of the bold insights this new field of microbiome-gut-brain interaction is bringing to the landscape of medicine, including psychiatry. It has also highlighted the previously underappreciated importance of nutrition in health and disease.20
References
1. Nasrallah HA. Psychoneurogastroenterology: the abdominal brain, the microbiome, and psychiatry. Current Psychiatry. 2015;14(5):10-11. 2. Dinan TG, Borre YE, Cryan JF. Genomics of schizophrenia: time to consider the gut microbiome? Mol Psychiatry. 2014;19(12):1252-1257. 3. Alam R, Abdolmaleky HM, Zhou JR. Microbiome, inflammation, epigenetic alterations, and mental diseases. Am J Med Genet B Neuropsychiatr Genet. 2017;174(6):651-660. 4. Lach G, Schellekens H, Dinan TG, et al. Anxiety, depression, and the microbiome: a role for gut peptides. Neurotherapeutics. 2018;15(1):36-59. 5. Kelly JR, Kennedy PJ, Cryan JF, et al. Breaking down the barriers: the gut microbiome, intestinal permeability and stress-related psychiatric disorders. Front Cell Neurosci. 2015;9:392. 6. Rodrigues-Amorim D, Rivera-Baltanás T, Regueiro B, et al. The role of the gut microbiota in schizophrenia: current and future perspectives. World J Biol Psychiatry. 2018;21:1-15. 7. Petra AI, Panagiotidou S, Hatziagelaki E, et al. Gut-microbiota-brain axis and its effect on neuropsychiatric disorders with suspected immune dysregulation. Clin Ther. 2015;37(5):984-995. 8. Lurie I, Yang YX, Haynes K, et al. Antibiotic exposure and the risk for depression, anxiety, or psychosis: a nested case-control study. J Clin Psychiatry. 2015;76(11):1522-1528. 9. He Y, Kosciolek T, Tang J, et al. Gut microbiome and magnetic resonance spectroscopy study of subjects at ultra-high risk for psychosis may support the membrane hypothesis. Eur Psychiatry. 2018;53:37-45. 10. Yuan X, Zhang P, Wang Y, et al. Changes in metabolism and microbiota after 24-week risperidone treatment in drug naïve, normal weight patients with first episode schizophrenia. Schizophr Res. 2018;pii: S0920-9964(18)30274-3. [Epub ahead of print]. doi: 10.1016/j.schres.2018.05.017. 11. Dickerson F, Severance E, Yolken R. The microbiome, immunity, and schizophrenia and bipolar disorder. Brain Behav Immun. 2017;62:46-52. 12. Huang R, Wang K, Hu J. Effect of probiotics on depression: a systematic review and meta-analysis of randomized controlled trials. Nutrients. 2016;8(8):pii: E483. doi: 10.3390/nu8080483. 13. Carding S, Verbeke K, Vipond DT, et al. Dysbiosis of the gut microbiota in disease. Microb Ecol Health Dis. 2015;26:26191. doi: 10.3402/mehd.v26.26191. 14. Thapar A, Cooper M, Eyre O, et al. Practitioner review: what have we learnt about the causes of ADHD? J Child Psychol Psychiatry. 2013;54(1):3-16. 15. Jiang C, Li G, Huang P, et al. The gut microbiota and Alzheimer’s disease. J Alzheimers Dis. 2017;58(1):1-15. 16. Kurokawa S, Kishimoto T, Mizuno S, et al. The effect of fecal microbiota transplantation on psychiatric symptoms among patients with irritable bowel syndrome, functional diarrhea and functional constipation: an open-label observational study. J Affect Disord. 2018;235:506-512. 17. Hillemacher T, Bachmann O, Kahl KG, et al. Alcohol, microbiome, and their effect on psychiatric disorders. Prog Neuropsychopharmacol Biol Psychiatry. 2018;85:105-115. 18. Doré J, Multon MC, Béhier JM; participants of Giens XXXII, Round Table No. 2. The human gut microbiome as source of innovation for health: which physiological and therapeutic outcomes could we expect? Therapie. 2017;72(1):21-38. 19. Vemuri RC, Gundamaraju R, Shinde T, et al. Therapeutic interventions for gut dysbiosis and related disorders in the elderly: antibiotics, probiotics or faecal microbiota transplantation? Benef Microbes. 2017;8(2):179-192. 20. Lombardi VC, De Meirleir KL, Subramanian K, et al. Nutritional modulation of the intestinal microbiota; future opportunities for the prevention and treatment of neuroimmune and neuroinflammatory disease. J Nutr Biochem. 2018;61:1-16.
What is the largest endocrine organ in the human body?
Here is a clue: It is also the largest immune organ in humans!
Still scratching your head? Here is another clue: This organ also contains a “second brain,” which is connected to big brain inside the head by the vagus nerve.
Okay, enough guessing: It’s the 30-foot long gastrointestinal (GI) tract, which is generally associated only with eating and digestion. But it is far more than a digestive tract. It is home to about 100 trillion diverse bacteria, including 1,000 known species, which together are known as “microbiota.” Its combined DNA is called the “microbiome” and is 10,000% larger than the human genome. Those trillions of bacteria in our guts are a symbiotic (commensal) organ that is vital for the normal functions of the human body.1
While this vast array of microorganisms is vital to sustaining a healthy human existence, it can also be involved in multiple psychiatric disorders, including depression, psychosis, anxiety, autism, and attention-deficit/hyperactivity disorder (ADHD). Humans acquire their unique sets of microbiota as they pass through the mother’s vagina at birth and while breastfeeding, as well as from exposure to various environmental sources in the first few months of life.2
The microbiota in the GI tract are an intimate neighbor of the “enteric brain,” comprised of 100 million neurons plus glia-like support cell structures. This “second brain” produces over 30 neurotransmitters, several of which (dopamine, serotonin, γ-aminobutyric acid [GABA], acetylcholine) have been implicated in major psychiatric disorders.3
The brain and gut have a dynamic bidirectional communication system, mediated by neural, hormonal, and immunological crosstalk and influences. The GI tract secretes dozens of peptides and other signaling molecules that influence the brain. The microbiota also interact with and are regulated by gut hormones such as oxytocin, ghrelin, neuropeptide Y, cholecystokinin, corticotrophin-releasing factor, and pancreatic polypeptide.4 The microbiota modulate brain development, functions, and behavior, and maintain the intestinal barrier, which, if disrupted, would result in the gut becoming “leaky” and triggering low-grade inflammation such as that associated with depression.5
Continue to: But don't overlook the importance of...
But don’t overlook the importance of diet. It is a major factor in shaping the composition of the microbiota. What we eat can have a preventative or reparative effect on neuroimmune or neuroinflammatory disease. An emerging body of evidence suggests that the diet and its effects on the gut microbiota can modify a person’s genes by epigenetic mechanisms (altering DNA methylation and histone effects). Probiotics can exert epigenetic effects by influencing cytokines, by producing short-chain fatty acids (SCFAs), by vitamin synthesis, and by producing several well-known neurotransmitters.6
The bidirectional trafficking across the microbiome-gut-brain axis includes reciprocal effects. The brain influences the microbiome composition by regulating satiety, the hypothalamic-pituitary axis, and with neuropeptides.7 In return, the microbiome conveys information to the brain about the intestinal status via infectious agents, intestinal neurotransmitters and modulators, cytokines, sensory vagal fibers, and various metabolites. Failure of these normal interactions can lead to a variety of pathological processes, including inflammatory, autoimmune, degenerative, metabolic, cognitive, mood, and behavioral adverse effects. Therapeutic interventions for these adverse consequences can be implemented through microbiome manipulations (such as fecal transplants), nutritional strategies, and reinforcement of the enteric and brain barriers.
Alterations in the microbiota, such as by the intake of antibiotics or by intestinal inflammation, can lead to psychiatric disorders.8 The following findings link gut microbiome disruptions with several psychiatric disorders:
Schizophrenia prodrome.Fecal bacteria show an increase in SCFAs, which can activate microglia (the initial step in triggering psychosis).9 These bacteria have been shown to lead to an increase in choline levels in the anterior cingulate, a known biomarker for membrane dysfunction, which is one of the biological models of schizophrenia.
Schizophrenia—first-episode.A recent study reported abnormalities in the gut microbiota of patients with first-episode psychosis, with a lower number of certain fecal bacteria (including bifidobacterium, E. coli, and lactobacillus) and high levels of Clostridium coccoides. After 6 months of risperidone treatment, the above changes were reversed.10
Continue to: Another study of fecal microbiota...
Another study of fecal microbiota in a first-episode psychosis cohort found significant differences in several bacterial strains compared with a healthy control group, and those with the strongest difference had more severe psychotic symptoms and poorer response after 12 months of antipsychotic treatment.11
Autism has been linked to increased microbiota diversity, and an excess of bacteroides has been associated with a higher diversity of autism. Fecal samples from autistic children were reported to have an increase in SCFAs. Interestingly, a certain strain of lactobacillus can modulate oxytocin or reverse some autistic symptoms.
Depression has been associated with increased diversity of microbiota alpha. Patients with depression have been reported to have low numbers of bifidobacterium and lactobacillus. Certain strains have been reported to reduce depression and anxiety behaviors in animal studies. The microbiota-friendly Mediterranean diet, but not the Western diet, appears to mitigate the risk of depression. Certain probiotics have been reported to increase resilience to stress.12,13
ADHD.Some studies suggest that ADHD may be linked to factors that can alter gut microbiota, including birthing mode, type of infant feeding, maternal health, and early stressors. In addition, dietary influences on gut microbiota can modify ADHD symptoms.14
Alzheimer’s disease.Metabolic dysregulation, such as obesity and diabetes, can inflame the gut microbiota, and are known risk factors for Alzheimer’s disease.15
Continue to: Irritable bowel sydrome...
Irritable bowel syndrome (IBS).Fecal microbiota transplantation has been shown to improve IBS by increasing the diversity of gut microbiota.16 It also improves patients’ mood, not just their IBS symptoms.
Alcohol use.Both alcohol consumption and alcohol withdrawal have been shown to cause immune dysregulation in the brain leading to neuroinflammation. This is attributed to the alteration in the composition of the microbiome (dysbiosis), which has a negative effect on the microbe-host homeostasis.17
The discovery of microbiome-gut-brain interactions and their bidirectional immune, endocrine, and neurotransmitter effects has been a momentous paradigm shift in health, neuroscience, and psychiatry.18 It has opened wide vistas of research for potential innovations in the prevention and treatment of various psychiatric disorders. Radical medical interventions that were previously inconceivable, such as fecal transplantation,19 are an example of the bold insights this new field of microbiome-gut-brain interaction is bringing to the landscape of medicine, including psychiatry. It has also highlighted the previously underappreciated importance of nutrition in health and disease.20
What is the largest endocrine organ in the human body?
Here is a clue: It is also the largest immune organ in humans!
Still scratching your head? Here is another clue: This organ also contains a “second brain,” which is connected to big brain inside the head by the vagus nerve.
Okay, enough guessing: It’s the 30-foot long gastrointestinal (GI) tract, which is generally associated only with eating and digestion. But it is far more than a digestive tract. It is home to about 100 trillion diverse bacteria, including 1,000 known species, which together are known as “microbiota.” Its combined DNA is called the “microbiome” and is 10,000% larger than the human genome. Those trillions of bacteria in our guts are a symbiotic (commensal) organ that is vital for the normal functions of the human body.1
While this vast array of microorganisms is vital to sustaining a healthy human existence, it can also be involved in multiple psychiatric disorders, including depression, psychosis, anxiety, autism, and attention-deficit/hyperactivity disorder (ADHD). Humans acquire their unique sets of microbiota as they pass through the mother’s vagina at birth and while breastfeeding, as well as from exposure to various environmental sources in the first few months of life.2
The microbiota in the GI tract are an intimate neighbor of the “enteric brain,” comprised of 100 million neurons plus glia-like support cell structures. This “second brain” produces over 30 neurotransmitters, several of which (dopamine, serotonin, γ-aminobutyric acid [GABA], acetylcholine) have been implicated in major psychiatric disorders.3
The brain and gut have a dynamic bidirectional communication system, mediated by neural, hormonal, and immunological crosstalk and influences. The GI tract secretes dozens of peptides and other signaling molecules that influence the brain. The microbiota also interact with and are regulated by gut hormones such as oxytocin, ghrelin, neuropeptide Y, cholecystokinin, corticotrophin-releasing factor, and pancreatic polypeptide.4 The microbiota modulate brain development, functions, and behavior, and maintain the intestinal barrier, which, if disrupted, would result in the gut becoming “leaky” and triggering low-grade inflammation such as that associated with depression.5
Continue to: But don't overlook the importance of...
But don’t overlook the importance of diet. It is a major factor in shaping the composition of the microbiota. What we eat can have a preventative or reparative effect on neuroimmune or neuroinflammatory disease. An emerging body of evidence suggests that the diet and its effects on the gut microbiota can modify a person’s genes by epigenetic mechanisms (altering DNA methylation and histone effects). Probiotics can exert epigenetic effects by influencing cytokines, by producing short-chain fatty acids (SCFAs), by vitamin synthesis, and by producing several well-known neurotransmitters.6
The bidirectional trafficking across the microbiome-gut-brain axis includes reciprocal effects. The brain influences the microbiome composition by regulating satiety, the hypothalamic-pituitary axis, and with neuropeptides.7 In return, the microbiome conveys information to the brain about the intestinal status via infectious agents, intestinal neurotransmitters and modulators, cytokines, sensory vagal fibers, and various metabolites. Failure of these normal interactions can lead to a variety of pathological processes, including inflammatory, autoimmune, degenerative, metabolic, cognitive, mood, and behavioral adverse effects. Therapeutic interventions for these adverse consequences can be implemented through microbiome manipulations (such as fecal transplants), nutritional strategies, and reinforcement of the enteric and brain barriers.
Alterations in the microbiota, such as by the intake of antibiotics or by intestinal inflammation, can lead to psychiatric disorders.8 The following findings link gut microbiome disruptions with several psychiatric disorders:
Schizophrenia prodrome.Fecal bacteria show an increase in SCFAs, which can activate microglia (the initial step in triggering psychosis).9 These bacteria have been shown to lead to an increase in choline levels in the anterior cingulate, a known biomarker for membrane dysfunction, which is one of the biological models of schizophrenia.
Schizophrenia—first-episode.A recent study reported abnormalities in the gut microbiota of patients with first-episode psychosis, with a lower number of certain fecal bacteria (including bifidobacterium, E. coli, and lactobacillus) and high levels of Clostridium coccoides. After 6 months of risperidone treatment, the above changes were reversed.10
Continue to: Another study of fecal microbiota...
Another study of fecal microbiota in a first-episode psychosis cohort found significant differences in several bacterial strains compared with a healthy control group, and those with the strongest difference had more severe psychotic symptoms and poorer response after 12 months of antipsychotic treatment.11
Autism has been linked to increased microbiota diversity, and an excess of bacteroides has been associated with a higher diversity of autism. Fecal samples from autistic children were reported to have an increase in SCFAs. Interestingly, a certain strain of lactobacillus can modulate oxytocin or reverse some autistic symptoms.
Depression has been associated with increased diversity of microbiota alpha. Patients with depression have been reported to have low numbers of bifidobacterium and lactobacillus. Certain strains have been reported to reduce depression and anxiety behaviors in animal studies. The microbiota-friendly Mediterranean diet, but not the Western diet, appears to mitigate the risk of depression. Certain probiotics have been reported to increase resilience to stress.12,13
ADHD.Some studies suggest that ADHD may be linked to factors that can alter gut microbiota, including birthing mode, type of infant feeding, maternal health, and early stressors. In addition, dietary influences on gut microbiota can modify ADHD symptoms.14
Alzheimer’s disease.Metabolic dysregulation, such as obesity and diabetes, can inflame the gut microbiota, and are known risk factors for Alzheimer’s disease.15
Continue to: Irritable bowel sydrome...
Irritable bowel syndrome (IBS).Fecal microbiota transplantation has been shown to improve IBS by increasing the diversity of gut microbiota.16 It also improves patients’ mood, not just their IBS symptoms.
Alcohol use.Both alcohol consumption and alcohol withdrawal have been shown to cause immune dysregulation in the brain leading to neuroinflammation. This is attributed to the alteration in the composition of the microbiome (dysbiosis), which has a negative effect on the microbe-host homeostasis.17
The discovery of microbiome-gut-brain interactions and their bidirectional immune, endocrine, and neurotransmitter effects has been a momentous paradigm shift in health, neuroscience, and psychiatry.18 It has opened wide vistas of research for potential innovations in the prevention and treatment of various psychiatric disorders. Radical medical interventions that were previously inconceivable, such as fecal transplantation,19 are an example of the bold insights this new field of microbiome-gut-brain interaction is bringing to the landscape of medicine, including psychiatry. It has also highlighted the previously underappreciated importance of nutrition in health and disease.20
References
1. Nasrallah HA. Psychoneurogastroenterology: the abdominal brain, the microbiome, and psychiatry. Current Psychiatry. 2015;14(5):10-11. 2. Dinan TG, Borre YE, Cryan JF. Genomics of schizophrenia: time to consider the gut microbiome? Mol Psychiatry. 2014;19(12):1252-1257. 3. Alam R, Abdolmaleky HM, Zhou JR. Microbiome, inflammation, epigenetic alterations, and mental diseases. Am J Med Genet B Neuropsychiatr Genet. 2017;174(6):651-660. 4. Lach G, Schellekens H, Dinan TG, et al. Anxiety, depression, and the microbiome: a role for gut peptides. Neurotherapeutics. 2018;15(1):36-59. 5. Kelly JR, Kennedy PJ, Cryan JF, et al. Breaking down the barriers: the gut microbiome, intestinal permeability and stress-related psychiatric disorders. Front Cell Neurosci. 2015;9:392. 6. Rodrigues-Amorim D, Rivera-Baltanás T, Regueiro B, et al. The role of the gut microbiota in schizophrenia: current and future perspectives. World J Biol Psychiatry. 2018;21:1-15. 7. Petra AI, Panagiotidou S, Hatziagelaki E, et al. Gut-microbiota-brain axis and its effect on neuropsychiatric disorders with suspected immune dysregulation. Clin Ther. 2015;37(5):984-995. 8. Lurie I, Yang YX, Haynes K, et al. Antibiotic exposure and the risk for depression, anxiety, or psychosis: a nested case-control study. J Clin Psychiatry. 2015;76(11):1522-1528. 9. He Y, Kosciolek T, Tang J, et al. Gut microbiome and magnetic resonance spectroscopy study of subjects at ultra-high risk for psychosis may support the membrane hypothesis. Eur Psychiatry. 2018;53:37-45. 10. Yuan X, Zhang P, Wang Y, et al. Changes in metabolism and microbiota after 24-week risperidone treatment in drug naïve, normal weight patients with first episode schizophrenia. Schizophr Res. 2018;pii: S0920-9964(18)30274-3. [Epub ahead of print]. doi: 10.1016/j.schres.2018.05.017. 11. Dickerson F, Severance E, Yolken R. The microbiome, immunity, and schizophrenia and bipolar disorder. Brain Behav Immun. 2017;62:46-52. 12. Huang R, Wang K, Hu J. Effect of probiotics on depression: a systematic review and meta-analysis of randomized controlled trials. Nutrients. 2016;8(8):pii: E483. doi: 10.3390/nu8080483. 13. Carding S, Verbeke K, Vipond DT, et al. Dysbiosis of the gut microbiota in disease. Microb Ecol Health Dis. 2015;26:26191. doi: 10.3402/mehd.v26.26191. 14. Thapar A, Cooper M, Eyre O, et al. Practitioner review: what have we learnt about the causes of ADHD? J Child Psychol Psychiatry. 2013;54(1):3-16. 15. Jiang C, Li G, Huang P, et al. The gut microbiota and Alzheimer’s disease. J Alzheimers Dis. 2017;58(1):1-15. 16. Kurokawa S, Kishimoto T, Mizuno S, et al. The effect of fecal microbiota transplantation on psychiatric symptoms among patients with irritable bowel syndrome, functional diarrhea and functional constipation: an open-label observational study. J Affect Disord. 2018;235:506-512. 17. Hillemacher T, Bachmann O, Kahl KG, et al. Alcohol, microbiome, and their effect on psychiatric disorders. Prog Neuropsychopharmacol Biol Psychiatry. 2018;85:105-115. 18. Doré J, Multon MC, Béhier JM; participants of Giens XXXII, Round Table No. 2. The human gut microbiome as source of innovation for health: which physiological and therapeutic outcomes could we expect? Therapie. 2017;72(1):21-38. 19. Vemuri RC, Gundamaraju R, Shinde T, et al. Therapeutic interventions for gut dysbiosis and related disorders in the elderly: antibiotics, probiotics or faecal microbiota transplantation? Benef Microbes. 2017;8(2):179-192. 20. Lombardi VC, De Meirleir KL, Subramanian K, et al. Nutritional modulation of the intestinal microbiota; future opportunities for the prevention and treatment of neuroimmune and neuroinflammatory disease. J Nutr Biochem. 2018;61:1-16.
References
1. Nasrallah HA. Psychoneurogastroenterology: the abdominal brain, the microbiome, and psychiatry. Current Psychiatry. 2015;14(5):10-11. 2. Dinan TG, Borre YE, Cryan JF. Genomics of schizophrenia: time to consider the gut microbiome? Mol Psychiatry. 2014;19(12):1252-1257. 3. Alam R, Abdolmaleky HM, Zhou JR. Microbiome, inflammation, epigenetic alterations, and mental diseases. Am J Med Genet B Neuropsychiatr Genet. 2017;174(6):651-660. 4. Lach G, Schellekens H, Dinan TG, et al. Anxiety, depression, and the microbiome: a role for gut peptides. Neurotherapeutics. 2018;15(1):36-59. 5. Kelly JR, Kennedy PJ, Cryan JF, et al. Breaking down the barriers: the gut microbiome, intestinal permeability and stress-related psychiatric disorders. Front Cell Neurosci. 2015;9:392. 6. Rodrigues-Amorim D, Rivera-Baltanás T, Regueiro B, et al. The role of the gut microbiota in schizophrenia: current and future perspectives. World J Biol Psychiatry. 2018;21:1-15. 7. Petra AI, Panagiotidou S, Hatziagelaki E, et al. Gut-microbiota-brain axis and its effect on neuropsychiatric disorders with suspected immune dysregulation. Clin Ther. 2015;37(5):984-995. 8. Lurie I, Yang YX, Haynes K, et al. Antibiotic exposure and the risk for depression, anxiety, or psychosis: a nested case-control study. J Clin Psychiatry. 2015;76(11):1522-1528. 9. He Y, Kosciolek T, Tang J, et al. Gut microbiome and magnetic resonance spectroscopy study of subjects at ultra-high risk for psychosis may support the membrane hypothesis. Eur Psychiatry. 2018;53:37-45. 10. Yuan X, Zhang P, Wang Y, et al. Changes in metabolism and microbiota after 24-week risperidone treatment in drug naïve, normal weight patients with first episode schizophrenia. Schizophr Res. 2018;pii: S0920-9964(18)30274-3. [Epub ahead of print]. doi: 10.1016/j.schres.2018.05.017. 11. Dickerson F, Severance E, Yolken R. The microbiome, immunity, and schizophrenia and bipolar disorder. Brain Behav Immun. 2017;62:46-52. 12. Huang R, Wang K, Hu J. Effect of probiotics on depression: a systematic review and meta-analysis of randomized controlled trials. Nutrients. 2016;8(8):pii: E483. doi: 10.3390/nu8080483. 13. Carding S, Verbeke K, Vipond DT, et al. Dysbiosis of the gut microbiota in disease. Microb Ecol Health Dis. 2015;26:26191. doi: 10.3402/mehd.v26.26191. 14. Thapar A, Cooper M, Eyre O, et al. Practitioner review: what have we learnt about the causes of ADHD? J Child Psychol Psychiatry. 2013;54(1):3-16. 15. Jiang C, Li G, Huang P, et al. The gut microbiota and Alzheimer’s disease. J Alzheimers Dis. 2017;58(1):1-15. 16. Kurokawa S, Kishimoto T, Mizuno S, et al. The effect of fecal microbiota transplantation on psychiatric symptoms among patients with irritable bowel syndrome, functional diarrhea and functional constipation: an open-label observational study. J Affect Disord. 2018;235:506-512. 17. Hillemacher T, Bachmann O, Kahl KG, et al. Alcohol, microbiome, and their effect on psychiatric disorders. Prog Neuropsychopharmacol Biol Psychiatry. 2018;85:105-115. 18. Doré J, Multon MC, Béhier JM; participants of Giens XXXII, Round Table No. 2. The human gut microbiome as source of innovation for health: which physiological and therapeutic outcomes could we expect? Therapie. 2017;72(1):21-38. 19. Vemuri RC, Gundamaraju R, Shinde T, et al. Therapeutic interventions for gut dysbiosis and related disorders in the elderly: antibiotics, probiotics or faecal microbiota transplantation? Benef Microbes. 2017;8(2):179-192. 20. Lombardi VC, De Meirleir KL, Subramanian K, et al. Nutritional modulation of the intestinal microbiota; future opportunities for the prevention and treatment of neuroimmune and neuroinflammatory disease. J Nutr Biochem. 2018;61:1-16.
Martha Boxer (not her real name) had mentally prepared herself that this could happen, but the news still hit hard. Her doctors on the leukemia service broke the facts as gently as we could: The chemotherapy she had been suffering through for the last 2 weeks hadn’t worked. The results of her latest bone marrow biopsy showed it remained packed with cancer cells.
As Martha absorbed the news quietly, her son, sitting next to her bedside with his hand on hers, spoke first. “What now?”
I looked at my attending and nodded, as we were fully ready to answer this question. From the outset, we knew that Martha’s leukemia carried a genetic mutation that unfortunately put her in a high-risk category. The chances of her cancer responding to the first round of chemotherapy were low. When this happens, what we typically do next is reinduction, we explained. It’s a different combination of chemotherapy drugs, with a somewhat different side effect profile. But it would give her the best chance of response, we believed. We could start the new chemotherapy as early as today, we said.
Martha took this in. “Okay,” she said pensively. “I’ve been thinking. And I think maybe … I won’t do chemotherapy anymore.”
Her words caught me off guard because, frankly, they seemed premature. Her leukemia had not budged with the first round of treatment. But we still had an option B, and then an option C. It was usually at a later, more dire stage – when multiple lines of treatment had not worked, and instead had only caused harm – or, when the decision was forced by the medical system’s admission that we had nothing left to offer – that I’d heard patients express similar preferences. It was then that I’d seen patients and their loved ones flip a mental switch and choose to focus the time they had left on what really mattered to them.
It didn’t feel like we were at that point.
And so, as we debriefed outside her room, my first instinct was to convince her otherwise.
However, Martha had other priorities, as I would come to learn. Above all else, she hated the hospital. She hated feeling trapped in a strange room that wasn’t hers; she hated how the chemotherapy stole her energy and made her feel too weak to even shower. She wanted to be in her own home. She wanted to eat her own food, sleep in her own bed, and be surrounded by what she recognized.
Dr. Ilana Yurkiewicz
But, she also wanted to live. Two paths lay ahead of her. It was a trade-off of more suffering with a small chance at remission, versus accepting no chance of cure but feeling well for as long as she could. She soon clarified that she wasn’t definitely against chemotherapy. She couldn’t decide. She needed more information from us to make this decision, the hardest of her life.
Over the next few days, I watched as our attending physician expertly provided just that. There were actually three options, she laid out. There was aggressive chemotherapy, entailing at least 3 more weeks in the hospital and coming with significant risk of infection, nausea, vomiting, and fatigue. The chances of inducing a remission were about one in three to one in two, and that remission would likely last between several months and 2 years before the leukemia would relapse. The second option was a chemotherapy pill she could take at home, an option with fewer side effects but no longer aimed at cure. The third option was home hospice support, focused on symptoms, without any anticancer medication.
I noticed a few things during those conversations. I noticed how my attending took a navigator role, not pushing Martha in one direction or another, but rather imparting all the relevant information to empower Martha to decide for herself. I noticed how she provided realistic estimates, not hedging away from numbers, but giving the honest, nitty-gritty facts, as best as she could predict. I noticed how she took the time and never rushed, even in spite of external pressures to discharge the patient from the hospital.
There was no right or wrong answer. I no longer felt that we had something in our grasp – a clear-cut, best decision – to persuade Martha toward. Is one in three good odds, or bad odds? Is 2 years a long period of time, or a short one? Of course, there is no actual answer to these questions; the answer is as elusive and personal as if we had asked Martha: What do you think?
What I learned from Martha is that, with a devastating diagnosis, there isn’t a right time to make this decision. There isn’t one defining moment where we flip a switch and change course. It isn’t only when we run out of treatment options that the choice to forgo it makes sense. That option is on a flexible line, different for every person and priority. As my attending later said, with Martha’s diagnosis and her values, it wouldn’t have been unreasonable to decide against chemotherapy from the start.
The language we use can sometimes mask that reality. As doctors, we may casually slip in words like “need” and “have to” in response to patients’ questions about what to do next. “You need more chemotherapy,” we might say. “We’d have to treat it.” We have “treatment,” after all, and so we go down the line of offering what’s next in the medical algorithm. That word, too, can be deceivingly tempting, enticing down a road that makes it seem like the obvious answer – or the only one. If the choices are treatment versus not, who wouldn’t want the treatment? But the details are where things get murky. What does that treatment involve? What are the chances it will work, and for how long?
Surreptitiously missing from this language is the fact that there’s a choice. There’s always a choice, and it’s on the table at any point. You can start chemotherapy without committing to stick it out until the end. You can go home, if that is what’s important to you. The best treatment option is the one the patient wants.
After 4 days, Martha decided to go home with palliative chemotherapy and a bridge to hospice. Each member of our team hugged her goodbye and wished her luck. She was nervous. But she packed her hospital room, and she left.
I recently pulled up her medical chart, bracing myself for bad news. But the interesting thing about hospice is that even though the focus is no longer on prolonging life, people sometimes live longer.
She felt well, the most recent palliative note said. She was spending her time writing, getting her finances in order, and finishing a legacy project for her grandchildren.
For Martha, it seemed to be the right choice.
Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.
Martha Boxer (not her real name) had mentally prepared herself that this could happen, but the news still hit hard. Her doctors on the leukemia service broke the facts as gently as we could: The chemotherapy she had been suffering through for the last 2 weeks hadn’t worked. The results of her latest bone marrow biopsy showed it remained packed with cancer cells.
As Martha absorbed the news quietly, her son, sitting next to her bedside with his hand on hers, spoke first. “What now?”
I looked at my attending and nodded, as we were fully ready to answer this question. From the outset, we knew that Martha’s leukemia carried a genetic mutation that unfortunately put her in a high-risk category. The chances of her cancer responding to the first round of chemotherapy were low. When this happens, what we typically do next is reinduction, we explained. It’s a different combination of chemotherapy drugs, with a somewhat different side effect profile. But it would give her the best chance of response, we believed. We could start the new chemotherapy as early as today, we said.
Martha took this in. “Okay,” she said pensively. “I’ve been thinking. And I think maybe … I won’t do chemotherapy anymore.”
Her words caught me off guard because, frankly, they seemed premature. Her leukemia had not budged with the first round of treatment. But we still had an option B, and then an option C. It was usually at a later, more dire stage – when multiple lines of treatment had not worked, and instead had only caused harm – or, when the decision was forced by the medical system’s admission that we had nothing left to offer – that I’d heard patients express similar preferences. It was then that I’d seen patients and their loved ones flip a mental switch and choose to focus the time they had left on what really mattered to them.
It didn’t feel like we were at that point.
And so, as we debriefed outside her room, my first instinct was to convince her otherwise.
However, Martha had other priorities, as I would come to learn. Above all else, she hated the hospital. She hated feeling trapped in a strange room that wasn’t hers; she hated how the chemotherapy stole her energy and made her feel too weak to even shower. She wanted to be in her own home. She wanted to eat her own food, sleep in her own bed, and be surrounded by what she recognized.
Dr. Ilana Yurkiewicz
But, she also wanted to live. Two paths lay ahead of her. It was a trade-off of more suffering with a small chance at remission, versus accepting no chance of cure but feeling well for as long as she could. She soon clarified that she wasn’t definitely against chemotherapy. She couldn’t decide. She needed more information from us to make this decision, the hardest of her life.
Over the next few days, I watched as our attending physician expertly provided just that. There were actually three options, she laid out. There was aggressive chemotherapy, entailing at least 3 more weeks in the hospital and coming with significant risk of infection, nausea, vomiting, and fatigue. The chances of inducing a remission were about one in three to one in two, and that remission would likely last between several months and 2 years before the leukemia would relapse. The second option was a chemotherapy pill she could take at home, an option with fewer side effects but no longer aimed at cure. The third option was home hospice support, focused on symptoms, without any anticancer medication.
I noticed a few things during those conversations. I noticed how my attending took a navigator role, not pushing Martha in one direction or another, but rather imparting all the relevant information to empower Martha to decide for herself. I noticed how she provided realistic estimates, not hedging away from numbers, but giving the honest, nitty-gritty facts, as best as she could predict. I noticed how she took the time and never rushed, even in spite of external pressures to discharge the patient from the hospital.
There was no right or wrong answer. I no longer felt that we had something in our grasp – a clear-cut, best decision – to persuade Martha toward. Is one in three good odds, or bad odds? Is 2 years a long period of time, or a short one? Of course, there is no actual answer to these questions; the answer is as elusive and personal as if we had asked Martha: What do you think?
What I learned from Martha is that, with a devastating diagnosis, there isn’t a right time to make this decision. There isn’t one defining moment where we flip a switch and change course. It isn’t only when we run out of treatment options that the choice to forgo it makes sense. That option is on a flexible line, different for every person and priority. As my attending later said, with Martha’s diagnosis and her values, it wouldn’t have been unreasonable to decide against chemotherapy from the start.
The language we use can sometimes mask that reality. As doctors, we may casually slip in words like “need” and “have to” in response to patients’ questions about what to do next. “You need more chemotherapy,” we might say. “We’d have to treat it.” We have “treatment,” after all, and so we go down the line of offering what’s next in the medical algorithm. That word, too, can be deceivingly tempting, enticing down a road that makes it seem like the obvious answer – or the only one. If the choices are treatment versus not, who wouldn’t want the treatment? But the details are where things get murky. What does that treatment involve? What are the chances it will work, and for how long?
Surreptitiously missing from this language is the fact that there’s a choice. There’s always a choice, and it’s on the table at any point. You can start chemotherapy without committing to stick it out until the end. You can go home, if that is what’s important to you. The best treatment option is the one the patient wants.
After 4 days, Martha decided to go home with palliative chemotherapy and a bridge to hospice. Each member of our team hugged her goodbye and wished her luck. She was nervous. But she packed her hospital room, and she left.
I recently pulled up her medical chart, bracing myself for bad news. But the interesting thing about hospice is that even though the focus is no longer on prolonging life, people sometimes live longer.
She felt well, the most recent palliative note said. She was spending her time writing, getting her finances in order, and finishing a legacy project for her grandchildren.
For Martha, it seemed to be the right choice.
Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.
Martha Boxer (not her real name) had mentally prepared herself that this could happen, but the news still hit hard. Her doctors on the leukemia service broke the facts as gently as we could: The chemotherapy she had been suffering through for the last 2 weeks hadn’t worked. The results of her latest bone marrow biopsy showed it remained packed with cancer cells.
As Martha absorbed the news quietly, her son, sitting next to her bedside with his hand on hers, spoke first. “What now?”
I looked at my attending and nodded, as we were fully ready to answer this question. From the outset, we knew that Martha’s leukemia carried a genetic mutation that unfortunately put her in a high-risk category. The chances of her cancer responding to the first round of chemotherapy were low. When this happens, what we typically do next is reinduction, we explained. It’s a different combination of chemotherapy drugs, with a somewhat different side effect profile. But it would give her the best chance of response, we believed. We could start the new chemotherapy as early as today, we said.
Martha took this in. “Okay,” she said pensively. “I’ve been thinking. And I think maybe … I won’t do chemotherapy anymore.”
Her words caught me off guard because, frankly, they seemed premature. Her leukemia had not budged with the first round of treatment. But we still had an option B, and then an option C. It was usually at a later, more dire stage – when multiple lines of treatment had not worked, and instead had only caused harm – or, when the decision was forced by the medical system’s admission that we had nothing left to offer – that I’d heard patients express similar preferences. It was then that I’d seen patients and their loved ones flip a mental switch and choose to focus the time they had left on what really mattered to them.
It didn’t feel like we were at that point.
And so, as we debriefed outside her room, my first instinct was to convince her otherwise.
However, Martha had other priorities, as I would come to learn. Above all else, she hated the hospital. She hated feeling trapped in a strange room that wasn’t hers; she hated how the chemotherapy stole her energy and made her feel too weak to even shower. She wanted to be in her own home. She wanted to eat her own food, sleep in her own bed, and be surrounded by what she recognized.
Dr. Ilana Yurkiewicz
But, she also wanted to live. Two paths lay ahead of her. It was a trade-off of more suffering with a small chance at remission, versus accepting no chance of cure but feeling well for as long as she could. She soon clarified that she wasn’t definitely against chemotherapy. She couldn’t decide. She needed more information from us to make this decision, the hardest of her life.
Over the next few days, I watched as our attending physician expertly provided just that. There were actually three options, she laid out. There was aggressive chemotherapy, entailing at least 3 more weeks in the hospital and coming with significant risk of infection, nausea, vomiting, and fatigue. The chances of inducing a remission were about one in three to one in two, and that remission would likely last between several months and 2 years before the leukemia would relapse. The second option was a chemotherapy pill she could take at home, an option with fewer side effects but no longer aimed at cure. The third option was home hospice support, focused on symptoms, without any anticancer medication.
I noticed a few things during those conversations. I noticed how my attending took a navigator role, not pushing Martha in one direction or another, but rather imparting all the relevant information to empower Martha to decide for herself. I noticed how she provided realistic estimates, not hedging away from numbers, but giving the honest, nitty-gritty facts, as best as she could predict. I noticed how she took the time and never rushed, even in spite of external pressures to discharge the patient from the hospital.
There was no right or wrong answer. I no longer felt that we had something in our grasp – a clear-cut, best decision – to persuade Martha toward. Is one in three good odds, or bad odds? Is 2 years a long period of time, or a short one? Of course, there is no actual answer to these questions; the answer is as elusive and personal as if we had asked Martha: What do you think?
What I learned from Martha is that, with a devastating diagnosis, there isn’t a right time to make this decision. There isn’t one defining moment where we flip a switch and change course. It isn’t only when we run out of treatment options that the choice to forgo it makes sense. That option is on a flexible line, different for every person and priority. As my attending later said, with Martha’s diagnosis and her values, it wouldn’t have been unreasonable to decide against chemotherapy from the start.
The language we use can sometimes mask that reality. As doctors, we may casually slip in words like “need” and “have to” in response to patients’ questions about what to do next. “You need more chemotherapy,” we might say. “We’d have to treat it.” We have “treatment,” after all, and so we go down the line of offering what’s next in the medical algorithm. That word, too, can be deceivingly tempting, enticing down a road that makes it seem like the obvious answer – or the only one. If the choices are treatment versus not, who wouldn’t want the treatment? But the details are where things get murky. What does that treatment involve? What are the chances it will work, and for how long?
Surreptitiously missing from this language is the fact that there’s a choice. There’s always a choice, and it’s on the table at any point. You can start chemotherapy without committing to stick it out until the end. You can go home, if that is what’s important to you. The best treatment option is the one the patient wants.
After 4 days, Martha decided to go home with palliative chemotherapy and a bridge to hospice. Each member of our team hugged her goodbye and wished her luck. She was nervous. But she packed her hospital room, and she left.
I recently pulled up her medical chart, bracing myself for bad news. But the interesting thing about hospice is that even though the focus is no longer on prolonging life, people sometimes live longer.
She felt well, the most recent palliative note said. She was spending her time writing, getting her finances in order, and finishing a legacy project for her grandchildren.
For Martha, it seemed to be the right choice.
Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.
I just finished reading Dr. Nasrallah’s editorial “The DNA of psychiatric practice: A covenant with our patients” (From the Editor, Current Psychiatry. May 2018, p. 20, 22). It offered very good messages. I can add a few more: “Make a commitment to life-long professional education. Understand how to critique research findings and their clinical applicability. Distinguish fad from science.”
David W. Goodman, MD, FAPA Assistant Professor Department of Psychiatry and Behavioral Sciences Johns Hopkins School of Medicine Baltimore, Maryland
Unfortunately, there is no way a physician who uses an electronic medical record can “Maintain total and unimpeachable confidentiality” as the “The medical record is a clinical, billing, legal, and research document.” Since 2003, patients no longer need to give consent for their medical records to be seen by the many staff members who work in treatment, payment, and health care operations, as long as these individuals follow the Health Insurance Portability and Accountability Act of 1996 (HIPAA). Even de-identified data is no longer safe because re-identification is still possible with all the databases available for cross-referencing (ie, Facebook and hospitals as one instance).
So, when a patient finally tells you about a history of sexual abuse, do you make it clear to him or her that although this information is no longer private, it can be expected to be kept confidential by all the business associates, covered entities, government agencies, etc., who see their records?
Maybe there also would be fewer physician suicides if they could be assured of receiving truly private, off-the-grid psychiatric treatment.
Susan Israel, MD Private psychiatric practice (retired) Woodbridge, Connecticut
I just read your excellent and exhaustive May editorial, which offered advice for new psychiatrists. I was surprised to see that nowhere on the list was “Please remember to practice what you preach and be vigilant about self-care. We have become increasingly aware of the high rates of burnout among physicians. Know your own limitations so that you can appreciate the work that you do.”
Hal D. Cash, MD Private psychiatric practice (retired) Mica Collaborative Wellesley, Massachusetts
Continue to: Dr. Nasrallah's editorial should have...
Dr. Nasrallah’s editorial should have listed something about the terms of payment for the psychiatrist who “provides” his or her clinical services to patients. This is an ethical issue. As you know, usually a corporation, rather than a patient, pays the psychiatrist. This payment may come from a health insurance company, government program, or (increasingly) a large clinic. When an organization pays the psychiatrist,it calls the tune for both the doctor’s employment and the patient’s access to quality care. Contracts between the hiring organization and psychiatrists are crucial, and therefore, most young doctors must join a hiring organization for financial reasons after completing their psychiatric residency. The young psychiatrists with whom I speak tell me they have no alternative but to be a “corporate dependent” in the world of 2018 psychiatric practice. They are aware of your (and my) noble principles, which should govern their relationships with patients. But the boss often does not agree with such principles.
In my book Passion for Patients1 and as President of the 501(c)3 Minnesota Physician-Patient Alliance think tank (www.physician-patient.org), I argue for empowering patients with the means to direct payments to their physicians. Allowing patients this option is especially important for forming and maintaining strong relationship-based psychiatric and other medical treatments. In 1996, I was fed up with being a psychiatric medical director for 5 years at a large Minnesota Preferred Provider Organization. For me, the saving grace was being able to have an independent, private psychiatric practice. Most of my patients agreed.Therefore, I suggest another principle: “Build and maintain an independent psychiatric practice as an escape option no matter what you do should you decide the ethical practice of psychiatry is not possible if you are employed by a given organization.”
Lee Beecher, MD Member Editorial Advisory Board Clinical Psychiatry News Adjunct Professor of Psychiatry University of Minnesota Minneapolis, Minnesota
Reference
1. Beecher L, Racer D. Passion for patients. St. Paul, MN: Alethos Press; 2017.
I agree with Dr. Nasrallah’s guiding principles of psychiatry, which he proposes to govern the relationships of psychiatrists with their patients. However, there is one glaring omission. The first principle should be “to appropriately diagnose the patient’s condition,” which may or may not be based in psychiatry. Misdiagnoses and inappropriate pharmacologic therapy have ruined the lives of some very good friends of mine, and the need to first do no harm by misdiagnosing the patient, especially in psychiatric emergency rooms and on inpatient units, cannot be overemphasized.
These situations may not rear their head in the everyday practice of psychiatry. However, medical malpractice, especially in the field of psychiatry, is a constant caution that all new physicians need to watch for.
I would like to thank Dr. Nasrallah for his efforts to strengthen the patient–psychiatrist contract.
Rama Kasturi, PhD Associate Professor (retired) Department of Pharmacology and Cell Biophysics Director (1999 to 2013) Medical Pharmacology Tutorial Program University of Cincinnati, College of Medicine Cincinnati, Ohio
Continue to: Dr. Nasrallah responds
Dr. Nasrallah responds
I thank my 5 colleagues for their perspectives on my editorial. You all made cogent points.
I agree with Dr. Israel that our patients’ records are now accessible by many entities due to the drastic changes in our health care delivery system. However, while I regard the basic psychiatric signs and symptoms as medical data, like heart disease or cancer, there are personal details that emerge during psychotherapy that should remain confidential and not be included in the written record, and thus are not accessible to billers, health insurance companies, or malpractice lawyers. As for physicians who consider suicide because of fear of the consequences of receiving psychiatric treatment that becomes a matter of record, that is a matter of the unfortunate stigma and ignorance about mental illness and how treatable it can be.
Regarding Dr. Cash’s comments, I agree that psychiatrists should be (and are almost always are) introspective about their vulnerabilities and limitations, and should act accordingly, which includes taking care of their needs to stay healthy and avoid burnout.
As Dr. Beecher pointed out, the employment model for psychiatrists does have many implications and constraints for patient care. I concur that having a small direct-care practice, sometimes called a“cash practice,” provides patients who can afford it the complete privacy they desire, with no one having access to their medical records except for their psychiatrist. Your book is a useful resource in that regard.
Dr. Kasturi is right about the importance of arriving at an accurate diagnosis before embarking on treatment; otherwise, patients will suffer from “therapeutic misadventures.” I have observed this being experienced by some of the patients referred to me because of “treatment resistance.”
Thanks again to my colleagues for their comments and suggestions to the newly minted psychiatrists for whom my editorial was intended.
Henry A. Nasrallah, MD The Sydney W. Souers Endowed ChairProfessor and Chairman Department of Psychiatry and Behavioral Neuroscience Saint Louis University School of Medicine St. Louis, Missouri
I just finished reading Dr. Nasrallah’s editorial “The DNA of psychiatric practice: A covenant with our patients” (From the Editor, Current Psychiatry. May 2018, p. 20, 22). It offered very good messages. I can add a few more: “Make a commitment to life-long professional education. Understand how to critique research findings and their clinical applicability. Distinguish fad from science.”
David W. Goodman, MD, FAPA Assistant Professor Department of Psychiatry and Behavioral Sciences Johns Hopkins School of Medicine Baltimore, Maryland
Unfortunately, there is no way a physician who uses an electronic medical record can “Maintain total and unimpeachable confidentiality” as the “The medical record is a clinical, billing, legal, and research document.” Since 2003, patients no longer need to give consent for their medical records to be seen by the many staff members who work in treatment, payment, and health care operations, as long as these individuals follow the Health Insurance Portability and Accountability Act of 1996 (HIPAA). Even de-identified data is no longer safe because re-identification is still possible with all the databases available for cross-referencing (ie, Facebook and hospitals as one instance).
So, when a patient finally tells you about a history of sexual abuse, do you make it clear to him or her that although this information is no longer private, it can be expected to be kept confidential by all the business associates, covered entities, government agencies, etc., who see their records?
Maybe there also would be fewer physician suicides if they could be assured of receiving truly private, off-the-grid psychiatric treatment.
Susan Israel, MD Private psychiatric practice (retired) Woodbridge, Connecticut
I just read your excellent and exhaustive May editorial, which offered advice for new psychiatrists. I was surprised to see that nowhere on the list was “Please remember to practice what you preach and be vigilant about self-care. We have become increasingly aware of the high rates of burnout among physicians. Know your own limitations so that you can appreciate the work that you do.”
Hal D. Cash, MD Private psychiatric practice (retired) Mica Collaborative Wellesley, Massachusetts
Continue to: Dr. Nasrallah's editorial should have...
Dr. Nasrallah’s editorial should have listed something about the terms of payment for the psychiatrist who “provides” his or her clinical services to patients. This is an ethical issue. As you know, usually a corporation, rather than a patient, pays the psychiatrist. This payment may come from a health insurance company, government program, or (increasingly) a large clinic. When an organization pays the psychiatrist,it calls the tune for both the doctor’s employment and the patient’s access to quality care. Contracts between the hiring organization and psychiatrists are crucial, and therefore, most young doctors must join a hiring organization for financial reasons after completing their psychiatric residency. The young psychiatrists with whom I speak tell me they have no alternative but to be a “corporate dependent” in the world of 2018 psychiatric practice. They are aware of your (and my) noble principles, which should govern their relationships with patients. But the boss often does not agree with such principles.
In my book Passion for Patients1 and as President of the 501(c)3 Minnesota Physician-Patient Alliance think tank (www.physician-patient.org), I argue for empowering patients with the means to direct payments to their physicians. Allowing patients this option is especially important for forming and maintaining strong relationship-based psychiatric and other medical treatments. In 1996, I was fed up with being a psychiatric medical director for 5 years at a large Minnesota Preferred Provider Organization. For me, the saving grace was being able to have an independent, private psychiatric practice. Most of my patients agreed.Therefore, I suggest another principle: “Build and maintain an independent psychiatric practice as an escape option no matter what you do should you decide the ethical practice of psychiatry is not possible if you are employed by a given organization.”
Lee Beecher, MD Member Editorial Advisory Board Clinical Psychiatry News Adjunct Professor of Psychiatry University of Minnesota Minneapolis, Minnesota
Reference
1. Beecher L, Racer D. Passion for patients. St. Paul, MN: Alethos Press; 2017.
I agree with Dr. Nasrallah’s guiding principles of psychiatry, which he proposes to govern the relationships of psychiatrists with their patients. However, there is one glaring omission. The first principle should be “to appropriately diagnose the patient’s condition,” which may or may not be based in psychiatry. Misdiagnoses and inappropriate pharmacologic therapy have ruined the lives of some very good friends of mine, and the need to first do no harm by misdiagnosing the patient, especially in psychiatric emergency rooms and on inpatient units, cannot be overemphasized.
These situations may not rear their head in the everyday practice of psychiatry. However, medical malpractice, especially in the field of psychiatry, is a constant caution that all new physicians need to watch for.
I would like to thank Dr. Nasrallah for his efforts to strengthen the patient–psychiatrist contract.
Rama Kasturi, PhD Associate Professor (retired) Department of Pharmacology and Cell Biophysics Director (1999 to 2013) Medical Pharmacology Tutorial Program University of Cincinnati, College of Medicine Cincinnati, Ohio
Continue to: Dr. Nasrallah responds
Dr. Nasrallah responds
I thank my 5 colleagues for their perspectives on my editorial. You all made cogent points.
I agree with Dr. Israel that our patients’ records are now accessible by many entities due to the drastic changes in our health care delivery system. However, while I regard the basic psychiatric signs and symptoms as medical data, like heart disease or cancer, there are personal details that emerge during psychotherapy that should remain confidential and not be included in the written record, and thus are not accessible to billers, health insurance companies, or malpractice lawyers. As for physicians who consider suicide because of fear of the consequences of receiving psychiatric treatment that becomes a matter of record, that is a matter of the unfortunate stigma and ignorance about mental illness and how treatable it can be.
Regarding Dr. Cash’s comments, I agree that psychiatrists should be (and are almost always are) introspective about their vulnerabilities and limitations, and should act accordingly, which includes taking care of their needs to stay healthy and avoid burnout.
As Dr. Beecher pointed out, the employment model for psychiatrists does have many implications and constraints for patient care. I concur that having a small direct-care practice, sometimes called a“cash practice,” provides patients who can afford it the complete privacy they desire, with no one having access to their medical records except for their psychiatrist. Your book is a useful resource in that regard.
Dr. Kasturi is right about the importance of arriving at an accurate diagnosis before embarking on treatment; otherwise, patients will suffer from “therapeutic misadventures.” I have observed this being experienced by some of the patients referred to me because of “treatment resistance.”
Thanks again to my colleagues for their comments and suggestions to the newly minted psychiatrists for whom my editorial was intended.
Henry A. Nasrallah, MD The Sydney W. Souers Endowed ChairProfessor and Chairman Department of Psychiatry and Behavioral Neuroscience Saint Louis University School of Medicine St. Louis, Missouri
I just finished reading Dr. Nasrallah’s editorial “The DNA of psychiatric practice: A covenant with our patients” (From the Editor, Current Psychiatry. May 2018, p. 20, 22). It offered very good messages. I can add a few more: “Make a commitment to life-long professional education. Understand how to critique research findings and their clinical applicability. Distinguish fad from science.”
David W. Goodman, MD, FAPA Assistant Professor Department of Psychiatry and Behavioral Sciences Johns Hopkins School of Medicine Baltimore, Maryland
Unfortunately, there is no way a physician who uses an electronic medical record can “Maintain total and unimpeachable confidentiality” as the “The medical record is a clinical, billing, legal, and research document.” Since 2003, patients no longer need to give consent for their medical records to be seen by the many staff members who work in treatment, payment, and health care operations, as long as these individuals follow the Health Insurance Portability and Accountability Act of 1996 (HIPAA). Even de-identified data is no longer safe because re-identification is still possible with all the databases available for cross-referencing (ie, Facebook and hospitals as one instance).
So, when a patient finally tells you about a history of sexual abuse, do you make it clear to him or her that although this information is no longer private, it can be expected to be kept confidential by all the business associates, covered entities, government agencies, etc., who see their records?
Maybe there also would be fewer physician suicides if they could be assured of receiving truly private, off-the-grid psychiatric treatment.
Susan Israel, MD Private psychiatric practice (retired) Woodbridge, Connecticut
I just read your excellent and exhaustive May editorial, which offered advice for new psychiatrists. I was surprised to see that nowhere on the list was “Please remember to practice what you preach and be vigilant about self-care. We have become increasingly aware of the high rates of burnout among physicians. Know your own limitations so that you can appreciate the work that you do.”
Hal D. Cash, MD Private psychiatric practice (retired) Mica Collaborative Wellesley, Massachusetts
Continue to: Dr. Nasrallah's editorial should have...
Dr. Nasrallah’s editorial should have listed something about the terms of payment for the psychiatrist who “provides” his or her clinical services to patients. This is an ethical issue. As you know, usually a corporation, rather than a patient, pays the psychiatrist. This payment may come from a health insurance company, government program, or (increasingly) a large clinic. When an organization pays the psychiatrist,it calls the tune for both the doctor’s employment and the patient’s access to quality care. Contracts between the hiring organization and psychiatrists are crucial, and therefore, most young doctors must join a hiring organization for financial reasons after completing their psychiatric residency. The young psychiatrists with whom I speak tell me they have no alternative but to be a “corporate dependent” in the world of 2018 psychiatric practice. They are aware of your (and my) noble principles, which should govern their relationships with patients. But the boss often does not agree with such principles.
In my book Passion for Patients1 and as President of the 501(c)3 Minnesota Physician-Patient Alliance think tank (www.physician-patient.org), I argue for empowering patients with the means to direct payments to their physicians. Allowing patients this option is especially important for forming and maintaining strong relationship-based psychiatric and other medical treatments. In 1996, I was fed up with being a psychiatric medical director for 5 years at a large Minnesota Preferred Provider Organization. For me, the saving grace was being able to have an independent, private psychiatric practice. Most of my patients agreed.Therefore, I suggest another principle: “Build and maintain an independent psychiatric practice as an escape option no matter what you do should you decide the ethical practice of psychiatry is not possible if you are employed by a given organization.”
Lee Beecher, MD Member Editorial Advisory Board Clinical Psychiatry News Adjunct Professor of Psychiatry University of Minnesota Minneapolis, Minnesota
Reference
1. Beecher L, Racer D. Passion for patients. St. Paul, MN: Alethos Press; 2017.
I agree with Dr. Nasrallah’s guiding principles of psychiatry, which he proposes to govern the relationships of psychiatrists with their patients. However, there is one glaring omission. The first principle should be “to appropriately diagnose the patient’s condition,” which may or may not be based in psychiatry. Misdiagnoses and inappropriate pharmacologic therapy have ruined the lives of some very good friends of mine, and the need to first do no harm by misdiagnosing the patient, especially in psychiatric emergency rooms and on inpatient units, cannot be overemphasized.
These situations may not rear their head in the everyday practice of psychiatry. However, medical malpractice, especially in the field of psychiatry, is a constant caution that all new physicians need to watch for.
I would like to thank Dr. Nasrallah for his efforts to strengthen the patient–psychiatrist contract.
Rama Kasturi, PhD Associate Professor (retired) Department of Pharmacology and Cell Biophysics Director (1999 to 2013) Medical Pharmacology Tutorial Program University of Cincinnati, College of Medicine Cincinnati, Ohio
Continue to: Dr. Nasrallah responds
Dr. Nasrallah responds
I thank my 5 colleagues for their perspectives on my editorial. You all made cogent points.
I agree with Dr. Israel that our patients’ records are now accessible by many entities due to the drastic changes in our health care delivery system. However, while I regard the basic psychiatric signs and symptoms as medical data, like heart disease or cancer, there are personal details that emerge during psychotherapy that should remain confidential and not be included in the written record, and thus are not accessible to billers, health insurance companies, or malpractice lawyers. As for physicians who consider suicide because of fear of the consequences of receiving psychiatric treatment that becomes a matter of record, that is a matter of the unfortunate stigma and ignorance about mental illness and how treatable it can be.
Regarding Dr. Cash’s comments, I agree that psychiatrists should be (and are almost always are) introspective about their vulnerabilities and limitations, and should act accordingly, which includes taking care of their needs to stay healthy and avoid burnout.
As Dr. Beecher pointed out, the employment model for psychiatrists does have many implications and constraints for patient care. I concur that having a small direct-care practice, sometimes called a“cash practice,” provides patients who can afford it the complete privacy they desire, with no one having access to their medical records except for their psychiatrist. Your book is a useful resource in that regard.
Dr. Kasturi is right about the importance of arriving at an accurate diagnosis before embarking on treatment; otherwise, patients will suffer from “therapeutic misadventures.” I have observed this being experienced by some of the patients referred to me because of “treatment resistance.”
Thanks again to my colleagues for their comments and suggestions to the newly minted psychiatrists for whom my editorial was intended.
Henry A. Nasrallah, MD The Sydney W. Souers Endowed ChairProfessor and Chairman Department of Psychiatry and Behavioral Neuroscience Saint Louis University School of Medicine St. Louis, Missouri
Hand, foot, and mouth disease (HFMD) has become a global challenge since its first description in 1957 in New Zealand and Canada. Clinicians readily recognize the characteristic syndrome in young children: fever associated with a papulovesicular rash affecting the palms or soles, or both, usually in spring, summer, or fall. In most cases the disease is self-limited, and brief. However, aseptic meningitis, brainstem encephalitis, acute flaccid paralysis or autonomic nervous system deregulation or cardiorespiratory failure may complicate the clinical course.
Copyright MidgleyDJ/Wikimedia Commons
HFMD is caused by enterovirus A (formerly called human enterovirus A) which consists of 25 serotypes including multiple coxsackie A viruses, multiple enteroviruses, simian enteroviruses, and baboon enterovirus A13. The clinical spectrum spans from herpangina, characterized by fever and painful mouth ulcers most prominent in the posterior oral cavity (uvula, tonsils, soft plates, and anterior pharyngeal folds), to HFMD with papulovesicular rash on palms and soles with or without mouth ulcers/vesicles.1 In atypical cases, the rash may be maculopapular and may include the buttocks, knees or elbows.
In the United States, the predominant cause is coxsackie A16. However, coxsackie A6 appears to be emerging; often more than one HFMD causing virus is circulating concurrently and clinically indistinguishable. Globally, especially, in Asia, enterovirus 1 is a major cause of HFMD and more often associated with prominent central nervous system involvement. Disease can be sporadic or epidemic. An outbreak is usually defined as two or more cases within a defined geographic area; global epidemics as large as 1.5 million cases (Taiwan, 1998) have been reported, and outbreaks in China involving tens of thousands with multiple deaths have been reported.
In 2015, an outbreak of HFMD occurred during basic military training at Lackland Air Force Base, Bexar County, Texas, due to coxsackie A6.2 The illness was characterized by prodromal symptoms of fever and malaise followed by erosive stomatitis and a rash that began on the palms and soles. The rate of infection among trainees was 4.7% (50 of 1,054 persons).
The differential diagnosis includes aphthous ulcers and herpetic gingivostomatitis.3 Aphthous ulcers are seen more commonly in older children and adolescents, are often recurrent, are not seasonal, and are not associated with rash. Herpes simplex virus gingivostomatitis usually has a febrile prodrome, perioral lesions are frequent in addition to gum and tongue involvement, and gingival bleeding is common. HFMD usually has an incubation period of 3-5 days and fever, malaise, and myalgia prodrome followed by onset of oral and dermatologic manifestations in sequence. The skin rash has features that may overlap with varicella, erythema multiforme (EM) or drug eruption. Varicella usually involves the face before spreading to the extremities, and the lesions are characterized by umbilication and subsequent crusting. EM is characterized by target lesions and drug eruptions are morbilliform or maculopapular. The majority of cases of HFMD are diagnosed clinically; polymerase chain reaction testing is available and best performed on throat or vesicle specimens. Serologic testing for A16 and enterovirus 71 (IgM) is available. Infected patients shed virus for 2-4 weeks and virus is stable in the environment resulting in fecal-oral or oral-oral transmission.
Atypical features of HFMD include occurrence in the winter (outbreak in Alabama in 2011/2012) or an atypical distribution of rash involving the antecubital and popliteal fossae distribution of rash, or “eczema coxsackium” – the accentuation of rash in areas previously affected by atopic dermatitis. Additional features may include nail dystrophies that manifest as Beau lines (deep grooved lines that run from side to side on the fingernail or the toenail) and nail shedding.
A spectrum of neurologic complications has been observed, more frequently with EV71 and more frequently in Asia. The spectrum includes aseptic meningitis and brainstem encephalitis. Progressive cardiopulmonary failure also can be observed in severe cases. The hallmark of severe disease is often presentation with high fever, sweating, mottled skin, and tachycardia. Early signs of CNS involvement include myoclonic jerks, ataxia, and “wandering eyes.”3 Elevated white blood count and/or hyperglycemia may distinguish children with severe disease from benign disease. Anecdotal reports of response to treatment with high-dose methylprednisolone and intravenous immune globulin suggest that the neurologic disease may be an autoimmune phenomenon.
Dr. Stephen I. Pelton
The clinician’s primary role is to accurately diagnose HFMD, provide supportive care for fever and dehydration, and identify those with early signs or laboratory features heralding a more severe course of disease.3 The Centers for Disease Control and Prevention recommends frequent hand washing after toileting and changing diapers, disinfecting surfaces such as toys, avoiding close contact with infected individuals or sharing of personal items for all affected patients. No antiviral treatment is available although improvement following early treatment with acyclovir has been reported anecdotally. Intravenous immunoglobulin has been used in severe cases in Asia with retrospective data analysis suggesting a potential for improvement when administered prior to cardiopulmonary arrest.1
Dr. Pelton is professor of pediatrics and epidemiology at Boston University. Dr. Pelton said he had no relevant financial disclosures. Email him at [email protected].
Hand, foot, and mouth disease (HFMD) has become a global challenge since its first description in 1957 in New Zealand and Canada. Clinicians readily recognize the characteristic syndrome in young children: fever associated with a papulovesicular rash affecting the palms or soles, or both, usually in spring, summer, or fall. In most cases the disease is self-limited, and brief. However, aseptic meningitis, brainstem encephalitis, acute flaccid paralysis or autonomic nervous system deregulation or cardiorespiratory failure may complicate the clinical course.
Copyright MidgleyDJ/Wikimedia Commons
HFMD is caused by enterovirus A (formerly called human enterovirus A) which consists of 25 serotypes including multiple coxsackie A viruses, multiple enteroviruses, simian enteroviruses, and baboon enterovirus A13. The clinical spectrum spans from herpangina, characterized by fever and painful mouth ulcers most prominent in the posterior oral cavity (uvula, tonsils, soft plates, and anterior pharyngeal folds), to HFMD with papulovesicular rash on palms and soles with or without mouth ulcers/vesicles.1 In atypical cases, the rash may be maculopapular and may include the buttocks, knees or elbows.
In the United States, the predominant cause is coxsackie A16. However, coxsackie A6 appears to be emerging; often more than one HFMD causing virus is circulating concurrently and clinically indistinguishable. Globally, especially, in Asia, enterovirus 1 is a major cause of HFMD and more often associated with prominent central nervous system involvement. Disease can be sporadic or epidemic. An outbreak is usually defined as two or more cases within a defined geographic area; global epidemics as large as 1.5 million cases (Taiwan, 1998) have been reported, and outbreaks in China involving tens of thousands with multiple deaths have been reported.
In 2015, an outbreak of HFMD occurred during basic military training at Lackland Air Force Base, Bexar County, Texas, due to coxsackie A6.2 The illness was characterized by prodromal symptoms of fever and malaise followed by erosive stomatitis and a rash that began on the palms and soles. The rate of infection among trainees was 4.7% (50 of 1,054 persons).
The differential diagnosis includes aphthous ulcers and herpetic gingivostomatitis.3 Aphthous ulcers are seen more commonly in older children and adolescents, are often recurrent, are not seasonal, and are not associated with rash. Herpes simplex virus gingivostomatitis usually has a febrile prodrome, perioral lesions are frequent in addition to gum and tongue involvement, and gingival bleeding is common. HFMD usually has an incubation period of 3-5 days and fever, malaise, and myalgia prodrome followed by onset of oral and dermatologic manifestations in sequence. The skin rash has features that may overlap with varicella, erythema multiforme (EM) or drug eruption. Varicella usually involves the face before spreading to the extremities, and the lesions are characterized by umbilication and subsequent crusting. EM is characterized by target lesions and drug eruptions are morbilliform or maculopapular. The majority of cases of HFMD are diagnosed clinically; polymerase chain reaction testing is available and best performed on throat or vesicle specimens. Serologic testing for A16 and enterovirus 71 (IgM) is available. Infected patients shed virus for 2-4 weeks and virus is stable in the environment resulting in fecal-oral or oral-oral transmission.
Atypical features of HFMD include occurrence in the winter (outbreak in Alabama in 2011/2012) or an atypical distribution of rash involving the antecubital and popliteal fossae distribution of rash, or “eczema coxsackium” – the accentuation of rash in areas previously affected by atopic dermatitis. Additional features may include nail dystrophies that manifest as Beau lines (deep grooved lines that run from side to side on the fingernail or the toenail) and nail shedding.
A spectrum of neurologic complications has been observed, more frequently with EV71 and more frequently in Asia. The spectrum includes aseptic meningitis and brainstem encephalitis. Progressive cardiopulmonary failure also can be observed in severe cases. The hallmark of severe disease is often presentation with high fever, sweating, mottled skin, and tachycardia. Early signs of CNS involvement include myoclonic jerks, ataxia, and “wandering eyes.”3 Elevated white blood count and/or hyperglycemia may distinguish children with severe disease from benign disease. Anecdotal reports of response to treatment with high-dose methylprednisolone and intravenous immune globulin suggest that the neurologic disease may be an autoimmune phenomenon.
Dr. Stephen I. Pelton
The clinician’s primary role is to accurately diagnose HFMD, provide supportive care for fever and dehydration, and identify those with early signs or laboratory features heralding a more severe course of disease.3 The Centers for Disease Control and Prevention recommends frequent hand washing after toileting and changing diapers, disinfecting surfaces such as toys, avoiding close contact with infected individuals or sharing of personal items for all affected patients. No antiviral treatment is available although improvement following early treatment with acyclovir has been reported anecdotally. Intravenous immunoglobulin has been used in severe cases in Asia with retrospective data analysis suggesting a potential for improvement when administered prior to cardiopulmonary arrest.1
Dr. Pelton is professor of pediatrics and epidemiology at Boston University. Dr. Pelton said he had no relevant financial disclosures. Email him at [email protected].
Hand, foot, and mouth disease (HFMD) has become a global challenge since its first description in 1957 in New Zealand and Canada. Clinicians readily recognize the characteristic syndrome in young children: fever associated with a papulovesicular rash affecting the palms or soles, or both, usually in spring, summer, or fall. In most cases the disease is self-limited, and brief. However, aseptic meningitis, brainstem encephalitis, acute flaccid paralysis or autonomic nervous system deregulation or cardiorespiratory failure may complicate the clinical course.
Copyright MidgleyDJ/Wikimedia Commons
HFMD is caused by enterovirus A (formerly called human enterovirus A) which consists of 25 serotypes including multiple coxsackie A viruses, multiple enteroviruses, simian enteroviruses, and baboon enterovirus A13. The clinical spectrum spans from herpangina, characterized by fever and painful mouth ulcers most prominent in the posterior oral cavity (uvula, tonsils, soft plates, and anterior pharyngeal folds), to HFMD with papulovesicular rash on palms and soles with or without mouth ulcers/vesicles.1 In atypical cases, the rash may be maculopapular and may include the buttocks, knees or elbows.
In the United States, the predominant cause is coxsackie A16. However, coxsackie A6 appears to be emerging; often more than one HFMD causing virus is circulating concurrently and clinically indistinguishable. Globally, especially, in Asia, enterovirus 1 is a major cause of HFMD and more often associated with prominent central nervous system involvement. Disease can be sporadic or epidemic. An outbreak is usually defined as two or more cases within a defined geographic area; global epidemics as large as 1.5 million cases (Taiwan, 1998) have been reported, and outbreaks in China involving tens of thousands with multiple deaths have been reported.
In 2015, an outbreak of HFMD occurred during basic military training at Lackland Air Force Base, Bexar County, Texas, due to coxsackie A6.2 The illness was characterized by prodromal symptoms of fever and malaise followed by erosive stomatitis and a rash that began on the palms and soles. The rate of infection among trainees was 4.7% (50 of 1,054 persons).
The differential diagnosis includes aphthous ulcers and herpetic gingivostomatitis.3 Aphthous ulcers are seen more commonly in older children and adolescents, are often recurrent, are not seasonal, and are not associated with rash. Herpes simplex virus gingivostomatitis usually has a febrile prodrome, perioral lesions are frequent in addition to gum and tongue involvement, and gingival bleeding is common. HFMD usually has an incubation period of 3-5 days and fever, malaise, and myalgia prodrome followed by onset of oral and dermatologic manifestations in sequence. The skin rash has features that may overlap with varicella, erythema multiforme (EM) or drug eruption. Varicella usually involves the face before spreading to the extremities, and the lesions are characterized by umbilication and subsequent crusting. EM is characterized by target lesions and drug eruptions are morbilliform or maculopapular. The majority of cases of HFMD are diagnosed clinically; polymerase chain reaction testing is available and best performed on throat or vesicle specimens. Serologic testing for A16 and enterovirus 71 (IgM) is available. Infected patients shed virus for 2-4 weeks and virus is stable in the environment resulting in fecal-oral or oral-oral transmission.
Atypical features of HFMD include occurrence in the winter (outbreak in Alabama in 2011/2012) or an atypical distribution of rash involving the antecubital and popliteal fossae distribution of rash, or “eczema coxsackium” – the accentuation of rash in areas previously affected by atopic dermatitis. Additional features may include nail dystrophies that manifest as Beau lines (deep grooved lines that run from side to side on the fingernail or the toenail) and nail shedding.
A spectrum of neurologic complications has been observed, more frequently with EV71 and more frequently in Asia. The spectrum includes aseptic meningitis and brainstem encephalitis. Progressive cardiopulmonary failure also can be observed in severe cases. The hallmark of severe disease is often presentation with high fever, sweating, mottled skin, and tachycardia. Early signs of CNS involvement include myoclonic jerks, ataxia, and “wandering eyes.”3 Elevated white blood count and/or hyperglycemia may distinguish children with severe disease from benign disease. Anecdotal reports of response to treatment with high-dose methylprednisolone and intravenous immune globulin suggest that the neurologic disease may be an autoimmune phenomenon.
Dr. Stephen I. Pelton
The clinician’s primary role is to accurately diagnose HFMD, provide supportive care for fever and dehydration, and identify those with early signs or laboratory features heralding a more severe course of disease.3 The Centers for Disease Control and Prevention recommends frequent hand washing after toileting and changing diapers, disinfecting surfaces such as toys, avoiding close contact with infected individuals or sharing of personal items for all affected patients. No antiviral treatment is available although improvement following early treatment with acyclovir has been reported anecdotally. Intravenous immunoglobulin has been used in severe cases in Asia with retrospective data analysis suggesting a potential for improvement when administered prior to cardiopulmonary arrest.1
Dr. Pelton is professor of pediatrics and epidemiology at Boston University. Dr. Pelton said he had no relevant financial disclosures. Email him at [email protected].
On Aug.16, the New York University School of Medicine announced it was offering full-tuition scholarships to all current and future students in its MD Program, regardless of need or merit – and that this policy also would apply to all matriculating students for the remainder of their medical school education at NYU.
Dr. Carol A. Bernstein
This bold initiative, they stated, was being instituted to simultaneously address the rising costs of medical education while still attracting the best and brightest to careers in medicine. In doing so, NYU School of Medicine (at which I hold a faculty appointment) became the first Top 10–ranked medical school in the nation to do so.
The symbolism of this announcement was noticeable: It was made at the medical school’s annual white coat ceremony, when each new student is presented with a white lab coat to mark the beginning of their medical education and training.
I count myself among many medical professionals and, indeed, others outside of medicine who have long advocated for free tuition for medical education, at the very least for those who have little or no means to pay. This particularly painful burden of debt often serves as a deterrent to many individuals who are considering a career in medicine or medical research.
According to the Association of American Medical Colleges, 75% of all U.S. doctors graduated with some degree of debt in 2017. For many, the total is staggering: The median current debt for a graduating medical student is $202,000, with debt for those pursuing private medical school education rising as high as $300,000.
What might develop as a result of NYU’s decision and that of several other schools who have adopted debt-reduction policies?
First, that these programs might have a ripple effect at other medical schools, and create a movement for more students to earn a medical degree without incurring a crushing financial burden. Some other schools, like Columbia University, already have taken steps, such as replacing all student loans with scholarships creating a “debt-free” medical school. It would, indeed, be a powerful message if other schools developed similar creative solutions to this problem.
Second, there is hope that debt relief will encourage more medical school graduates to pursue careers in such specialties as family medicine, psychiatry, pediatrics, and geriatrics – because they will not have the additional financial pressure to pursue careers in more lucrative specialties in order to pay off debt. While many medical school graduates point to other issues like complex reimbursement as a greater deterrent to a specific specialty choice, I certainly hope that debt relief will have a positive effect in shifting the subspecialty paradigm.
Third, these actions might incentivize the federal government to establish an AmeriCorps-type program, in which the cost of a medical education is covered in return for a commitment to practice medicine for a period of time in underserved areas of the country. Such an approach also might motivate more medical school graduates to pursue careers in primary care specialties and help address some of the ongoing concerns related to the uneven distribution of physicians in the United States.
Another issue that often comes up is the impact of debt burden on “burnout” among medical students. This is a complex subject – and one that actually affects physicians beyond medical school and into residency training and medical practice.
There is no doubt that debt weighs heavily on the minds of medical students – and many enter medical school having sustained significant debt already from previous education in colleges and universities. However, the causes and influences on burnout in training are multifactorial. Earlier in medical school, the impact of debt obligation may be less apparent because of the other challenges students face when beginning medical school.
However, once trainees begin residency and fellowship training – and especially during early career years when many are beginning to have families – concerns about increasing financial strain become even more prominent. For many young physicians, already stressed by other extenuating factors, it would be a tremendous relief not to have that debt pursuing them.
As someone who teaches and mentors medical students and residents, I firmly believe that most students pursue a career in medicine for altruistic reasons: to help cure illness and take care of patients, to make new scientific discoveries, and to train the next generation of physicians who will follow them into the medical profession. Unfortunately, outside economic influences – such as increased competition among health care systems, shrinking reimbursements, loss of joy and meaning in medicine, increasing isolation of the caregiver from the patient and the significant cost of a medical education – lead many physicians to burn out prematurely and, for some, to leave the profession altogether.
By eliminating medical school debt, we can remove one of these constraints and make the practice of medicine as rewarding and gratifying as it has been in the past, and more accessible to those who truly wish to care for others.
Dr. Bernstein is a professor in the departments of psychiatry and neurology at New York University and a past president of the American Psychiatric Association.
On Aug.16, the New York University School of Medicine announced it was offering full-tuition scholarships to all current and future students in its MD Program, regardless of need or merit – and that this policy also would apply to all matriculating students for the remainder of their medical school education at NYU.
Dr. Carol A. Bernstein
This bold initiative, they stated, was being instituted to simultaneously address the rising costs of medical education while still attracting the best and brightest to careers in medicine. In doing so, NYU School of Medicine (at which I hold a faculty appointment) became the first Top 10–ranked medical school in the nation to do so.
The symbolism of this announcement was noticeable: It was made at the medical school’s annual white coat ceremony, when each new student is presented with a white lab coat to mark the beginning of their medical education and training.
I count myself among many medical professionals and, indeed, others outside of medicine who have long advocated for free tuition for medical education, at the very least for those who have little or no means to pay. This particularly painful burden of debt often serves as a deterrent to many individuals who are considering a career in medicine or medical research.
According to the Association of American Medical Colleges, 75% of all U.S. doctors graduated with some degree of debt in 2017. For many, the total is staggering: The median current debt for a graduating medical student is $202,000, with debt for those pursuing private medical school education rising as high as $300,000.
What might develop as a result of NYU’s decision and that of several other schools who have adopted debt-reduction policies?
First, that these programs might have a ripple effect at other medical schools, and create a movement for more students to earn a medical degree without incurring a crushing financial burden. Some other schools, like Columbia University, already have taken steps, such as replacing all student loans with scholarships creating a “debt-free” medical school. It would, indeed, be a powerful message if other schools developed similar creative solutions to this problem.
Second, there is hope that debt relief will encourage more medical school graduates to pursue careers in such specialties as family medicine, psychiatry, pediatrics, and geriatrics – because they will not have the additional financial pressure to pursue careers in more lucrative specialties in order to pay off debt. While many medical school graduates point to other issues like complex reimbursement as a greater deterrent to a specific specialty choice, I certainly hope that debt relief will have a positive effect in shifting the subspecialty paradigm.
Third, these actions might incentivize the federal government to establish an AmeriCorps-type program, in which the cost of a medical education is covered in return for a commitment to practice medicine for a period of time in underserved areas of the country. Such an approach also might motivate more medical school graduates to pursue careers in primary care specialties and help address some of the ongoing concerns related to the uneven distribution of physicians in the United States.
Another issue that often comes up is the impact of debt burden on “burnout” among medical students. This is a complex subject – and one that actually affects physicians beyond medical school and into residency training and medical practice.
There is no doubt that debt weighs heavily on the minds of medical students – and many enter medical school having sustained significant debt already from previous education in colleges and universities. However, the causes and influences on burnout in training are multifactorial. Earlier in medical school, the impact of debt obligation may be less apparent because of the other challenges students face when beginning medical school.
However, once trainees begin residency and fellowship training – and especially during early career years when many are beginning to have families – concerns about increasing financial strain become even more prominent. For many young physicians, already stressed by other extenuating factors, it would be a tremendous relief not to have that debt pursuing them.
As someone who teaches and mentors medical students and residents, I firmly believe that most students pursue a career in medicine for altruistic reasons: to help cure illness and take care of patients, to make new scientific discoveries, and to train the next generation of physicians who will follow them into the medical profession. Unfortunately, outside economic influences – such as increased competition among health care systems, shrinking reimbursements, loss of joy and meaning in medicine, increasing isolation of the caregiver from the patient and the significant cost of a medical education – lead many physicians to burn out prematurely and, for some, to leave the profession altogether.
By eliminating medical school debt, we can remove one of these constraints and make the practice of medicine as rewarding and gratifying as it has been in the past, and more accessible to those who truly wish to care for others.
Dr. Bernstein is a professor in the departments of psychiatry and neurology at New York University and a past president of the American Psychiatric Association.
On Aug.16, the New York University School of Medicine announced it was offering full-tuition scholarships to all current and future students in its MD Program, regardless of need or merit – and that this policy also would apply to all matriculating students for the remainder of their medical school education at NYU.
Dr. Carol A. Bernstein
This bold initiative, they stated, was being instituted to simultaneously address the rising costs of medical education while still attracting the best and brightest to careers in medicine. In doing so, NYU School of Medicine (at which I hold a faculty appointment) became the first Top 10–ranked medical school in the nation to do so.
The symbolism of this announcement was noticeable: It was made at the medical school’s annual white coat ceremony, when each new student is presented with a white lab coat to mark the beginning of their medical education and training.
I count myself among many medical professionals and, indeed, others outside of medicine who have long advocated for free tuition for medical education, at the very least for those who have little or no means to pay. This particularly painful burden of debt often serves as a deterrent to many individuals who are considering a career in medicine or medical research.
According to the Association of American Medical Colleges, 75% of all U.S. doctors graduated with some degree of debt in 2017. For many, the total is staggering: The median current debt for a graduating medical student is $202,000, with debt for those pursuing private medical school education rising as high as $300,000.
What might develop as a result of NYU’s decision and that of several other schools who have adopted debt-reduction policies?
First, that these programs might have a ripple effect at other medical schools, and create a movement for more students to earn a medical degree without incurring a crushing financial burden. Some other schools, like Columbia University, already have taken steps, such as replacing all student loans with scholarships creating a “debt-free” medical school. It would, indeed, be a powerful message if other schools developed similar creative solutions to this problem.
Second, there is hope that debt relief will encourage more medical school graduates to pursue careers in such specialties as family medicine, psychiatry, pediatrics, and geriatrics – because they will not have the additional financial pressure to pursue careers in more lucrative specialties in order to pay off debt. While many medical school graduates point to other issues like complex reimbursement as a greater deterrent to a specific specialty choice, I certainly hope that debt relief will have a positive effect in shifting the subspecialty paradigm.
Third, these actions might incentivize the federal government to establish an AmeriCorps-type program, in which the cost of a medical education is covered in return for a commitment to practice medicine for a period of time in underserved areas of the country. Such an approach also might motivate more medical school graduates to pursue careers in primary care specialties and help address some of the ongoing concerns related to the uneven distribution of physicians in the United States.
Another issue that often comes up is the impact of debt burden on “burnout” among medical students. This is a complex subject – and one that actually affects physicians beyond medical school and into residency training and medical practice.
There is no doubt that debt weighs heavily on the minds of medical students – and many enter medical school having sustained significant debt already from previous education in colleges and universities. However, the causes and influences on burnout in training are multifactorial. Earlier in medical school, the impact of debt obligation may be less apparent because of the other challenges students face when beginning medical school.
However, once trainees begin residency and fellowship training – and especially during early career years when many are beginning to have families – concerns about increasing financial strain become even more prominent. For many young physicians, already stressed by other extenuating factors, it would be a tremendous relief not to have that debt pursuing them.
As someone who teaches and mentors medical students and residents, I firmly believe that most students pursue a career in medicine for altruistic reasons: to help cure illness and take care of patients, to make new scientific discoveries, and to train the next generation of physicians who will follow them into the medical profession. Unfortunately, outside economic influences – such as increased competition among health care systems, shrinking reimbursements, loss of joy and meaning in medicine, increasing isolation of the caregiver from the patient and the significant cost of a medical education – lead many physicians to burn out prematurely and, for some, to leave the profession altogether.
By eliminating medical school debt, we can remove one of these constraints and make the practice of medicine as rewarding and gratifying as it has been in the past, and more accessible to those who truly wish to care for others.
Dr. Bernstein is a professor in the departments of psychiatry and neurology at New York University and a past president of the American Psychiatric Association.
The management of bipolar disorder during pregnancy is a critical clinical situation demanding great attention to issues such as reproductive safety of psychiatric medications used by women with bipolar disorder to maintain emotional well-being, compared with the established risk of relapse if patients stopped those medications.
Antonio_Diaz/Thinkstock
Treatment of bipolar disorder frequently includes mainstay treatment with mood stabilizers such as sodium valproate, lithium, lamotrigine, and second-generation atypical antipsychotics. While we have robust information regarding the reproductive safety of sodium valproate, it is a teratogen with a very high risk for neural tube defects. In contrast, data over the 15 years have been very supportive of the reproductive safety of lamotrigine. The last decade has seen growing use of second-generation antipsychotics, so-called atypical antipsychotics. There has been growing interest in the reproductive safety of these medicines given their use both for acute mania and for prophylaxis of bipolar disorder; they also are used as an adjunct to treat patients with major depression. Atypical antipsychotics are widely used off-label to treat obsessive compulsive disorder, other anxiety disorders, and a spectrum of psychiatric illness.
Until relatively recently, data on the reproductive safety of second-generation atypical antipsychotics has been relatively sparse, with the small number of prospective studies yielding a small total number of patients. Over the same period of time, the National Pregnancy Registry for Atypical Antipsychotics (NPRAA) at Massachusetts General Hospital (MGH) was established, modeled after the North American Antiepileptic Drug Registry as a prospective registry of women with histories of first trimester exposure to atypical antipsychotics.
Over the last several years, the MGH NPRAA has accumulated very rigorous, prospectively ascertained data on outcomes following first trimester exposure to the atypical antipsychotics. Given the high prevalence of the use of this class of medications in reproductive-age women, data on the reproductive safety of atypical antipsychotics has been anxiously awaited and also has been relatively reassuring based on sources such as the NPRAA and also analyses of data from large administrative databases. For example, a recent paper published in JAMA Psychiatry by KF Huybrechts and her colleagues of 1,360,101 pregnant women who were enrolled in the Medicaid Analytic Extract database found an adjusted relative risk of 1.05 for congenital malformations in births for patients exposed to atypical antipsychotics (2016;73[9]:938-46).
Patients most often present with questions not about the reproductive safety of a class of medications, but about the safety of a particular medicine. A recent paper from our own group published in the American Journal of Psychiatry using data from the MGH NPRAA–described outcome of fetal exposure to quetiapine with a total of 152 women exposed to quetiapine and 205 unexposed patients. These patients were prospectively followed and compared with controls not exposed to the atypical antipsychotic but having a history of psychiatric morbidity. There was a 1.29% risk of major malformations in women exposed to quetiapine vs. 1.43% in the unexposed population (2018 Aug 16. doi: 10.1176/appi.ajp.2018.18010098).
The positive features of the MGH NPRAA include the careful rigorous assessments of patients over time as well as review of their obstetric, neonatal, and pediatric records up to 6 months, with blinded adjudication of outcome. The limitation of the small sample size remains with findings including relatively wide confidence intervals. With that being said, included in the paper in the discussion section is a pooled analysis of prospective data regarding quetiapine from the world’s literature that supports the findings of even this small prospective study in our registry, namely flat risk or absence of data suggesting that quetiapine is a major teratogen (pooled risk ratio, 1.03; 95% confidence interval, 0.89-1.19).
The delineation of risk for atypical antipsychotics is an extremely important area of research from a clinical point of view because it may help inform choices made by women with bipolar disorder who are well and maintained on these medicines as they wrestle with risk of relapse when agents are discontinued on one hand and reproductive safety concerns on the other.
Although not as widely used as perhaps a decade ago, data on the reproductive safety of lithium only continue to grow and become more refined. Use of lithium, a known teratogen with studies dating back to the 1970s, has an increased risk for cardiovascular malformations with the classic reference being to the small heightened risk of Ebstein’s anomaly (0.05%-0.1%). More recent studies from large administrative databases have been published with new data regarding risk of fetal exposure to lithium.
Two recent studies on lithium help to clarify some lingering questions about lithium use during pregnancy and risk for cardiovascular malformations. In one study published in the New England Journal of Medicine, researchers have demonstrated a small increased risk for cardiac malformations associated with using lithium during the first trimester (2017;376:2245-54). After researchers controlled for potential confounding factors, the adjusted risk ratio for cardiac malformations among infants exposed to lithium was 1.65 (95% CI, 1.02-2.68), compared with nonexposed infants. In a second study published in Lancet Psychiatry (2018 Aug;5[8]:644-52), a primary data meta-analysis of pregnant women and their children from six international cohorts in Denmark, Sweden, and Canada, there was no significant difference in major cardiac malformations between the lithium-exposed group, 2.1% (0.5%-3.7%), and the reference group, 1.6% (1.0%-2.1%).
Women with particularly brittle bipolar disorder or with histories of response to lithium may, in consultation with their doctors, consider use of lithium during pregnancy given the almost 50-year history of data accumulation on its reproductive safety, compared with some of the other mood stabilizers for which there is either confirmed teratogenicity (sodium valproate) or still incomplete data. Moreover, given the high risk for postpartum relapse of mood disorder in women who suffer from bipolar disorder, it is important to remember that the most robust data on prophylactic benefit of mood stabilizer during the peripartum period are with lithium.
Dr. Lee S. Cohen
Reproductive age women with bipolar disorder have for decades been caught between a teratologic rock and a clinical hard place. More recent data that have emerged from rigorously conducted registries and carefully analyzed administrative databases allow for more effective collaboration between patient and doctor as together they make personal decisions that match individual clinical situations with personal wishes.
Dr. Cohen is the director of the Ammon-Pinizzotto Center for Women’s Mental Health at Massachusetts General Hospital in Boston, which provides information resources and conducts clinical care and research in reproductive mental health. He has been a consultant to manufacturers of psychiatric medications. Email him at [email protected].
The management of bipolar disorder during pregnancy is a critical clinical situation demanding great attention to issues such as reproductive safety of psychiatric medications used by women with bipolar disorder to maintain emotional well-being, compared with the established risk of relapse if patients stopped those medications.
Antonio_Diaz/Thinkstock
Treatment of bipolar disorder frequently includes mainstay treatment with mood stabilizers such as sodium valproate, lithium, lamotrigine, and second-generation atypical antipsychotics. While we have robust information regarding the reproductive safety of sodium valproate, it is a teratogen with a very high risk for neural tube defects. In contrast, data over the 15 years have been very supportive of the reproductive safety of lamotrigine. The last decade has seen growing use of second-generation antipsychotics, so-called atypical antipsychotics. There has been growing interest in the reproductive safety of these medicines given their use both for acute mania and for prophylaxis of bipolar disorder; they also are used as an adjunct to treat patients with major depression. Atypical antipsychotics are widely used off-label to treat obsessive compulsive disorder, other anxiety disorders, and a spectrum of psychiatric illness.
Until relatively recently, data on the reproductive safety of second-generation atypical antipsychotics has been relatively sparse, with the small number of prospective studies yielding a small total number of patients. Over the same period of time, the National Pregnancy Registry for Atypical Antipsychotics (NPRAA) at Massachusetts General Hospital (MGH) was established, modeled after the North American Antiepileptic Drug Registry as a prospective registry of women with histories of first trimester exposure to atypical antipsychotics.
Over the last several years, the MGH NPRAA has accumulated very rigorous, prospectively ascertained data on outcomes following first trimester exposure to the atypical antipsychotics. Given the high prevalence of the use of this class of medications in reproductive-age women, data on the reproductive safety of atypical antipsychotics has been anxiously awaited and also has been relatively reassuring based on sources such as the NPRAA and also analyses of data from large administrative databases. For example, a recent paper published in JAMA Psychiatry by KF Huybrechts and her colleagues of 1,360,101 pregnant women who were enrolled in the Medicaid Analytic Extract database found an adjusted relative risk of 1.05 for congenital malformations in births for patients exposed to atypical antipsychotics (2016;73[9]:938-46).
Patients most often present with questions not about the reproductive safety of a class of medications, but about the safety of a particular medicine. A recent paper from our own group published in the American Journal of Psychiatry using data from the MGH NPRAA–described outcome of fetal exposure to quetiapine with a total of 152 women exposed to quetiapine and 205 unexposed patients. These patients were prospectively followed and compared with controls not exposed to the atypical antipsychotic but having a history of psychiatric morbidity. There was a 1.29% risk of major malformations in women exposed to quetiapine vs. 1.43% in the unexposed population (2018 Aug 16. doi: 10.1176/appi.ajp.2018.18010098).
The positive features of the MGH NPRAA include the careful rigorous assessments of patients over time as well as review of their obstetric, neonatal, and pediatric records up to 6 months, with blinded adjudication of outcome. The limitation of the small sample size remains with findings including relatively wide confidence intervals. With that being said, included in the paper in the discussion section is a pooled analysis of prospective data regarding quetiapine from the world’s literature that supports the findings of even this small prospective study in our registry, namely flat risk or absence of data suggesting that quetiapine is a major teratogen (pooled risk ratio, 1.03; 95% confidence interval, 0.89-1.19).
The delineation of risk for atypical antipsychotics is an extremely important area of research from a clinical point of view because it may help inform choices made by women with bipolar disorder who are well and maintained on these medicines as they wrestle with risk of relapse when agents are discontinued on one hand and reproductive safety concerns on the other.
Although not as widely used as perhaps a decade ago, data on the reproductive safety of lithium only continue to grow and become more refined. Use of lithium, a known teratogen with studies dating back to the 1970s, has an increased risk for cardiovascular malformations with the classic reference being to the small heightened risk of Ebstein’s anomaly (0.05%-0.1%). More recent studies from large administrative databases have been published with new data regarding risk of fetal exposure to lithium.
Two recent studies on lithium help to clarify some lingering questions about lithium use during pregnancy and risk for cardiovascular malformations. In one study published in the New England Journal of Medicine, researchers have demonstrated a small increased risk for cardiac malformations associated with using lithium during the first trimester (2017;376:2245-54). After researchers controlled for potential confounding factors, the adjusted risk ratio for cardiac malformations among infants exposed to lithium was 1.65 (95% CI, 1.02-2.68), compared with nonexposed infants. In a second study published in Lancet Psychiatry (2018 Aug;5[8]:644-52), a primary data meta-analysis of pregnant women and their children from six international cohorts in Denmark, Sweden, and Canada, there was no significant difference in major cardiac malformations between the lithium-exposed group, 2.1% (0.5%-3.7%), and the reference group, 1.6% (1.0%-2.1%).
Women with particularly brittle bipolar disorder or with histories of response to lithium may, in consultation with their doctors, consider use of lithium during pregnancy given the almost 50-year history of data accumulation on its reproductive safety, compared with some of the other mood stabilizers for which there is either confirmed teratogenicity (sodium valproate) or still incomplete data. Moreover, given the high risk for postpartum relapse of mood disorder in women who suffer from bipolar disorder, it is important to remember that the most robust data on prophylactic benefit of mood stabilizer during the peripartum period are with lithium.
Dr. Lee S. Cohen
Reproductive age women with bipolar disorder have for decades been caught between a teratologic rock and a clinical hard place. More recent data that have emerged from rigorously conducted registries and carefully analyzed administrative databases allow for more effective collaboration between patient and doctor as together they make personal decisions that match individual clinical situations with personal wishes.
Dr. Cohen is the director of the Ammon-Pinizzotto Center for Women’s Mental Health at Massachusetts General Hospital in Boston, which provides information resources and conducts clinical care and research in reproductive mental health. He has been a consultant to manufacturers of psychiatric medications. Email him at [email protected].
The management of bipolar disorder during pregnancy is a critical clinical situation demanding great attention to issues such as reproductive safety of psychiatric medications used by women with bipolar disorder to maintain emotional well-being, compared with the established risk of relapse if patients stopped those medications.
Antonio_Diaz/Thinkstock
Treatment of bipolar disorder frequently includes mainstay treatment with mood stabilizers such as sodium valproate, lithium, lamotrigine, and second-generation atypical antipsychotics. While we have robust information regarding the reproductive safety of sodium valproate, it is a teratogen with a very high risk for neural tube defects. In contrast, data over the 15 years have been very supportive of the reproductive safety of lamotrigine. The last decade has seen growing use of second-generation antipsychotics, so-called atypical antipsychotics. There has been growing interest in the reproductive safety of these medicines given their use both for acute mania and for prophylaxis of bipolar disorder; they also are used as an adjunct to treat patients with major depression. Atypical antipsychotics are widely used off-label to treat obsessive compulsive disorder, other anxiety disorders, and a spectrum of psychiatric illness.
Until relatively recently, data on the reproductive safety of second-generation atypical antipsychotics has been relatively sparse, with the small number of prospective studies yielding a small total number of patients. Over the same period of time, the National Pregnancy Registry for Atypical Antipsychotics (NPRAA) at Massachusetts General Hospital (MGH) was established, modeled after the North American Antiepileptic Drug Registry as a prospective registry of women with histories of first trimester exposure to atypical antipsychotics.
Over the last several years, the MGH NPRAA has accumulated very rigorous, prospectively ascertained data on outcomes following first trimester exposure to the atypical antipsychotics. Given the high prevalence of the use of this class of medications in reproductive-age women, data on the reproductive safety of atypical antipsychotics has been anxiously awaited and also has been relatively reassuring based on sources such as the NPRAA and also analyses of data from large administrative databases. For example, a recent paper published in JAMA Psychiatry by KF Huybrechts and her colleagues of 1,360,101 pregnant women who were enrolled in the Medicaid Analytic Extract database found an adjusted relative risk of 1.05 for congenital malformations in births for patients exposed to atypical antipsychotics (2016;73[9]:938-46).
Patients most often present with questions not about the reproductive safety of a class of medications, but about the safety of a particular medicine. A recent paper from our own group published in the American Journal of Psychiatry using data from the MGH NPRAA–described outcome of fetal exposure to quetiapine with a total of 152 women exposed to quetiapine and 205 unexposed patients. These patients were prospectively followed and compared with controls not exposed to the atypical antipsychotic but having a history of psychiatric morbidity. There was a 1.29% risk of major malformations in women exposed to quetiapine vs. 1.43% in the unexposed population (2018 Aug 16. doi: 10.1176/appi.ajp.2018.18010098).
The positive features of the MGH NPRAA include the careful rigorous assessments of patients over time as well as review of their obstetric, neonatal, and pediatric records up to 6 months, with blinded adjudication of outcome. The limitation of the small sample size remains with findings including relatively wide confidence intervals. With that being said, included in the paper in the discussion section is a pooled analysis of prospective data regarding quetiapine from the world’s literature that supports the findings of even this small prospective study in our registry, namely flat risk or absence of data suggesting that quetiapine is a major teratogen (pooled risk ratio, 1.03; 95% confidence interval, 0.89-1.19).
The delineation of risk for atypical antipsychotics is an extremely important area of research from a clinical point of view because it may help inform choices made by women with bipolar disorder who are well and maintained on these medicines as they wrestle with risk of relapse when agents are discontinued on one hand and reproductive safety concerns on the other.
Although not as widely used as perhaps a decade ago, data on the reproductive safety of lithium only continue to grow and become more refined. Use of lithium, a known teratogen with studies dating back to the 1970s, has an increased risk for cardiovascular malformations with the classic reference being to the small heightened risk of Ebstein’s anomaly (0.05%-0.1%). More recent studies from large administrative databases have been published with new data regarding risk of fetal exposure to lithium.
Two recent studies on lithium help to clarify some lingering questions about lithium use during pregnancy and risk for cardiovascular malformations. In one study published in the New England Journal of Medicine, researchers have demonstrated a small increased risk for cardiac malformations associated with using lithium during the first trimester (2017;376:2245-54). After researchers controlled for potential confounding factors, the adjusted risk ratio for cardiac malformations among infants exposed to lithium was 1.65 (95% CI, 1.02-2.68), compared with nonexposed infants. In a second study published in Lancet Psychiatry (2018 Aug;5[8]:644-52), a primary data meta-analysis of pregnant women and their children from six international cohorts in Denmark, Sweden, and Canada, there was no significant difference in major cardiac malformations between the lithium-exposed group, 2.1% (0.5%-3.7%), and the reference group, 1.6% (1.0%-2.1%).
Women with particularly brittle bipolar disorder or with histories of response to lithium may, in consultation with their doctors, consider use of lithium during pregnancy given the almost 50-year history of data accumulation on its reproductive safety, compared with some of the other mood stabilizers for which there is either confirmed teratogenicity (sodium valproate) or still incomplete data. Moreover, given the high risk for postpartum relapse of mood disorder in women who suffer from bipolar disorder, it is important to remember that the most robust data on prophylactic benefit of mood stabilizer during the peripartum period are with lithium.
Dr. Lee S. Cohen
Reproductive age women with bipolar disorder have for decades been caught between a teratologic rock and a clinical hard place. More recent data that have emerged from rigorously conducted registries and carefully analyzed administrative databases allow for more effective collaboration between patient and doctor as together they make personal decisions that match individual clinical situations with personal wishes.
Dr. Cohen is the director of the Ammon-Pinizzotto Center for Women’s Mental Health at Massachusetts General Hospital in Boston, which provides information resources and conducts clinical care and research in reproductive mental health. He has been a consultant to manufacturers of psychiatric medications. Email him at [email protected].
I want to start with a disclaimer: I don’t have a website for my private practice, and I have no formal education in marketing. My opinions on what should and should not be on physician practice websites are my own, and as you take my thoughts into account, remember that others have different opinions about what belongs on a website.
Dr. Dinah Miller
Periodically, I look at websites my colleagues have set up, and I have noted some interesting differences in how detailed they are, the photos that are chosen, the information that is listed, the editing, and how the doctor presents himself or herself. It seems like a wonderful way to both “advertise” and to have people know about the doctor in advance. Practice websites can save time for everyone: A patient can weed out psychiatrists who don’t treat the condition he or she has, and the doctor can refer to the website rather than having long phone conversations with someone who would not want to see them for any number of reasons. In theory, websites can include ways for patients to schedule their own appointments, but I have not yet seen this software on any psychiatry sites.
Psychiatrist websites often start with some biographical and training issues on either the home or Welcome page or in a specific About section. They may give helpful information, such as directions to the office, parking instructions, and what conditions the doctor treats. It’s important to have a clear link to the site’s menu, and I’m not sure that older users always know that the “hamburger” icon of three horizontal lines is a menu link. It’s nice if there is a picture of the doctor, and I’ve even seen a few sites where there is a photo of the doctor’s office; it seems like a nice touch and may allay some anxiety for new patients if the doctor and his or her space feel familiar and nonthreatening. As with everything on the website, the artwork and graphics reflect something about the doctor. Many psychotherapists will use nature photos; others feature stethoscopes and lab coats for a more medical feel. Some psychiatrists opt for more opaque graphics – geometric shapes, for example.
Dr. Jeff SoulenMost psychiatrists put up something about their treatment orientation, and sometimes a statement about goals that include more than illness and symptom management. Jeffrey Soulen, MD, a psychiatrist in Ellicott City, Md., notes on his welcome page, “My practice is dedicated to helping people enhance and sustain long-term mental health. I encourage development of awareness and skills that help us see our problems more clearly and respond to them with greater flexibility, adaptability, stability, and resilience. When we become more aware and skillful, we experience increased feelings of self-mastery, freedom, well-being, and hope.” While Dr. Soulen uses the traditional treatments of medications and psychotherapy, he goes on to note that his practice has been informed by the disciplines of yoga, meditation, tai chi, and qi gong, and he uses these practices with people who are both interested and as appropriate.
Psychiatrists differ as to the tone of the websites, with a range from chatty to purely informative. Some are done in the third person, as though written by an agent for the doctor, while others, like Dr. Soulen’s, are written in the first person with a conversational feel. Several psychiatrists I know in solo practice use the first-person plural voice of “we/our” to discuss their practice. It is probably best to choose a single option and stick to it; it can sound awkward if a solo practitioner mixes both “I” and “we,” and a prospective patient may not be sure if he is to meet with one person or a team.
Dr. Joseph AndrewsJoseph Andrews, MD, is a psychiatrist in Baltimore and founder of the Via Clinic. While Dr. Andrews is in solo practice, he references “we/our” on his website. “I did this for two reasons,” he said, “First, I felt it was important that the website emphasize the practice and not myself. This also gives room to grow and add colleagues. Second, I want patients to feel like they are joining a collaborative venture in getting well and that they belong as mutual partners. I don’t want to give the impression this is a passive journey for them.”
A website can be a painless way to let prospective patients know about insurance participation, fees, and payment policies before the first meeting. Some psychiatrists list their fees and others choose not to. Many doctors list their cancellation policies, and this also seems reasonable. I, personally, find it off-putting when a psychiatrist gets too detailed about money, and there may be better venues for telling patients very specific practice policies such as the price per page for copying records or the consequences of arriving late to a session. In my practice, I don’t charge patients to call or send in prescriptions between sessions, but it does take up physician time, so I have mixed feelings when I see a website that lists a price for this service. I might also worry that patients would stop their medications and risk relapse if they had to worry about paying a fee to have a medication renewal sent in to the pharmacy.
It’s important to remember that patients want a psychiatrist who cares about them, and too much website emphasis on fee collection or office rules may give prospective patients the impression that financial issues take precedence. While many psychiatrists list detailed office policies with grace, I have occasionally seen sites filled with rules such that they almost read, “Here is what I won’t do for you.” Practice ground rules and policies are helpful and set useful boundaries, but a website might not be the best place to announce every policy with every contingency, and doing so may create the impression – accurate or not – that the psychiatrist is rigid and uncaring. And they may hedge the doctor in such that it’s harder to be flexible when a situation warrants doing something other than what is publicly proclaimed.
Many psychiatrists also use their practice websites as a place to offer something more: a blog where they post information on psychiatric conditions, a video of a talk they have given, recommendations for helpful books or articles, and links to other resources. It can be an efficient way of communicating with patients, prospective patients, family members, or referral sources.
Finally, in our age of information overload and Yelp doctor reviews, a practice website allows the physician some control over what a person might learn on a Google search. It doesn’t make negative information go away, but it gives the physician a place to have a say and put up information he or she wants others to see.
Websites come in a variety of formats: Some doctors have them professionally designed; others use free templates. Whatever option one chooses, it’s important to think about how the site will be perceived and to check carefully for spelling and grammar mistakes. Abbreviations should also be avoided; while many patients know what ECT or SSRIs are, it’s best to assume that site visitors may not be familiar with psychiatric lingo.
“A website is a modern-day storefront. I feel it is important to have something that is professional,” Dr. Andrews said.
I want to start with a disclaimer: I don’t have a website for my private practice, and I have no formal education in marketing. My opinions on what should and should not be on physician practice websites are my own, and as you take my thoughts into account, remember that others have different opinions about what belongs on a website.
Dr. Dinah Miller
Periodically, I look at websites my colleagues have set up, and I have noted some interesting differences in how detailed they are, the photos that are chosen, the information that is listed, the editing, and how the doctor presents himself or herself. It seems like a wonderful way to both “advertise” and to have people know about the doctor in advance. Practice websites can save time for everyone: A patient can weed out psychiatrists who don’t treat the condition he or she has, and the doctor can refer to the website rather than having long phone conversations with someone who would not want to see them for any number of reasons. In theory, websites can include ways for patients to schedule their own appointments, but I have not yet seen this software on any psychiatry sites.
Psychiatrist websites often start with some biographical and training issues on either the home or Welcome page or in a specific About section. They may give helpful information, such as directions to the office, parking instructions, and what conditions the doctor treats. It’s important to have a clear link to the site’s menu, and I’m not sure that older users always know that the “hamburger” icon of three horizontal lines is a menu link. It’s nice if there is a picture of the doctor, and I’ve even seen a few sites where there is a photo of the doctor’s office; it seems like a nice touch and may allay some anxiety for new patients if the doctor and his or her space feel familiar and nonthreatening. As with everything on the website, the artwork and graphics reflect something about the doctor. Many psychotherapists will use nature photos; others feature stethoscopes and lab coats for a more medical feel. Some psychiatrists opt for more opaque graphics – geometric shapes, for example.
Dr. Jeff SoulenMost psychiatrists put up something about their treatment orientation, and sometimes a statement about goals that include more than illness and symptom management. Jeffrey Soulen, MD, a psychiatrist in Ellicott City, Md., notes on his welcome page, “My practice is dedicated to helping people enhance and sustain long-term mental health. I encourage development of awareness and skills that help us see our problems more clearly and respond to them with greater flexibility, adaptability, stability, and resilience. When we become more aware and skillful, we experience increased feelings of self-mastery, freedom, well-being, and hope.” While Dr. Soulen uses the traditional treatments of medications and psychotherapy, he goes on to note that his practice has been informed by the disciplines of yoga, meditation, tai chi, and qi gong, and he uses these practices with people who are both interested and as appropriate.
Psychiatrists differ as to the tone of the websites, with a range from chatty to purely informative. Some are done in the third person, as though written by an agent for the doctor, while others, like Dr. Soulen’s, are written in the first person with a conversational feel. Several psychiatrists I know in solo practice use the first-person plural voice of “we/our” to discuss their practice. It is probably best to choose a single option and stick to it; it can sound awkward if a solo practitioner mixes both “I” and “we,” and a prospective patient may not be sure if he is to meet with one person or a team.
Dr. Joseph AndrewsJoseph Andrews, MD, is a psychiatrist in Baltimore and founder of the Via Clinic. While Dr. Andrews is in solo practice, he references “we/our” on his website. “I did this for two reasons,” he said, “First, I felt it was important that the website emphasize the practice and not myself. This also gives room to grow and add colleagues. Second, I want patients to feel like they are joining a collaborative venture in getting well and that they belong as mutual partners. I don’t want to give the impression this is a passive journey for them.”
A website can be a painless way to let prospective patients know about insurance participation, fees, and payment policies before the first meeting. Some psychiatrists list their fees and others choose not to. Many doctors list their cancellation policies, and this also seems reasonable. I, personally, find it off-putting when a psychiatrist gets too detailed about money, and there may be better venues for telling patients very specific practice policies such as the price per page for copying records or the consequences of arriving late to a session. In my practice, I don’t charge patients to call or send in prescriptions between sessions, but it does take up physician time, so I have mixed feelings when I see a website that lists a price for this service. I might also worry that patients would stop their medications and risk relapse if they had to worry about paying a fee to have a medication renewal sent in to the pharmacy.
It’s important to remember that patients want a psychiatrist who cares about them, and too much website emphasis on fee collection or office rules may give prospective patients the impression that financial issues take precedence. While many psychiatrists list detailed office policies with grace, I have occasionally seen sites filled with rules such that they almost read, “Here is what I won’t do for you.” Practice ground rules and policies are helpful and set useful boundaries, but a website might not be the best place to announce every policy with every contingency, and doing so may create the impression – accurate or not – that the psychiatrist is rigid and uncaring. And they may hedge the doctor in such that it’s harder to be flexible when a situation warrants doing something other than what is publicly proclaimed.
Many psychiatrists also use their practice websites as a place to offer something more: a blog where they post information on psychiatric conditions, a video of a talk they have given, recommendations for helpful books or articles, and links to other resources. It can be an efficient way of communicating with patients, prospective patients, family members, or referral sources.
Finally, in our age of information overload and Yelp doctor reviews, a practice website allows the physician some control over what a person might learn on a Google search. It doesn’t make negative information go away, but it gives the physician a place to have a say and put up information he or she wants others to see.
Websites come in a variety of formats: Some doctors have them professionally designed; others use free templates. Whatever option one chooses, it’s important to think about how the site will be perceived and to check carefully for spelling and grammar mistakes. Abbreviations should also be avoided; while many patients know what ECT or SSRIs are, it’s best to assume that site visitors may not be familiar with psychiatric lingo.
“A website is a modern-day storefront. I feel it is important to have something that is professional,” Dr. Andrews said.
I want to start with a disclaimer: I don’t have a website for my private practice, and I have no formal education in marketing. My opinions on what should and should not be on physician practice websites are my own, and as you take my thoughts into account, remember that others have different opinions about what belongs on a website.
Dr. Dinah Miller
Periodically, I look at websites my colleagues have set up, and I have noted some interesting differences in how detailed they are, the photos that are chosen, the information that is listed, the editing, and how the doctor presents himself or herself. It seems like a wonderful way to both “advertise” and to have people know about the doctor in advance. Practice websites can save time for everyone: A patient can weed out psychiatrists who don’t treat the condition he or she has, and the doctor can refer to the website rather than having long phone conversations with someone who would not want to see them for any number of reasons. In theory, websites can include ways for patients to schedule their own appointments, but I have not yet seen this software on any psychiatry sites.
Psychiatrist websites often start with some biographical and training issues on either the home or Welcome page or in a specific About section. They may give helpful information, such as directions to the office, parking instructions, and what conditions the doctor treats. It’s important to have a clear link to the site’s menu, and I’m not sure that older users always know that the “hamburger” icon of three horizontal lines is a menu link. It’s nice if there is a picture of the doctor, and I’ve even seen a few sites where there is a photo of the doctor’s office; it seems like a nice touch and may allay some anxiety for new patients if the doctor and his or her space feel familiar and nonthreatening. As with everything on the website, the artwork and graphics reflect something about the doctor. Many psychotherapists will use nature photos; others feature stethoscopes and lab coats for a more medical feel. Some psychiatrists opt for more opaque graphics – geometric shapes, for example.
Dr. Jeff SoulenMost psychiatrists put up something about their treatment orientation, and sometimes a statement about goals that include more than illness and symptom management. Jeffrey Soulen, MD, a psychiatrist in Ellicott City, Md., notes on his welcome page, “My practice is dedicated to helping people enhance and sustain long-term mental health. I encourage development of awareness and skills that help us see our problems more clearly and respond to them with greater flexibility, adaptability, stability, and resilience. When we become more aware and skillful, we experience increased feelings of self-mastery, freedom, well-being, and hope.” While Dr. Soulen uses the traditional treatments of medications and psychotherapy, he goes on to note that his practice has been informed by the disciplines of yoga, meditation, tai chi, and qi gong, and he uses these practices with people who are both interested and as appropriate.
Psychiatrists differ as to the tone of the websites, with a range from chatty to purely informative. Some are done in the third person, as though written by an agent for the doctor, while others, like Dr. Soulen’s, are written in the first person with a conversational feel. Several psychiatrists I know in solo practice use the first-person plural voice of “we/our” to discuss their practice. It is probably best to choose a single option and stick to it; it can sound awkward if a solo practitioner mixes both “I” and “we,” and a prospective patient may not be sure if he is to meet with one person or a team.
Dr. Joseph AndrewsJoseph Andrews, MD, is a psychiatrist in Baltimore and founder of the Via Clinic. While Dr. Andrews is in solo practice, he references “we/our” on his website. “I did this for two reasons,” he said, “First, I felt it was important that the website emphasize the practice and not myself. This also gives room to grow and add colleagues. Second, I want patients to feel like they are joining a collaborative venture in getting well and that they belong as mutual partners. I don’t want to give the impression this is a passive journey for them.”
A website can be a painless way to let prospective patients know about insurance participation, fees, and payment policies before the first meeting. Some psychiatrists list their fees and others choose not to. Many doctors list their cancellation policies, and this also seems reasonable. I, personally, find it off-putting when a psychiatrist gets too detailed about money, and there may be better venues for telling patients very specific practice policies such as the price per page for copying records or the consequences of arriving late to a session. In my practice, I don’t charge patients to call or send in prescriptions between sessions, but it does take up physician time, so I have mixed feelings when I see a website that lists a price for this service. I might also worry that patients would stop their medications and risk relapse if they had to worry about paying a fee to have a medication renewal sent in to the pharmacy.
It’s important to remember that patients want a psychiatrist who cares about them, and too much website emphasis on fee collection or office rules may give prospective patients the impression that financial issues take precedence. While many psychiatrists list detailed office policies with grace, I have occasionally seen sites filled with rules such that they almost read, “Here is what I won’t do for you.” Practice ground rules and policies are helpful and set useful boundaries, but a website might not be the best place to announce every policy with every contingency, and doing so may create the impression – accurate or not – that the psychiatrist is rigid and uncaring. And they may hedge the doctor in such that it’s harder to be flexible when a situation warrants doing something other than what is publicly proclaimed.
Many psychiatrists also use their practice websites as a place to offer something more: a blog where they post information on psychiatric conditions, a video of a talk they have given, recommendations for helpful books or articles, and links to other resources. It can be an efficient way of communicating with patients, prospective patients, family members, or referral sources.
Finally, in our age of information overload and Yelp doctor reviews, a practice website allows the physician some control over what a person might learn on a Google search. It doesn’t make negative information go away, but it gives the physician a place to have a say and put up information he or she wants others to see.
Websites come in a variety of formats: Some doctors have them professionally designed; others use free templates. Whatever option one chooses, it’s important to think about how the site will be perceived and to check carefully for spelling and grammar mistakes. Abbreviations should also be avoided; while many patients know what ECT or SSRIs are, it’s best to assume that site visitors may not be familiar with psychiatric lingo.
“A website is a modern-day storefront. I feel it is important to have something that is professional,” Dr. Andrews said.
Cervical dysplasia is commonly diagnosed in women who have completed childbearing and don’t desire future fertility. While diagnostic and/or definitive therapy for cervical dysplasia can include hysterectomy, there are important considerations to make when offering this procedure to patients.
Dr. Emma C. Rossi
Pitfalls
Hysterectomy is commonly requested by patients upon learning of cervical dysplasia, particularly if they have chronic human papillomavirus (HPV) infection and have experienced years of frequent surveillance and interventions. They may see hysterectomy as an option to avoid this close surveillance and to be free of their dysplasia. There are two main concerns with offering hysterectomy as the primary surgical option for the management of dysplasia. Firstly, it may not be curative, and secondly, it may be an inadequate excisional procedure, particularly if the patient has occult invasive disease that has not been adequately diagnosed with a loop electrosurgical excision procedure (LEEP) or a cone biopsy procedure.
It is important to counsel these patients that surgery is not a treatment for high-risk HPV infection, which is the underlying etiology of their disease. With that etiology, HPV infection is likely to persist after hysterectomy and they may develop vaginal or vulvar dysplasia. Therefore, the American Society for Colposcopy and Cervical Pathology recommends that cytology and/or high-risk HPV surveillance continue following hysterectomy if that surgery was performed for dysplasia.1 Hysterectomy is not a means to avoid years of surveillance testing. Approximately 10% of women who have hysterectomy for cervical dysplasia develop vaginal dysplasia or cancer after surgery.2,3 This is similar to the likelihood of recurrent dysplasia after an alternative excisional procedure. In my experience, this diagnosis is often met with enormous frustration for the patient who thought that her hysterectomy would be the cure of her HPV-related disease. Thorough colposcopic evaluation of the vagina can be technically challenging after hysterectomy because of difficulty adequately visualizing lesions within the vaginal rugations, particularly within the puckered lateral vaginal fornices, the most common location for dysplasia.3 We will explore the diagnosis and treatment options for vaginal dysplasia further in a future column.
It is critical that, if patients are offered hysterectomy for treatment of cervical dysplasia, they are counseled that it may not be curative, that they will require long-term vaginal surveillance, and that they are at continued risk for vaginal and vulvar cancer.
An additional concern with performing hysterectomy for definitive management of cervical dysplasia is the concern that occult cancer may be missed preoperatively, and that the hysterectomy is inadequate surgical clearance of the disease. Approximately 2%-5% of patients with a high-grade squamous intraepithelial lesion or equivocal Pap test have occult cervical cancer.4 A similar proportion of patients with cervical intraepithelial neoplasia stage III or adenocarcinoma in situ on colposcopy biopsy have invasive carcinoma on evaluation of an excisional specimen.5 The traditional surgical approach has dictated that a modified (type II) or extended (type III) radical hysterectomy be performed in the setting of FIGO stage IA2 or greater cervical cancer. Radical hysterectomies remove parametrial tissue, effectively achieving a wider margin around the primary lesion. This is important because cervical cancer primarily spreads via direct extension.
The appropriate radicality of surgery for microscopic lesions is debated. It has been proposed that for very small, low-risk lesions, a traditional extrafascial hysterectomy or trachelectomy, or possibly even a large conization, may be adequate.6 However, this is controversial, and National Comprehensive Cancer Network guidelines still advocate for radical procedures for these lesions.7 Certainly an excisional procedure (LEEP or cone) should first be performed to define the size and histologic features of the lesion, and ideally, evaluation and counseling with a gynecologic oncologist should be performed prior to offering patients with a stage IA2 or greater lesion an extrafascial hysterectomy. Additionally, a separate decision would need to be made regarding the need for lymphadenectomy, as this is typically recommended for patients with stage IA2 or greater lesions.
Patients should be counseled that, if extrafascial (simple) hysterectomy is chosen as the primary excisional procedure, they may require additional therapy (additional surgery, or radiation and possibly chemotherapy) if cancer is found in the specimen and the parametrial margin is inadequate. Additionally, and of more concern, if the lesion is a bulky lesion extending into the parametrium and not recognized preoperatively, a “cut-through” hysterectomy will be inadvertently performed (in which margins are grossly positive). These situations typically feature heavy blood loss with patients at increased risk for immediate surgical complications. Postoperatively, prognosis is substantially worse for patients who have had a cut-through hysterectomy, compared stage for stage with patients who primarily received a radical procedure with negative margins or primary chemotherapy and radiation.8 Otherwise said, their risk for death is higher if this error is made. Therefore a thorough examination is essential prior to performing hysterectomy for dysplasia. Any suspicion of bulky cancer should be considered a contraindication for proceeding.
Preoperative evaluation
As a rule, no patient should transition directly from cytologic evaluation with Pap screening to hysterectomy. A colposcopic evaluation of the cervix and vagina accompanied with a thorough bimanual rectovaginal examination should always be performed first. Biopsies of the ectocervix and ideally the endocervix should be obtained because the accuracy of histology is greater than that of cytology. For patients with cervical intraepithelial neoplasia stage I lesions, hysterectomy is not appropriate, as these patients have an extremely low risk for the development of cervical cancer, and the risks and costs of hysterectomy are not justified in such a population.
Surgeons should wait at least 6 weeks following conization or LEEP before performing hysterectomy in order to minimize the likelihood of perioperative complications.9
Substituting LEEP or cone with hysterectomy
In general, it is the most prudent approach to first perform a diagnostic excision with LEEP or cone biopsy before proceeding with hysterectomy for definitive surgery. However, there may be some situations in which this is not feasible. In patients whose cervix is very small and flush with the vagina, an excisional procedure may not be technically possible without concern for damage to adjacent structures. In these patients, after a thorough exam has evaluated for gross disease, a hysterectomy may be the only way to adequately diagnose and treat high-grade dysplasia through excision. For patients with limited access to resources, transportation, or a concern for noncompliance with follow-up, surgeons may wish to offer patients primary hysterectomy rather than a staged procedure.
Hysterectomy remains a potential option for treatment of cervical dysplasia. However, patients should be made aware of the risks of undertreatment of occult cancers, the need for long-term surveillance testing, and the risk for future vaginal dysplasia or cancer. Ideally a comprehensive, stepwise assessment from cytology to colposcopy and examination to diagnostic excisional procedure will first take place to proceed safely with this approach.
References
1. Saslow D et al. American Cancer Society, American Society for Colposcopy and Cervical Pathology, and American Society for Clinical Pathology screening guidelines for the prevention and early detection of cervical cancer. CA Cancer J Clin. 2012 May-Jun;62(3):147-72.
2. Schockaert S et al. Incidence of vaginal intraepithelial neoplasia after hysterectomy for cervical intraepithelial neoplasia: a retrospective study. Am J Obstet Gynecol. 2008 Aug;199(2):113.e1-5.
3. Kalogirou D et al. Vaginal intraepithelial neoplasia (VAIN) following hysterectomy in patients treated for carcinoma in situ of the cervix. Eur J Gynaecol Oncol. 1997;18(3):188-91.
5. Latif NA et al. Management of adenocarcinoma in situ of the uterine cervix: a comparison of loop electrosurgical excision procedure and cold knife conization. J Low Genit Tract Dis. 2015 Apr;19(2):97-102.
8. Barber HR et al. Operative management of patients previously operated upon for a benign lesion with cervical cancer as a surprise finding. Am J Obstet Gynecol. 1968 Aug 1;101(7):959-65.
9. Sullivan SA et al. Association between timing of cervical excision procedure to minimally invasive hysterectomy and surgical complications. Gynecol Oncol. 2017 Feb;144(2):294-298.
Cervical dysplasia is commonly diagnosed in women who have completed childbearing and don’t desire future fertility. While diagnostic and/or definitive therapy for cervical dysplasia can include hysterectomy, there are important considerations to make when offering this procedure to patients.
Dr. Emma C. Rossi
Pitfalls
Hysterectomy is commonly requested by patients upon learning of cervical dysplasia, particularly if they have chronic human papillomavirus (HPV) infection and have experienced years of frequent surveillance and interventions. They may see hysterectomy as an option to avoid this close surveillance and to be free of their dysplasia. There are two main concerns with offering hysterectomy as the primary surgical option for the management of dysplasia. Firstly, it may not be curative, and secondly, it may be an inadequate excisional procedure, particularly if the patient has occult invasive disease that has not been adequately diagnosed with a loop electrosurgical excision procedure (LEEP) or a cone biopsy procedure.
It is important to counsel these patients that surgery is not a treatment for high-risk HPV infection, which is the underlying etiology of their disease. With that etiology, HPV infection is likely to persist after hysterectomy and they may develop vaginal or vulvar dysplasia. Therefore, the American Society for Colposcopy and Cervical Pathology recommends that cytology and/or high-risk HPV surveillance continue following hysterectomy if that surgery was performed for dysplasia.1 Hysterectomy is not a means to avoid years of surveillance testing. Approximately 10% of women who have hysterectomy for cervical dysplasia develop vaginal dysplasia or cancer after surgery.2,3 This is similar to the likelihood of recurrent dysplasia after an alternative excisional procedure. In my experience, this diagnosis is often met with enormous frustration for the patient who thought that her hysterectomy would be the cure of her HPV-related disease. Thorough colposcopic evaluation of the vagina can be technically challenging after hysterectomy because of difficulty adequately visualizing lesions within the vaginal rugations, particularly within the puckered lateral vaginal fornices, the most common location for dysplasia.3 We will explore the diagnosis and treatment options for vaginal dysplasia further in a future column.
It is critical that, if patients are offered hysterectomy for treatment of cervical dysplasia, they are counseled that it may not be curative, that they will require long-term vaginal surveillance, and that they are at continued risk for vaginal and vulvar cancer.
An additional concern with performing hysterectomy for definitive management of cervical dysplasia is the concern that occult cancer may be missed preoperatively, and that the hysterectomy is inadequate surgical clearance of the disease. Approximately 2%-5% of patients with a high-grade squamous intraepithelial lesion or equivocal Pap test have occult cervical cancer.4 A similar proportion of patients with cervical intraepithelial neoplasia stage III or adenocarcinoma in situ on colposcopy biopsy have invasive carcinoma on evaluation of an excisional specimen.5 The traditional surgical approach has dictated that a modified (type II) or extended (type III) radical hysterectomy be performed in the setting of FIGO stage IA2 or greater cervical cancer. Radical hysterectomies remove parametrial tissue, effectively achieving a wider margin around the primary lesion. This is important because cervical cancer primarily spreads via direct extension.
The appropriate radicality of surgery for microscopic lesions is debated. It has been proposed that for very small, low-risk lesions, a traditional extrafascial hysterectomy or trachelectomy, or possibly even a large conization, may be adequate.6 However, this is controversial, and National Comprehensive Cancer Network guidelines still advocate for radical procedures for these lesions.7 Certainly an excisional procedure (LEEP or cone) should first be performed to define the size and histologic features of the lesion, and ideally, evaluation and counseling with a gynecologic oncologist should be performed prior to offering patients with a stage IA2 or greater lesion an extrafascial hysterectomy. Additionally, a separate decision would need to be made regarding the need for lymphadenectomy, as this is typically recommended for patients with stage IA2 or greater lesions.
Patients should be counseled that, if extrafascial (simple) hysterectomy is chosen as the primary excisional procedure, they may require additional therapy (additional surgery, or radiation and possibly chemotherapy) if cancer is found in the specimen and the parametrial margin is inadequate. Additionally, and of more concern, if the lesion is a bulky lesion extending into the parametrium and not recognized preoperatively, a “cut-through” hysterectomy will be inadvertently performed (in which margins are grossly positive). These situations typically feature heavy blood loss with patients at increased risk for immediate surgical complications. Postoperatively, prognosis is substantially worse for patients who have had a cut-through hysterectomy, compared stage for stage with patients who primarily received a radical procedure with negative margins or primary chemotherapy and radiation.8 Otherwise said, their risk for death is higher if this error is made. Therefore a thorough examination is essential prior to performing hysterectomy for dysplasia. Any suspicion of bulky cancer should be considered a contraindication for proceeding.
Preoperative evaluation
As a rule, no patient should transition directly from cytologic evaluation with Pap screening to hysterectomy. A colposcopic evaluation of the cervix and vagina accompanied with a thorough bimanual rectovaginal examination should always be performed first. Biopsies of the ectocervix and ideally the endocervix should be obtained because the accuracy of histology is greater than that of cytology. For patients with cervical intraepithelial neoplasia stage I lesions, hysterectomy is not appropriate, as these patients have an extremely low risk for the development of cervical cancer, and the risks and costs of hysterectomy are not justified in such a population.
Surgeons should wait at least 6 weeks following conization or LEEP before performing hysterectomy in order to minimize the likelihood of perioperative complications.9
Substituting LEEP or cone with hysterectomy
In general, it is the most prudent approach to first perform a diagnostic excision with LEEP or cone biopsy before proceeding with hysterectomy for definitive surgery. However, there may be some situations in which this is not feasible. In patients whose cervix is very small and flush with the vagina, an excisional procedure may not be technically possible without concern for damage to adjacent structures. In these patients, after a thorough exam has evaluated for gross disease, a hysterectomy may be the only way to adequately diagnose and treat high-grade dysplasia through excision. For patients with limited access to resources, transportation, or a concern for noncompliance with follow-up, surgeons may wish to offer patients primary hysterectomy rather than a staged procedure.
Hysterectomy remains a potential option for treatment of cervical dysplasia. However, patients should be made aware of the risks of undertreatment of occult cancers, the need for long-term surveillance testing, and the risk for future vaginal dysplasia or cancer. Ideally a comprehensive, stepwise assessment from cytology to colposcopy and examination to diagnostic excisional procedure will first take place to proceed safely with this approach.
References
1. Saslow D et al. American Cancer Society, American Society for Colposcopy and Cervical Pathology, and American Society for Clinical Pathology screening guidelines for the prevention and early detection of cervical cancer. CA Cancer J Clin. 2012 May-Jun;62(3):147-72.
2. Schockaert S et al. Incidence of vaginal intraepithelial neoplasia after hysterectomy for cervical intraepithelial neoplasia: a retrospective study. Am J Obstet Gynecol. 2008 Aug;199(2):113.e1-5.
3. Kalogirou D et al. Vaginal intraepithelial neoplasia (VAIN) following hysterectomy in patients treated for carcinoma in situ of the cervix. Eur J Gynaecol Oncol. 1997;18(3):188-91.
5. Latif NA et al. Management of adenocarcinoma in situ of the uterine cervix: a comparison of loop electrosurgical excision procedure and cold knife conization. J Low Genit Tract Dis. 2015 Apr;19(2):97-102.
8. Barber HR et al. Operative management of patients previously operated upon for a benign lesion with cervical cancer as a surprise finding. Am J Obstet Gynecol. 1968 Aug 1;101(7):959-65.
9. Sullivan SA et al. Association between timing of cervical excision procedure to minimally invasive hysterectomy and surgical complications. Gynecol Oncol. 2017 Feb;144(2):294-298.
Cervical dysplasia is commonly diagnosed in women who have completed childbearing and don’t desire future fertility. While diagnostic and/or definitive therapy for cervical dysplasia can include hysterectomy, there are important considerations to make when offering this procedure to patients.
Dr. Emma C. Rossi
Pitfalls
Hysterectomy is commonly requested by patients upon learning of cervical dysplasia, particularly if they have chronic human papillomavirus (HPV) infection and have experienced years of frequent surveillance and interventions. They may see hysterectomy as an option to avoid this close surveillance and to be free of their dysplasia. There are two main concerns with offering hysterectomy as the primary surgical option for the management of dysplasia. Firstly, it may not be curative, and secondly, it may be an inadequate excisional procedure, particularly if the patient has occult invasive disease that has not been adequately diagnosed with a loop electrosurgical excision procedure (LEEP) or a cone biopsy procedure.
It is important to counsel these patients that surgery is not a treatment for high-risk HPV infection, which is the underlying etiology of their disease. With that etiology, HPV infection is likely to persist after hysterectomy and they may develop vaginal or vulvar dysplasia. Therefore, the American Society for Colposcopy and Cervical Pathology recommends that cytology and/or high-risk HPV surveillance continue following hysterectomy if that surgery was performed for dysplasia.1 Hysterectomy is not a means to avoid years of surveillance testing. Approximately 10% of women who have hysterectomy for cervical dysplasia develop vaginal dysplasia or cancer after surgery.2,3 This is similar to the likelihood of recurrent dysplasia after an alternative excisional procedure. In my experience, this diagnosis is often met with enormous frustration for the patient who thought that her hysterectomy would be the cure of her HPV-related disease. Thorough colposcopic evaluation of the vagina can be technically challenging after hysterectomy because of difficulty adequately visualizing lesions within the vaginal rugations, particularly within the puckered lateral vaginal fornices, the most common location for dysplasia.3 We will explore the diagnosis and treatment options for vaginal dysplasia further in a future column.
It is critical that, if patients are offered hysterectomy for treatment of cervical dysplasia, they are counseled that it may not be curative, that they will require long-term vaginal surveillance, and that they are at continued risk for vaginal and vulvar cancer.
An additional concern with performing hysterectomy for definitive management of cervical dysplasia is the concern that occult cancer may be missed preoperatively, and that the hysterectomy is inadequate surgical clearance of the disease. Approximately 2%-5% of patients with a high-grade squamous intraepithelial lesion or equivocal Pap test have occult cervical cancer.4 A similar proportion of patients with cervical intraepithelial neoplasia stage III or adenocarcinoma in situ on colposcopy biopsy have invasive carcinoma on evaluation of an excisional specimen.5 The traditional surgical approach has dictated that a modified (type II) or extended (type III) radical hysterectomy be performed in the setting of FIGO stage IA2 or greater cervical cancer. Radical hysterectomies remove parametrial tissue, effectively achieving a wider margin around the primary lesion. This is important because cervical cancer primarily spreads via direct extension.
The appropriate radicality of surgery for microscopic lesions is debated. It has been proposed that for very small, low-risk lesions, a traditional extrafascial hysterectomy or trachelectomy, or possibly even a large conization, may be adequate.6 However, this is controversial, and National Comprehensive Cancer Network guidelines still advocate for radical procedures for these lesions.7 Certainly an excisional procedure (LEEP or cone) should first be performed to define the size and histologic features of the lesion, and ideally, evaluation and counseling with a gynecologic oncologist should be performed prior to offering patients with a stage IA2 or greater lesion an extrafascial hysterectomy. Additionally, a separate decision would need to be made regarding the need for lymphadenectomy, as this is typically recommended for patients with stage IA2 or greater lesions.
Patients should be counseled that, if extrafascial (simple) hysterectomy is chosen as the primary excisional procedure, they may require additional therapy (additional surgery, or radiation and possibly chemotherapy) if cancer is found in the specimen and the parametrial margin is inadequate. Additionally, and of more concern, if the lesion is a bulky lesion extending into the parametrium and not recognized preoperatively, a “cut-through” hysterectomy will be inadvertently performed (in which margins are grossly positive). These situations typically feature heavy blood loss with patients at increased risk for immediate surgical complications. Postoperatively, prognosis is substantially worse for patients who have had a cut-through hysterectomy, compared stage for stage with patients who primarily received a radical procedure with negative margins or primary chemotherapy and radiation.8 Otherwise said, their risk for death is higher if this error is made. Therefore a thorough examination is essential prior to performing hysterectomy for dysplasia. Any suspicion of bulky cancer should be considered a contraindication for proceeding.
Preoperative evaluation
As a rule, no patient should transition directly from cytologic evaluation with Pap screening to hysterectomy. A colposcopic evaluation of the cervix and vagina accompanied with a thorough bimanual rectovaginal examination should always be performed first. Biopsies of the ectocervix and ideally the endocervix should be obtained because the accuracy of histology is greater than that of cytology. For patients with cervical intraepithelial neoplasia stage I lesions, hysterectomy is not appropriate, as these patients have an extremely low risk for the development of cervical cancer, and the risks and costs of hysterectomy are not justified in such a population.
Surgeons should wait at least 6 weeks following conization or LEEP before performing hysterectomy in order to minimize the likelihood of perioperative complications.9
Substituting LEEP or cone with hysterectomy
In general, it is the most prudent approach to first perform a diagnostic excision with LEEP or cone biopsy before proceeding with hysterectomy for definitive surgery. However, there may be some situations in which this is not feasible. In patients whose cervix is very small and flush with the vagina, an excisional procedure may not be technically possible without concern for damage to adjacent structures. In these patients, after a thorough exam has evaluated for gross disease, a hysterectomy may be the only way to adequately diagnose and treat high-grade dysplasia through excision. For patients with limited access to resources, transportation, or a concern for noncompliance with follow-up, surgeons may wish to offer patients primary hysterectomy rather than a staged procedure.
Hysterectomy remains a potential option for treatment of cervical dysplasia. However, patients should be made aware of the risks of undertreatment of occult cancers, the need for long-term surveillance testing, and the risk for future vaginal dysplasia or cancer. Ideally a comprehensive, stepwise assessment from cytology to colposcopy and examination to diagnostic excisional procedure will first take place to proceed safely with this approach.
References
1. Saslow D et al. American Cancer Society, American Society for Colposcopy and Cervical Pathology, and American Society for Clinical Pathology screening guidelines for the prevention and early detection of cervical cancer. CA Cancer J Clin. 2012 May-Jun;62(3):147-72.
2. Schockaert S et al. Incidence of vaginal intraepithelial neoplasia after hysterectomy for cervical intraepithelial neoplasia: a retrospective study. Am J Obstet Gynecol. 2008 Aug;199(2):113.e1-5.
3. Kalogirou D et al. Vaginal intraepithelial neoplasia (VAIN) following hysterectomy in patients treated for carcinoma in situ of the cervix. Eur J Gynaecol Oncol. 1997;18(3):188-91.
5. Latif NA et al. Management of adenocarcinoma in situ of the uterine cervix: a comparison of loop electrosurgical excision procedure and cold knife conization. J Low Genit Tract Dis. 2015 Apr;19(2):97-102.
8. Barber HR et al. Operative management of patients previously operated upon for a benign lesion with cervical cancer as a surprise finding. Am J Obstet Gynecol. 1968 Aug 1;101(7):959-65.
9. Sullivan SA et al. Association between timing of cervical excision procedure to minimally invasive hysterectomy and surgical complications. Gynecol Oncol. 2017 Feb;144(2):294-298.
“Suicide rates are increasing,” Dr. Igor Galynker said, “and I believe they will continue to rise. These are deaths of despair, and despair is increasing in our society.”
Dr. Igor GalynkerSuicide is a psychiatric issue, it’s a public health issue, and it’s a societal issue. After a celebrity dies, the message to the public is both amplified and simplified: Get help. But getting help is only part of the solution; sometimes people seek help, find it, and still die.
That said, I listened with interest to the May 16 MDedge Psychcast, “Approach assesses imminent suicide risk,” an interview with Igor Galynker, MD, PhD, author of “The Suicidal Crisis” and director of the Galynker Suicide Research Laboratory at the Icahn School of Medicine at Mount Sinai in New York. In the podcast, Dr. Galynker talked about techniques for identifying those at risk for suicide among the patients psychiatrists see for evaluation and treatment.
“Using suicidal ideation as a risk factor is flawed,” he contended. “Asking about suicidal thoughts leaves us to miss 75% of people who go on to die by suicide.” Dr. Galynker noted that suicidal thoughts are often absent or not endorsed at all and clinicians should view other factors – such as the patient’s sense of being entrapped and the clinician’s own emotional responses to the patient – as more sensitive measures of elevated suicide risk.
This informative podcast left me with more questions, so I called Dr. Galynker. Suicide remains a rare phenomenon, and most psychiatrists will have limited experience with completed suicide during the course of a career. Dr. Galynker’s interest in suicide as an area of research began after he had a patient die the year after he finished residency training. Since then, he’s had one more patient suicide, and he’s aware of eight people who have died after leaving his care. “It can be devastating,” he said.
I wanted to know what psychiatrists should be doing differently after we have identified a patient at risk. While it seems obvious that a depressed patient should be treated for major depression, it also seems obvious that our interventions are imprecisely targeted and not fully successful.
Dr. Dinah Miller
We talked about the role of hospitalization in preventing suicide. Dr. Galynker has mixed opinions on this. He noted that suicide rates skyrocket in the time right after psychiatric hospitalization. “For women, the rate is 250 times higher at the time of hospital discharge; for men it’s 100 times higher. But hospitalization may help someone to survive a transitional period and to gather their support systems.”
Dr. Galynker noted that since the podcast in May aired, the Centers for Disease Control and Prevention published findings on suicide rates in the United States. He summarized some of the key points from the findings.
“Suicide rates were going down until 1999. From 2000 to 2006, suicide rates increased by 1% per year. From 2006 until 2016, rates have increased by 2% per year. Most people who die by suicide don’t have a diagnosis of a mental illness. And finally – and what has gone unnoticed – most people who die by suicide do not express suicidal intent. In fact, in that study, suicide intent was disclosed by less than a quarter of persons both with and without known mental health conditions.”
Dr. Galynker talked about safety plans and emphasized means restriction as ways to prevent suicide, including limiting access to firearms, placing netting under bridges, and providing medications in smaller containers.
“Suicidal ideation comes late; it may happen 15 minutes before a suicidal act or attempt. We need to alert people that there are certainly things that put them at risk, and we need to look at the drivers.
“Sometimes, people die for trivial reasons.” He noted instances where a susceptible person might attempt or complete suicide after an argument or perceived slight. Work is being done to look at outreach interventions to those at risk, including phone contacts and postcards.
Untreated mental illness is often considered as a cause of suicide. Dr. Galynker, however, notes that the story is more complicated.
“We don’t have a suicide-specific diagnosis ... and people die for other reasons besides mental illness. Final romantic rejection, terminal illness, and humiliating failures in business all place people at elevated risk. We need to work to change the suicidal narrative for people away from one where life has no future; we need to help them open doors.”
Dr. Miller is the coauthor of “Committed: The Battle Over Involuntary Psychiatric Care,” (Baltimore: Johns Hopkins University Press, 2016).
“Suicide rates are increasing,” Dr. Igor Galynker said, “and I believe they will continue to rise. These are deaths of despair, and despair is increasing in our society.”
Dr. Igor GalynkerSuicide is a psychiatric issue, it’s a public health issue, and it’s a societal issue. After a celebrity dies, the message to the public is both amplified and simplified: Get help. But getting help is only part of the solution; sometimes people seek help, find it, and still die.
That said, I listened with interest to the May 16 MDedge Psychcast, “Approach assesses imminent suicide risk,” an interview with Igor Galynker, MD, PhD, author of “The Suicidal Crisis” and director of the Galynker Suicide Research Laboratory at the Icahn School of Medicine at Mount Sinai in New York. In the podcast, Dr. Galynker talked about techniques for identifying those at risk for suicide among the patients psychiatrists see for evaluation and treatment.
“Using suicidal ideation as a risk factor is flawed,” he contended. “Asking about suicidal thoughts leaves us to miss 75% of people who go on to die by suicide.” Dr. Galynker noted that suicidal thoughts are often absent or not endorsed at all and clinicians should view other factors – such as the patient’s sense of being entrapped and the clinician’s own emotional responses to the patient – as more sensitive measures of elevated suicide risk.
This informative podcast left me with more questions, so I called Dr. Galynker. Suicide remains a rare phenomenon, and most psychiatrists will have limited experience with completed suicide during the course of a career. Dr. Galynker’s interest in suicide as an area of research began after he had a patient die the year after he finished residency training. Since then, he’s had one more patient suicide, and he’s aware of eight people who have died after leaving his care. “It can be devastating,” he said.
I wanted to know what psychiatrists should be doing differently after we have identified a patient at risk. While it seems obvious that a depressed patient should be treated for major depression, it also seems obvious that our interventions are imprecisely targeted and not fully successful.
Dr. Dinah Miller
We talked about the role of hospitalization in preventing suicide. Dr. Galynker has mixed opinions on this. He noted that suicide rates skyrocket in the time right after psychiatric hospitalization. “For women, the rate is 250 times higher at the time of hospital discharge; for men it’s 100 times higher. But hospitalization may help someone to survive a transitional period and to gather their support systems.”
Dr. Galynker noted that since the podcast in May aired, the Centers for Disease Control and Prevention published findings on suicide rates in the United States. He summarized some of the key points from the findings.
“Suicide rates were going down until 1999. From 2000 to 2006, suicide rates increased by 1% per year. From 2006 until 2016, rates have increased by 2% per year. Most people who die by suicide don’t have a diagnosis of a mental illness. And finally – and what has gone unnoticed – most people who die by suicide do not express suicidal intent. In fact, in that study, suicide intent was disclosed by less than a quarter of persons both with and without known mental health conditions.”
Dr. Galynker talked about safety plans and emphasized means restriction as ways to prevent suicide, including limiting access to firearms, placing netting under bridges, and providing medications in smaller containers.
“Suicidal ideation comes late; it may happen 15 minutes before a suicidal act or attempt. We need to alert people that there are certainly things that put them at risk, and we need to look at the drivers.
“Sometimes, people die for trivial reasons.” He noted instances where a susceptible person might attempt or complete suicide after an argument or perceived slight. Work is being done to look at outreach interventions to those at risk, including phone contacts and postcards.
Untreated mental illness is often considered as a cause of suicide. Dr. Galynker, however, notes that the story is more complicated.
“We don’t have a suicide-specific diagnosis ... and people die for other reasons besides mental illness. Final romantic rejection, terminal illness, and humiliating failures in business all place people at elevated risk. We need to work to change the suicidal narrative for people away from one where life has no future; we need to help them open doors.”
Dr. Miller is the coauthor of “Committed: The Battle Over Involuntary Psychiatric Care,” (Baltimore: Johns Hopkins University Press, 2016).
“Suicide rates are increasing,” Dr. Igor Galynker said, “and I believe they will continue to rise. These are deaths of despair, and despair is increasing in our society.”
Dr. Igor GalynkerSuicide is a psychiatric issue, it’s a public health issue, and it’s a societal issue. After a celebrity dies, the message to the public is both amplified and simplified: Get help. But getting help is only part of the solution; sometimes people seek help, find it, and still die.
That said, I listened with interest to the May 16 MDedge Psychcast, “Approach assesses imminent suicide risk,” an interview with Igor Galynker, MD, PhD, author of “The Suicidal Crisis” and director of the Galynker Suicide Research Laboratory at the Icahn School of Medicine at Mount Sinai in New York. In the podcast, Dr. Galynker talked about techniques for identifying those at risk for suicide among the patients psychiatrists see for evaluation and treatment.
“Using suicidal ideation as a risk factor is flawed,” he contended. “Asking about suicidal thoughts leaves us to miss 75% of people who go on to die by suicide.” Dr. Galynker noted that suicidal thoughts are often absent or not endorsed at all and clinicians should view other factors – such as the patient’s sense of being entrapped and the clinician’s own emotional responses to the patient – as more sensitive measures of elevated suicide risk.
This informative podcast left me with more questions, so I called Dr. Galynker. Suicide remains a rare phenomenon, and most psychiatrists will have limited experience with completed suicide during the course of a career. Dr. Galynker’s interest in suicide as an area of research began after he had a patient die the year after he finished residency training. Since then, he’s had one more patient suicide, and he’s aware of eight people who have died after leaving his care. “It can be devastating,” he said.
I wanted to know what psychiatrists should be doing differently after we have identified a patient at risk. While it seems obvious that a depressed patient should be treated for major depression, it also seems obvious that our interventions are imprecisely targeted and not fully successful.
Dr. Dinah Miller
We talked about the role of hospitalization in preventing suicide. Dr. Galynker has mixed opinions on this. He noted that suicide rates skyrocket in the time right after psychiatric hospitalization. “For women, the rate is 250 times higher at the time of hospital discharge; for men it’s 100 times higher. But hospitalization may help someone to survive a transitional period and to gather their support systems.”
Dr. Galynker noted that since the podcast in May aired, the Centers for Disease Control and Prevention published findings on suicide rates in the United States. He summarized some of the key points from the findings.
“Suicide rates were going down until 1999. From 2000 to 2006, suicide rates increased by 1% per year. From 2006 until 2016, rates have increased by 2% per year. Most people who die by suicide don’t have a diagnosis of a mental illness. And finally – and what has gone unnoticed – most people who die by suicide do not express suicidal intent. In fact, in that study, suicide intent was disclosed by less than a quarter of persons both with and without known mental health conditions.”
Dr. Galynker talked about safety plans and emphasized means restriction as ways to prevent suicide, including limiting access to firearms, placing netting under bridges, and providing medications in smaller containers.
“Suicidal ideation comes late; it may happen 15 minutes before a suicidal act or attempt. We need to alert people that there are certainly things that put them at risk, and we need to look at the drivers.
“Sometimes, people die for trivial reasons.” He noted instances where a susceptible person might attempt or complete suicide after an argument or perceived slight. Work is being done to look at outreach interventions to those at risk, including phone contacts and postcards.
Untreated mental illness is often considered as a cause of suicide. Dr. Galynker, however, notes that the story is more complicated.
“We don’t have a suicide-specific diagnosis ... and people die for other reasons besides mental illness. Final romantic rejection, terminal illness, and humiliating failures in business all place people at elevated risk. We need to work to change the suicidal narrative for people away from one where life has no future; we need to help them open doors.”
Dr. Miller is the coauthor of “Committed: The Battle Over Involuntary Psychiatric Care,” (Baltimore: Johns Hopkins University Press, 2016).
