Perspectives

As the end of the academic year approaches, I always think of one last message to send to the freshly minted psychiatrists who will complete their 4 years of post-MD training. This year, I thought of emphasizing the principles of psychiatric practice, which the graduates will deliver for the next 4 to 5 decades of their professional lives. Those essential principles are coded in the DNA of psychiatric practice, just as the construction of all organs in the human body is coded within the DNA of the 22,000 genes that comprise our 23 chromosomes.

So here are the principles of psych­iatry that I propose govern the relationship of psychiatrists with their patients, encrypted within the DNA of our esteemed medical specialty:

• Provide total dedication to helping psychiatric patients recover from their illness and regain their wellness.
• Maintain total and unimpeachable confidentiality.
• Demonstrate unconditional acceptance and respect to every patient.
• Adopt a nonjudgmental stance toward all patients.
• Establish a strong therapeutic alliance as early as possible. It is the center of the doctor–patient relationship.
• Provide the same standard of care to all patients—the same care you would want your family members to receive.
• Provide evidence-based treatments first, and if no response, use unapproved treatments judiciously, but above all, do no harm.
• Educate patients, and their families, about the illness, and discuss the benefits and risks of various treatments.
• Do not practice “naked psychopharmacology.” Psychotherapy must always be provided side-by-side with medications.
• Support the patient’s family. Their burden often is very heavy.
• Emphasize adherence as a key patient responsibility, and address it at every visit.
• Do not hesitate to consult a seasoned colleague about your complex clinical cases.
• Deal effectively with negative countertransference. Recognize it, and refer the patient to another colleague if you cannot resolve it.
• Always inquire about thoughts of harming self or others and act accordingly.
• Always ask about alcohol and substance use, and about over-the-counter drugs as well. They all can complicate your patient’s treatment course and outcome.
• Never breach boundaries with your patient, and firmly guide the patient about breaching boundaries with you.
• Uphold the medical tenet that all “mental” disorders of thought, mood, affect, behavior, and cognition are generated by disruptions of brain structure and/or function, whether molecular, cellular, or connectomic, caused by various combinations of genetic and/or environmental etiologies.
• Check your patients’ physical health status, including all treatments they received from other specialists, and always rule out iatrogenesis and disruptive pharmacokinetic interactions that may trigger or exacerbate psychiatric symptoms.
• Learn and use clinical rating scales to quantify symptom severity and adverse effects at baseline and at each visit. Measuring the severity of psychosis, depression, or anxiety in psychiatry is like measuring fasting glucose, triglycerides, or blood pressure in internal medicine.
• Use rational adjunctive and augmentation therapies when indicated, but avoid irrational and hazardous polypharmacy.
• Document your clinical findings, diagnosis, and treatment plan conscientiously and accurately. The medical record is a clinical, billing, legal, and research document.
• Advocate tirelessly for psychiatric patients to increase their access to care, and fight the unfair and hurtful stigma vigorously until it is completely erased. A psychiatric disorder should have no more stigma than a broken leg or peptic ulcer, and insurance parity must be identical as well.
• Establish collaborative care for each of your patients and link them to a primary care provider if they do not already have one. Disorders of the body and the brain are bidirectional in their effects and psychiatric patients often suffer from multiple organ diseases.
• Do some pro bono care for indigent or uninsured patients, and actively ask companies to provide free drugs to patients who cannot afford the medication you believe they need.
• Recognize that every treatment you use as the current standard of care was at one time a research project. Know that the research of today is the treatment of tomorrow. So support the creation of new medical knowledge by referring patients to FDA clinical trials or to National Institutes of Health–funded biologic investigations.
• No matter how busy you are, write a case report or a letter to the editor about an unusual response or adverse effect. This generates hypotheses that researchers can pursue and test.
• Volunteer to serve as a clinical supervisor for medical students and residents from your local medical school. Most academic departments of psychiatry appreciate their community-based volunteer faculty.

You, the readers of Current Psychiatry, include thousands of experienced psychiatrists with years of practice in the real world. I invite you to add to this list of principles by writing to me at [email protected]. Join me in providing the freshly minted psychiatrists words of wisdom about the DNA of psychiatry to guide them before they embark on their careers as psychiatric physicians.

As the end of the academic year approaches, I always think of one last message to send to the freshly minted psychiatrists who will complete their 4 years of post-MD training. This year, I thought of emphasizing the principles of psychiatric practice, which the graduates will deliver for the next 4 to 5 decades of their professional lives. Those essential principles are coded in the DNA of psychiatric practice, just as the construction of all organs in the human body is coded within the DNA of the 22,000 genes that comprise our 23 chromosomes.

So here are the principles of psych­iatry that I propose govern the relationship of psychiatrists with their patients, encrypted within the DNA of our esteemed medical specialty:

• Provide total dedication to helping psychiatric patients recover from their illness and regain their wellness.
• Maintain total and unimpeachable confidentiality.
• Demonstrate unconditional acceptance and respect to every patient.
• Adopt a nonjudgmental stance toward all patients.
• Establish a strong therapeutic alliance as early as possible. It is the center of the doctor–patient relationship.
• Provide the same standard of care to all patients—the same care you would want your family members to receive.
• Provide evidence-based treatments first, and if no response, use unapproved treatments judiciously, but above all, do no harm.
• Educate patients, and their families, about the illness, and discuss the benefits and risks of various treatments.
• Do not practice “naked psychopharmacology.” Psychotherapy must always be provided side-by-side with medications.
• Support the patient’s family. Their burden often is very heavy.
• Emphasize adherence as a key patient responsibility, and address it at every visit.
• Do not hesitate to consult a seasoned colleague about your complex clinical cases.
• Deal effectively with negative countertransference. Recognize it, and refer the patient to another colleague if you cannot resolve it.
• Always inquire about thoughts of harming self or others and act accordingly.
• Always ask about alcohol and substance use, and about over-the-counter drugs as well. They all can complicate your patient’s treatment course and outcome.
• Never breach boundaries with your patient, and firmly guide the patient about breaching boundaries with you.
• Uphold the medical tenet that all “mental” disorders of thought, mood, affect, behavior, and cognition are generated by disruptions of brain structure and/or function, whether molecular, cellular, or connectomic, caused by various combinations of genetic and/or environmental etiologies.
• Check your patients’ physical health status, including all treatments they received from other specialists, and always rule out iatrogenesis and disruptive pharmacokinetic interactions that may trigger or exacerbate psychiatric symptoms.
• Learn and use clinical rating scales to quantify symptom severity and adverse effects at baseline and at each visit. Measuring the severity of psychosis, depression, or anxiety in psychiatry is like measuring fasting glucose, triglycerides, or blood pressure in internal medicine.
• Use rational adjunctive and augmentation therapies when indicated, but avoid irrational and hazardous polypharmacy.
• Document your clinical findings, diagnosis, and treatment plan conscientiously and accurately. The medical record is a clinical, billing, legal, and research document.
• Advocate tirelessly for psychiatric patients to increase their access to care, and fight the unfair and hurtful stigma vigorously until it is completely erased. A psychiatric disorder should have no more stigma than a broken leg or peptic ulcer, and insurance parity must be identical as well.
• Establish collaborative care for each of your patients and link them to a primary care provider if they do not already have one. Disorders of the body and the brain are bidirectional in their effects and psychiatric patients often suffer from multiple organ diseases.
• Do some pro bono care for indigent or uninsured patients, and actively ask companies to provide free drugs to patients who cannot afford the medication you believe they need.
• Recognize that every treatment you use as the current standard of care was at one time a research project. Know that the research of today is the treatment of tomorrow. So support the creation of new medical knowledge by referring patients to FDA clinical trials or to National Institutes of Health–funded biologic investigations.
• No matter how busy you are, write a case report or a letter to the editor about an unusual response or adverse effect. This generates hypotheses that researchers can pursue and test.
• Volunteer to serve as a clinical supervisor for medical students and residents from your local medical school. Most academic departments of psychiatry appreciate their community-based volunteer faculty.

You, the readers of Current Psychiatry, include thousands of experienced psychiatrists with years of practice in the real world. I invite you to add to this list of principles by writing to me at [email protected]. Join me in providing the freshly minted psychiatrists words of wisdom about the DNA of psychiatry to guide them before they embark on their careers as psychiatric physicians.

As the end of the academic year approaches, I always think of one last message to send to the freshly minted psychiatrists who will complete their 4 years of post-MD training. This year, I thought of emphasizing the principles of psychiatric practice, which the graduates will deliver for the next 4 to 5 decades of their professional lives. Those essential principles are coded in the DNA of psychiatric practice, just as the construction of all organs in the human body is coded within the DNA of the 22,000 genes that comprise our 23 chromosomes.

So here are the principles of psych­iatry that I propose govern the relationship of psychiatrists with their patients, encrypted within the DNA of our esteemed medical specialty:

• Provide total dedication to helping psychiatric patients recover from their illness and regain their wellness.
• Maintain total and unimpeachable confidentiality.
• Demonstrate unconditional acceptance and respect to every patient.
• Adopt a nonjudgmental stance toward all patients.
• Establish a strong therapeutic alliance as early as possible. It is the center of the doctor–patient relationship.
• Provide the same standard of care to all patients—the same care you would want your family members to receive.
• Provide evidence-based treatments first, and if no response, use unapproved treatments judiciously, but above all, do no harm.
• Educate patients, and their families, about the illness, and discuss the benefits and risks of various treatments.
• Do not practice “naked psychopharmacology.” Psychotherapy must always be provided side-by-side with medications.
• Support the patient’s family. Their burden often is very heavy.
• Emphasize adherence as a key patient responsibility, and address it at every visit.
• Do not hesitate to consult a seasoned colleague about your complex clinical cases.
• Deal effectively with negative countertransference. Recognize it, and refer the patient to another colleague if you cannot resolve it.
• Always inquire about thoughts of harming self or others and act accordingly.
• Always ask about alcohol and substance use, and about over-the-counter drugs as well. They all can complicate your patient’s treatment course and outcome.
• Never breach boundaries with your patient, and firmly guide the patient about breaching boundaries with you.
• Uphold the medical tenet that all “mental” disorders of thought, mood, affect, behavior, and cognition are generated by disruptions of brain structure and/or function, whether molecular, cellular, or connectomic, caused by various combinations of genetic and/or environmental etiologies.
• Check your patients’ physical health status, including all treatments they received from other specialists, and always rule out iatrogenesis and disruptive pharmacokinetic interactions that may trigger or exacerbate psychiatric symptoms.
• Learn and use clinical rating scales to quantify symptom severity and adverse effects at baseline and at each visit. Measuring the severity of psychosis, depression, or anxiety in psychiatry is like measuring fasting glucose, triglycerides, or blood pressure in internal medicine.
• Use rational adjunctive and augmentation therapies when indicated, but avoid irrational and hazardous polypharmacy.
• Document your clinical findings, diagnosis, and treatment plan conscientiously and accurately. The medical record is a clinical, billing, legal, and research document.
• Advocate tirelessly for psychiatric patients to increase their access to care, and fight the unfair and hurtful stigma vigorously until it is completely erased. A psychiatric disorder should have no more stigma than a broken leg or peptic ulcer, and insurance parity must be identical as well.
• Establish collaborative care for each of your patients and link them to a primary care provider if they do not already have one. Disorders of the body and the brain are bidirectional in their effects and psychiatric patients often suffer from multiple organ diseases.
• Do some pro bono care for indigent or uninsured patients, and actively ask companies to provide free drugs to patients who cannot afford the medication you believe they need.
• Recognize that every treatment you use as the current standard of care was at one time a research project. Know that the research of today is the treatment of tomorrow. So support the creation of new medical knowledge by referring patients to FDA clinical trials or to National Institutes of Health–funded biologic investigations.
• No matter how busy you are, write a case report or a letter to the editor about an unusual response or adverse effect. This generates hypotheses that researchers can pursue and test.
• Volunteer to serve as a clinical supervisor for medical students and residents from your local medical school. Most academic departments of psychiatry appreciate their community-based volunteer faculty.

You, the readers of Current Psychiatry, include thousands of experienced psychiatrists with years of practice in the real world. I invite you to add to this list of principles by writing to me at [email protected]. Join me in providing the freshly minted psychiatrists words of wisdom about the DNA of psychiatry to guide them before they embark on their careers as psychiatric physicians.

The Goldwater Rule and free speech

In his editorial, “The toxic zeitgeist of hyper-partisanship: A psychiatric perspective” (From the Editor, Current Psychiatry, February 2018, p. 17-18), Dr. Nasrallah notes that he “adheres” to the APA’s Goldwater Rule. The Goldwater Rule and the reason for its creation and current implementation in the United States cannot be fully understood without appreciating the political circumstances that led to its creation in 1964. The conservative movement had been using the slogan “better dead than red” to criticize Democrats who they felt were soft on communism. Unfortunately, some psychiatrists took these words and the views of Arizona senator Barry Goldwater quite literally. They claimed they understood his psychological structure by listening to his political views, and feared that he would risk starting a nuclear war. Of course, no psychiatrist actually examined senator Goldwater. During the 1964 presidential campaign, a television commercial from President Lyndon B. Johnson’s campaign included a mushroom cloud of a nuclear explosion with an implicit reference to senator Goldwater and the “better dead than red” slogan. In the end, psychiatry, and particularly psychoanalysis, as well as President Johnson’s campaign, were embarrassed.

One’s political views do not inform us of his or her mental health status. This appreciation can be obtained only by a thorough psychological assessment. This is the basis of the Goldwater Rule, coupled with the ethical responsibility not to discuss patients’ private communications.

Today, this rule is tested by the behavior and actions of President Donald Trump. Proponents of the Goldwater Rule state that a psychiatrist cannot diagnose someone without performing a face-to-face diagnostic evaluation. This assumes psychiatrists diagnose patients only by interviewing them. However, any psychiatrist who has worked in an emergency room has signed involuntary commitment papers for a patient who refuses to talk to them. This clinical action typically is based on reports of the patient’s potential dangerousness from family, friends, or the police.

The diagnostic criteria for some personality disorders are based only on observed or reported behavior. They do not indicate a need for an interview.  The diagnosis of a personality disorder cannot be made solely by interviewing an individual without knowledge of his or her behavior. Interviewing Bernie Madoff would not have revealed his sociopathic behavior.

The critical question may not be whether one could ethically make a psychiatric diagnosis of the President (I believe you can), but rather would it indicate or imply that he is dangerous? History informs us that the existence of a psychiatric disorder does not determine a politician’s fitness for office or if they are dangerous. Behavioral accounts of President Abraham Lincoln and his self-reports seem to confirm that at times he was depressed, but he clearly served our country with distinction.

Finally, it is not clear whether the Goldwater Rule is legal. It arguably interferes with a psychiatrist’s right of free speech without the risk of being accused of unethical behavior. I wonder what would happen if it were tested in court. Does the First Amendment of the U.S. Constitution protect a psychiatrist’s right to speak freely?

Sidney Weissman, MD
Clinical Professor of Psychiatry and Behavioral Science
Feinberg School of Medicine
Northwestern University
Chicago, Illinois

The current ‘political morass’

Thank you, Dr. Nasrallah, for the wonderful synopsis of the current political morass in your editorial (From the Editor, Current Psychiatry, February 2018, p. 17-18). You followed Descartes’ dictum: you thought about matters in a novel fashion. I will assertively share this with others. It is a good piece of teaching.

James Gallagher, MD
Private psychiatric practice
Des Moines, Iowa

Continue to: The biological etiology of compulsive sexual behavior

Dr. Grant’s article, “Compulsive sexual behavior: A nonjudgmental approach” (Evidence-Based Reviews, Current Psychiatry, February 2018, p. 34,38-40,45-46), puts a well-deserved spotlight on a relatively underrecognized problem that most psychiatrists will encounter at least once during clinical practice. While the article is overall helpful, it completely leaves out any possible biological etiology and underpinnings to the condition that may be important to address while evaluating someone with compulsive sexual behavior. Specifically, are there any endocrine issues that should be considered that may also impact our approach to its treatment?

Mukesh Sanghadia, MD, MRCPsych (UK), Diplomate ABPN
PsychiatristCommunity Research Foundation
San Diego, California

The author responds

Dr. Sanghadia highlights the lack of possible biological etiology of compulsive sexual behavior (CSB) in my article. This is a fair comment. The lack of agreed-upon diagnostic criteria, however, has resulted in a vast literature discussing sexual behaviors that may or may not be related to each other, and even suggest that what is currently referred to as CSB may in fact be quite heterogeneous. My article mentions the few neuroimaging and neurocognitive studies that address a more rigorously defined CSB. Other possible etiologies have been suggested for a range of out-of-control sexual behaviors, but have not been studied with a focus on this formal diagnostic category. For example, endocrine issues have been explored to some extent in individuals with paraphilic sexual behaviors (behaviors that appear to many to have no relationship to CSB as discussed in my article), and in those cases of paraphilic sexual behavior, a range of endocrine hormones have been examined—gonadotropin-releasing hormone, follicle-stimulating hormone, luteinizing hormone, testosterone/dihydrotestosterone, and estrogen/progesterone. But these studies have yielded no conclusive outcomes in terms of findings or treatments.

In summary, the biology of CSB lags far behind that of other mental health disorders (and even other psychiatric disorders lack conclusive biological etiologies). Establishing this behavior as a legitimate diagnostic entity with agreed-upon criteria may be the first step in furthering our understanding of its possible biology.

Jon E. Grant, JD, MD, MPH
Professor
Department of Psychiatry and Behavioral Neuroscience
University of Chicago, Pritzker School of Medicine
Chicago, Illinois

Continue to: A different view of patients with schizophrenia

After treating patients with schizophrenia for more than 30 years, I’ve observed a continuous flood of information about them. This overload has been consistent since my residency back in the 1980s. Theories ranging from the psychoanalytic to the biologic are numerous and valuable additions to our understanding of those who suffer with this malady, yet they provide no summation or overview with which to understand it.

For instance, we know that schizophrenia usually begins in the late teens or early twenties. We know that antidopaminergic medications usually help to varying degrees. Psychosocial interventions may contribute greatly to the ultimate outcome. Substance use invariably makes it worse. Establishing a connection with the patient can often be helpful. Medication compliance is crucial.

It is more or less accepted that there is deterioration of higher brain functions, hypofrontality, as well as so-called dysconnectivity of white matter. There is a genetic vulnerability, and there seems to be an excess of inflammation and changes in mitochondria. Most patients have low functioning, poor compensation, and a lack of social adeptness. However, some patients can recover quite nicely. Although most of us would agree that this is not dementia, we’d also concede that these patients’ cognitive functioning is not what it used to be. Electroconvulsive therapy also can sometimes be helpful.

So, how are we to view our patients with schizophrenia in a way that can be illuminating and give us a deeper sense of understanding this quizzical disorder? It has been helpful to me to regard these individuals as a people whose brain function has been usurped by a more primitive organization that is characterized by:

• a reduction in mental development, where patients function in a more childlike way with magical thinking and impaired reality-testing
• atrophy of higher brain structures, leading to hallucinatory experiences
• a hyper-dominergic state
• a usually gradual onset with some evidence of struggle between the old and new brain organizations
• impaired prepulse inhibition that’s likely secondary to diffuseness of thought
• eventual demise of higher brain structures with an inability to respond to anti-dopaminergics. (Antipsychotics can push the brain organization closer to the adult structure attained before the onset of the disease, at least initially.)

The list goes on. Thinking about patients with schizophrenia in this way allows me to appreciate what I feel is a more encompassing view of who they are and how they got there. I have some theories about where this more primitive organization may have originated, but whatever its origin, in a small percentage of people it is there, ready to assume control of their thinking just as they are reaching reproductive age. Early intervention and medication compliance may minimize damage.

If a theory helps us gain a greater understanding of our patients, then it’s worth considering. This proposition fits much of what we know about schizophrenia. Reading patients’ firsthand accounts of the illness helps confirm, in my opinion, this point of view.

Steven Lesk, MD
Private psychiatric practice
Fridley, Minnesota

Continue to: Cognitive impairment in schizophrenia

The authors of “Suspicious, sleepless, and smoking” (Cases That Test Your Skills, Current Psychiatry, September 2017, p. 49-50,52-54) assert that “…the severity of cognitive impairment in schizophrenia has no association with the positive symptoms of schizophrenia” and they add, “Treatment of the cognitive symptoms of schizophrenia with antipsychotics has been largely ineffective.” However, in the case they present, Mr. F appears to demonstrate just the opposite: He is given antipsychotics, and over the course of his hospital stay, both his positive symptoms and his cognition improve. His scores on the Montreal Cognitive Assessment increase from 9 (Day 11) to 15 (Day 16) to 21 (Day 24). Thus, in this particular case, treatment with antipsychotics is clearly associated with cognitive improvement.

During the past 15 years, I have routinely measured cognitive functioning in patients with schizophrenia. Some have no impairment, some have severe impairment, and some fall in between these extremes. Most often, impairment occurs in the area of executive function, which can lead to significant disability. Indeed, positive symptoms can clear up completely with treatment, but the deficits in executive functioning can remain.

I think it is fair to say that cognitive impairment is a common, although not nearly universal, feature of schizophrenia that sometimes improves with antipsychotic medication. I look forward to the advent of more clinicians paying attention to the issue of cognition in schizophrenia and, hopefully, better treatments for it.

John M. Mahoney, PhD
Shasta Psychiatric Hospital
Redding, California

The authors respond

We thank Dr. Mahoney for his thoughtful letter and queries into the case of Mr. F.

First, regarding the prevalence of cognitive impairment in schizophrenia, it is our opinion that cognitive impairment is a distinct, core, and nearly universal feature of schizophrenia. This also is the conclusion of many clinicians and researchers based on their significant work in the field; still, just as in our initial case study, we concede that these symptoms are not part of the DSM-5’s formal diagnostic criteria.

The core question Dr. Mahoney seems to pose is whether we contradicted ourselves. We assert that cognitive impairment in schizophrenia is not effectively treated with existing medications, and yet we described Mr. F’s cognitive improvement after he received risperidone, 2 mg/d, titrated up to 2 mg twice daily. We first pointed out that part of our treatment strategy was to target comorbid depression in this patient; nonetheless, Dr. Mahoney’s question remains valid, and we will attempt to answer.

Dr. Mahoney has observed that his patients with schizophrenia variably experience improved cognition, and notes that executive function is a particularly common lingering impairment. On this we wholly agree; this is a helpful point of clarification, and a useful distinction in light of the above question. Improvement in positive and negative symptoms of schizophrenia, as psychosis resolves, is a well-known and studied effect of antipsychotic therapy. As a result, the sensorium becomes more congruent with external reality, and one would expect the patient to display improved orientation. This then might be reasonably expected to produce mental status improvements; however, while some improvement is frequently observed, this is neither consistent nor complete improvement. In the case of Mr. F, we document improvement, but also significant continued impairment. Thus, we maintain that treating the cognitive symptoms of schizophrenia with antipsychotics has been largely ineffective.

We do not see this as a slight distinction or an argument of minutiae. That patients frequently experience some degree of lingering impairment is a salient point. Neurocognitive impairment is a strong contributor to and predictor of disability in schizophrenia, and neurocognitive abilities most strongly predict functional outcomes. From a patient’s point of view, these symptoms have real-world consequences. Thus, we believe they should be evaluated and treated as aggressively and consistently as other schizophrenia symptoms.

In our case, we attempted to convey one primary message: Despite the challenges of treatment, there are viable options that should be pursued in the treatment of schizophrenia-related cognitive impairments. Nonpharmacologic modalities have shown encouraging results. Cognitive remediation therapy produces durable cognitive improvement—especially when combined with adjunctive therapies, such as small group therapy and vocational rehabilitation, and when comorbid conditions (major depressive disorder in Mr. F’s case) are treated.

In summary, we reiterate that cognitive impairments in schizophrenia represent a strong predictor of patient-oriented outcomes; we maintain our assertion regarding their inadequate treatment with existing medications; and we suggest that future trials attempt to find effective alternative strategies. We encourage psychiatric clinicians to approach treatment of this facet of pathology with an open mind, and to utilize alternative multi-modal therapies for the benefit of their patients with schizophrenia while waiting for new safe and effective pharmaceutical regimens.

Jarrett Dawson, MD
Family medicine resident
Department of Psychiatry
Saint Louis University
St. Louis, Missouri

Catalina Belean, MD
Assistant Professor
Department of Psychiatry
Saint Louis University
St. Louis, Missouri

The Goldwater Rule and free speech

In his editorial, “The toxic zeitgeist of hyper-partisanship: A psychiatric perspective” (From the Editor, Current Psychiatry, February 2018, p. 17-18), Dr. Nasrallah notes that he “adheres” to the APA’s Goldwater Rule. The Goldwater Rule and the reason for its creation and current implementation in the United States cannot be fully understood without appreciating the political circumstances that led to its creation in 1964. The conservative movement had been using the slogan “better dead than red” to criticize Democrats who they felt were soft on communism. Unfortunately, some psychiatrists took these words and the views of Arizona senator Barry Goldwater quite literally. They claimed they understood his psychological structure by listening to his political views, and feared that he would risk starting a nuclear war. Of course, no psychiatrist actually examined senator Goldwater. During the 1964 presidential campaign, a television commercial from President Lyndon B. Johnson’s campaign included a mushroom cloud of a nuclear explosion with an implicit reference to senator Goldwater and the “better dead than red” slogan. In the end, psychiatry, and particularly psychoanalysis, as well as President Johnson’s campaign, were embarrassed.

One’s political views do not inform us of his or her mental health status. This appreciation can be obtained only by a thorough psychological assessment. This is the basis of the Goldwater Rule, coupled with the ethical responsibility not to discuss patients’ private communications.

Today, this rule is tested by the behavior and actions of President Donald Trump. Proponents of the Goldwater Rule state that a psychiatrist cannot diagnose someone without performing a face-to-face diagnostic evaluation. This assumes psychiatrists diagnose patients only by interviewing them. However, any psychiatrist who has worked in an emergency room has signed involuntary commitment papers for a patient who refuses to talk to them. This clinical action typically is based on reports of the patient’s potential dangerousness from family, friends, or the police.

The diagnostic criteria for some personality disorders are based only on observed or reported behavior. They do not indicate a need for an interview.  The diagnosis of a personality disorder cannot be made solely by interviewing an individual without knowledge of his or her behavior. Interviewing Bernie Madoff would not have revealed his sociopathic behavior.

The critical question may not be whether one could ethically make a psychiatric diagnosis of the President (I believe you can), but rather would it indicate or imply that he is dangerous? History informs us that the existence of a psychiatric disorder does not determine a politician’s fitness for office or if they are dangerous. Behavioral accounts of President Abraham Lincoln and his self-reports seem to confirm that at times he was depressed, but he clearly served our country with distinction.

Finally, it is not clear whether the Goldwater Rule is legal. It arguably interferes with a psychiatrist’s right of free speech without the risk of being accused of unethical behavior. I wonder what would happen if it were tested in court. Does the First Amendment of the U.S. Constitution protect a psychiatrist’s right to speak freely?

Sidney Weissman, MD
Clinical Professor of Psychiatry and Behavioral Science
Feinberg School of Medicine
Northwestern University
Chicago, Illinois

The current ‘political morass’

Thank you, Dr. Nasrallah, for the wonderful synopsis of the current political morass in your editorial (From the Editor, Current Psychiatry, February 2018, p. 17-18). You followed Descartes’ dictum: you thought about matters in a novel fashion. I will assertively share this with others. It is a good piece of teaching.

James Gallagher, MD
Private psychiatric practice
Des Moines, Iowa

Continue to: The biological etiology of compulsive sexual behavior

Dr. Grant’s article, “Compulsive sexual behavior: A nonjudgmental approach” (Evidence-Based Reviews, Current Psychiatry, February 2018, p. 34,38-40,45-46), puts a well-deserved spotlight on a relatively underrecognized problem that most psychiatrists will encounter at least once during clinical practice. While the article is overall helpful, it completely leaves out any possible biological etiology and underpinnings to the condition that may be important to address while evaluating someone with compulsive sexual behavior. Specifically, are there any endocrine issues that should be considered that may also impact our approach to its treatment?

Mukesh Sanghadia, MD, MRCPsych (UK), Diplomate ABPN
PsychiatristCommunity Research Foundation
San Diego, California

The author responds

Dr. Sanghadia highlights the lack of possible biological etiology of compulsive sexual behavior (CSB) in my article. This is a fair comment. The lack of agreed-upon diagnostic criteria, however, has resulted in a vast literature discussing sexual behaviors that may or may not be related to each other, and even suggest that what is currently referred to as CSB may in fact be quite heterogeneous. My article mentions the few neuroimaging and neurocognitive studies that address a more rigorously defined CSB. Other possible etiologies have been suggested for a range of out-of-control sexual behaviors, but have not been studied with a focus on this formal diagnostic category. For example, endocrine issues have been explored to some extent in individuals with paraphilic sexual behaviors (behaviors that appear to many to have no relationship to CSB as discussed in my article), and in those cases of paraphilic sexual behavior, a range of endocrine hormones have been examined—gonadotropin-releasing hormone, follicle-stimulating hormone, luteinizing hormone, testosterone/dihydrotestosterone, and estrogen/progesterone. But these studies have yielded no conclusive outcomes in terms of findings or treatments.

In summary, the biology of CSB lags far behind that of other mental health disorders (and even other psychiatric disorders lack conclusive biological etiologies). Establishing this behavior as a legitimate diagnostic entity with agreed-upon criteria may be the first step in furthering our understanding of its possible biology.

Jon E. Grant, JD, MD, MPH
Professor
Department of Psychiatry and Behavioral Neuroscience
University of Chicago, Pritzker School of Medicine
Chicago, Illinois

Continue to: A different view of patients with schizophrenia

After treating patients with schizophrenia for more than 30 years, I’ve observed a continuous flood of information about them. This overload has been consistent since my residency back in the 1980s. Theories ranging from the psychoanalytic to the biologic are numerous and valuable additions to our understanding of those who suffer with this malady, yet they provide no summation or overview with which to understand it.

For instance, we know that schizophrenia usually begins in the late teens or early twenties. We know that antidopaminergic medications usually help to varying degrees. Psychosocial interventions may contribute greatly to the ultimate outcome. Substance use invariably makes it worse. Establishing a connection with the patient can often be helpful. Medication compliance is crucial.

It is more or less accepted that there is deterioration of higher brain functions, hypofrontality, as well as so-called dysconnectivity of white matter. There is a genetic vulnerability, and there seems to be an excess of inflammation and changes in mitochondria. Most patients have low functioning, poor compensation, and a lack of social adeptness. However, some patients can recover quite nicely. Although most of us would agree that this is not dementia, we’d also concede that these patients’ cognitive functioning is not what it used to be. Electroconvulsive therapy also can sometimes be helpful.

So, how are we to view our patients with schizophrenia in a way that can be illuminating and give us a deeper sense of understanding this quizzical disorder? It has been helpful to me to regard these individuals as a people whose brain function has been usurped by a more primitive organization that is characterized by:

• a reduction in mental development, where patients function in a more childlike way with magical thinking and impaired reality-testing
• atrophy of higher brain structures, leading to hallucinatory experiences
• a hyper-dominergic state
• a usually gradual onset with some evidence of struggle between the old and new brain organizations
• impaired prepulse inhibition that’s likely secondary to diffuseness of thought
• eventual demise of higher brain structures with an inability to respond to anti-dopaminergics. (Antipsychotics can push the brain organization closer to the adult structure attained before the onset of the disease, at least initially.)

The list goes on. Thinking about patients with schizophrenia in this way allows me to appreciate what I feel is a more encompassing view of who they are and how they got there. I have some theories about where this more primitive organization may have originated, but whatever its origin, in a small percentage of people it is there, ready to assume control of their thinking just as they are reaching reproductive age. Early intervention and medication compliance may minimize damage.

If a theory helps us gain a greater understanding of our patients, then it’s worth considering. This proposition fits much of what we know about schizophrenia. Reading patients’ firsthand accounts of the illness helps confirm, in my opinion, this point of view.

Steven Lesk, MD
Private psychiatric practice
Fridley, Minnesota

Continue to: Cognitive impairment in schizophrenia

The authors of “Suspicious, sleepless, and smoking” (Cases That Test Your Skills, Current Psychiatry, September 2017, p. 49-50,52-54) assert that “…the severity of cognitive impairment in schizophrenia has no association with the positive symptoms of schizophrenia” and they add, “Treatment of the cognitive symptoms of schizophrenia with antipsychotics has been largely ineffective.” However, in the case they present, Mr. F appears to demonstrate just the opposite: He is given antipsychotics, and over the course of his hospital stay, both his positive symptoms and his cognition improve. His scores on the Montreal Cognitive Assessment increase from 9 (Day 11) to 15 (Day 16) to 21 (Day 24). Thus, in this particular case, treatment with antipsychotics is clearly associated with cognitive improvement.

During the past 15 years, I have routinely measured cognitive functioning in patients with schizophrenia. Some have no impairment, some have severe impairment, and some fall in between these extremes. Most often, impairment occurs in the area of executive function, which can lead to significant disability. Indeed, positive symptoms can clear up completely with treatment, but the deficits in executive functioning can remain.

I think it is fair to say that cognitive impairment is a common, although not nearly universal, feature of schizophrenia that sometimes improves with antipsychotic medication. I look forward to the advent of more clinicians paying attention to the issue of cognition in schizophrenia and, hopefully, better treatments for it.

John M. Mahoney, PhD
Shasta Psychiatric Hospital
Redding, California

The authors respond

We thank Dr. Mahoney for his thoughtful letter and queries into the case of Mr. F.

First, regarding the prevalence of cognitive impairment in schizophrenia, it is our opinion that cognitive impairment is a distinct, core, and nearly universal feature of schizophrenia. This also is the conclusion of many clinicians and researchers based on their significant work in the field; still, just as in our initial case study, we concede that these symptoms are not part of the DSM-5’s formal diagnostic criteria.

The core question Dr. Mahoney seems to pose is whether we contradicted ourselves. We assert that cognitive impairment in schizophrenia is not effectively treated with existing medications, and yet we described Mr. F’s cognitive improvement after he received risperidone, 2 mg/d, titrated up to 2 mg twice daily. We first pointed out that part of our treatment strategy was to target comorbid depression in this patient; nonetheless, Dr. Mahoney’s question remains valid, and we will attempt to answer.

Dr. Mahoney has observed that his patients with schizophrenia variably experience improved cognition, and notes that executive function is a particularly common lingering impairment. On this we wholly agree; this is a helpful point of clarification, and a useful distinction in light of the above question. Improvement in positive and negative symptoms of schizophrenia, as psychosis resolves, is a well-known and studied effect of antipsychotic therapy. As a result, the sensorium becomes more congruent with external reality, and one would expect the patient to display improved orientation. This then might be reasonably expected to produce mental status improvements; however, while some improvement is frequently observed, this is neither consistent nor complete improvement. In the case of Mr. F, we document improvement, but also significant continued impairment. Thus, we maintain that treating the cognitive symptoms of schizophrenia with antipsychotics has been largely ineffective.

We do not see this as a slight distinction or an argument of minutiae. That patients frequently experience some degree of lingering impairment is a salient point. Neurocognitive impairment is a strong contributor to and predictor of disability in schizophrenia, and neurocognitive abilities most strongly predict functional outcomes. From a patient’s point of view, these symptoms have real-world consequences. Thus, we believe they should be evaluated and treated as aggressively and consistently as other schizophrenia symptoms.

In our case, we attempted to convey one primary message: Despite the challenges of treatment, there are viable options that should be pursued in the treatment of schizophrenia-related cognitive impairments. Nonpharmacologic modalities have shown encouraging results. Cognitive remediation therapy produces durable cognitive improvement—especially when combined with adjunctive therapies, such as small group therapy and vocational rehabilitation, and when comorbid conditions (major depressive disorder in Mr. F’s case) are treated.

In summary, we reiterate that cognitive impairments in schizophrenia represent a strong predictor of patient-oriented outcomes; we maintain our assertion regarding their inadequate treatment with existing medications; and we suggest that future trials attempt to find effective alternative strategies. We encourage psychiatric clinicians to approach treatment of this facet of pathology with an open mind, and to utilize alternative multi-modal therapies for the benefit of their patients with schizophrenia while waiting for new safe and effective pharmaceutical regimens.

Jarrett Dawson, MD
Family medicine resident
Department of Psychiatry
Saint Louis University
St. Louis, Missouri

Catalina Belean, MD
Assistant Professor
Department of Psychiatry
Saint Louis University
St. Louis, Missouri

The Goldwater Rule and free speech

In his editorial, “The toxic zeitgeist of hyper-partisanship: A psychiatric perspective” (From the Editor, Current Psychiatry, February 2018, p. 17-18), Dr. Nasrallah notes that he “adheres” to the APA’s Goldwater Rule. The Goldwater Rule and the reason for its creation and current implementation in the United States cannot be fully understood without appreciating the political circumstances that led to its creation in 1964. The conservative movement had been using the slogan “better dead than red” to criticize Democrats who they felt were soft on communism. Unfortunately, some psychiatrists took these words and the views of Arizona senator Barry Goldwater quite literally. They claimed they understood his psychological structure by listening to his political views, and feared that he would risk starting a nuclear war. Of course, no psychiatrist actually examined senator Goldwater. During the 1964 presidential campaign, a television commercial from President Lyndon B. Johnson’s campaign included a mushroom cloud of a nuclear explosion with an implicit reference to senator Goldwater and the “better dead than red” slogan. In the end, psychiatry, and particularly psychoanalysis, as well as President Johnson’s campaign, were embarrassed.

One’s political views do not inform us of his or her mental health status. This appreciation can be obtained only by a thorough psychological assessment. This is the basis of the Goldwater Rule, coupled with the ethical responsibility not to discuss patients’ private communications.

Today, this rule is tested by the behavior and actions of President Donald Trump. Proponents of the Goldwater Rule state that a psychiatrist cannot diagnose someone without performing a face-to-face diagnostic evaluation. This assumes psychiatrists diagnose patients only by interviewing them. However, any psychiatrist who has worked in an emergency room has signed involuntary commitment papers for a patient who refuses to talk to them. This clinical action typically is based on reports of the patient’s potential dangerousness from family, friends, or the police.

The diagnostic criteria for some personality disorders are based only on observed or reported behavior. They do not indicate a need for an interview.  The diagnosis of a personality disorder cannot be made solely by interviewing an individual without knowledge of his or her behavior. Interviewing Bernie Madoff would not have revealed his sociopathic behavior.

The critical question may not be whether one could ethically make a psychiatric diagnosis of the President (I believe you can), but rather would it indicate or imply that he is dangerous? History informs us that the existence of a psychiatric disorder does not determine a politician’s fitness for office or if they are dangerous. Behavioral accounts of President Abraham Lincoln and his self-reports seem to confirm that at times he was depressed, but he clearly served our country with distinction.

Finally, it is not clear whether the Goldwater Rule is legal. It arguably interferes with a psychiatrist’s right of free speech without the risk of being accused of unethical behavior. I wonder what would happen if it were tested in court. Does the First Amendment of the U.S. Constitution protect a psychiatrist’s right to speak freely?

Sidney Weissman, MD
Clinical Professor of Psychiatry and Behavioral Science
Feinberg School of Medicine
Northwestern University
Chicago, Illinois

The current ‘political morass’

Thank you, Dr. Nasrallah, for the wonderful synopsis of the current political morass in your editorial (From the Editor, Current Psychiatry, February 2018, p. 17-18). You followed Descartes’ dictum: you thought about matters in a novel fashion. I will assertively share this with others. It is a good piece of teaching.

James Gallagher, MD
Private psychiatric practice
Des Moines, Iowa

Continue to: The biological etiology of compulsive sexual behavior

Dr. Grant’s article, “Compulsive sexual behavior: A nonjudgmental approach” (Evidence-Based Reviews, Current Psychiatry, February 2018, p. 34,38-40,45-46), puts a well-deserved spotlight on a relatively underrecognized problem that most psychiatrists will encounter at least once during clinical practice. While the article is overall helpful, it completely leaves out any possible biological etiology and underpinnings to the condition that may be important to address while evaluating someone with compulsive sexual behavior. Specifically, are there any endocrine issues that should be considered that may also impact our approach to its treatment?

Mukesh Sanghadia, MD, MRCPsych (UK), Diplomate ABPN
PsychiatristCommunity Research Foundation
San Diego, California

The author responds

Dr. Sanghadia highlights the lack of possible biological etiology of compulsive sexual behavior (CSB) in my article. This is a fair comment. The lack of agreed-upon diagnostic criteria, however, has resulted in a vast literature discussing sexual behaviors that may or may not be related to each other, and even suggest that what is currently referred to as CSB may in fact be quite heterogeneous. My article mentions the few neuroimaging and neurocognitive studies that address a more rigorously defined CSB. Other possible etiologies have been suggested for a range of out-of-control sexual behaviors, but have not been studied with a focus on this formal diagnostic category. For example, endocrine issues have been explored to some extent in individuals with paraphilic sexual behaviors (behaviors that appear to many to have no relationship to CSB as discussed in my article), and in those cases of paraphilic sexual behavior, a range of endocrine hormones have been examined—gonadotropin-releasing hormone, follicle-stimulating hormone, luteinizing hormone, testosterone/dihydrotestosterone, and estrogen/progesterone. But these studies have yielded no conclusive outcomes in terms of findings or treatments.

In summary, the biology of CSB lags far behind that of other mental health disorders (and even other psychiatric disorders lack conclusive biological etiologies). Establishing this behavior as a legitimate diagnostic entity with agreed-upon criteria may be the first step in furthering our understanding of its possible biology.

Jon E. Grant, JD, MD, MPH
Professor
Department of Psychiatry and Behavioral Neuroscience
University of Chicago, Pritzker School of Medicine
Chicago, Illinois

Continue to: A different view of patients with schizophrenia

After treating patients with schizophrenia for more than 30 years, I’ve observed a continuous flood of information about them. This overload has been consistent since my residency back in the 1980s. Theories ranging from the psychoanalytic to the biologic are numerous and valuable additions to our understanding of those who suffer with this malady, yet they provide no summation or overview with which to understand it.

For instance, we know that schizophrenia usually begins in the late teens or early twenties. We know that antidopaminergic medications usually help to varying degrees. Psychosocial interventions may contribute greatly to the ultimate outcome. Substance use invariably makes it worse. Establishing a connection with the patient can often be helpful. Medication compliance is crucial.

It is more or less accepted that there is deterioration of higher brain functions, hypofrontality, as well as so-called dysconnectivity of white matter. There is a genetic vulnerability, and there seems to be an excess of inflammation and changes in mitochondria. Most patients have low functioning, poor compensation, and a lack of social adeptness. However, some patients can recover quite nicely. Although most of us would agree that this is not dementia, we’d also concede that these patients’ cognitive functioning is not what it used to be. Electroconvulsive therapy also can sometimes be helpful.

So, how are we to view our patients with schizophrenia in a way that can be illuminating and give us a deeper sense of understanding this quizzical disorder? It has been helpful to me to regard these individuals as a people whose brain function has been usurped by a more primitive organization that is characterized by:

• a reduction in mental development, where patients function in a more childlike way with magical thinking and impaired reality-testing
• atrophy of higher brain structures, leading to hallucinatory experiences
• a hyper-dominergic state
• a usually gradual onset with some evidence of struggle between the old and new brain organizations
• impaired prepulse inhibition that’s likely secondary to diffuseness of thought
• eventual demise of higher brain structures with an inability to respond to anti-dopaminergics. (Antipsychotics can push the brain organization closer to the adult structure attained before the onset of the disease, at least initially.)

The list goes on. Thinking about patients with schizophrenia in this way allows me to appreciate what I feel is a more encompassing view of who they are and how they got there. I have some theories about where this more primitive organization may have originated, but whatever its origin, in a small percentage of people it is there, ready to assume control of their thinking just as they are reaching reproductive age. Early intervention and medication compliance may minimize damage.

If a theory helps us gain a greater understanding of our patients, then it’s worth considering. This proposition fits much of what we know about schizophrenia. Reading patients’ firsthand accounts of the illness helps confirm, in my opinion, this point of view.

Steven Lesk, MD
Private psychiatric practice
Fridley, Minnesota

Continue to: Cognitive impairment in schizophrenia

The authors of “Suspicious, sleepless, and smoking” (Cases That Test Your Skills, Current Psychiatry, September 2017, p. 49-50,52-54) assert that “…the severity of cognitive impairment in schizophrenia has no association with the positive symptoms of schizophrenia” and they add, “Treatment of the cognitive symptoms of schizophrenia with antipsychotics has been largely ineffective.” However, in the case they present, Mr. F appears to demonstrate just the opposite: He is given antipsychotics, and over the course of his hospital stay, both his positive symptoms and his cognition improve. His scores on the Montreal Cognitive Assessment increase from 9 (Day 11) to 15 (Day 16) to 21 (Day 24). Thus, in this particular case, treatment with antipsychotics is clearly associated with cognitive improvement.

During the past 15 years, I have routinely measured cognitive functioning in patients with schizophrenia. Some have no impairment, some have severe impairment, and some fall in between these extremes. Most often, impairment occurs in the area of executive function, which can lead to significant disability. Indeed, positive symptoms can clear up completely with treatment, but the deficits in executive functioning can remain.

I think it is fair to say that cognitive impairment is a common, although not nearly universal, feature of schizophrenia that sometimes improves with antipsychotic medication. I look forward to the advent of more clinicians paying attention to the issue of cognition in schizophrenia and, hopefully, better treatments for it.

John M. Mahoney, PhD
Shasta Psychiatric Hospital
Redding, California

The authors respond

We thank Dr. Mahoney for his thoughtful letter and queries into the case of Mr. F.

First, regarding the prevalence of cognitive impairment in schizophrenia, it is our opinion that cognitive impairment is a distinct, core, and nearly universal feature of schizophrenia. This also is the conclusion of many clinicians and researchers based on their significant work in the field; still, just as in our initial case study, we concede that these symptoms are not part of the DSM-5’s formal diagnostic criteria.

The core question Dr. Mahoney seems to pose is whether we contradicted ourselves. We assert that cognitive impairment in schizophrenia is not effectively treated with existing medications, and yet we described Mr. F’s cognitive improvement after he received risperidone, 2 mg/d, titrated up to 2 mg twice daily. We first pointed out that part of our treatment strategy was to target comorbid depression in this patient; nonetheless, Dr. Mahoney’s question remains valid, and we will attempt to answer.

Dr. Mahoney has observed that his patients with schizophrenia variably experience improved cognition, and notes that executive function is a particularly common lingering impairment. On this we wholly agree; this is a helpful point of clarification, and a useful distinction in light of the above question. Improvement in positive and negative symptoms of schizophrenia, as psychosis resolves, is a well-known and studied effect of antipsychotic therapy. As a result, the sensorium becomes more congruent with external reality, and one would expect the patient to display improved orientation. This then might be reasonably expected to produce mental status improvements; however, while some improvement is frequently observed, this is neither consistent nor complete improvement. In the case of Mr. F, we document improvement, but also significant continued impairment. Thus, we maintain that treating the cognitive symptoms of schizophrenia with antipsychotics has been largely ineffective.

We do not see this as a slight distinction or an argument of minutiae. That patients frequently experience some degree of lingering impairment is a salient point. Neurocognitive impairment is a strong contributor to and predictor of disability in schizophrenia, and neurocognitive abilities most strongly predict functional outcomes. From a patient’s point of view, these symptoms have real-world consequences. Thus, we believe they should be evaluated and treated as aggressively and consistently as other schizophrenia symptoms.

In our case, we attempted to convey one primary message: Despite the challenges of treatment, there are viable options that should be pursued in the treatment of schizophrenia-related cognitive impairments. Nonpharmacologic modalities have shown encouraging results. Cognitive remediation therapy produces durable cognitive improvement—especially when combined with adjunctive therapies, such as small group therapy and vocational rehabilitation, and when comorbid conditions (major depressive disorder in Mr. F’s case) are treated.

In summary, we reiterate that cognitive impairments in schizophrenia represent a strong predictor of patient-oriented outcomes; we maintain our assertion regarding their inadequate treatment with existing medications; and we suggest that future trials attempt to find effective alternative strategies. We encourage psychiatric clinicians to approach treatment of this facet of pathology with an open mind, and to utilize alternative multi-modal therapies for the benefit of their patients with schizophrenia while waiting for new safe and effective pharmaceutical regimens.

Jarrett Dawson, MD
Family medicine resident
Department of Psychiatry
Saint Louis University
St. Louis, Missouri

Catalina Belean, MD
Assistant Professor
Department of Psychiatry
Saint Louis University
St. Louis, Missouri

The last two decades have seen an ever-growing number of reports on risks of fetal exposure to medicines used to treat depression during pregnancy. These reports have described issues ranging from estimated risk of congenital malformations following fetal exposure to various psychotropics such as SSRIs or atypical antipsychotics to adverse neonatal effects such as poor neonatal adaptation syndrome. More recent reports, derived primarily from large administrative databases, have focused on concerns regarding both risk for later childhood psychopathology such as autism or ADHD or neurobehavioral sequelae such as motor or speech delay following fetal exposure to antidepressants.

When considering the potential risks of fetal exposure to antidepressants on the spectrum of relevant outcomes, it is important to keep in mind the risks of not receiving antidepressant treatment. Data on known risks of antidepressant use during pregnancy are well described, but the literature supporting adverse effects of untreated depression during pregnancy has also grown substantially. For example, accumulated data over the last several years supports heightened risk for obstetrical and neonatal complications among women who suffer from untreated depression and recent data is inconclusive regarding the effects of untreated maternal depression on gene expression in the CNS during gestation and the effects of depression during pregnancy on development of actual brain structures in areas of the brain that modulate emotion and behavior.

monkeybusinessimages/Thinkstock

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.

The last two decades have seen an ever-growing number of reports on risks of fetal exposure to medicines used to treat depression during pregnancy. These reports have described issues ranging from estimated risk of congenital malformations following fetal exposure to various psychotropics such as SSRIs or atypical antipsychotics to adverse neonatal effects such as poor neonatal adaptation syndrome. More recent reports, derived primarily from large administrative databases, have focused on concerns regarding both risk for later childhood psychopathology such as autism or ADHD or neurobehavioral sequelae such as motor or speech delay following fetal exposure to antidepressants.

When considering the potential risks of fetal exposure to antidepressants on the spectrum of relevant outcomes, it is important to keep in mind the risks of not receiving antidepressant treatment. Data on known risks of antidepressant use during pregnancy are well described, but the literature supporting adverse effects of untreated depression during pregnancy has also grown substantially. For example, accumulated data over the last several years supports heightened risk for obstetrical and neonatal complications among women who suffer from untreated depression and recent data is inconclusive regarding the effects of untreated maternal depression on gene expression in the CNS during gestation and the effects of depression during pregnancy on development of actual brain structures in areas of the brain that modulate emotion and behavior.

monkeybusinessimages/Thinkstock

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.

The last two decades have seen an ever-growing number of reports on risks of fetal exposure to medicines used to treat depression during pregnancy. These reports have described issues ranging from estimated risk of congenital malformations following fetal exposure to various psychotropics such as SSRIs or atypical antipsychotics to adverse neonatal effects such as poor neonatal adaptation syndrome. More recent reports, derived primarily from large administrative databases, have focused on concerns regarding both risk for later childhood psychopathology such as autism or ADHD or neurobehavioral sequelae such as motor or speech delay following fetal exposure to antidepressants.

When considering the potential risks of fetal exposure to antidepressants on the spectrum of relevant outcomes, it is important to keep in mind the risks of not receiving antidepressant treatment. Data on known risks of antidepressant use during pregnancy are well described, but the literature supporting adverse effects of untreated depression during pregnancy has also grown substantially. For example, accumulated data over the last several years supports heightened risk for obstetrical and neonatal complications among women who suffer from untreated depression and recent data is inconclusive regarding the effects of untreated maternal depression on gene expression in the CNS during gestation and the effects of depression during pregnancy on development of actual brain structures in areas of the brain that modulate emotion and behavior.

monkeybusinessimages/Thinkstock

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.

Ovarian cancer most commonly follows a pattern of intraperitoneal spread, and even in the setting of bulky extra-ovarian disease, it can be thought of as being largely localized to the peritoneal compartment. This forms some of the rationale for performing extensive cytoreductive surgery (CRS) on ovarian cancer metastatic within the peritoneal cavity, and also some of the rationale for delivery of cytotoxic therapy directly to this compartment (intraperitoneal or “IP” chemotherapy). To be most effective, IP chemotherapy should be able to contact all peritoneal surfaces and be exposed to very low volume tumors (ideally no thicker than 2-mm implants).

There is a large body of evidence demonstrating the benefits of conventional IP chemotherapy in women who have received complete or “optimal” CRS to disease measuring less than 1 cm³.¹ However, IP chemotherapy is complicated by difficult administration and can be difficult for patients to tolerate. It is associated with significant toxicity, more so than what is seen from intravenous chemotherapy, and this toxicity is drawn out over the 18 (or more) weeks of therapy. It requires placement of an intraperitoneal port, and there are many problems associated with this foreign body including infection, malposition, and even erosions into underlying visceral structures. There are also concerns regarding the ability of the intraperitoneal infusions to reach all peritoneal surfaces when postoperative adhesions may have formed to pocket-off areas of the peritoneal cavity.

Hyperthermic intraperitoneal chemotherapy (HIPEC), at the time of CRS, is a strategy that has been explored to overcome some of these challenges.² HIPEC has the most history as an adjunct to the surgical management of gastrointestinal cancers (particularly appendiceal and colorectal). The technique first described by Dr. Paul H. Sugarbaker for gastrointestinal tumors remains similar to that performed in ovarian cancer.³ Patients first undergo extensive CRS until there is no macroscopic residual disease. Immediately following cytoreduction, catheters are placed into the peritoneal cavity, the main incision is temporarily closed (to prevent spillage), and an infusion of cytotoxic agents (commonly cisplatin, often with a second agent such as mitomycin C or doxorubicin) is warmed and then distilled into the peritoneal cavity until it is “moderately distended.” The patient’s body is then rolled back and forth to “wash” down the entire peritoneal cavity. All peritoneal surfaces can be touched by the agent as this procedure is happening intraoperatively prior to adhesion formation.

The “H” in HIPEC stands for hyperthermic, which is a key differentiator from traditional intraperitoneal and intravenous chemotherapy administration. Some chemotherapy agents, such as cisplatin, have a synergistic effect with hyperthermia. Some of these effects include increased oxygen free radical formation, increased cellular uptake of drug, reversal of mechanisms of drug resistance, and increases in DNA damage. The ideal range of hyperthermia is between 41° C and 44° C. At higher temperatures, infusions rates can be faster; however, higher temperatures are associated with more toxicity, particularly of the small bowel.⁴

Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill.

References

1. Armstrong DK et al. Intraperitoneal cisplatin and paclitaxel in ovarian cancer. N Engl J Med. 2006;354:34-43.

2. Helm CW et al. Hyperthermic intraperitoneal chemotherapy with and without cytoreductive surgery for epithelial ovarian cancer. J Surg Oncol. 2008;98(4):283-90.

3. Glehen O et al. Hyperthermic intraperitoneal chemotherapy: nomenclature and modalities of perfusion. J Surg Oncol. 2008;98(4):242-6.

4. Kusamura S et al. Drugs, carrier solutions and temperature in hyperthermic intraperitoneal chemotherapy. J Surg Oncol. 2008;98(4):247-52.

5. Kusamura S et al. Impact of cytoreductive surgery and hyperthermic intraperitoneal chemotherapy on systemic toxicity. Ann Surg Oncol. 2007;14(9):2550-8.

6. van Driel WJ et al. Hyperthermic Intraperitoneal Chemotherapy in Ovarian Cancer. N Engl J Med. 2018 Jan;378(3):230-240.

Ovarian cancer most commonly follows a pattern of intraperitoneal spread, and even in the setting of bulky extra-ovarian disease, it can be thought of as being largely localized to the peritoneal compartment. This forms some of the rationale for performing extensive cytoreductive surgery (CRS) on ovarian cancer metastatic within the peritoneal cavity, and also some of the rationale for delivery of cytotoxic therapy directly to this compartment (intraperitoneal or “IP” chemotherapy). To be most effective, IP chemotherapy should be able to contact all peritoneal surfaces and be exposed to very low volume tumors (ideally no thicker than 2-mm implants).

There is a large body of evidence demonstrating the benefits of conventional IP chemotherapy in women who have received complete or “optimal” CRS to disease measuring less than 1 cm³.¹ However, IP chemotherapy is complicated by difficult administration and can be difficult for patients to tolerate. It is associated with significant toxicity, more so than what is seen from intravenous chemotherapy, and this toxicity is drawn out over the 18 (or more) weeks of therapy. It requires placement of an intraperitoneal port, and there are many problems associated with this foreign body including infection, malposition, and even erosions into underlying visceral structures. There are also concerns regarding the ability of the intraperitoneal infusions to reach all peritoneal surfaces when postoperative adhesions may have formed to pocket-off areas of the peritoneal cavity.

Hyperthermic intraperitoneal chemotherapy (HIPEC), at the time of CRS, is a strategy that has been explored to overcome some of these challenges.² HIPEC has the most history as an adjunct to the surgical management of gastrointestinal cancers (particularly appendiceal and colorectal). The technique first described by Dr. Paul H. Sugarbaker for gastrointestinal tumors remains similar to that performed in ovarian cancer.³ Patients first undergo extensive CRS until there is no macroscopic residual disease. Immediately following cytoreduction, catheters are placed into the peritoneal cavity, the main incision is temporarily closed (to prevent spillage), and an infusion of cytotoxic agents (commonly cisplatin, often with a second agent such as mitomycin C or doxorubicin) is warmed and then distilled into the peritoneal cavity until it is “moderately distended.” The patient’s body is then rolled back and forth to “wash” down the entire peritoneal cavity. All peritoneal surfaces can be touched by the agent as this procedure is happening intraoperatively prior to adhesion formation.

The “H” in HIPEC stands for hyperthermic, which is a key differentiator from traditional intraperitoneal and intravenous chemotherapy administration. Some chemotherapy agents, such as cisplatin, have a synergistic effect with hyperthermia. Some of these effects include increased oxygen free radical formation, increased cellular uptake of drug, reversal of mechanisms of drug resistance, and increases in DNA damage. The ideal range of hyperthermia is between 41° C and 44° C. At higher temperatures, infusions rates can be faster; however, higher temperatures are associated with more toxicity, particularly of the small bowel.⁴

Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill.

References

1. Armstrong DK et al. Intraperitoneal cisplatin and paclitaxel in ovarian cancer. N Engl J Med. 2006;354:34-43.

2. Helm CW et al. Hyperthermic intraperitoneal chemotherapy with and without cytoreductive surgery for epithelial ovarian cancer. J Surg Oncol. 2008;98(4):283-90.

3. Glehen O et al. Hyperthermic intraperitoneal chemotherapy: nomenclature and modalities of perfusion. J Surg Oncol. 2008;98(4):242-6.

4. Kusamura S et al. Drugs, carrier solutions and temperature in hyperthermic intraperitoneal chemotherapy. J Surg Oncol. 2008;98(4):247-52.

5. Kusamura S et al. Impact of cytoreductive surgery and hyperthermic intraperitoneal chemotherapy on systemic toxicity. Ann Surg Oncol. 2007;14(9):2550-8.

6. van Driel WJ et al. Hyperthermic Intraperitoneal Chemotherapy in Ovarian Cancer. N Engl J Med. 2018 Jan;378(3):230-240.

Ovarian cancer most commonly follows a pattern of intraperitoneal spread, and even in the setting of bulky extra-ovarian disease, it can be thought of as being largely localized to the peritoneal compartment. This forms some of the rationale for performing extensive cytoreductive surgery (CRS) on ovarian cancer metastatic within the peritoneal cavity, and also some of the rationale for delivery of cytotoxic therapy directly to this compartment (intraperitoneal or “IP” chemotherapy). To be most effective, IP chemotherapy should be able to contact all peritoneal surfaces and be exposed to very low volume tumors (ideally no thicker than 2-mm implants).

There is a large body of evidence demonstrating the benefits of conventional IP chemotherapy in women who have received complete or “optimal” CRS to disease measuring less than 1 cm³.¹ However, IP chemotherapy is complicated by difficult administration and can be difficult for patients to tolerate. It is associated with significant toxicity, more so than what is seen from intravenous chemotherapy, and this toxicity is drawn out over the 18 (or more) weeks of therapy. It requires placement of an intraperitoneal port, and there are many problems associated with this foreign body including infection, malposition, and even erosions into underlying visceral structures. There are also concerns regarding the ability of the intraperitoneal infusions to reach all peritoneal surfaces when postoperative adhesions may have formed to pocket-off areas of the peritoneal cavity.

Hyperthermic intraperitoneal chemotherapy (HIPEC), at the time of CRS, is a strategy that has been explored to overcome some of these challenges.² HIPEC has the most history as an adjunct to the surgical management of gastrointestinal cancers (particularly appendiceal and colorectal). The technique first described by Dr. Paul H. Sugarbaker for gastrointestinal tumors remains similar to that performed in ovarian cancer.³ Patients first undergo extensive CRS until there is no macroscopic residual disease. Immediately following cytoreduction, catheters are placed into the peritoneal cavity, the main incision is temporarily closed (to prevent spillage), and an infusion of cytotoxic agents (commonly cisplatin, often with a second agent such as mitomycin C or doxorubicin) is warmed and then distilled into the peritoneal cavity until it is “moderately distended.” The patient’s body is then rolled back and forth to “wash” down the entire peritoneal cavity. All peritoneal surfaces can be touched by the agent as this procedure is happening intraoperatively prior to adhesion formation.

The “H” in HIPEC stands for hyperthermic, which is a key differentiator from traditional intraperitoneal and intravenous chemotherapy administration. Some chemotherapy agents, such as cisplatin, have a synergistic effect with hyperthermia. Some of these effects include increased oxygen free radical formation, increased cellular uptake of drug, reversal of mechanisms of drug resistance, and increases in DNA damage. The ideal range of hyperthermia is between 41° C and 44° C. At higher temperatures, infusions rates can be faster; however, higher temperatures are associated with more toxicity, particularly of the small bowel.⁴

Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill.

References

1. Armstrong DK et al. Intraperitoneal cisplatin and paclitaxel in ovarian cancer. N Engl J Med. 2006;354:34-43.

2. Helm CW et al. Hyperthermic intraperitoneal chemotherapy with and without cytoreductive surgery for epithelial ovarian cancer. J Surg Oncol. 2008;98(4):283-90.

3. Glehen O et al. Hyperthermic intraperitoneal chemotherapy: nomenclature and modalities of perfusion. J Surg Oncol. 2008;98(4):242-6.

4. Kusamura S et al. Drugs, carrier solutions and temperature in hyperthermic intraperitoneal chemotherapy. J Surg Oncol. 2008;98(4):247-52.

5. Kusamura S et al. Impact of cytoreductive surgery and hyperthermic intraperitoneal chemotherapy on systemic toxicity. Ann Surg Oncol. 2007;14(9):2550-8.

6. van Driel WJ et al. Hyperthermic Intraperitoneal Chemotherapy in Ovarian Cancer. N Engl J Med. 2018 Jan;378(3):230-240.

It is well established that general medical conditions can be associated with various psychiatric disorders. But the reverse is less recognized: That serious mental illness is associated with many physical maladies, often leading to early mortality. Thus, it is a bidirectional medical reality.

The multisystem adverse effects of psycho­tropic medications, such as metabolic dysregulation, often are blamed for the serious medical problems afflicting psychiatrically ill patients. However, evidence is mounting that while iatrogenic effects play a role, the larger effect appears to be due to a genetic link between psychiatric disorders and cardiovascular risk.¹ Unhealthy lifestyles, including sedentary living, poor dietary habits, smoking, and alcohol/substance use, also play a role in the rapid deterioration of physical health and early mortality of individuals afflicted by mood disorders, psychotic disorders, and anxiety disorders. The mantra of “healthy body, healthy mind” is well known, but “unhealthy mind, unhealthy body” should be equally emphasized as a reason for high morbidity and premature mortality in patients with serious mental disorders.

Consider the following alarming findings:

• A recent study revealed that even before the onset of the first psychotic episode, young patients with schizophrenia already suffer from a wide variety of medical conditions.² In a large sample of 954,351 Danish persons followed from birth to adulthood, of whom 4,371 developed schizophrenia, 95.6% of patients with schizophrenia had a history of hospitalization for somatic problems, including gastrointestinal, endocrine, genitourinary, metabolic, and circulatory system diseases; cancer; and epilepsy. Those findings suggest genetic, physiological, immunological, or developmental overlap between schizophrenia and medical conditions.
• A survey of 67,609 individuals with mood, anxiety, eating, impulse control, or substance use disorders followed for 10 years found that persons with those psychiatric disorders had a significantly higher risk of chronic medical conditions, including heart disease, stroke, hypertension, diabetes, asthma, arthritis, lung disease, peptic ulcer, and cancer.³
• A 7-year follow-up study of 1,138,853 individuals with schizophrenia in the United States found a 350% increase in mortality among this group of patients, who ranged in age from 20 to 64 years, compared with the general population, matched for age, sex, race, ethnicity, and geographic regions.⁴ An editorial accompanying this study urged psychiatrists to urgently address the “deadly consequences” of major psychiatric disorders.⁵
• A study of 18,380 individuals with schizophrenia, schizoaffective disorder, or bipolar disorder in London found that these patients were frequently hospitalized for general medical conditions, most commonly urinary, digestive, respiratory, endocrine/metabolic, hematologic, neurologic, dermatologic, and infectious disorders, neoplasm, and poisoning.⁶ The authors attributed those nonpsychiatric hospitalizations to self-neglect, self-harm, and poor health care access, as well as to “medically unexplained” causes.
• An extremely elevated mortality rate (24-fold higher than the general population) was reported in a 12-month study of young individuals (age 16 to 30 years) diagnosed with psychosis.⁷ The investigators also found that 61% of the cohort did not fill their antipsychotic prescriptions during that year, and 62% had ≥1 hospitalizations and/or emergency room visits during that year. The relationship between high mortality and lack of treatment with antipsychotics in schizophrenia was confirmed by another recent study,⁸ a 7-year follow-up of 29,823 persons with schizophrenia in Sweden that measured all-cause mortality. These researchers found the highest mortality among patients not receiving any antipsychotics, while the lowest mortality was among those receiving a long-acting injectable second-generation antipsychotic.
• A recent systematic review of 16 studies that examined glucose homeostasis in first-episode psychosis⁹ revealed that even at the onset of schizophrenia, glucose homeostasis was already altered, suggesting that predisposition to type 2 diabetes mellitus is a medical condition associated with schizophrenia, and not simply an iatrogenic effect of antipsychotic pharmacotherapy. This adds fodder to the possibility of a genetic overlap between schizophrenia and somatic disorders, including diabetes.¹⁰
• In a meta-analysis of 47 studies of young people at “ultra-high risk” for schizophrenia, cardiovascular risk was found to be high, mostly as a result of lifestyle factors such as low levels of physical activity and high rates of smoking and alcohol use, even before the onset of psychosis.¹¹
• The risk of stroke was found to be higher in 80,569 patients with schizophrenia compared with 241,707 age- and sex-matched control subjects.¹²
• A meta-analysis of the risk of stroke in 6 cohorts with schizophrenia found that there is a higher risk for stroke in schizophrenia, and that this may be related to natural history of the illness itself, not just due to comorbid metabolic risk factors.¹³
• The high rate of cardiovascular disease in depression has been attributed to neuroinflammation¹⁴ or possibly to increased platelet reactivity.¹⁵

Continue to: As psychiatric physicians...

As psychiatric physicians, we always screen our patients for past and current medical conditions that are comorbid with their psychiatric disorders. We are aware of the lifestyle factors that increase these patients’ physical morbidity and mortality, above and beyond their suicide-related mortality. Our patients with schizophrenia and mood disorders have triple the smoking rates of the general population, and they tend to be sedentary with poor eating habits that lead to obesity, obstructive sleep apnea, diabetes, hypertension, and dyslipidemia, which increases their risk for heart attack, stroke, and cancer. Self-neglect during acute episodes of depression or psychosis increases the risk of infection, malnutrition, and tooth decay. We also see skin damage in obsessive-compulsive disorder patients who are compelled to wash their hands numerous times a day, the life-threatening effects of anorexia nervosa, and various types of medical ailments caused by incomplete suicidal attempts. Poverty and substance use among chronically mentally ill patients also increase the odds of physical ailments.

So we need to act diligently to reduce the alarming medical morbidity and mortality of the psychiatric population. Collaborative care with a primary care provider is a must, not an option, for every patient, because studies indicate that without collaborative care, patients receive inadequate primary care.¹⁶ Providing rapid access to standard medical care is the single most critical step for the prevention or amelioration of physical disorders in our psychiatric patients, concurrently with stabilizing their ailing brains and minds. If we focus only on treating psychopathology, then we will win the battle against mental illness, but lose the war of life and death.

It is well established that general medical conditions can be associated with various psychiatric disorders. But the reverse is less recognized: That serious mental illness is associated with many physical maladies, often leading to early mortality. Thus, it is a bidirectional medical reality.

The multisystem adverse effects of psycho­tropic medications, such as metabolic dysregulation, often are blamed for the serious medical problems afflicting psychiatrically ill patients. However, evidence is mounting that while iatrogenic effects play a role, the larger effect appears to be due to a genetic link between psychiatric disorders and cardiovascular risk.¹ Unhealthy lifestyles, including sedentary living, poor dietary habits, smoking, and alcohol/substance use, also play a role in the rapid deterioration of physical health and early mortality of individuals afflicted by mood disorders, psychotic disorders, and anxiety disorders. The mantra of “healthy body, healthy mind” is well known, but “unhealthy mind, unhealthy body” should be equally emphasized as a reason for high morbidity and premature mortality in patients with serious mental disorders.

Consider the following alarming findings:

• A recent study revealed that even before the onset of the first psychotic episode, young patients with schizophrenia already suffer from a wide variety of medical conditions.² In a large sample of 954,351 Danish persons followed from birth to adulthood, of whom 4,371 developed schizophrenia, 95.6% of patients with schizophrenia had a history of hospitalization for somatic problems, including gastrointestinal, endocrine, genitourinary, metabolic, and circulatory system diseases; cancer; and epilepsy. Those findings suggest genetic, physiological, immunological, or developmental overlap between schizophrenia and medical conditions.
• A survey of 67,609 individuals with mood, anxiety, eating, impulse control, or substance use disorders followed for 10 years found that persons with those psychiatric disorders had a significantly higher risk of chronic medical conditions, including heart disease, stroke, hypertension, diabetes, asthma, arthritis, lung disease, peptic ulcer, and cancer.³
• A 7-year follow-up study of 1,138,853 individuals with schizophrenia in the United States found a 350% increase in mortality among this group of patients, who ranged in age from 20 to 64 years, compared with the general population, matched for age, sex, race, ethnicity, and geographic regions.⁴ An editorial accompanying this study urged psychiatrists to urgently address the “deadly consequences” of major psychiatric disorders.⁵
• A study of 18,380 individuals with schizophrenia, schizoaffective disorder, or bipolar disorder in London found that these patients were frequently hospitalized for general medical conditions, most commonly urinary, digestive, respiratory, endocrine/metabolic, hematologic, neurologic, dermatologic, and infectious disorders, neoplasm, and poisoning.⁶ The authors attributed those nonpsychiatric hospitalizations to self-neglect, self-harm, and poor health care access, as well as to “medically unexplained” causes.
• An extremely elevated mortality rate (24-fold higher than the general population) was reported in a 12-month study of young individuals (age 16 to 30 years) diagnosed with psychosis.⁷ The investigators also found that 61% of the cohort did not fill their antipsychotic prescriptions during that year, and 62% had ≥1 hospitalizations and/or emergency room visits during that year. The relationship between high mortality and lack of treatment with antipsychotics in schizophrenia was confirmed by another recent study,⁸ a 7-year follow-up of 29,823 persons with schizophrenia in Sweden that measured all-cause mortality. These researchers found the highest mortality among patients not receiving any antipsychotics, while the lowest mortality was among those receiving a long-acting injectable second-generation antipsychotic.
• A recent systematic review of 16 studies that examined glucose homeostasis in first-episode psychosis⁹ revealed that even at the onset of schizophrenia, glucose homeostasis was already altered, suggesting that predisposition to type 2 diabetes mellitus is a medical condition associated with schizophrenia, and not simply an iatrogenic effect of antipsychotic pharmacotherapy. This adds fodder to the possibility of a genetic overlap between schizophrenia and somatic disorders, including diabetes.¹⁰
• In a meta-analysis of 47 studies of young people at “ultra-high risk” for schizophrenia, cardiovascular risk was found to be high, mostly as a result of lifestyle factors such as low levels of physical activity and high rates of smoking and alcohol use, even before the onset of psychosis.¹¹
• The risk of stroke was found to be higher in 80,569 patients with schizophrenia compared with 241,707 age- and sex-matched control subjects.¹²
• A meta-analysis of the risk of stroke in 6 cohorts with schizophrenia found that there is a higher risk for stroke in schizophrenia, and that this may be related to natural history of the illness itself, not just due to comorbid metabolic risk factors.¹³
• The high rate of cardiovascular disease in depression has been attributed to neuroinflammation¹⁴ or possibly to increased platelet reactivity.¹⁵

Continue to: As psychiatric physicians...

As psychiatric physicians, we always screen our patients for past and current medical conditions that are comorbid with their psychiatric disorders. We are aware of the lifestyle factors that increase these patients’ physical morbidity and mortality, above and beyond their suicide-related mortality. Our patients with schizophrenia and mood disorders have triple the smoking rates of the general population, and they tend to be sedentary with poor eating habits that lead to obesity, obstructive sleep apnea, diabetes, hypertension, and dyslipidemia, which increases their risk for heart attack, stroke, and cancer. Self-neglect during acute episodes of depression or psychosis increases the risk of infection, malnutrition, and tooth decay. We also see skin damage in obsessive-compulsive disorder patients who are compelled to wash their hands numerous times a day, the life-threatening effects of anorexia nervosa, and various types of medical ailments caused by incomplete suicidal attempts. Poverty and substance use among chronically mentally ill patients also increase the odds of physical ailments.

So we need to act diligently to reduce the alarming medical morbidity and mortality of the psychiatric population. Collaborative care with a primary care provider is a must, not an option, for every patient, because studies indicate that without collaborative care, patients receive inadequate primary care.¹⁶ Providing rapid access to standard medical care is the single most critical step for the prevention or amelioration of physical disorders in our psychiatric patients, concurrently with stabilizing their ailing brains and minds. If we focus only on treating psychopathology, then we will win the battle against mental illness, but lose the war of life and death.

It is well established that general medical conditions can be associated with various psychiatric disorders. But the reverse is less recognized: That serious mental illness is associated with many physical maladies, often leading to early mortality. Thus, it is a bidirectional medical reality.

The multisystem adverse effects of psycho­tropic medications, such as metabolic dysregulation, often are blamed for the serious medical problems afflicting psychiatrically ill patients. However, evidence is mounting that while iatrogenic effects play a role, the larger effect appears to be due to a genetic link between psychiatric disorders and cardiovascular risk.¹ Unhealthy lifestyles, including sedentary living, poor dietary habits, smoking, and alcohol/substance use, also play a role in the rapid deterioration of physical health and early mortality of individuals afflicted by mood disorders, psychotic disorders, and anxiety disorders. The mantra of “healthy body, healthy mind” is well known, but “unhealthy mind, unhealthy body” should be equally emphasized as a reason for high morbidity and premature mortality in patients with serious mental disorders.

Consider the following alarming findings:

• A recent study revealed that even before the onset of the first psychotic episode, young patients with schizophrenia already suffer from a wide variety of medical conditions.² In a large sample of 954,351 Danish persons followed from birth to adulthood, of whom 4,371 developed schizophrenia, 95.6% of patients with schizophrenia had a history of hospitalization for somatic problems, including gastrointestinal, endocrine, genitourinary, metabolic, and circulatory system diseases; cancer; and epilepsy. Those findings suggest genetic, physiological, immunological, or developmental overlap between schizophrenia and medical conditions.
• A survey of 67,609 individuals with mood, anxiety, eating, impulse control, or substance use disorders followed for 10 years found that persons with those psychiatric disorders had a significantly higher risk of chronic medical conditions, including heart disease, stroke, hypertension, diabetes, asthma, arthritis, lung disease, peptic ulcer, and cancer.³
• A 7-year follow-up study of 1,138,853 individuals with schizophrenia in the United States found a 350% increase in mortality among this group of patients, who ranged in age from 20 to 64 years, compared with the general population, matched for age, sex, race, ethnicity, and geographic regions.⁴ An editorial accompanying this study urged psychiatrists to urgently address the “deadly consequences” of major psychiatric disorders.⁵
• A study of 18,380 individuals with schizophrenia, schizoaffective disorder, or bipolar disorder in London found that these patients were frequently hospitalized for general medical conditions, most commonly urinary, digestive, respiratory, endocrine/metabolic, hematologic, neurologic, dermatologic, and infectious disorders, neoplasm, and poisoning.⁶ The authors attributed those nonpsychiatric hospitalizations to self-neglect, self-harm, and poor health care access, as well as to “medically unexplained” causes.
• An extremely elevated mortality rate (24-fold higher than the general population) was reported in a 12-month study of young individuals (age 16 to 30 years) diagnosed with psychosis.⁷ The investigators also found that 61% of the cohort did not fill their antipsychotic prescriptions during that year, and 62% had ≥1 hospitalizations and/or emergency room visits during that year. The relationship between high mortality and lack of treatment with antipsychotics in schizophrenia was confirmed by another recent study,⁸ a 7-year follow-up of 29,823 persons with schizophrenia in Sweden that measured all-cause mortality. These researchers found the highest mortality among patients not receiving any antipsychotics, while the lowest mortality was among those receiving a long-acting injectable second-generation antipsychotic.
• A recent systematic review of 16 studies that examined glucose homeostasis in first-episode psychosis⁹ revealed that even at the onset of schizophrenia, glucose homeostasis was already altered, suggesting that predisposition to type 2 diabetes mellitus is a medical condition associated with schizophrenia, and not simply an iatrogenic effect of antipsychotic pharmacotherapy. This adds fodder to the possibility of a genetic overlap between schizophrenia and somatic disorders, including diabetes.¹⁰
• In a meta-analysis of 47 studies of young people at “ultra-high risk” for schizophrenia, cardiovascular risk was found to be high, mostly as a result of lifestyle factors such as low levels of physical activity and high rates of smoking and alcohol use, even before the onset of psychosis.¹¹
• The risk of stroke was found to be higher in 80,569 patients with schizophrenia compared with 241,707 age- and sex-matched control subjects.¹²
• A meta-analysis of the risk of stroke in 6 cohorts with schizophrenia found that there is a higher risk for stroke in schizophrenia, and that this may be related to natural history of the illness itself, not just due to comorbid metabolic risk factors.¹³
• The high rate of cardiovascular disease in depression has been attributed to neuroinflammation¹⁴ or possibly to increased platelet reactivity.¹⁵

Continue to: As psychiatric physicians...

As psychiatric physicians, we always screen our patients for past and current medical conditions that are comorbid with their psychiatric disorders. We are aware of the lifestyle factors that increase these patients’ physical morbidity and mortality, above and beyond their suicide-related mortality. Our patients with schizophrenia and mood disorders have triple the smoking rates of the general population, and they tend to be sedentary with poor eating habits that lead to obesity, obstructive sleep apnea, diabetes, hypertension, and dyslipidemia, which increases their risk for heart attack, stroke, and cancer. Self-neglect during acute episodes of depression or psychosis increases the risk of infection, malnutrition, and tooth decay. We also see skin damage in obsessive-compulsive disorder patients who are compelled to wash their hands numerous times a day, the life-threatening effects of anorexia nervosa, and various types of medical ailments caused by incomplete suicidal attempts. Poverty and substance use among chronically mentally ill patients also increase the odds of physical ailments.

So we need to act diligently to reduce the alarming medical morbidity and mortality of the psychiatric population. Collaborative care with a primary care provider is a must, not an option, for every patient, because studies indicate that without collaborative care, patients receive inadequate primary care.¹⁶ Providing rapid access to standard medical care is the single most critical step for the prevention or amelioration of physical disorders in our psychiatric patients, concurrently with stabilizing their ailing brains and minds. If we focus only on treating psychopathology, then we will win the battle against mental illness, but lose the war of life and death.

How precision psychiatry helped my patient

I applaud Dr. Nasrallah’s editorial “The dawn of precision psychiatry” (From the Editor, Current Psychiatry. December 2017, p. 7-8,11). Since the late 1990s, I have been practicing psychiatry in this mode in increasingly greater degree. I thought you would be interested in a recent case that demonstrates the application of precision psychiatry in an adolescent patient previously diagnosed with an attention disorder, an anxiety disorder, and a possible dissociative disorder.

Ms. G, age 14, presented with periodic emotional “meltdowns,” which would occur in any setting, and I determined that they were precipitated by a high glycemic intake. By carefully controlling her glycemic intake and starting her on caprylic acid (a medium-chain triglyceride, which was used to maintain a ketotic state), 1 tablespoon 3 times daily, we were able to reduce the frequency of her episodes by 80% to 90%. Using data from commercially available DNA testing, I determined that she had single nucleotide polymorphisms (SNPs) in an alpha-ketoglutarate dehydrogenase gene, which is primarily located in the prefrontal cortex (PFC), and whose function is supported by thiamine and impaired by high glycemic intake.¹ After adding oral thiamine hydrochloride, 100 mg twice a day, and correcting other abnormalities (eg, she was hypothyroid), her episodes are now rare. She is functioning well, has been getting high grades, and recently wrote a 40-page short story.

Once she improved, she was able to describe having a partial seizure, with a rising sensation, which often improves with ketosis. Clearly, disruption of her PFC energetics due to the SNPs described above contributed to the disinhibition of the temporal lobe structures. Furthermore, she has an APOE3/4 status, which puts her at risk for Alzheimer’s disease. Her mother was educated about the importance of good health habits, which is personalized and preventative medicine.

Robert Hedaya, MD, DLFAPA
Clinical Professor
MedStar Georgetown University Hospital
Washington, DC
Faculty
Institute for Functional Medicine
Gig Harbor, Washington, DC
Founder
National Center for Whole Psychiatry
Rockville, Maryland

Reference
1. Tretter L, Adam-Vizi V. Alpha-ketoglutarate dehydrogenase: a target and generator of oxidative stress. Philos Trans R Soc Lond B Biol Sci. 2005;360(1464):2335-2345.

Dr. Nasrallah responds

My thanks to Dr. Hedaya for his letter and for providing an excellent example of precision psychiatry. His brief case vignette brings it to life! I commend him for practicing on the cutting-edge of psychiatry’s scientific frontier.

Continue to: Ketamine: The next 'opioid crisis'?

Ketamine: The next ‘opioid crisis’?

The chief of the FDA, Scott Gottlieb, MD, recently discussed the need to learn from the mistakes that contributed to the current opioid epidemic¹ and how to curb this crisis. Understanding some of the potential pitfalls could help us prevent, or better manage, the next crisis. Despite the bad press about the opioid crisis,² there seems to be growing promise of another: ketamine. Although ketamine is classified as a Schedule III drug by the Drug Enforcement Agency³ and has a well-documented potential for dependency,⁴ this medication is now being considered a potential treatment for acute suicidality and depression.

There are many similarities between the use of opioids to treat pain and the potential use of ketamine to treat suicidality. Physical and mental pain are subjective, qualitative, and difficult to quantify, which makes it difficult to develop accurate measurements of symptom severity. Chronic physical pain and suicidality are not illnesses, but symptoms of myriad types of pathologies with differing etiologies and treatment options.⁵ Due to the ambiguous and subjective experience of physical and mental pain, we tend to lump them together as 1 pathological category without understanding pathophysiologic differences. The most commonly reported types of pain include low back pain, migraine/headache, neck pain, and facial pain.⁶ However, each of these pain types would likely have a different pathophysiology and treatment. Likewise, suicide can be associated with various psychiatric conditions,⁷ and suicidality resulting from these conditions may require a different etiology and treatment.

We already know that both opioids and ketamine are addictive. For example, there is a report of a nurse stealing a hospital’s supply of ketamine and self-treating for depression, which led to an inpatient detox admission after she developed toxicity and addiction.⁸ Some ketamine research supports its safe use, but it may be biased due to conflicts of interest. For example, several authors of a recent study proclaiming the effectiveness of a single dose of ketamine in treating suicidal ideation are named on patents or are employed by companies named on patents related to ketamine and would financially benefit from FDA-approval of ketamine for the treatment of psychiatric disorders.⁹

Warnings stating how both opioid and ketamine should be used were published years ago but have since been ignored. For example, a 1977 article advocated that opioids should only be used for a “short duration and limited to patients with acute diseases or inoperable or metastatic cancer who require long-term relief.”¹⁰ The rationale for this distinction was foretelling of the current opioid epidemic: “Continued and prolonged use of narcotics in patients with chronic benign pain is not recommended because of serious behavioral consequences, the development of tolerance, and addiction liability. Long-term use of analgesic drugs in chronic pain usually produces negative behavioral complications that are more difficult to manage than the pain it was desired to eliminate.”¹⁰ We knew better then.

The earliest report of ketamine dependency I could find was published in 1987, which predates its classification as a controlled substance.¹¹ More recently, ketamine dependency has been associated with adverse effects that are similar to “not only cocaine and amphetamine but also with opiates, alcohol and cannabis, as well as the psychological attractions of its distinctive psychedelic properties.”¹² We should consider ourselves warned.

Michael Shapiro, MD
Assistant Professor
Department of Psychiatry
University of Florida
Gainesville, Florida

References
1. Jayne O’Donnell. FDA chief supports opioid prescription limits, regrets agency’s prior inaction. USA TODAY. https://www.usatoday.com/story/news/politics/2017/10/23/fda-chief-supports-opioid-prescription-limits-regrets-agencys-prior-inaction/774007001. Published October 23, 2017. Accessed January 25, 2018.
2. Bill Whitaker. Ex-DEA agent: opioid crisis fueled by drug industry and Congress. CBS News. https://www.cbsnews.com/news/ex-dea-agent-opioid-crisis-fueled-by-drug-industry-and-congress. Published October 15, 2017. Accessed January 25, 2018.
3. Drug Enforcement Administration. Diversion of Control Division. Ketamine. https://www.deadiversion.usdoj.gov/drug_chem_info/ketamine.pdf. Published August 2013. Accessed January 25, 2018.
4. Bell RF. Ketamine for chronic noncancer pain: concerns regarding toxicity. Curr Opin Support Palliat Care. 2012;6(2):183-187.
5. Barzilay S, Apter A. Psychological models of suicide. Arch Suicide Res. 2014;18(4):295-312.
6. American Academy of Pain Medicine. AAPM facts and figures on pain. http://www.painmed.org/patientcenter/facts_on_pain.aspx.
7. Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
8. Bonnet U. Long-term ketamine self-injections in major depressive disorder: focus on tolerance in ketamine’s antidepressant response and the development of ketamine addiction. J Psychoactive Drugs. 2015;47(4):276-85.
9. Wilkinson ST, Ballard ED, Bloch MH, et al. The effect of a single dose of intravenous ketamine on suicidal ideation: a systematic review and individual participant data meta-analysis. Am J Psychiatry 2017. https://doi.org/10.1176/appi.ajp.2017.17040472
10. Halpern LM. Analgesic drugs in the management of pain. Arch Surg. 1977;112(7):861-869.
11. Kamaya H, Krishna PR. Anesthesiology. 1987;67(5):861-862.
12. Jansen KL, Darracot-Cankovic R. The nonmedical use of ketamine, part two: a review of problem use and dependence. J Psychoactive Drugs. 2001;33(2):151-158.

How precision psychiatry helped my patient

I applaud Dr. Nasrallah’s editorial “The dawn of precision psychiatry” (From the Editor, Current Psychiatry. December 2017, p. 7-8,11). Since the late 1990s, I have been practicing psychiatry in this mode in increasingly greater degree. I thought you would be interested in a recent case that demonstrates the application of precision psychiatry in an adolescent patient previously diagnosed with an attention disorder, an anxiety disorder, and a possible dissociative disorder.

Ms. G, age 14, presented with periodic emotional “meltdowns,” which would occur in any setting, and I determined that they were precipitated by a high glycemic intake. By carefully controlling her glycemic intake and starting her on caprylic acid (a medium-chain triglyceride, which was used to maintain a ketotic state), 1 tablespoon 3 times daily, we were able to reduce the frequency of her episodes by 80% to 90%. Using data from commercially available DNA testing, I determined that she had single nucleotide polymorphisms (SNPs) in an alpha-ketoglutarate dehydrogenase gene, which is primarily located in the prefrontal cortex (PFC), and whose function is supported by thiamine and impaired by high glycemic intake.¹ After adding oral thiamine hydrochloride, 100 mg twice a day, and correcting other abnormalities (eg, she was hypothyroid), her episodes are now rare. She is functioning well, has been getting high grades, and recently wrote a 40-page short story.

Once she improved, she was able to describe having a partial seizure, with a rising sensation, which often improves with ketosis. Clearly, disruption of her PFC energetics due to the SNPs described above contributed to the disinhibition of the temporal lobe structures. Furthermore, she has an APOE3/4 status, which puts her at risk for Alzheimer’s disease. Her mother was educated about the importance of good health habits, which is personalized and preventative medicine.

Robert Hedaya, MD, DLFAPA
Clinical Professor
MedStar Georgetown University Hospital
Washington, DC
Faculty
Institute for Functional Medicine
Gig Harbor, Washington, DC
Founder
National Center for Whole Psychiatry
Rockville, Maryland

Reference
1. Tretter L, Adam-Vizi V. Alpha-ketoglutarate dehydrogenase: a target and generator of oxidative stress. Philos Trans R Soc Lond B Biol Sci. 2005;360(1464):2335-2345.

Dr. Nasrallah responds

My thanks to Dr. Hedaya for his letter and for providing an excellent example of precision psychiatry. His brief case vignette brings it to life! I commend him for practicing on the cutting-edge of psychiatry’s scientific frontier.

Continue to: Ketamine: The next 'opioid crisis'?

Ketamine: The next ‘opioid crisis’?

The chief of the FDA, Scott Gottlieb, MD, recently discussed the need to learn from the mistakes that contributed to the current opioid epidemic¹ and how to curb this crisis. Understanding some of the potential pitfalls could help us prevent, or better manage, the next crisis. Despite the bad press about the opioid crisis,² there seems to be growing promise of another: ketamine. Although ketamine is classified as a Schedule III drug by the Drug Enforcement Agency³ and has a well-documented potential for dependency,⁴ this medication is now being considered a potential treatment for acute suicidality and depression.

There are many similarities between the use of opioids to treat pain and the potential use of ketamine to treat suicidality. Physical and mental pain are subjective, qualitative, and difficult to quantify, which makes it difficult to develop accurate measurements of symptom severity. Chronic physical pain and suicidality are not illnesses, but symptoms of myriad types of pathologies with differing etiologies and treatment options.⁵ Due to the ambiguous and subjective experience of physical and mental pain, we tend to lump them together as 1 pathological category without understanding pathophysiologic differences. The most commonly reported types of pain include low back pain, migraine/headache, neck pain, and facial pain.⁶ However, each of these pain types would likely have a different pathophysiology and treatment. Likewise, suicide can be associated with various psychiatric conditions,⁷ and suicidality resulting from these conditions may require a different etiology and treatment.

We already know that both opioids and ketamine are addictive. For example, there is a report of a nurse stealing a hospital’s supply of ketamine and self-treating for depression, which led to an inpatient detox admission after she developed toxicity and addiction.⁸ Some ketamine research supports its safe use, but it may be biased due to conflicts of interest. For example, several authors of a recent study proclaiming the effectiveness of a single dose of ketamine in treating suicidal ideation are named on patents or are employed by companies named on patents related to ketamine and would financially benefit from FDA-approval of ketamine for the treatment of psychiatric disorders.⁹

Warnings stating how both opioid and ketamine should be used were published years ago but have since been ignored. For example, a 1977 article advocated that opioids should only be used for a “short duration and limited to patients with acute diseases or inoperable or metastatic cancer who require long-term relief.”¹⁰ The rationale for this distinction was foretelling of the current opioid epidemic: “Continued and prolonged use of narcotics in patients with chronic benign pain is not recommended because of serious behavioral consequences, the development of tolerance, and addiction liability. Long-term use of analgesic drugs in chronic pain usually produces negative behavioral complications that are more difficult to manage than the pain it was desired to eliminate.”¹⁰ We knew better then.

The earliest report of ketamine dependency I could find was published in 1987, which predates its classification as a controlled substance.¹¹ More recently, ketamine dependency has been associated with adverse effects that are similar to “not only cocaine and amphetamine but also with opiates, alcohol and cannabis, as well as the psychological attractions of its distinctive psychedelic properties.”¹² We should consider ourselves warned.

Michael Shapiro, MD
Assistant Professor
Department of Psychiatry
University of Florida
Gainesville, Florida

References
1. Jayne O’Donnell. FDA chief supports opioid prescription limits, regrets agency’s prior inaction. USA TODAY. https://www.usatoday.com/story/news/politics/2017/10/23/fda-chief-supports-opioid-prescription-limits-regrets-agencys-prior-inaction/774007001. Published October 23, 2017. Accessed January 25, 2018.
2. Bill Whitaker. Ex-DEA agent: opioid crisis fueled by drug industry and Congress. CBS News. https://www.cbsnews.com/news/ex-dea-agent-opioid-crisis-fueled-by-drug-industry-and-congress. Published October 15, 2017. Accessed January 25, 2018.
3. Drug Enforcement Administration. Diversion of Control Division. Ketamine. https://www.deadiversion.usdoj.gov/drug_chem_info/ketamine.pdf. Published August 2013. Accessed January 25, 2018.
4. Bell RF. Ketamine for chronic noncancer pain: concerns regarding toxicity. Curr Opin Support Palliat Care. 2012;6(2):183-187.
5. Barzilay S, Apter A. Psychological models of suicide. Arch Suicide Res. 2014;18(4):295-312.
6. American Academy of Pain Medicine. AAPM facts and figures on pain. http://www.painmed.org/patientcenter/facts_on_pain.aspx.
7. Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
8. Bonnet U. Long-term ketamine self-injections in major depressive disorder: focus on tolerance in ketamine’s antidepressant response and the development of ketamine addiction. J Psychoactive Drugs. 2015;47(4):276-85.
9. Wilkinson ST, Ballard ED, Bloch MH, et al. The effect of a single dose of intravenous ketamine on suicidal ideation: a systematic review and individual participant data meta-analysis. Am J Psychiatry 2017. https://doi.org/10.1176/appi.ajp.2017.17040472
10. Halpern LM. Analgesic drugs in the management of pain. Arch Surg. 1977;112(7):861-869.
11. Kamaya H, Krishna PR. Anesthesiology. 1987;67(5):861-862.
12. Jansen KL, Darracot-Cankovic R. The nonmedical use of ketamine, part two: a review of problem use and dependence. J Psychoactive Drugs. 2001;33(2):151-158.

How precision psychiatry helped my patient

I applaud Dr. Nasrallah’s editorial “The dawn of precision psychiatry” (From the Editor, Current Psychiatry. December 2017, p. 7-8,11). Since the late 1990s, I have been practicing psychiatry in this mode in increasingly greater degree. I thought you would be interested in a recent case that demonstrates the application of precision psychiatry in an adolescent patient previously diagnosed with an attention disorder, an anxiety disorder, and a possible dissociative disorder.

Ms. G, age 14, presented with periodic emotional “meltdowns,” which would occur in any setting, and I determined that they were precipitated by a high glycemic intake. By carefully controlling her glycemic intake and starting her on caprylic acid (a medium-chain triglyceride, which was used to maintain a ketotic state), 1 tablespoon 3 times daily, we were able to reduce the frequency of her episodes by 80% to 90%. Using data from commercially available DNA testing, I determined that she had single nucleotide polymorphisms (SNPs) in an alpha-ketoglutarate dehydrogenase gene, which is primarily located in the prefrontal cortex (PFC), and whose function is supported by thiamine and impaired by high glycemic intake.¹ After adding oral thiamine hydrochloride, 100 mg twice a day, and correcting other abnormalities (eg, she was hypothyroid), her episodes are now rare. She is functioning well, has been getting high grades, and recently wrote a 40-page short story.

Once she improved, she was able to describe having a partial seizure, with a rising sensation, which often improves with ketosis. Clearly, disruption of her PFC energetics due to the SNPs described above contributed to the disinhibition of the temporal lobe structures. Furthermore, she has an APOE3/4 status, which puts her at risk for Alzheimer’s disease. Her mother was educated about the importance of good health habits, which is personalized and preventative medicine.

Robert Hedaya, MD, DLFAPA
Clinical Professor
MedStar Georgetown University Hospital
Washington, DC
Faculty
Institute for Functional Medicine
Gig Harbor, Washington, DC
Founder
National Center for Whole Psychiatry
Rockville, Maryland

Reference
1. Tretter L, Adam-Vizi V. Alpha-ketoglutarate dehydrogenase: a target and generator of oxidative stress. Philos Trans R Soc Lond B Biol Sci. 2005;360(1464):2335-2345.

Dr. Nasrallah responds

My thanks to Dr. Hedaya for his letter and for providing an excellent example of precision psychiatry. His brief case vignette brings it to life! I commend him for practicing on the cutting-edge of psychiatry’s scientific frontier.

Continue to: Ketamine: The next 'opioid crisis'?

Ketamine: The next ‘opioid crisis’?

The chief of the FDA, Scott Gottlieb, MD, recently discussed the need to learn from the mistakes that contributed to the current opioid epidemic¹ and how to curb this crisis. Understanding some of the potential pitfalls could help us prevent, or better manage, the next crisis. Despite the bad press about the opioid crisis,² there seems to be growing promise of another: ketamine. Although ketamine is classified as a Schedule III drug by the Drug Enforcement Agency³ and has a well-documented potential for dependency,⁴ this medication is now being considered a potential treatment for acute suicidality and depression.

There are many similarities between the use of opioids to treat pain and the potential use of ketamine to treat suicidality. Physical and mental pain are subjective, qualitative, and difficult to quantify, which makes it difficult to develop accurate measurements of symptom severity. Chronic physical pain and suicidality are not illnesses, but symptoms of myriad types of pathologies with differing etiologies and treatment options.⁵ Due to the ambiguous and subjective experience of physical and mental pain, we tend to lump them together as 1 pathological category without understanding pathophysiologic differences. The most commonly reported types of pain include low back pain, migraine/headache, neck pain, and facial pain.⁶ However, each of these pain types would likely have a different pathophysiology and treatment. Likewise, suicide can be associated with various psychiatric conditions,⁷ and suicidality resulting from these conditions may require a different etiology and treatment.

We already know that both opioids and ketamine are addictive. For example, there is a report of a nurse stealing a hospital’s supply of ketamine and self-treating for depression, which led to an inpatient detox admission after she developed toxicity and addiction.⁸ Some ketamine research supports its safe use, but it may be biased due to conflicts of interest. For example, several authors of a recent study proclaiming the effectiveness of a single dose of ketamine in treating suicidal ideation are named on patents or are employed by companies named on patents related to ketamine and would financially benefit from FDA-approval of ketamine for the treatment of psychiatric disorders.⁹

Warnings stating how both opioid and ketamine should be used were published years ago but have since been ignored. For example, a 1977 article advocated that opioids should only be used for a “short duration and limited to patients with acute diseases or inoperable or metastatic cancer who require long-term relief.”¹⁰ The rationale for this distinction was foretelling of the current opioid epidemic: “Continued and prolonged use of narcotics in patients with chronic benign pain is not recommended because of serious behavioral consequences, the development of tolerance, and addiction liability. Long-term use of analgesic drugs in chronic pain usually produces negative behavioral complications that are more difficult to manage than the pain it was desired to eliminate.”¹⁰ We knew better then.

The earliest report of ketamine dependency I could find was published in 1987, which predates its classification as a controlled substance.¹¹ More recently, ketamine dependency has been associated with adverse effects that are similar to “not only cocaine and amphetamine but also with opiates, alcohol and cannabis, as well as the psychological attractions of its distinctive psychedelic properties.”¹² We should consider ourselves warned.

Michael Shapiro, MD
Assistant Professor
Department of Psychiatry
University of Florida
Gainesville, Florida

References
1. Jayne O’Donnell. FDA chief supports opioid prescription limits, regrets agency’s prior inaction. USA TODAY. https://www.usatoday.com/story/news/politics/2017/10/23/fda-chief-supports-opioid-prescription-limits-regrets-agencys-prior-inaction/774007001. Published October 23, 2017. Accessed January 25, 2018.
2. Bill Whitaker. Ex-DEA agent: opioid crisis fueled by drug industry and Congress. CBS News. https://www.cbsnews.com/news/ex-dea-agent-opioid-crisis-fueled-by-drug-industry-and-congress. Published October 15, 2017. Accessed January 25, 2018.
3. Drug Enforcement Administration. Diversion of Control Division. Ketamine. https://www.deadiversion.usdoj.gov/drug_chem_info/ketamine.pdf. Published August 2013. Accessed January 25, 2018.
4. Bell RF. Ketamine for chronic noncancer pain: concerns regarding toxicity. Curr Opin Support Palliat Care. 2012;6(2):183-187.
5. Barzilay S, Apter A. Psychological models of suicide. Arch Suicide Res. 2014;18(4):295-312.
6. American Academy of Pain Medicine. AAPM facts and figures on pain. http://www.painmed.org/patientcenter/facts_on_pain.aspx.
7. Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
8. Bonnet U. Long-term ketamine self-injections in major depressive disorder: focus on tolerance in ketamine’s antidepressant response and the development of ketamine addiction. J Psychoactive Drugs. 2015;47(4):276-85.
9. Wilkinson ST, Ballard ED, Bloch MH, et al. The effect of a single dose of intravenous ketamine on suicidal ideation: a systematic review and individual participant data meta-analysis. Am J Psychiatry 2017. https://doi.org/10.1176/appi.ajp.2017.17040472
10. Halpern LM. Analgesic drugs in the management of pain. Arch Surg. 1977;112(7):861-869.
11. Kamaya H, Krishna PR. Anesthesiology. 1987;67(5):861-862.
12. Jansen KL, Darracot-Cankovic R. The nonmedical use of ketamine, part two: a review of problem use and dependence. J Psychoactive Drugs. 2001;33(2):151-158.

The evening before the March For Our Lives rally in Washington, I was hard at work on my sign. Making a statement is important, but at the Women’s March last January, I discovered that a sign was invaluable for keeping friends together in a crowd. Since my Women’s March sign read “Make America Kind Again,” I opted to keep with the theme, and I created a “Make America Safe Again” sign for gun control. My daughter looked at my sign skeptically. “It’s too vague and nondirective,” she declared. Now challenged, I added the following directives: “Universal Background Checks,” “Ban Assault Weapons,” and “Smart Guns.” My sign was now complete.

I was surprised when my daughter – our family Jeopardy! whiz – asked, “What’s a smart gun?” When we arrived to join friends, their daughter – a doctoral student – also looked at the sign and asked me what a smart gun is. I explained to both young women that a smart gun – like an iPhone – relies on a biometric such as a fingerprint so that it can be used only by authorized users. This technology would reduce the flow of firearms to illegal owners, prevent accidental discharge by children, protect rightful owners and law enforcement officers from having their own weapons used against them by criminals, and decrease the number of suicides by family members of gun owners. In my state of Maryland, there have been two school shootings, one as recently as March 20, and both were committed by boys who took a parent’s firearm to school.

Courtesy Dr. Dinah Miller

We arrived at the rally and found a spot in front of the Newseum, with two jumbotrons in sight, right in the middle of the crowd. The young people who spoke were inspirational. Regardless of one’s political views or thoughts on gun control, they were bright, articulate, fearless, passionate, and determined. The show was stolen by Naomi Wadler, a precocious 11-year-old girl who is destined to be a member of Congress (if not president) one day, and by Dr. Martin Luther King Jr.’s 9-year-old granddaughter, Yolanda Renee King.

The rest of the speakers were teenagers, all of whom had lost someone to gunfire. There were speakers from Parkland, Fla., who talked about the raw losses they were feeling, and the student who wasn’t celebrating his 18th birthday on March 24. Matthew Soto from Newtown, Conn., talked about losing his sister, a first-grade teacher, in the Sandy Hook shooting.

But the rally wasn’t just about mass murders and school shootings: Zion Kelly talked about the death of his twin, a teen who was killed when he stopped at a convenience store on the way home from school in Washington, only to have his promising life snuffed out during a holdup. We heard about shootings in the bullet-riddled streets of Chicago and Los Angeles and the toll they have taken. The losses to gun violence have been felt most strongly in communities of color. While it was mentioned that the majority of gun deaths are suicides, there were no speakers from families of people who died from suicide. The final speaker was Emma Gonzalez, a young woman from Parkland who took the stage for 6 minutes and 20 seconds - the duration of the shooter’s rampage - and closed with a powerful moment of silence.*  The rally closed with a performance of Bob Dylan’s “The Times They Are a-Changin’ ” by Jennifer Hudson, whose mother, brother, and nephew were murdered by a gunman.

The teens talked about what changes they wanted to see enacted. They talked about closing loopholes to background checks, and I was pleased that one young man specifically mentioned keeping guns from those who are violent, but did not mention mental illness as a reason to block gun ownership. A call to resume a ban on assault weapons was made repeatedly as was a call to raise the age (to 21) at which an individual can purchase a gun. Military-style weapons are not necessary for hunting or self-defense, and they enable the rapid-fire assassinations we have seen in mass shootings, so they remain an easy target of gun control advocacy. But in terms of numbers, these firearms are responsible for a small fraction of gun deaths. I was surprised, but the teens did not mention “smart gun” legislation as a way to reduce gun deaths.

Guns, and gun deaths, are a part of American society. While the majority of Americans favor stronger regulation of gun ownership, legislation that would end gun ownership is not likely to go anywhere. Smart guns, however, are different. Forty percent of polled gun owners have said they would swap their firearm for a smart firearm. So given the appeal of a firearm that can’t be diverted or stolen, used against the owner, discharged accidentally by a child, or used for suicide or homicide by a distressed family member, why don’t these weapons exist for use by the American people? Numerous technologies exist, dating back to 1975, and the first fingerprint-enabled gun was invented by Kai Kloepfer, an 18-year-old high school student, in 2015. People want these guns and the protections they offer, yet they have never been produced and made available to either the American public or to our law enforcement officers.

So where are these firearms, and why aren’t our Parkland teens asking for them? The answer to the first part of that question lies with the National Rifle Association (NRA) and the state of New Jersey. In 2003, New Jersey passed the Childproof Handgun bill, which requires that all guns sold in the state be smart guns within 3 years of their availability. The NRA has vigorously opposed any legislation that would require all guns to be smart guns. Because the availability of these weapons would trigger the New Jersey bill, California and Maryland have been prevented from importing smart firearms from a German company. Perhaps, however, New Jersey does not need to bear all the blame; in 1999, 4 years before the passage of the bill, the NRA and its members boycotted Smith & Wesson when the gun manufacturer revealed plans to develop a smart gun for the government. The NRA’s public stance is that it does not oppose smart guns for those who want them, but it opposes legislation that would eliminate the sale of conventional firearms. The organization has voiced concerns that technology fails and that it potentially slows down firing the weapon. It doesn’t talk about dead toddlers, or about police officers who’ve been killed when their weapons were taken from them.

As for the Parkland students, I don’t know why they aren’t asking for smart gun technology while they have the attention of the country. Perhaps they, like the young women I was with, don’t know it’s an option. Perhaps it’s too removed from the issue of mass murders and an assault weapon ban feels more attainable. Or perhaps the NRA’s mission has too much of a stronghold in Florida. I don’t know why they aren’t asking for smart gun production, but I know they should be.

*Correction, 3/27/2018: An earlier version of this story misstated the duration of Emma Gonzalez's moment of silence.

Dr. Miller is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press), 2016. She practices in Baltimore.

The evening before the March For Our Lives rally in Washington, I was hard at work on my sign. Making a statement is important, but at the Women’s March last January, I discovered that a sign was invaluable for keeping friends together in a crowd. Since my Women’s March sign read “Make America Kind Again,” I opted to keep with the theme, and I created a “Make America Safe Again” sign for gun control. My daughter looked at my sign skeptically. “It’s too vague and nondirective,” she declared. Now challenged, I added the following directives: “Universal Background Checks,” “Ban Assault Weapons,” and “Smart Guns.” My sign was now complete.

I was surprised when my daughter – our family Jeopardy! whiz – asked, “What’s a smart gun?” When we arrived to join friends, their daughter – a doctoral student – also looked at the sign and asked me what a smart gun is. I explained to both young women that a smart gun – like an iPhone – relies on a biometric such as a fingerprint so that it can be used only by authorized users. This technology would reduce the flow of firearms to illegal owners, prevent accidental discharge by children, protect rightful owners and law enforcement officers from having their own weapons used against them by criminals, and decrease the number of suicides by family members of gun owners. In my state of Maryland, there have been two school shootings, one as recently as March 20, and both were committed by boys who took a parent’s firearm to school.

Courtesy Dr. Dinah Miller

We arrived at the rally and found a spot in front of the Newseum, with two jumbotrons in sight, right in the middle of the crowd. The young people who spoke were inspirational. Regardless of one’s political views or thoughts on gun control, they were bright, articulate, fearless, passionate, and determined. The show was stolen by Naomi Wadler, a precocious 11-year-old girl who is destined to be a member of Congress (if not president) one day, and by Dr. Martin Luther King Jr.’s 9-year-old granddaughter, Yolanda Renee King.

The rest of the speakers were teenagers, all of whom had lost someone to gunfire. There were speakers from Parkland, Fla., who talked about the raw losses they were feeling, and the student who wasn’t celebrating his 18th birthday on March 24. Matthew Soto from Newtown, Conn., talked about losing his sister, a first-grade teacher, in the Sandy Hook shooting.

But the rally wasn’t just about mass murders and school shootings: Zion Kelly talked about the death of his twin, a teen who was killed when he stopped at a convenience store on the way home from school in Washington, only to have his promising life snuffed out during a holdup. We heard about shootings in the bullet-riddled streets of Chicago and Los Angeles and the toll they have taken. The losses to gun violence have been felt most strongly in communities of color. While it was mentioned that the majority of gun deaths are suicides, there were no speakers from families of people who died from suicide. The final speaker was Emma Gonzalez, a young woman from Parkland who took the stage for 6 minutes and 20 seconds - the duration of the shooter’s rampage - and closed with a powerful moment of silence.*  The rally closed with a performance of Bob Dylan’s “The Times They Are a-Changin’ ” by Jennifer Hudson, whose mother, brother, and nephew were murdered by a gunman.

The teens talked about what changes they wanted to see enacted. They talked about closing loopholes to background checks, and I was pleased that one young man specifically mentioned keeping guns from those who are violent, but did not mention mental illness as a reason to block gun ownership. A call to resume a ban on assault weapons was made repeatedly as was a call to raise the age (to 21) at which an individual can purchase a gun. Military-style weapons are not necessary for hunting or self-defense, and they enable the rapid-fire assassinations we have seen in mass shootings, so they remain an easy target of gun control advocacy. But in terms of numbers, these firearms are responsible for a small fraction of gun deaths. I was surprised, but the teens did not mention “smart gun” legislation as a way to reduce gun deaths.

Guns, and gun deaths, are a part of American society. While the majority of Americans favor stronger regulation of gun ownership, legislation that would end gun ownership is not likely to go anywhere. Smart guns, however, are different. Forty percent of polled gun owners have said they would swap their firearm for a smart firearm. So given the appeal of a firearm that can’t be diverted or stolen, used against the owner, discharged accidentally by a child, or used for suicide or homicide by a distressed family member, why don’t these weapons exist for use by the American people? Numerous technologies exist, dating back to 1975, and the first fingerprint-enabled gun was invented by Kai Kloepfer, an 18-year-old high school student, in 2015. People want these guns and the protections they offer, yet they have never been produced and made available to either the American public or to our law enforcement officers.

So where are these firearms, and why aren’t our Parkland teens asking for them? The answer to the first part of that question lies with the National Rifle Association (NRA) and the state of New Jersey. In 2003, New Jersey passed the Childproof Handgun bill, which requires that all guns sold in the state be smart guns within 3 years of their availability. The NRA has vigorously opposed any legislation that would require all guns to be smart guns. Because the availability of these weapons would trigger the New Jersey bill, California and Maryland have been prevented from importing smart firearms from a German company. Perhaps, however, New Jersey does not need to bear all the blame; in 1999, 4 years before the passage of the bill, the NRA and its members boycotted Smith & Wesson when the gun manufacturer revealed plans to develop a smart gun for the government. The NRA’s public stance is that it does not oppose smart guns for those who want them, but it opposes legislation that would eliminate the sale of conventional firearms. The organization has voiced concerns that technology fails and that it potentially slows down firing the weapon. It doesn’t talk about dead toddlers, or about police officers who’ve been killed when their weapons were taken from them.

As for the Parkland students, I don’t know why they aren’t asking for smart gun technology while they have the attention of the country. Perhaps they, like the young women I was with, don’t know it’s an option. Perhaps it’s too removed from the issue of mass murders and an assault weapon ban feels more attainable. Or perhaps the NRA’s mission has too much of a stronghold in Florida. I don’t know why they aren’t asking for smart gun production, but I know they should be.

*Correction, 3/27/2018: An earlier version of this story misstated the duration of Emma Gonzalez's moment of silence.

Dr. Miller is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press), 2016. She practices in Baltimore.

The evening before the March For Our Lives rally in Washington, I was hard at work on my sign. Making a statement is important, but at the Women’s March last January, I discovered that a sign was invaluable for keeping friends together in a crowd. Since my Women’s March sign read “Make America Kind Again,” I opted to keep with the theme, and I created a “Make America Safe Again” sign for gun control. My daughter looked at my sign skeptically. “It’s too vague and nondirective,” she declared. Now challenged, I added the following directives: “Universal Background Checks,” “Ban Assault Weapons,” and “Smart Guns.” My sign was now complete.

I was surprised when my daughter – our family Jeopardy! whiz – asked, “What’s a smart gun?” When we arrived to join friends, their daughter – a doctoral student – also looked at the sign and asked me what a smart gun is. I explained to both young women that a smart gun – like an iPhone – relies on a biometric such as a fingerprint so that it can be used only by authorized users. This technology would reduce the flow of firearms to illegal owners, prevent accidental discharge by children, protect rightful owners and law enforcement officers from having their own weapons used against them by criminals, and decrease the number of suicides by family members of gun owners. In my state of Maryland, there have been two school shootings, one as recently as March 20, and both were committed by boys who took a parent’s firearm to school.

Courtesy Dr. Dinah Miller

We arrived at the rally and found a spot in front of the Newseum, with two jumbotrons in sight, right in the middle of the crowd. The young people who spoke were inspirational. Regardless of one’s political views or thoughts on gun control, they were bright, articulate, fearless, passionate, and determined. The show was stolen by Naomi Wadler, a precocious 11-year-old girl who is destined to be a member of Congress (if not president) one day, and by Dr. Martin Luther King Jr.’s 9-year-old granddaughter, Yolanda Renee King.

The rest of the speakers were teenagers, all of whom had lost someone to gunfire. There were speakers from Parkland, Fla., who talked about the raw losses they were feeling, and the student who wasn’t celebrating his 18th birthday on March 24. Matthew Soto from Newtown, Conn., talked about losing his sister, a first-grade teacher, in the Sandy Hook shooting.

But the rally wasn’t just about mass murders and school shootings: Zion Kelly talked about the death of his twin, a teen who was killed when he stopped at a convenience store on the way home from school in Washington, only to have his promising life snuffed out during a holdup. We heard about shootings in the bullet-riddled streets of Chicago and Los Angeles and the toll they have taken. The losses to gun violence have been felt most strongly in communities of color. While it was mentioned that the majority of gun deaths are suicides, there were no speakers from families of people who died from suicide. The final speaker was Emma Gonzalez, a young woman from Parkland who took the stage for 6 minutes and 20 seconds - the duration of the shooter’s rampage - and closed with a powerful moment of silence.*  The rally closed with a performance of Bob Dylan’s “The Times They Are a-Changin’ ” by Jennifer Hudson, whose mother, brother, and nephew were murdered by a gunman.

The teens talked about what changes they wanted to see enacted. They talked about closing loopholes to background checks, and I was pleased that one young man specifically mentioned keeping guns from those who are violent, but did not mention mental illness as a reason to block gun ownership. A call to resume a ban on assault weapons was made repeatedly as was a call to raise the age (to 21) at which an individual can purchase a gun. Military-style weapons are not necessary for hunting or self-defense, and they enable the rapid-fire assassinations we have seen in mass shootings, so they remain an easy target of gun control advocacy. But in terms of numbers, these firearms are responsible for a small fraction of gun deaths. I was surprised, but the teens did not mention “smart gun” legislation as a way to reduce gun deaths.

Guns, and gun deaths, are a part of American society. While the majority of Americans favor stronger regulation of gun ownership, legislation that would end gun ownership is not likely to go anywhere. Smart guns, however, are different. Forty percent of polled gun owners have said they would swap their firearm for a smart firearm. So given the appeal of a firearm that can’t be diverted or stolen, used against the owner, discharged accidentally by a child, or used for suicide or homicide by a distressed family member, why don’t these weapons exist for use by the American people? Numerous technologies exist, dating back to 1975, and the first fingerprint-enabled gun was invented by Kai Kloepfer, an 18-year-old high school student, in 2015. People want these guns and the protections they offer, yet they have never been produced and made available to either the American public or to our law enforcement officers.

So where are these firearms, and why aren’t our Parkland teens asking for them? The answer to the first part of that question lies with the National Rifle Association (NRA) and the state of New Jersey. In 2003, New Jersey passed the Childproof Handgun bill, which requires that all guns sold in the state be smart guns within 3 years of their availability. The NRA has vigorously opposed any legislation that would require all guns to be smart guns. Because the availability of these weapons would trigger the New Jersey bill, California and Maryland have been prevented from importing smart firearms from a German company. Perhaps, however, New Jersey does not need to bear all the blame; in 1999, 4 years before the passage of the bill, the NRA and its members boycotted Smith & Wesson when the gun manufacturer revealed plans to develop a smart gun for the government. The NRA’s public stance is that it does not oppose smart guns for those who want them, but it opposes legislation that would eliminate the sale of conventional firearms. The organization has voiced concerns that technology fails and that it potentially slows down firing the weapon. It doesn’t talk about dead toddlers, or about police officers who’ve been killed when their weapons were taken from them.

As for the Parkland students, I don’t know why they aren’t asking for smart gun technology while they have the attention of the country. Perhaps they, like the young women I was with, don’t know it’s an option. Perhaps it’s too removed from the issue of mass murders and an assault weapon ban feels more attainable. Or perhaps the NRA’s mission has too much of a stronghold in Florida. I don’t know why they aren’t asking for smart gun production, but I know they should be.

*Correction, 3/27/2018: An earlier version of this story misstated the duration of Emma Gonzalez's moment of silence.

Dr. Miller is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press), 2016. She practices in Baltimore.

There is an increased focus on reducing the costs of health care delivery, and one major driver of surgical cost is length of hospitalization. A minimally invasive surgical approach to hysterectomy is a strategy that significantly enhances recovery and shortens hospital stay, although many patients who can safely be considered for same-day discharge (SDD), including many with cancer, are still admitted to the hospital overnight. Much has been published on the predictors and pathways for successful same-day discharge after minimally invasive hysterectomy, and in this column we will review how to best predict who is a good candidate for SDD and how to optimize the success of this approach with respect to safety and patient satisfaction.

What are the benefits to SDD?

Certainly, decreased hospitalization costs are an attractive feature of SDD following hysterectomy, although surgeons should also be mindful that patient-centered outcomes, such as pain control, managing nausea, and patient satisfaction, also are considered with equal emphasis. Several studies have shown that, in appropriate candidates and when proactive pathways are used, patient satisfaction is preserved with SDD following hysterectomy.¹

Choosing patient candidates

Same day discharge is most successfully accomplished in patients of good general baseline health.² Diabetic patients, particularly those on insulin, are generally not good candidates for SDD because it is important to monitor and intervene in blood glucose changes that are influenced by a nothing-by-mouth status and surgical stress. We recommend observing patients overnight with a history of pulmonary disease who may have transient increased postoperative O₂ needs. Similarly, patients with significant cardiac disease (including heart failure and coronary disease) may benefit from prolonged overnight observation.

Particular caution should be paid to patients with obstructive sleep apnea, which may be occult but anticipated in patients with very high body mass indexes (greater than 40 kg/m²). General anesthetic drugs, the trauma of intubation, and opioids all couple with the underlying airway compromise such that these patients are at risk for postoperative apnea, which, in severe cases, can result in anoxia and death. These patients should be considered for continuous pulse-ox monitoring for at least 12-24 hours postoperatively and are not good candidates for same-day discharge.

Patients who have baseline anticoagulation that has been stopped or bridged preoperatively should have prolonged observation with recheck of their postoperative hemoglobin prior to discharge.

Patients who live alone or are very elderly with baseline frailty are poor candidates for SDD and may benefit from nursing observation overnight while they metabolize their anesthesia. Patients who have chronic opioid dependency present a greater challenge to control postoperative pain; these patients are generally less good candidates for SDD.

Studies have shown that the indication for the procedure (for example, cancer with staging, fibroids, endometriosis) is less critical in determining who is a good candidate for SDD.³ However, successful SDD rates are highest in more straightforward cases with few or no prior surgeries, small uteri (less than 14 weeks), a surgical duration of less than 3 hours, and a surgical start time before 2 p.m. Longer, more complex cases are typically associated with more blood loss, higher risk for occult complications, and more time under anesthesia (and in Trendelenburg), which can exacerbate airway edema. In preparation for such cases, it might be wise to prepare patients for the possibility that they may not be good candidates for discharge on the same day. In general, most SDD pathways exclude patients with very high BMI (greater than 50 kg/m²) because of concern for airway patency and because these cases may be more complex with higher underlying risk. In addition, many of these patients have diabetes and require perioperative metabolic interventions.

Patient preparation

A key component to successful SDD is setting patient expectations. Patients should be informed at their preoperative visit that, unless there is an unexpected occurrence or response to the surgery, they will be discharged to home the same day. This allows them to prepare their home (including transportation needs) in advance. They should be provided with information about what to expect that first night after surgery (including potential residual drowsiness or nausea from anesthesia and immediate postoperative pain).

On the day of surgery, under the influence of anesthesia and pain medication, patients will have difficulty retaining complex discharge instructions. The preoperative visit is critically important because it’s the best time to provide them with this information, including postoperative activity limitations, wound and dressing care, and follow-up instructions. This is also the best time to provide prescriptions for postoperative pain, nausea, and constipation prophylaxis with detailed instructions about best use. Patients should be encouraged to fill these prescriptions preoperatively so that they have these medications on hand on the evening of their discharge.

Many programs utilize a combination of educational strategies (in person, written, video) to maximize the likelihood of retention.¹ It is also important to offer an opportunity for patients to ask questions about this information after they have received it (for example, by phoning the patients prior to their procedure).
 

Preoperative strategies

Intraoperative strategies

Consider in-and-out catheterization rather than placement of an indwelling catheter for anticipated short cases without complex bladder dissection.⁵ Minimize blood loss and maximally evacuate blood and clots with suction because hemoperitoneum can induce nausea and pain.

Pain from retained gas under the diaphragm can be reduced by bathing the diaphragms with 400 cc of dilute local anesthetic made by mixing 50 mL of 0.5% bupivacaine in 1000 mL normal saline prior to removal of pneumoperitoneum and while still in Trendelenburg. Ensure there is minimal retained intraperitoneal CO₂ at the completion of the surgery by asking the anesthesiologists to perform positive pressure ventilations prior to fascial closure. Consider injecting port sites (including the peritoneal and fascial layers) with a mixture of immediate and long-acting local anesthetics. Request that the anesthesia staff administer intraoperative doses of IV ketorolac, acetaminophen, and tramadol (in preference to opioids) and an aggressive perioperative cocktail of antiemetics.

Management in the recovery room

Surgeons should ensure that recovery room staff are well versed in the pathway for patients who are selected for SDD to ensure proactive implementation of analgesic and antiemetic regimens and to fast-track the various tasks and education required for discharge.⁵

Patients should be started on their home postoperative medication regimen in the recovery room, including an anti-inflammatory such as diclofenac, sublingual tramadol (in preference to an opioid, such as hydrocodone), docusate, and sennosides. IV opioids should be avoided because they can result in somnolence and nausea.

If placed intraoperatively, the Foley catheter should be removed early to allow adequate time to void. Backfilling the bladder prior to removal can hasten the urge to void and help objectively document completeness of evacuation. All patients should be seen by the anesthesiologist and/or surgeon prior to discharge.

For patients who are discharged same day, a follow-up phone call on postoperative day 1 is valuable to ensure that they have continued their successful postoperative transition to the home and to intervene early if there are concerns for patient satisfaction.

Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill.

References

1. Fountain CR et al. Promoting same-day discharge for gynecologic oncology patients in minimally invasive hysterectomy. J Minim Invasive Gynecol. 2017 Sep-Oct;24(6):932-9.

2. Rivard C et al. Factors influencing same-day hospital discharge and risk factors for readmission after robotic surgery in the gynecologic oncology patient population. J Minim Invasive Gynecol. 2015 Feb;22(2):219-26.

3. Lee SJ et al. The feasibility and safety of same-day discharge after robotic-assisted hysterectomy alone or with other procedures for benign and malignant indications. Gynecol Oncol. 2014 Jun;133(3):552-5.

4. Elia N et al. Does multimodal analgesia with acetaminophen, nonsteroidal antiinflammatory drugs, or selective cyclooxygenase-2 inhibitors and patient-controlled analgesia morphine offer advantages over morphine alone? Meta-analyses of randomized trials. Anesthesiology. 2005 Dec;103(6):1296-304.

5. Donnez O et al. Low pain score after total laparoscopic hysterectomy and same-day discharge within less than 5 hours: Results of a prospective observational study. J Minim Invasive Gynecol. 2015 Nov-Dec;22(7):1293-9.

There is an increased focus on reducing the costs of health care delivery, and one major driver of surgical cost is length of hospitalization. A minimally invasive surgical approach to hysterectomy is a strategy that significantly enhances recovery and shortens hospital stay, although many patients who can safely be considered for same-day discharge (SDD), including many with cancer, are still admitted to the hospital overnight. Much has been published on the predictors and pathways for successful same-day discharge after minimally invasive hysterectomy, and in this column we will review how to best predict who is a good candidate for SDD and how to optimize the success of this approach with respect to safety and patient satisfaction.

What are the benefits to SDD?

Certainly, decreased hospitalization costs are an attractive feature of SDD following hysterectomy, although surgeons should also be mindful that patient-centered outcomes, such as pain control, managing nausea, and patient satisfaction, also are considered with equal emphasis. Several studies have shown that, in appropriate candidates and when proactive pathways are used, patient satisfaction is preserved with SDD following hysterectomy.¹

Choosing patient candidates

Same day discharge is most successfully accomplished in patients of good general baseline health.² Diabetic patients, particularly those on insulin, are generally not good candidates for SDD because it is important to monitor and intervene in blood glucose changes that are influenced by a nothing-by-mouth status and surgical stress. We recommend observing patients overnight with a history of pulmonary disease who may have transient increased postoperative O₂ needs. Similarly, patients with significant cardiac disease (including heart failure and coronary disease) may benefit from prolonged overnight observation.

Particular caution should be paid to patients with obstructive sleep apnea, which may be occult but anticipated in patients with very high body mass indexes (greater than 40 kg/m²). General anesthetic drugs, the trauma of intubation, and opioids all couple with the underlying airway compromise such that these patients are at risk for postoperative apnea, which, in severe cases, can result in anoxia and death. These patients should be considered for continuous pulse-ox monitoring for at least 12-24 hours postoperatively and are not good candidates for same-day discharge.

Patients who have baseline anticoagulation that has been stopped or bridged preoperatively should have prolonged observation with recheck of their postoperative hemoglobin prior to discharge.

Patients who live alone or are very elderly with baseline frailty are poor candidates for SDD and may benefit from nursing observation overnight while they metabolize their anesthesia. Patients who have chronic opioid dependency present a greater challenge to control postoperative pain; these patients are generally less good candidates for SDD.

Studies have shown that the indication for the procedure (for example, cancer with staging, fibroids, endometriosis) is less critical in determining who is a good candidate for SDD.³ However, successful SDD rates are highest in more straightforward cases with few or no prior surgeries, small uteri (less than 14 weeks), a surgical duration of less than 3 hours, and a surgical start time before 2 p.m. Longer, more complex cases are typically associated with more blood loss, higher risk for occult complications, and more time under anesthesia (and in Trendelenburg), which can exacerbate airway edema. In preparation for such cases, it might be wise to prepare patients for the possibility that they may not be good candidates for discharge on the same day. In general, most SDD pathways exclude patients with very high BMI (greater than 50 kg/m²) because of concern for airway patency and because these cases may be more complex with higher underlying risk. In addition, many of these patients have diabetes and require perioperative metabolic interventions.

Patient preparation

A key component to successful SDD is setting patient expectations. Patients should be informed at their preoperative visit that, unless there is an unexpected occurrence or response to the surgery, they will be discharged to home the same day. This allows them to prepare their home (including transportation needs) in advance. They should be provided with information about what to expect that first night after surgery (including potential residual drowsiness or nausea from anesthesia and immediate postoperative pain).

On the day of surgery, under the influence of anesthesia and pain medication, patients will have difficulty retaining complex discharge instructions. The preoperative visit is critically important because it’s the best time to provide them with this information, including postoperative activity limitations, wound and dressing care, and follow-up instructions. This is also the best time to provide prescriptions for postoperative pain, nausea, and constipation prophylaxis with detailed instructions about best use. Patients should be encouraged to fill these prescriptions preoperatively so that they have these medications on hand on the evening of their discharge.

Many programs utilize a combination of educational strategies (in person, written, video) to maximize the likelihood of retention.¹ It is also important to offer an opportunity for patients to ask questions about this information after they have received it (for example, by phoning the patients prior to their procedure).
 

Preoperative strategies

Intraoperative strategies

Consider in-and-out catheterization rather than placement of an indwelling catheter for anticipated short cases without complex bladder dissection.⁵ Minimize blood loss and maximally evacuate blood and clots with suction because hemoperitoneum can induce nausea and pain.

Pain from retained gas under the diaphragm can be reduced by bathing the diaphragms with 400 cc of dilute local anesthetic made by mixing 50 mL of 0.5% bupivacaine in 1000 mL normal saline prior to removal of pneumoperitoneum and while still in Trendelenburg. Ensure there is minimal retained intraperitoneal CO₂ at the completion of the surgery by asking the anesthesiologists to perform positive pressure ventilations prior to fascial closure. Consider injecting port sites (including the peritoneal and fascial layers) with a mixture of immediate and long-acting local anesthetics. Request that the anesthesia staff administer intraoperative doses of IV ketorolac, acetaminophen, and tramadol (in preference to opioids) and an aggressive perioperative cocktail of antiemetics.

Management in the recovery room

Surgeons should ensure that recovery room staff are well versed in the pathway for patients who are selected for SDD to ensure proactive implementation of analgesic and antiemetic regimens and to fast-track the various tasks and education required for discharge.⁵

Patients should be started on their home postoperative medication regimen in the recovery room, including an anti-inflammatory such as diclofenac, sublingual tramadol (in preference to an opioid, such as hydrocodone), docusate, and sennosides. IV opioids should be avoided because they can result in somnolence and nausea.

If placed intraoperatively, the Foley catheter should be removed early to allow adequate time to void. Backfilling the bladder prior to removal can hasten the urge to void and help objectively document completeness of evacuation. All patients should be seen by the anesthesiologist and/or surgeon prior to discharge.

For patients who are discharged same day, a follow-up phone call on postoperative day 1 is valuable to ensure that they have continued their successful postoperative transition to the home and to intervene early if there are concerns for patient satisfaction.

Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill.

References

1. Fountain CR et al. Promoting same-day discharge for gynecologic oncology patients in minimally invasive hysterectomy. J Minim Invasive Gynecol. 2017 Sep-Oct;24(6):932-9.

2. Rivard C et al. Factors influencing same-day hospital discharge and risk factors for readmission after robotic surgery in the gynecologic oncology patient population. J Minim Invasive Gynecol. 2015 Feb;22(2):219-26.

3. Lee SJ et al. The feasibility and safety of same-day discharge after robotic-assisted hysterectomy alone or with other procedures for benign and malignant indications. Gynecol Oncol. 2014 Jun;133(3):552-5.

4. Elia N et al. Does multimodal analgesia with acetaminophen, nonsteroidal antiinflammatory drugs, or selective cyclooxygenase-2 inhibitors and patient-controlled analgesia morphine offer advantages over morphine alone? Meta-analyses of randomized trials. Anesthesiology. 2005 Dec;103(6):1296-304.

5. Donnez O et al. Low pain score after total laparoscopic hysterectomy and same-day discharge within less than 5 hours: Results of a prospective observational study. J Minim Invasive Gynecol. 2015 Nov-Dec;22(7):1293-9.

There is an increased focus on reducing the costs of health care delivery, and one major driver of surgical cost is length of hospitalization. A minimally invasive surgical approach to hysterectomy is a strategy that significantly enhances recovery and shortens hospital stay, although many patients who can safely be considered for same-day discharge (SDD), including many with cancer, are still admitted to the hospital overnight. Much has been published on the predictors and pathways for successful same-day discharge after minimally invasive hysterectomy, and in this column we will review how to best predict who is a good candidate for SDD and how to optimize the success of this approach with respect to safety and patient satisfaction.

What are the benefits to SDD?

Certainly, decreased hospitalization costs are an attractive feature of SDD following hysterectomy, although surgeons should also be mindful that patient-centered outcomes, such as pain control, managing nausea, and patient satisfaction, also are considered with equal emphasis. Several studies have shown that, in appropriate candidates and when proactive pathways are used, patient satisfaction is preserved with SDD following hysterectomy.¹

Choosing patient candidates

Same day discharge is most successfully accomplished in patients of good general baseline health.² Diabetic patients, particularly those on insulin, are generally not good candidates for SDD because it is important to monitor and intervene in blood glucose changes that are influenced by a nothing-by-mouth status and surgical stress. We recommend observing patients overnight with a history of pulmonary disease who may have transient increased postoperative O₂ needs. Similarly, patients with significant cardiac disease (including heart failure and coronary disease) may benefit from prolonged overnight observation.

Particular caution should be paid to patients with obstructive sleep apnea, which may be occult but anticipated in patients with very high body mass indexes (greater than 40 kg/m²). General anesthetic drugs, the trauma of intubation, and opioids all couple with the underlying airway compromise such that these patients are at risk for postoperative apnea, which, in severe cases, can result in anoxia and death. These patients should be considered for continuous pulse-ox monitoring for at least 12-24 hours postoperatively and are not good candidates for same-day discharge.

Patients who have baseline anticoagulation that has been stopped or bridged preoperatively should have prolonged observation with recheck of their postoperative hemoglobin prior to discharge.

Patients who live alone or are very elderly with baseline frailty are poor candidates for SDD and may benefit from nursing observation overnight while they metabolize their anesthesia. Patients who have chronic opioid dependency present a greater challenge to control postoperative pain; these patients are generally less good candidates for SDD.

Studies have shown that the indication for the procedure (for example, cancer with staging, fibroids, endometriosis) is less critical in determining who is a good candidate for SDD.³ However, successful SDD rates are highest in more straightforward cases with few or no prior surgeries, small uteri (less than 14 weeks), a surgical duration of less than 3 hours, and a surgical start time before 2 p.m. Longer, more complex cases are typically associated with more blood loss, higher risk for occult complications, and more time under anesthesia (and in Trendelenburg), which can exacerbate airway edema. In preparation for such cases, it might be wise to prepare patients for the possibility that they may not be good candidates for discharge on the same day. In general, most SDD pathways exclude patients with very high BMI (greater than 50 kg/m²) because of concern for airway patency and because these cases may be more complex with higher underlying risk. In addition, many of these patients have diabetes and require perioperative metabolic interventions.

Patient preparation

A key component to successful SDD is setting patient expectations. Patients should be informed at their preoperative visit that, unless there is an unexpected occurrence or response to the surgery, they will be discharged to home the same day. This allows them to prepare their home (including transportation needs) in advance. They should be provided with information about what to expect that first night after surgery (including potential residual drowsiness or nausea from anesthesia and immediate postoperative pain).

On the day of surgery, under the influence of anesthesia and pain medication, patients will have difficulty retaining complex discharge instructions. The preoperative visit is critically important because it’s the best time to provide them with this information, including postoperative activity limitations, wound and dressing care, and follow-up instructions. This is also the best time to provide prescriptions for postoperative pain, nausea, and constipation prophylaxis with detailed instructions about best use. Patients should be encouraged to fill these prescriptions preoperatively so that they have these medications on hand on the evening of their discharge.

Many programs utilize a combination of educational strategies (in person, written, video) to maximize the likelihood of retention.¹ It is also important to offer an opportunity for patients to ask questions about this information after they have received it (for example, by phoning the patients prior to their procedure).
 

Preoperative strategies

Intraoperative strategies

Consider in-and-out catheterization rather than placement of an indwelling catheter for anticipated short cases without complex bladder dissection.⁵ Minimize blood loss and maximally evacuate blood and clots with suction because hemoperitoneum can induce nausea and pain.

Pain from retained gas under the diaphragm can be reduced by bathing the diaphragms with 400 cc of dilute local anesthetic made by mixing 50 mL of 0.5% bupivacaine in 1000 mL normal saline prior to removal of pneumoperitoneum and while still in Trendelenburg. Ensure there is minimal retained intraperitoneal CO₂ at the completion of the surgery by asking the anesthesiologists to perform positive pressure ventilations prior to fascial closure. Consider injecting port sites (including the peritoneal and fascial layers) with a mixture of immediate and long-acting local anesthetics. Request that the anesthesia staff administer intraoperative doses of IV ketorolac, acetaminophen, and tramadol (in preference to opioids) and an aggressive perioperative cocktail of antiemetics.

Management in the recovery room

Surgeons should ensure that recovery room staff are well versed in the pathway for patients who are selected for SDD to ensure proactive implementation of analgesic and antiemetic regimens and to fast-track the various tasks and education required for discharge.⁵

Patients should be started on their home postoperative medication regimen in the recovery room, including an anti-inflammatory such as diclofenac, sublingual tramadol (in preference to an opioid, such as hydrocodone), docusate, and sennosides. IV opioids should be avoided because they can result in somnolence and nausea.

If placed intraoperatively, the Foley catheter should be removed early to allow adequate time to void. Backfilling the bladder prior to removal can hasten the urge to void and help objectively document completeness of evacuation. All patients should be seen by the anesthesiologist and/or surgeon prior to discharge.

For patients who are discharged same day, a follow-up phone call on postoperative day 1 is valuable to ensure that they have continued their successful postoperative transition to the home and to intervene early if there are concerns for patient satisfaction.

Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill.

References

1. Fountain CR et al. Promoting same-day discharge for gynecologic oncology patients in minimally invasive hysterectomy. J Minim Invasive Gynecol. 2017 Sep-Oct;24(6):932-9.

2. Rivard C et al. Factors influencing same-day hospital discharge and risk factors for readmission after robotic surgery in the gynecologic oncology patient population. J Minim Invasive Gynecol. 2015 Feb;22(2):219-26.

3. Lee SJ et al. The feasibility and safety of same-day discharge after robotic-assisted hysterectomy alone or with other procedures for benign and malignant indications. Gynecol Oncol. 2014 Jun;133(3):552-5.

4. Elia N et al. Does multimodal analgesia with acetaminophen, nonsteroidal antiinflammatory drugs, or selective cyclooxygenase-2 inhibitors and patient-controlled analgesia morphine offer advantages over morphine alone? Meta-analyses of randomized trials. Anesthesiology. 2005 Dec;103(6):1296-304.

5. Donnez O et al. Low pain score after total laparoscopic hysterectomy and same-day discharge within less than 5 hours: Results of a prospective observational study. J Minim Invasive Gynecol. 2015 Nov-Dec;22(7):1293-9.

Over the last few years, I have spoken to many people about their experiences with involuntary psychiatric hospitalizations. While the stories I’ve heard are anecdotes, often from people who have reached out to me, and not randomized, controlled studies, I’ve taken the liberty of coming to a few conclusions. First, involuntary hospitalizations help people. Most people say that they left the hospital with fewer symptoms than they had when they entered. Second, many of those people, helped though they may have been, are angry about the treatment they received. An unknown percentage feel traumatized by their psychiatric treatment, and years later they dwell on a perception of injustice and injury.

It’s perplexing that this negative residue remains given that involuntary psychiatric care often helps people to escape from the torment of psychosis or from soul-crushing depressions. While many feel it should be easier to involuntarily treat psychiatric disorders, there are no groups of patients asking for easier access to involuntary care. One group, Mad in America – formed by journalist Robert Whitaker – takes the position that psychiatric medications don’t just harm people, but that psychotropic medications actually cause psychiatric disorders in people who would have fared better without them. It now offers CME activities through its conferences and website!

I wanted to know what psychiatrists might learn from his experiences with involuntary care. Weinstein hesitated. “It wasn’t the best experience, and I felt there had to be a better way, but I know everyone was trying to help me, and I want my overall message to be one of hope. I don’t want to complain, because I’ve ended up in a much better place, I’m back at work, enjoying my family, and I feel joy now.”

For psychiatrists, this is the best outcome from a story such as Dr. Weinstein’s. He’s much better, in a scenario where he could have just as easily have died, and he wasn’t traumatized by his care. However, he avoided returning to inpatient care at a precarious time, and he’s left asking if there weren’t a gentler way this could have transpired. These questions are easier to look at from the perspective of a Monday morning quarterback than they are to look at from the perspective of a treatment team dealing with a very sick and combative patient. Still, I hope we all continue to question patients about their experiences and ask if there might be better ways.
 

Dr. Miller, who practices in Baltimore, is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Care” (Baltimore: Johns Hopkins University Press, 2016).

Over the last few years, I have spoken to many people about their experiences with involuntary psychiatric hospitalizations. While the stories I’ve heard are anecdotes, often from people who have reached out to me, and not randomized, controlled studies, I’ve taken the liberty of coming to a few conclusions. First, involuntary hospitalizations help people. Most people say that they left the hospital with fewer symptoms than they had when they entered. Second, many of those people, helped though they may have been, are angry about the treatment they received. An unknown percentage feel traumatized by their psychiatric treatment, and years later they dwell on a perception of injustice and injury.

It’s perplexing that this negative residue remains given that involuntary psychiatric care often helps people to escape from the torment of psychosis or from soul-crushing depressions. While many feel it should be easier to involuntarily treat psychiatric disorders, there are no groups of patients asking for easier access to involuntary care. One group, Mad in America – formed by journalist Robert Whitaker – takes the position that psychiatric medications don’t just harm people, but that psychotropic medications actually cause psychiatric disorders in people who would have fared better without them. It now offers CME activities through its conferences and website!

I wanted to know what psychiatrists might learn from his experiences with involuntary care. Weinstein hesitated. “It wasn’t the best experience, and I felt there had to be a better way, but I know everyone was trying to help me, and I want my overall message to be one of hope. I don’t want to complain, because I’ve ended up in a much better place, I’m back at work, enjoying my family, and I feel joy now.”

For psychiatrists, this is the best outcome from a story such as Dr. Weinstein’s. He’s much better, in a scenario where he could have just as easily have died, and he wasn’t traumatized by his care. However, he avoided returning to inpatient care at a precarious time, and he’s left asking if there weren’t a gentler way this could have transpired. These questions are easier to look at from the perspective of a Monday morning quarterback than they are to look at from the perspective of a treatment team dealing with a very sick and combative patient. Still, I hope we all continue to question patients about their experiences and ask if there might be better ways.
 

Dr. Miller, who practices in Baltimore, is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Care” (Baltimore: Johns Hopkins University Press, 2016).

Over the last few years, I have spoken to many people about their experiences with involuntary psychiatric hospitalizations. While the stories I’ve heard are anecdotes, often from people who have reached out to me, and not randomized, controlled studies, I’ve taken the liberty of coming to a few conclusions. First, involuntary hospitalizations help people. Most people say that they left the hospital with fewer symptoms than they had when they entered. Second, many of those people, helped though they may have been, are angry about the treatment they received. An unknown percentage feel traumatized by their psychiatric treatment, and years later they dwell on a perception of injustice and injury.

It’s perplexing that this negative residue remains given that involuntary psychiatric care often helps people to escape from the torment of psychosis or from soul-crushing depressions. While many feel it should be easier to involuntarily treat psychiatric disorders, there are no groups of patients asking for easier access to involuntary care. One group, Mad in America – formed by journalist Robert Whitaker – takes the position that psychiatric medications don’t just harm people, but that psychotropic medications actually cause psychiatric disorders in people who would have fared better without them. It now offers CME activities through its conferences and website!

I wanted to know what psychiatrists might learn from his experiences with involuntary care. Weinstein hesitated. “It wasn’t the best experience, and I felt there had to be a better way, but I know everyone was trying to help me, and I want my overall message to be one of hope. I don’t want to complain, because I’ve ended up in a much better place, I’m back at work, enjoying my family, and I feel joy now.”

For psychiatrists, this is the best outcome from a story such as Dr. Weinstein’s. He’s much better, in a scenario where he could have just as easily have died, and he wasn’t traumatized by his care. However, he avoided returning to inpatient care at a precarious time, and he’s left asking if there weren’t a gentler way this could have transpired. These questions are easier to look at from the perspective of a Monday morning quarterback than they are to look at from the perspective of a treatment team dealing with a very sick and combative patient. Still, I hope we all continue to question patients about their experiences and ask if there might be better ways.
 

Dr. Miller, who practices in Baltimore, is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Care” (Baltimore: Johns Hopkins University Press, 2016).

Hearing a diagnosis of cancer is one of the most significant moments of a patient’s life and informing a patient of her diagnosis is an emotionally and technically challenging task for an obstetrician gynecologist who is frequently on the front line of making this diagnosis. In this column, we will explore some patient-centered strategies to perform this difficult task well so that patients come away informed but with the highest chance for positive emotional adjustment.

Fewer than 10% of physicians report receiving formal training in techniques of breaking bad news. For the majority of clinicians concerns are centered on being honest and not taking away hope, and in responding to a patient’s emotions.¹ The SPIKES approach was developed to arm physicians with strategies to discuss a cancer diagnosis with their patients. This approach includes six key elements to incorporate during the encounter. These strategies are not meant to be formulaic but rather consistent principles that can be adjusted for individual patient needs.

Setting up the discussion

Breaking bad news should not be a one-size-fits-all approach. Age, educational level, culture, religion, race and ethnicity, and socioeconomic opportunities each affects what and how patients may want to have this kind of information communicated to them. So how do you know how best to deliver a patient-centered approach for your patient? I recommend this simple strategy: Ask her. When ordering a test or performing a biopsy, let the patient know then why you are ordering the test and inform her of the possibility that the results may show cancer. Ask her how she would like for you to communicate that result. Would she like to be called by phone, the benefit of which is quick dissemination of information? Or would she like to receive the information face to face in the office? Research supports that most patients prefer to learn the result in the office.2 If so, I recommend scheduling a follow-up appointment in advance to prevent delays. Ask her if she would like a family member or a supportive friend to be present for the conveying of results so that she will have time to make these arrangements. Ask her if she would prefer for an alternate person to be provided with the results on her behalf.

When preparing to speak with the patient, it is valuable to mentally rehearse the words that you’ll use. Arrange for privacy and manage time constraints and interruptions (silence pagers and phones, ensure there is adequate time allocated in the schedule). Sit down to deliver the news and make a connection with eye contact and, if appropriate, touch.

Assessing the patient’s perception. Before you tell, ask. For example, “what is your understanding about why we did the biopsy?” This will guide you in where her head and heart are and can ensure you meet her wherever she is.

Obtaining the patient’s invitation. Ask the patient what she would like to be told and how much information. What would she like you to focus on? What does she not want to hear?

Giving knowledge and information to the patient. Especially now, it is important to avoid jargon and use nontechnical terms. However, do not shy away from using specific words like “cancer” by substituting them for more vague and confusing terms such as “malignancy” or “tumor.” It is important to find the balance between expressing information without being overly emotive, while avoiding excessive bluntness. Word choice is critical. Communication styles in the breaking of bad news can be separated broadly into three styles: disease centered, emotion centered, and patient-centered.³ The patient-centered approach is achieved by balancing emotional connection, information sharing, nondominance, and conveying hope. (For example, “I have some disappointing news to share. Shall we talk about the next steps in treatment? I understand this is that this is difficult for you.”) In general, this approach is most valued by patients and is associated with better information recall.

Addressing the patient’s emotions with empathetic responses. It is important that physicians take a moment to pause after communicating the test result. Even if prepared, most patients will still have a moment of shock, and their minds will likely spin through a multitude of thoughts preventing them from being able to “hear” and focus on the subsequent information. This is a moment to reflect on her reactions, her body language, and nonverbal communications to guide you on how to approach the rest of the encounter. Offer her your comfort and condolence in whichever way feels appropriate for you and her.

Beware of your own inclinations to “soften the blow.” It is a natural, compassionate instinct to follow-up giving a bad piece of information by balancing a good piece of information. For example, after just telling a woman that she has endometrial cancer, following with a statement such as “but it’s just stage 1 and is curable with surgery.” While this certainly may have immediate comforting effects, it has a couple of unintended consequences. First, it can result in difficulties later adjusting to a change in diagnosis when more information comes in (for example, upstaging after surgery or imaging). It is better to be honest and tell patients only what you know for sure in these immediate first moments of diagnosis when complete information is lacking. A more general statement such as “for most women, this is found at an early stage and is highly treatable” may be more appropriate and still provide some comfort. Second, attempts to soften the blow with a qualifying statement of positivity, such as “this is a good kind of cancer to have” might be interpreted by some patients as failing to acknowledge their devastation. She may feel that you are minimizing her condition and not allowing her to grieve or be distressed.

Strategy and summary. Patients who leave the encounter with some kind of plan for the future feel less distressed and anxious. The direction at this point of the encounter should be led by the patient. What are her greatest concerns (such as mortality, loss of fertility, time off work for treatment), and what does she want to know right now? Most patients express a desire to know more about treatment or prognosis.^2,4 Unfortunately, it often is not possible to furnish this yet, particularly if this falls into the realm of a subspecialist, and prognostication typically requires more information than a provider has at initial diagnosis. However, leaving these questions unanswered is likely to result in a patient feeling helpless. For example, if an ob.gyn. discovers an apparent advanced ovarian cancer on a CT scan, tell her that, despite its apparent advanced case, it is usually treatable and that a gynecologic oncologist will discuss those best treatment options with her. Assure her that you will expeditiously refer her to a specialist who will provide her with those specifics.
 

The aftermath

That interval between initial diagnosis and specialist consultation is extraordinarily difficult and a high anxiety time. It is not unreasonable, in such cases, to recommend the patient to reputable online information sources, such as the Society of Gynecologic Oncology or American Cancer Society websites so that she and her family can do some research prior to that visit in order to prepare them better and give them a sense of understanding in their disease.

It is a particularly compassionate touch to reach out to the patient in the days following her cancer diagnosis, even if she has moved on to a specialist. Patients often tell me that they felt enormous reassurance and appreciation when their ob.gyn. reached out to them to “check on how they are doing.” This can usually reasonably be done by phone. This second contact serves another critical purpose: it allows for repetition of the diagnosis and initial plan, and the ability to fill in the blanks of what the patient may have missed during the prior visit, if her mind was, naturally, elsewhere. It also, quite simply, shows that you care.

Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill. She reports no relevant financial disclosures.

References

1. Baile WF et al. Oncologist. 2000;5(4):302-11.

2. Girgis A et al. Behav Med. 1999 Summer;25(2):69-77.

3. Schmid MM et al. Patient Educ Couns. 2005 Sep;58(3):244-51.

4. Girgis A et al. J Clin Oncol. 1995 Sep;13(9):2449-56.



5. Marscholiek P et al. J Cancer Educ. 2018 Feb 5. doi: 10.1007/s13187-017-1315-3.
 

Hearing a diagnosis of cancer is one of the most significant moments of a patient’s life and informing a patient of her diagnosis is an emotionally and technically challenging task for an obstetrician gynecologist who is frequently on the front line of making this diagnosis. In this column, we will explore some patient-centered strategies to perform this difficult task well so that patients come away informed but with the highest chance for positive emotional adjustment.

Fewer than 10% of physicians report receiving formal training in techniques of breaking bad news. For the majority of clinicians concerns are centered on being honest and not taking away hope, and in responding to a patient’s emotions.¹ The SPIKES approach was developed to arm physicians with strategies to discuss a cancer diagnosis with their patients. This approach includes six key elements to incorporate during the encounter. These strategies are not meant to be formulaic but rather consistent principles that can be adjusted for individual patient needs.

Setting up the discussion

Breaking bad news should not be a one-size-fits-all approach. Age, educational level, culture, religion, race and ethnicity, and socioeconomic opportunities each affects what and how patients may want to have this kind of information communicated to them. So how do you know how best to deliver a patient-centered approach for your patient? I recommend this simple strategy: Ask her. When ordering a test or performing a biopsy, let the patient know then why you are ordering the test and inform her of the possibility that the results may show cancer. Ask her how she would like for you to communicate that result. Would she like to be called by phone, the benefit of which is quick dissemination of information? Or would she like to receive the information face to face in the office? Research supports that most patients prefer to learn the result in the office.2 If so, I recommend scheduling a follow-up appointment in advance to prevent delays. Ask her if she would like a family member or a supportive friend to be present for the conveying of results so that she will have time to make these arrangements. Ask her if she would prefer for an alternate person to be provided with the results on her behalf.

When preparing to speak with the patient, it is valuable to mentally rehearse the words that you’ll use. Arrange for privacy and manage time constraints and interruptions (silence pagers and phones, ensure there is adequate time allocated in the schedule). Sit down to deliver the news and make a connection with eye contact and, if appropriate, touch.

Assessing the patient’s perception. Before you tell, ask. For example, “what is your understanding about why we did the biopsy?” This will guide you in where her head and heart are and can ensure you meet her wherever she is.

Obtaining the patient’s invitation. Ask the patient what she would like to be told and how much information. What would she like you to focus on? What does she not want to hear?

Giving knowledge and information to the patient. Especially now, it is important to avoid jargon and use nontechnical terms. However, do not shy away from using specific words like “cancer” by substituting them for more vague and confusing terms such as “malignancy” or “tumor.” It is important to find the balance between expressing information without being overly emotive, while avoiding excessive bluntness. Word choice is critical. Communication styles in the breaking of bad news can be separated broadly into three styles: disease centered, emotion centered, and patient-centered.³ The patient-centered approach is achieved by balancing emotional connection, information sharing, nondominance, and conveying hope. (For example, “I have some disappointing news to share. Shall we talk about the next steps in treatment? I understand this is that this is difficult for you.”) In general, this approach is most valued by patients and is associated with better information recall.

Addressing the patient’s emotions with empathetic responses. It is important that physicians take a moment to pause after communicating the test result. Even if prepared, most patients will still have a moment of shock, and their minds will likely spin through a multitude of thoughts preventing them from being able to “hear” and focus on the subsequent information. This is a moment to reflect on her reactions, her body language, and nonverbal communications to guide you on how to approach the rest of the encounter. Offer her your comfort and condolence in whichever way feels appropriate for you and her.

Beware of your own inclinations to “soften the blow.” It is a natural, compassionate instinct to follow-up giving a bad piece of information by balancing a good piece of information. For example, after just telling a woman that she has endometrial cancer, following with a statement such as “but it’s just stage 1 and is curable with surgery.” While this certainly may have immediate comforting effects, it has a couple of unintended consequences. First, it can result in difficulties later adjusting to a change in diagnosis when more information comes in (for example, upstaging after surgery or imaging). It is better to be honest and tell patients only what you know for sure in these immediate first moments of diagnosis when complete information is lacking. A more general statement such as “for most women, this is found at an early stage and is highly treatable” may be more appropriate and still provide some comfort. Second, attempts to soften the blow with a qualifying statement of positivity, such as “this is a good kind of cancer to have” might be interpreted by some patients as failing to acknowledge their devastation. She may feel that you are minimizing her condition and not allowing her to grieve or be distressed.

Strategy and summary. Patients who leave the encounter with some kind of plan for the future feel less distressed and anxious. The direction at this point of the encounter should be led by the patient. What are her greatest concerns (such as mortality, loss of fertility, time off work for treatment), and what does she want to know right now? Most patients express a desire to know more about treatment or prognosis.^2,4 Unfortunately, it often is not possible to furnish this yet, particularly if this falls into the realm of a subspecialist, and prognostication typically requires more information than a provider has at initial diagnosis. However, leaving these questions unanswered is likely to result in a patient feeling helpless. For example, if an ob.gyn. discovers an apparent advanced ovarian cancer on a CT scan, tell her that, despite its apparent advanced case, it is usually treatable and that a gynecologic oncologist will discuss those best treatment options with her. Assure her that you will expeditiously refer her to a specialist who will provide her with those specifics.
 

The aftermath

That interval between initial diagnosis and specialist consultation is extraordinarily difficult and a high anxiety time. It is not unreasonable, in such cases, to recommend the patient to reputable online information sources, such as the Society of Gynecologic Oncology or American Cancer Society websites so that she and her family can do some research prior to that visit in order to prepare them better and give them a sense of understanding in their disease.

It is a particularly compassionate touch to reach out to the patient in the days following her cancer diagnosis, even if she has moved on to a specialist. Patients often tell me that they felt enormous reassurance and appreciation when their ob.gyn. reached out to them to “check on how they are doing.” This can usually reasonably be done by phone. This second contact serves another critical purpose: it allows for repetition of the diagnosis and initial plan, and the ability to fill in the blanks of what the patient may have missed during the prior visit, if her mind was, naturally, elsewhere. It also, quite simply, shows that you care.

Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill. She reports no relevant financial disclosures.

References

1. Baile WF et al. Oncologist. 2000;5(4):302-11.

2. Girgis A et al. Behav Med. 1999 Summer;25(2):69-77.

3. Schmid MM et al. Patient Educ Couns. 2005 Sep;58(3):244-51.

4. Girgis A et al. J Clin Oncol. 1995 Sep;13(9):2449-56.



5. Marscholiek P et al. J Cancer Educ. 2018 Feb 5. doi: 10.1007/s13187-017-1315-3.
 

Hearing a diagnosis of cancer is one of the most significant moments of a patient’s life and informing a patient of her diagnosis is an emotionally and technically challenging task for an obstetrician gynecologist who is frequently on the front line of making this diagnosis. In this column, we will explore some patient-centered strategies to perform this difficult task well so that patients come away informed but with the highest chance for positive emotional adjustment.

Fewer than 10% of physicians report receiving formal training in techniques of breaking bad news. For the majority of clinicians concerns are centered on being honest and not taking away hope, and in responding to a patient’s emotions.¹ The SPIKES approach was developed to arm physicians with strategies to discuss a cancer diagnosis with their patients. This approach includes six key elements to incorporate during the encounter. These strategies are not meant to be formulaic but rather consistent principles that can be adjusted for individual patient needs.

Setting up the discussion

Breaking bad news should not be a one-size-fits-all approach. Age, educational level, culture, religion, race and ethnicity, and socioeconomic opportunities each affects what and how patients may want to have this kind of information communicated to them. So how do you know how best to deliver a patient-centered approach for your patient? I recommend this simple strategy: Ask her. When ordering a test or performing a biopsy, let the patient know then why you are ordering the test and inform her of the possibility that the results may show cancer. Ask her how she would like for you to communicate that result. Would she like to be called by phone, the benefit of which is quick dissemination of information? Or would she like to receive the information face to face in the office? Research supports that most patients prefer to learn the result in the office.2 If so, I recommend scheduling a follow-up appointment in advance to prevent delays. Ask her if she would like a family member or a supportive friend to be present for the conveying of results so that she will have time to make these arrangements. Ask her if she would prefer for an alternate person to be provided with the results on her behalf.

When preparing to speak with the patient, it is valuable to mentally rehearse the words that you’ll use. Arrange for privacy and manage time constraints and interruptions (silence pagers and phones, ensure there is adequate time allocated in the schedule). Sit down to deliver the news and make a connection with eye contact and, if appropriate, touch.

Assessing the patient’s perception. Before you tell, ask. For example, “what is your understanding about why we did the biopsy?” This will guide you in where her head and heart are and can ensure you meet her wherever she is.

Obtaining the patient’s invitation. Ask the patient what she would like to be told and how much information. What would she like you to focus on? What does she not want to hear?

Giving knowledge and information to the patient. Especially now, it is important to avoid jargon and use nontechnical terms. However, do not shy away from using specific words like “cancer” by substituting them for more vague and confusing terms such as “malignancy” or “tumor.” It is important to find the balance between expressing information without being overly emotive, while avoiding excessive bluntness. Word choice is critical. Communication styles in the breaking of bad news can be separated broadly into three styles: disease centered, emotion centered, and patient-centered.³ The patient-centered approach is achieved by balancing emotional connection, information sharing, nondominance, and conveying hope. (For example, “I have some disappointing news to share. Shall we talk about the next steps in treatment? I understand this is that this is difficult for you.”) In general, this approach is most valued by patients and is associated with better information recall.

Addressing the patient’s emotions with empathetic responses. It is important that physicians take a moment to pause after communicating the test result. Even if prepared, most patients will still have a moment of shock, and their minds will likely spin through a multitude of thoughts preventing them from being able to “hear” and focus on the subsequent information. This is a moment to reflect on her reactions, her body language, and nonverbal communications to guide you on how to approach the rest of the encounter. Offer her your comfort and condolence in whichever way feels appropriate for you and her.

Beware of your own inclinations to “soften the blow.” It is a natural, compassionate instinct to follow-up giving a bad piece of information by balancing a good piece of information. For example, after just telling a woman that she has endometrial cancer, following with a statement such as “but it’s just stage 1 and is curable with surgery.” While this certainly may have immediate comforting effects, it has a couple of unintended consequences. First, it can result in difficulties later adjusting to a change in diagnosis when more information comes in (for example, upstaging after surgery or imaging). It is better to be honest and tell patients only what you know for sure in these immediate first moments of diagnosis when complete information is lacking. A more general statement such as “for most women, this is found at an early stage and is highly treatable” may be more appropriate and still provide some comfort. Second, attempts to soften the blow with a qualifying statement of positivity, such as “this is a good kind of cancer to have” might be interpreted by some patients as failing to acknowledge their devastation. She may feel that you are minimizing her condition and not allowing her to grieve or be distressed.

Strategy and summary. Patients who leave the encounter with some kind of plan for the future feel less distressed and anxious. The direction at this point of the encounter should be led by the patient. What are her greatest concerns (such as mortality, loss of fertility, time off work for treatment), and what does she want to know right now? Most patients express a desire to know more about treatment or prognosis.^2,4 Unfortunately, it often is not possible to furnish this yet, particularly if this falls into the realm of a subspecialist, and prognostication typically requires more information than a provider has at initial diagnosis. However, leaving these questions unanswered is likely to result in a patient feeling helpless. For example, if an ob.gyn. discovers an apparent advanced ovarian cancer on a CT scan, tell her that, despite its apparent advanced case, it is usually treatable and that a gynecologic oncologist will discuss those best treatment options with her. Assure her that you will expeditiously refer her to a specialist who will provide her with those specifics.
 

The aftermath

That interval between initial diagnosis and specialist consultation is extraordinarily difficult and a high anxiety time. It is not unreasonable, in such cases, to recommend the patient to reputable online information sources, such as the Society of Gynecologic Oncology or American Cancer Society websites so that she and her family can do some research prior to that visit in order to prepare them better and give them a sense of understanding in their disease.

It is a particularly compassionate touch to reach out to the patient in the days following her cancer diagnosis, even if she has moved on to a specialist. Patients often tell me that they felt enormous reassurance and appreciation when their ob.gyn. reached out to them to “check on how they are doing.” This can usually reasonably be done by phone. This second contact serves another critical purpose: it allows for repetition of the diagnosis and initial plan, and the ability to fill in the blanks of what the patient may have missed during the prior visit, if her mind was, naturally, elsewhere. It also, quite simply, shows that you care.

Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill. She reports no relevant financial disclosures.

References

1. Baile WF et al. Oncologist. 2000;5(4):302-11.

2. Girgis A et al. Behav Med. 1999 Summer;25(2):69-77.

3. Schmid MM et al. Patient Educ Couns. 2005 Sep;58(3):244-51.

4. Girgis A et al. J Clin Oncol. 1995 Sep;13(9):2449-56.



5. Marscholiek P et al. J Cancer Educ. 2018 Feb 5. doi: 10.1007/s13187-017-1315-3.