From the Editor

Imagine being able to precisely select the medication with the optimal efficacy, safety, and tolerability at the outset of treatment for every psychiatric patient who needs pharma­cotherapy. Imagine how much the patient would appreciate not receiving a series of drugs and suffering multiple adverse effects and unremitting symptoms until the “right medication” is identified. Imagine how gratifying it would be for you as a psychiatrist to watch every one of your patients improve rapidly with minimal complaints or adverse effects.

Precision psychiatry is the indispensable vehicle to achieve personalized medicine for psychiatric patients. Precision psychiatry is a cherished goal, but it remains an aspirational objective. Other medical specialties, especially oncology and cardiology, have made remarkable strides in precision medicine, but the journey to precision psychiatry is still in its early stages. Yet there is every reason to believe that we are making progress toward that cherished goal.

To implement precision psychiatry, we must be able to identify the biosignature of each patient’s psychiatric brain disorder. But there is a formidable challenge to overcome: the complex, extensive heterogeneity of psychiatric disorders, which requires intense and inspired neurobiology research. So, while clinicians go on with the mundane trial-and-error approach of contemporary psychopharmacology, psychiatric neuroscientists are diligently deconstructing major psychiatric disorders into specific biotypes with unique biosignatures that will one day guide accurate and prompt clinical management.

Psychiatric practitioners may be too busy to keep tabs on the progress being made in identifying various biomarkers that are the key ingredients to decoding the biosignature of each psychiatric patient. Take schizophrenia, for example. There are myriad clinical variations that comprise this heterogeneous brain syndrome, including level of premorbid functioning; acute vs gradual onset of psychosis; the type and severity of hallucinations or delusions; the dimensional spectrum of negative symptoms and cognitive impairments; the presence and intensity of suicidal or homicidal urges; and the type of medical and psychiatric comorbidities. No wonder every patient is a unique and fascinating clinical puzzle, and yet, patients with schizophrenia are still being homogenized under a single DSM diagnostic category.

Precision psychiatry will ultimately enable practitioners to recognize various psychotic diseases that are more specific than the current DSM psychosis categories. Further, precision psychiatry will provide guidance as to which member within a class of so-called “me-too” drugs is the optimal match for each patient. This will stand in stark contrast to the chaotic hit-or-miss approach.

Precision psychiatry also will reveal the absurdity of current FDA clinical trials design for drug development. How can a molecule with a putative mechanism of action relevant to a specific biotype be administered to a hodgepodge of heterogeneous biotypes that have been lumped in 1 clinical category, and yet be expected to exert efficacy in most biotypes? It is a small miracle that some new drugs beat placebo despite the extensive variability in both placebo responses and drug responses. But it is well known that in all FDA placebo-controlled trials, the therapeutic response across the patient population varies from extremely high to extremely low, and worsening may even occur in a subset of patients receiving either the active drug or placebo. Perhaps drug response should be used as 1 methodology to classify biotypes of patients encompassed within a heterogeneous syndrome such as schizophrenia.

Precision psychiatry will represent a huge paradigm shift in the science and practice of our specialty. In his landmark book, Thomas Kuhn defined a paradigm as “an entire worldview in which a theory exists and all the implications that come from that view.”² Precision psychiatry will completely disrupt the current antiquated clinical paradigm, transforming psychiatry into the clinical neuroscience it is. Many “omics,” such as genomics, epigenomics, transcriptomics, proteomics, metabolomics, lipidomics, and metagenomics, will inevitably find their way into the jargon of psychiatrists.³

A marriage of science and technology is essential for the emergence of precision psychiatry. To achieve this transformative amalgamation, we need to reconfigure our concepts, reengineer our methods, reinvent our models, and redesign our approaches to patient care.

As Peter Drucker said, “The best way to predict the future is to create it.”⁴ Precision psychiatry is our future. Let’s create it!

Imagine being able to precisely select the medication with the optimal efficacy, safety, and tolerability at the outset of treatment for every psychiatric patient who needs pharma­cotherapy. Imagine how much the patient would appreciate not receiving a series of drugs and suffering multiple adverse effects and unremitting symptoms until the “right medication” is identified. Imagine how gratifying it would be for you as a psychiatrist to watch every one of your patients improve rapidly with minimal complaints or adverse effects.

Precision psychiatry is the indispensable vehicle to achieve personalized medicine for psychiatric patients. Precision psychiatry is a cherished goal, but it remains an aspirational objective. Other medical specialties, especially oncology and cardiology, have made remarkable strides in precision medicine, but the journey to precision psychiatry is still in its early stages. Yet there is every reason to believe that we are making progress toward that cherished goal.

To implement precision psychiatry, we must be able to identify the biosignature of each patient’s psychiatric brain disorder. But there is a formidable challenge to overcome: the complex, extensive heterogeneity of psychiatric disorders, which requires intense and inspired neurobiology research. So, while clinicians go on with the mundane trial-and-error approach of contemporary psychopharmacology, psychiatric neuroscientists are diligently deconstructing major psychiatric disorders into specific biotypes with unique biosignatures that will one day guide accurate and prompt clinical management.

Psychiatric practitioners may be too busy to keep tabs on the progress being made in identifying various biomarkers that are the key ingredients to decoding the biosignature of each psychiatric patient. Take schizophrenia, for example. There are myriad clinical variations that comprise this heterogeneous brain syndrome, including level of premorbid functioning; acute vs gradual onset of psychosis; the type and severity of hallucinations or delusions; the dimensional spectrum of negative symptoms and cognitive impairments; the presence and intensity of suicidal or homicidal urges; and the type of medical and psychiatric comorbidities. No wonder every patient is a unique and fascinating clinical puzzle, and yet, patients with schizophrenia are still being homogenized under a single DSM diagnostic category.

Precision psychiatry will ultimately enable practitioners to recognize various psychotic diseases that are more specific than the current DSM psychosis categories. Further, precision psychiatry will provide guidance as to which member within a class of so-called “me-too” drugs is the optimal match for each patient. This will stand in stark contrast to the chaotic hit-or-miss approach.

Precision psychiatry also will reveal the absurdity of current FDA clinical trials design for drug development. How can a molecule with a putative mechanism of action relevant to a specific biotype be administered to a hodgepodge of heterogeneous biotypes that have been lumped in 1 clinical category, and yet be expected to exert efficacy in most biotypes? It is a small miracle that some new drugs beat placebo despite the extensive variability in both placebo responses and drug responses. But it is well known that in all FDA placebo-controlled trials, the therapeutic response across the patient population varies from extremely high to extremely low, and worsening may even occur in a subset of patients receiving either the active drug or placebo. Perhaps drug response should be used as 1 methodology to classify biotypes of patients encompassed within a heterogeneous syndrome such as schizophrenia.

Precision psychiatry will represent a huge paradigm shift in the science and practice of our specialty. In his landmark book, Thomas Kuhn defined a paradigm as “an entire worldview in which a theory exists and all the implications that come from that view.”² Precision psychiatry will completely disrupt the current antiquated clinical paradigm, transforming psychiatry into the clinical neuroscience it is. Many “omics,” such as genomics, epigenomics, transcriptomics, proteomics, metabolomics, lipidomics, and metagenomics, will inevitably find their way into the jargon of psychiatrists.³

A marriage of science and technology is essential for the emergence of precision psychiatry. To achieve this transformative amalgamation, we need to reconfigure our concepts, reengineer our methods, reinvent our models, and redesign our approaches to patient care.

As Peter Drucker said, “The best way to predict the future is to create it.”⁴ Precision psychiatry is our future. Let’s create it!

Imagine being able to precisely select the medication with the optimal efficacy, safety, and tolerability at the outset of treatment for every psychiatric patient who needs pharma­cotherapy. Imagine how much the patient would appreciate not receiving a series of drugs and suffering multiple adverse effects and unremitting symptoms until the “right medication” is identified. Imagine how gratifying it would be for you as a psychiatrist to watch every one of your patients improve rapidly with minimal complaints or adverse effects.

Precision psychiatry is the indispensable vehicle to achieve personalized medicine for psychiatric patients. Precision psychiatry is a cherished goal, but it remains an aspirational objective. Other medical specialties, especially oncology and cardiology, have made remarkable strides in precision medicine, but the journey to precision psychiatry is still in its early stages. Yet there is every reason to believe that we are making progress toward that cherished goal.

To implement precision psychiatry, we must be able to identify the biosignature of each patient’s psychiatric brain disorder. But there is a formidable challenge to overcome: the complex, extensive heterogeneity of psychiatric disorders, which requires intense and inspired neurobiology research. So, while clinicians go on with the mundane trial-and-error approach of contemporary psychopharmacology, psychiatric neuroscientists are diligently deconstructing major psychiatric disorders into specific biotypes with unique biosignatures that will one day guide accurate and prompt clinical management.

Psychiatric practitioners may be too busy to keep tabs on the progress being made in identifying various biomarkers that are the key ingredients to decoding the biosignature of each psychiatric patient. Take schizophrenia, for example. There are myriad clinical variations that comprise this heterogeneous brain syndrome, including level of premorbid functioning; acute vs gradual onset of psychosis; the type and severity of hallucinations or delusions; the dimensional spectrum of negative symptoms and cognitive impairments; the presence and intensity of suicidal or homicidal urges; and the type of medical and psychiatric comorbidities. No wonder every patient is a unique and fascinating clinical puzzle, and yet, patients with schizophrenia are still being homogenized under a single DSM diagnostic category.

Precision psychiatry will ultimately enable practitioners to recognize various psychotic diseases that are more specific than the current DSM psychosis categories. Further, precision psychiatry will provide guidance as to which member within a class of so-called “me-too” drugs is the optimal match for each patient. This will stand in stark contrast to the chaotic hit-or-miss approach.

Precision psychiatry also will reveal the absurdity of current FDA clinical trials design for drug development. How can a molecule with a putative mechanism of action relevant to a specific biotype be administered to a hodgepodge of heterogeneous biotypes that have been lumped in 1 clinical category, and yet be expected to exert efficacy in most biotypes? It is a small miracle that some new drugs beat placebo despite the extensive variability in both placebo responses and drug responses. But it is well known that in all FDA placebo-controlled trials, the therapeutic response across the patient population varies from extremely high to extremely low, and worsening may even occur in a subset of patients receiving either the active drug or placebo. Perhaps drug response should be used as 1 methodology to classify biotypes of patients encompassed within a heterogeneous syndrome such as schizophrenia.

Precision psychiatry will represent a huge paradigm shift in the science and practice of our specialty. In his landmark book, Thomas Kuhn defined a paradigm as “an entire worldview in which a theory exists and all the implications that come from that view.”² Precision psychiatry will completely disrupt the current antiquated clinical paradigm, transforming psychiatry into the clinical neuroscience it is. Many “omics,” such as genomics, epigenomics, transcriptomics, proteomics, metabolomics, lipidomics, and metagenomics, will inevitably find their way into the jargon of psychiatrists.³

A marriage of science and technology is essential for the emergence of precision psychiatry. To achieve this transformative amalgamation, we need to reconfigure our concepts, reengineer our methods, reinvent our models, and redesign our approaches to patient care.

As Peter Drucker said, “The best way to predict the future is to create it.”⁴ Precision psychiatry is our future. Let’s create it!

Timely access to cancer care can translate into improved outcomes and quality of care, better patient quality of life, and cost savings for patients, practices, and society alike. There are many ways to facilitate such access, starting with educating patients and caregivers about its importance and that ensuring routine screening recommendations are followed to increase the likelihood of earlier-stage diagnosis and therefore earlier therapy initiation. But literal access – physically getting to the point of care – can also be an issue. For patients who live in rural or remote areas or those of low socioeconomic status, even in an urban area, the cost and logistics of getting to the point of care for treatment can be prohibitive, especially if the various components of care are not consolidated. Two articles in this issue focus on access to care and the impact on outcomes.

On page e263, Margaret Kemeny reports on the impact on outcomes and quality of care in patients of low socioeconomic status who were treated for breast cancer at a centralized cancer care center. The center was established at a public hospital in Queens, New York, to provide single-site, comprehensive care encompassing the clinical, supportive, and clerical-financial aspects of care during all phases of the disease trajectory. Kemeny compared the data of breast cancer patients treated at the hospital before the center was established with the five-year data of those treated at the cancer care center. She found that several factors changed, among them, that there was an increase in the number of patients diagnosed with earlier-stage breast cancer, an increase in the use of lumpectomies, and an increase in survival for patients with stage 3 disease. Not only are the findings of this study compelling, but the introduction and discussion sections provide a useful review of related literature as well as some practical “how-to” pointers for anyone thinking about setting up a similar center.

Gilbertson-White and colleagues continue with the theme of access to care in cancer patients, but shift the focus in their systemic literature review to supportive and palliative interventions for patients with advanced disease who live in rural communities (p. e248). Compared with urban communities, the rates of late-stage cancer and mortality are higher in rural communities, where low socioeconomic status, inadequate health coverage, and less workplace flexibility and social support hamper access to care. The findings show that the interventions resulted in a reduction in physical and emotional symptoms; improvement in patient quality of life and well-being, access to health care services, and quality of care; and cost savings for patients who received care from rural- instead of urban-based hospitals. The authors emphasize the importance of technology, especially tele- and video-conferencing, in delivering palliative and supportive care to underserved communities.

Patient-reported outcomes have been described as a picture of the patient perspective on treatment and its side effects, and they are increasingly being included in clinical trials and incorporated into the delivery of quality care. Valenti and colleagues studied the impact of cancer-therapy–related adverse events (AEs) on patient quality of life (p. e256). They compared the impact on quality of life reported by cancer patients who had experienced a particular AE with the impact envisioned by participants from the general public who had not experienced AEs and found that those who had experienced AEs perceived a lower impact on quality of life compared with the general public participants who had not experienced the AEs.

Also in this issue are a pertinent and comprehensive review of the latest in breast cancer therapies, specifically targeted therapies for multiple subtypes (p. e277); two Case Reports, one on managing tonsillar carcinoma with advanced radiation and chemotherapy techniques (p. e268), another on familial essential thrombocythemia associated with JAK2 V617F mutation in siblings (p. e274); and Community Translations articles on the approvals of atezolizumab for non–small-cell lung cancer (p. e 242)and lenlidomide for multiple myeloma in the maintenance setting (p. e245).

Timely access to cancer care can translate into improved outcomes and quality of care, better patient quality of life, and cost savings for patients, practices, and society alike. There are many ways to facilitate such access, starting with educating patients and caregivers about its importance and that ensuring routine screening recommendations are followed to increase the likelihood of earlier-stage diagnosis and therefore earlier therapy initiation. But literal access – physically getting to the point of care – can also be an issue. For patients who live in rural or remote areas or those of low socioeconomic status, even in an urban area, the cost and logistics of getting to the point of care for treatment can be prohibitive, especially if the various components of care are not consolidated. Two articles in this issue focus on access to care and the impact on outcomes.

On page e263, Margaret Kemeny reports on the impact on outcomes and quality of care in patients of low socioeconomic status who were treated for breast cancer at a centralized cancer care center. The center was established at a public hospital in Queens, New York, to provide single-site, comprehensive care encompassing the clinical, supportive, and clerical-financial aspects of care during all phases of the disease trajectory. Kemeny compared the data of breast cancer patients treated at the hospital before the center was established with the five-year data of those treated at the cancer care center. She found that several factors changed, among them, that there was an increase in the number of patients diagnosed with earlier-stage breast cancer, an increase in the use of lumpectomies, and an increase in survival for patients with stage 3 disease. Not only are the findings of this study compelling, but the introduction and discussion sections provide a useful review of related literature as well as some practical “how-to” pointers for anyone thinking about setting up a similar center.

Gilbertson-White and colleagues continue with the theme of access to care in cancer patients, but shift the focus in their systemic literature review to supportive and palliative interventions for patients with advanced disease who live in rural communities (p. e248). Compared with urban communities, the rates of late-stage cancer and mortality are higher in rural communities, where low socioeconomic status, inadequate health coverage, and less workplace flexibility and social support hamper access to care. The findings show that the interventions resulted in a reduction in physical and emotional symptoms; improvement in patient quality of life and well-being, access to health care services, and quality of care; and cost savings for patients who received care from rural- instead of urban-based hospitals. The authors emphasize the importance of technology, especially tele- and video-conferencing, in delivering palliative and supportive care to underserved communities.

Patient-reported outcomes have been described as a picture of the patient perspective on treatment and its side effects, and they are increasingly being included in clinical trials and incorporated into the delivery of quality care. Valenti and colleagues studied the impact of cancer-therapy–related adverse events (AEs) on patient quality of life (p. e256). They compared the impact on quality of life reported by cancer patients who had experienced a particular AE with the impact envisioned by participants from the general public who had not experienced AEs and found that those who had experienced AEs perceived a lower impact on quality of life compared with the general public participants who had not experienced the AEs.

Also in this issue are a pertinent and comprehensive review of the latest in breast cancer therapies, specifically targeted therapies for multiple subtypes (p. e277); two Case Reports, one on managing tonsillar carcinoma with advanced radiation and chemotherapy techniques (p. e268), another on familial essential thrombocythemia associated with JAK2 V617F mutation in siblings (p. e274); and Community Translations articles on the approvals of atezolizumab for non–small-cell lung cancer (p. e 242)and lenlidomide for multiple myeloma in the maintenance setting (p. e245).

Timely access to cancer care can translate into improved outcomes and quality of care, better patient quality of life, and cost savings for patients, practices, and society alike. There are many ways to facilitate such access, starting with educating patients and caregivers about its importance and that ensuring routine screening recommendations are followed to increase the likelihood of earlier-stage diagnosis and therefore earlier therapy initiation. But literal access – physically getting to the point of care – can also be an issue. For patients who live in rural or remote areas or those of low socioeconomic status, even in an urban area, the cost and logistics of getting to the point of care for treatment can be prohibitive, especially if the various components of care are not consolidated. Two articles in this issue focus on access to care and the impact on outcomes.

On page e263, Margaret Kemeny reports on the impact on outcomes and quality of care in patients of low socioeconomic status who were treated for breast cancer at a centralized cancer care center. The center was established at a public hospital in Queens, New York, to provide single-site, comprehensive care encompassing the clinical, supportive, and clerical-financial aspects of care during all phases of the disease trajectory. Kemeny compared the data of breast cancer patients treated at the hospital before the center was established with the five-year data of those treated at the cancer care center. She found that several factors changed, among them, that there was an increase in the number of patients diagnosed with earlier-stage breast cancer, an increase in the use of lumpectomies, and an increase in survival for patients with stage 3 disease. Not only are the findings of this study compelling, but the introduction and discussion sections provide a useful review of related literature as well as some practical “how-to” pointers for anyone thinking about setting up a similar center.

Gilbertson-White and colleagues continue with the theme of access to care in cancer patients, but shift the focus in their systemic literature review to supportive and palliative interventions for patients with advanced disease who live in rural communities (p. e248). Compared with urban communities, the rates of late-stage cancer and mortality are higher in rural communities, where low socioeconomic status, inadequate health coverage, and less workplace flexibility and social support hamper access to care. The findings show that the interventions resulted in a reduction in physical and emotional symptoms; improvement in patient quality of life and well-being, access to health care services, and quality of care; and cost savings for patients who received care from rural- instead of urban-based hospitals. The authors emphasize the importance of technology, especially tele- and video-conferencing, in delivering palliative and supportive care to underserved communities.

Patient-reported outcomes have been described as a picture of the patient perspective on treatment and its side effects, and they are increasingly being included in clinical trials and incorporated into the delivery of quality care. Valenti and colleagues studied the impact of cancer-therapy–related adverse events (AEs) on patient quality of life (p. e256). They compared the impact on quality of life reported by cancer patients who had experienced a particular AE with the impact envisioned by participants from the general public who had not experienced AEs and found that those who had experienced AEs perceived a lower impact on quality of life compared with the general public participants who had not experienced the AEs.

Also in this issue are a pertinent and comprehensive review of the latest in breast cancer therapies, specifically targeted therapies for multiple subtypes (p. e277); two Case Reports, one on managing tonsillar carcinoma with advanced radiation and chemotherapy techniques (p. e268), another on familial essential thrombocythemia associated with JAK2 V617F mutation in siblings (p. e274); and Community Translations articles on the approvals of atezolizumab for non–small-cell lung cancer (p. e 242)and lenlidomide for multiple myeloma in the maintenance setting (p. e245).

Illustration: Kimberly Martens for OBG Management

All mammalian life is dependent on a continuous supply of molecular oxygen. Molecular oxygen is carried to cells by noncovalent binding to the iron moiety in the hemoglobin of red blood cells. It is utilized within cells by noncovalent binding to the iron moiety in various microsomal and mitochondrial proteins, including myoglobin and cytochromes. Consequently, to efficiently utilize molecular oxygen all mammalian life is dependent on an adequate supply of iron. Surprisingly, in an era of high technology precision medicine, many pregnant women are iron deficient, anemic, and not receiving adequate iron supplementation.

Iron deficiency is prevalent in women and pregnant women

Women often become iron deficient because of pregnancy or heavy menstrual bleeding. During pregnancy, maternal iron is provided to supply the needs of the fetus and placenta. Additional iron is needed to expand maternal red blood cell volume and replace iron lost due to bleeding at delivery. In the National Health and Nutrition Examination Survey (NHANES) of 1988–1994, 11% of women aged 16 to 49 years were iron deficient. By contrast, less than 1% of men aged 16 to 49 years were iron deficient.¹

In a NHANES study from 1999–2006, risk factors for iron deficiency included multiparity, current pregnancy, and regular menstrual cycles. Use of hormonal contraception reduced the rate of iron deficiency.² Using the same data, the prevalences of iron deficiency during the first, second, and third trimesters of pregnancy were reported to be 7%, 14%, and 30%, respectively.³ In addition to pregnancy and menstrual bleeding there are many other medical problems that may contribute to iron deficiency, including Helicobacter pylori (H pylori) infection, gastritis, celiac disease, and bariatric surgery.

Iron deficiency anemia may be associated with adverse pregnancy outcomes

In a retrospective study of 75,660 singleton pregnancies, 7,977 women were diagnosed with iron deficiency anemia when they were admitted for delivery. Compared with pregnant women without iron deficiency, the presence of iron deficiency increased the risk of:

• blood transfusion (odds ratio [OR], 5.48; 95% confidence interval [CI], 4.57–6.58)
• preterm delivery (OR, 1.54; 95% CI, 1.36–1.76)
• cesarean delivery (OR, 1.30; 95% CI, 1.13–1.49)
• 5-minute Apgar score <7 (OR, 2.21; 95% CI, 1.84–2.64)
• intensive care unit (ICU) admission (OR, 1.28; 95% CI, 1.20–1.39).⁴

In a systematic review and meta-analysis of 26 studies, maternal anemia (mostly iron deficiency anemia) was associated with a higher risk of low birth weight (relative risk [RR], 1.31; 95% CI, 1.13–1.51), preterm birth (RR, 1.63; 95% CI, 1.33–2.01), perinatal mortality (RR, 1.51; 95% CI, 1.30–1.76), and neonatal mortality (RR, 2.72; 95% CI, 1.19–6.25).⁵

In a clinical trial, pregnant women were randomly assigned to receive folic acid alone; folic acid plus iron supplements; or 15 vitamins and minerals, including folic acid and iron. At delivery, women in the iron-folic acid and the 15 vitamin and minerals groups had higher hemoglobin concentrations than the folic acid monotherapy group. Among 4,697 live births, women in the iron-folic acid group had significantly fewer preterm births (<34 weeks’ gestation) than the folic acid group (RR, 0.50; 95% CI, 0.27–0.94; P = .031).⁶ Data from additional randomized trials are needed to further clarify the effect of iron supplementation on obstetric outcomes.

Related article:
Treating polycystic ovary syndrome: Start using dual medical therapy

The diagnosis of iron deficiency is optimized by measuring serum ferritin

Serum ferritin measurement is an excellent test of iron deficiency. We recommend that all pregnant women have serum ferritin measured at the first prenatal visit and at the beginning of the third trimester to assess maternal iron stores. In pregnancy, the Centers for Disease Control and Prevention and the World Health Organization define anemia as a hemoglobin level of less than 11 g/dL or hematocrit less than 33% in the first and third trimesters. If a pregnant woman is not anemic, a serum ferritin level less than 15 ng/mL indicates iron deficiency.⁷ Some experts believe that in pregnant women who are not anemic, a serum ferritin level between 15 and 30 ng/mL may also indicate iron deficiency.⁸ If the pregnant woman is anemic and does not have another cause of the anemia, a serum ferritin level less than 40 ng/mL is indicative of iron deficiency.⁷

Ferritin is an acute phase reactant and levels may be falsely elevated due to chronic or acute inflammation, liver disease, renal failure, metabolic syndrome, or malignancy. Some women with iron deficiency due to bariatric surgery or malabsorption also have vitamin B12 and, less commonly, folate deficiency, which can contribute to the development of anemia (see “Diagnosis of anemia, iron deficiency, and iron deficiency anemia in pregnancy.”) Clinicians are often advised that a mean corpuscular volume demonstrating microcytosis is the “best test” to assess a patient for iron deficiency. However, reduced iron availability and low ferritin precede microcytosis. Hence microcytosis is a lagging measure and iron deficiency is diagnosed at an earlier stage by ferritin.

Dietary iron

Iron in food is present in heme (meat, poultry, fish) and non-heme forms (grains, plant food, supplements). Heme iron is better absorbed than non-heme iron. Foods rich in non-heme iron include spinach, lentils, prune juice, dried prunes, and fortified cereals. Absorption of non-heme iron can be increased by vitamin C or vitamin C–rich foods (broccoli, bell peppers, cantaloupe, grapefruit, oranges, strawberries, and tomatoes). Absorption of non-heme iron is reduced by consumption of dairy products, coffee, tea, and chocolate.

Oral iron treatment

Oral iron is an effective treatment for iron deficiency^9,10 and is inexpensive, safe, and widely available. The CDC recommends that all pregnant women take a 30 mg/day iron supplement, unless they have hemochromatosis.¹¹ For women with a low ferritin level and anemia, iron supplementation should be increased to 30 to 120 mg daily.¹¹ Not all prenatal vitamins contain iron; those that do typically contain 17 to 28 mg of elemental iron per dose.

Many pregnant women taking oral iron, especially at doses greater than 30 mg daily, have gastrointestinal side effects, which cause them to discontinue the iron therapy.¹² Taking iron supplementation on an intermittent basis may help to reduce gastrointestinal side effects and improve iron stores.¹³

In the past, a standard approach to the treatment of iron deficiency anemia was oral ferrous sulfate 325 mg (65 mg elemental iron) spaced in 3 doses each day for a total daily dose of 195 mg elemental iron. However, recent absorption studies concluded that maximal absorption of iron occurs with a dose in the range of 40 to 80 mg of elemental iron daily. Greater doses do not result in more iron absorption and are associated with more side effects.^14,15 (See “Start using alternate-day oral iron dosing, and stop using daily iron dosing.”)

Oral iron should not be taken in close approximation to the consumption of milk, cereals, tea, coffee, eggs, or calcium supplements. The absorption of oral iron is enhanced by the consumption of orange juice or 250 mg of vitamin C. Gastrointestinal side effects include nausea, flatulence, constipation, diarrhea, epigastric distress, and vomiting. If gastrointestinal side effects occur, interventions that might improve tolerability include: reduce the dose of iron or administer intermittently or use a low dose of oral iron, where dosing can be more easily titrated.

We re-check ferritin and hemoglobin levels 2 to 4 weeks after initiation of oral iron therapy and expect to see a hemoglobin rise of 1 g/dL if the therapy is effective.

Intravenous iron treatment

For women with iron deficiency anemia who cannot tolerate oral iron or in whom oral iron treatment has not resolved their anemia, intravenous (IV) iron treatment may be an optimal approach. Women in the third trimester of pregnancy with iron deficiency anemia have very little time to consume sufficient quantities of oral iron in food and supplements to restore their deficiency and reverse their anemia. Consequently, treatment with IV iron may be especially appropriate for women with iron deficiency anemia in the third trimester of pregnancy. Prior gastric surgery, including gastric bypass, results in reduced gastric acid production and causes severe impairment of intestinal absorption of iron. Patients with malabsorption syndromes, including celiac disease, also may have limited absorption of oral iron. These populations of pregnant women may particularly benefit from the use of IV iron. In pregnant women IV iron has fewer gastrointestinal side effects than oral iron.¹⁶

Many severely iron deficient patients need 1,000 mg of iron to resolve their deficit. In order to avoid giving multiple standard doses (200 mg per infusion, with 5 infusions over many days), some centers have explored the use of 1 large dose of IV iron (1,000 mg of low molecular weight iron dextran administered over 1 hour) (INFeD, Watson Pharma).^17–19 This is not a regimen that is specifically approved by the US Food and Drug Administration. An alternative regimen is to administer 750 mg of ferrous carboxymaltose (Injectafer, Luitpold Pharmaceuticals) over 15 minutes, which is an FDA-approved regimen.¹⁸ Many hematologists prefer to administer multiple smaller doses of iron. For example, in our practice, pregnant women are commonly treated with IV iron sucrose (300 mg) every 2 weeks for 3 doses. To increase access of pregnant women to IV iron treatment, obstetricians need to work with hematologists and infusion centers to create collaborative protocols to expeditiously treat women in the third trimester.

There is an epidemic of iron deficiency in pregnant women in the United States. In an era of high technology medicine, it is surprising that iron deficiency remains an unsolved obstetric problem in our country.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Illustration: Kimberly Martens for OBG Management

All mammalian life is dependent on a continuous supply of molecular oxygen. Molecular oxygen is carried to cells by noncovalent binding to the iron moiety in the hemoglobin of red blood cells. It is utilized within cells by noncovalent binding to the iron moiety in various microsomal and mitochondrial proteins, including myoglobin and cytochromes. Consequently, to efficiently utilize molecular oxygen all mammalian life is dependent on an adequate supply of iron. Surprisingly, in an era of high technology precision medicine, many pregnant women are iron deficient, anemic, and not receiving adequate iron supplementation.

Iron deficiency is prevalent in women and pregnant women

Women often become iron deficient because of pregnancy or heavy menstrual bleeding. During pregnancy, maternal iron is provided to supply the needs of the fetus and placenta. Additional iron is needed to expand maternal red blood cell volume and replace iron lost due to bleeding at delivery. In the National Health and Nutrition Examination Survey (NHANES) of 1988–1994, 11% of women aged 16 to 49 years were iron deficient. By contrast, less than 1% of men aged 16 to 49 years were iron deficient.¹

In a NHANES study from 1999–2006, risk factors for iron deficiency included multiparity, current pregnancy, and regular menstrual cycles. Use of hormonal contraception reduced the rate of iron deficiency.² Using the same data, the prevalences of iron deficiency during the first, second, and third trimesters of pregnancy were reported to be 7%, 14%, and 30%, respectively.³ In addition to pregnancy and menstrual bleeding there are many other medical problems that may contribute to iron deficiency, including Helicobacter pylori (H pylori) infection, gastritis, celiac disease, and bariatric surgery.

Iron deficiency anemia may be associated with adverse pregnancy outcomes

In a retrospective study of 75,660 singleton pregnancies, 7,977 women were diagnosed with iron deficiency anemia when they were admitted for delivery. Compared with pregnant women without iron deficiency, the presence of iron deficiency increased the risk of:

• blood transfusion (odds ratio [OR], 5.48; 95% confidence interval [CI], 4.57–6.58)
• preterm delivery (OR, 1.54; 95% CI, 1.36–1.76)
• cesarean delivery (OR, 1.30; 95% CI, 1.13–1.49)
• 5-minute Apgar score <7 (OR, 2.21; 95% CI, 1.84–2.64)
• intensive care unit (ICU) admission (OR, 1.28; 95% CI, 1.20–1.39).⁴

In a systematic review and meta-analysis of 26 studies, maternal anemia (mostly iron deficiency anemia) was associated with a higher risk of low birth weight (relative risk [RR], 1.31; 95% CI, 1.13–1.51), preterm birth (RR, 1.63; 95% CI, 1.33–2.01), perinatal mortality (RR, 1.51; 95% CI, 1.30–1.76), and neonatal mortality (RR, 2.72; 95% CI, 1.19–6.25).⁵

In a clinical trial, pregnant women were randomly assigned to receive folic acid alone; folic acid plus iron supplements; or 15 vitamins and minerals, including folic acid and iron. At delivery, women in the iron-folic acid and the 15 vitamin and minerals groups had higher hemoglobin concentrations than the folic acid monotherapy group. Among 4,697 live births, women in the iron-folic acid group had significantly fewer preterm births (<34 weeks’ gestation) than the folic acid group (RR, 0.50; 95% CI, 0.27–0.94; P = .031).⁶ Data from additional randomized trials are needed to further clarify the effect of iron supplementation on obstetric outcomes.

Related article:
Treating polycystic ovary syndrome: Start using dual medical therapy

The diagnosis of iron deficiency is optimized by measuring serum ferritin

Serum ferritin measurement is an excellent test of iron deficiency. We recommend that all pregnant women have serum ferritin measured at the first prenatal visit and at the beginning of the third trimester to assess maternal iron stores. In pregnancy, the Centers for Disease Control and Prevention and the World Health Organization define anemia as a hemoglobin level of less than 11 g/dL or hematocrit less than 33% in the first and third trimesters. If a pregnant woman is not anemic, a serum ferritin level less than 15 ng/mL indicates iron deficiency.⁷ Some experts believe that in pregnant women who are not anemic, a serum ferritin level between 15 and 30 ng/mL may also indicate iron deficiency.⁸ If the pregnant woman is anemic and does not have another cause of the anemia, a serum ferritin level less than 40 ng/mL is indicative of iron deficiency.⁷

Ferritin is an acute phase reactant and levels may be falsely elevated due to chronic or acute inflammation, liver disease, renal failure, metabolic syndrome, or malignancy. Some women with iron deficiency due to bariatric surgery or malabsorption also have vitamin B12 and, less commonly, folate deficiency, which can contribute to the development of anemia (see “Diagnosis of anemia, iron deficiency, and iron deficiency anemia in pregnancy.”) Clinicians are often advised that a mean corpuscular volume demonstrating microcytosis is the “best test” to assess a patient for iron deficiency. However, reduced iron availability and low ferritin precede microcytosis. Hence microcytosis is a lagging measure and iron deficiency is diagnosed at an earlier stage by ferritin.

Dietary iron

Iron in food is present in heme (meat, poultry, fish) and non-heme forms (grains, plant food, supplements). Heme iron is better absorbed than non-heme iron. Foods rich in non-heme iron include spinach, lentils, prune juice, dried prunes, and fortified cereals. Absorption of non-heme iron can be increased by vitamin C or vitamin C–rich foods (broccoli, bell peppers, cantaloupe, grapefruit, oranges, strawberries, and tomatoes). Absorption of non-heme iron is reduced by consumption of dairy products, coffee, tea, and chocolate.

Oral iron treatment

Oral iron is an effective treatment for iron deficiency^9,10 and is inexpensive, safe, and widely available. The CDC recommends that all pregnant women take a 30 mg/day iron supplement, unless they have hemochromatosis.¹¹ For women with a low ferritin level and anemia, iron supplementation should be increased to 30 to 120 mg daily.¹¹ Not all prenatal vitamins contain iron; those that do typically contain 17 to 28 mg of elemental iron per dose.

Many pregnant women taking oral iron, especially at doses greater than 30 mg daily, have gastrointestinal side effects, which cause them to discontinue the iron therapy.¹² Taking iron supplementation on an intermittent basis may help to reduce gastrointestinal side effects and improve iron stores.¹³

In the past, a standard approach to the treatment of iron deficiency anemia was oral ferrous sulfate 325 mg (65 mg elemental iron) spaced in 3 doses each day for a total daily dose of 195 mg elemental iron. However, recent absorption studies concluded that maximal absorption of iron occurs with a dose in the range of 40 to 80 mg of elemental iron daily. Greater doses do not result in more iron absorption and are associated with more side effects.^14,15 (See “Start using alternate-day oral iron dosing, and stop using daily iron dosing.”)

Oral iron should not be taken in close approximation to the consumption of milk, cereals, tea, coffee, eggs, or calcium supplements. The absorption of oral iron is enhanced by the consumption of orange juice or 250 mg of vitamin C. Gastrointestinal side effects include nausea, flatulence, constipation, diarrhea, epigastric distress, and vomiting. If gastrointestinal side effects occur, interventions that might improve tolerability include: reduce the dose of iron or administer intermittently or use a low dose of oral iron, where dosing can be more easily titrated.

We re-check ferritin and hemoglobin levels 2 to 4 weeks after initiation of oral iron therapy and expect to see a hemoglobin rise of 1 g/dL if the therapy is effective.

Intravenous iron treatment

For women with iron deficiency anemia who cannot tolerate oral iron or in whom oral iron treatment has not resolved their anemia, intravenous (IV) iron treatment may be an optimal approach. Women in the third trimester of pregnancy with iron deficiency anemia have very little time to consume sufficient quantities of oral iron in food and supplements to restore their deficiency and reverse their anemia. Consequently, treatment with IV iron may be especially appropriate for women with iron deficiency anemia in the third trimester of pregnancy. Prior gastric surgery, including gastric bypass, results in reduced gastric acid production and causes severe impairment of intestinal absorption of iron. Patients with malabsorption syndromes, including celiac disease, also may have limited absorption of oral iron. These populations of pregnant women may particularly benefit from the use of IV iron. In pregnant women IV iron has fewer gastrointestinal side effects than oral iron.¹⁶

Many severely iron deficient patients need 1,000 mg of iron to resolve their deficit. In order to avoid giving multiple standard doses (200 mg per infusion, with 5 infusions over many days), some centers have explored the use of 1 large dose of IV iron (1,000 mg of low molecular weight iron dextran administered over 1 hour) (INFeD, Watson Pharma).^17–19 This is not a regimen that is specifically approved by the US Food and Drug Administration. An alternative regimen is to administer 750 mg of ferrous carboxymaltose (Injectafer, Luitpold Pharmaceuticals) over 15 minutes, which is an FDA-approved regimen.¹⁸ Many hematologists prefer to administer multiple smaller doses of iron. For example, in our practice, pregnant women are commonly treated with IV iron sucrose (300 mg) every 2 weeks for 3 doses. To increase access of pregnant women to IV iron treatment, obstetricians need to work with hematologists and infusion centers to create collaborative protocols to expeditiously treat women in the third trimester.

There is an epidemic of iron deficiency in pregnant women in the United States. In an era of high technology medicine, it is surprising that iron deficiency remains an unsolved obstetric problem in our country.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Illustration: Kimberly Martens for OBG Management

All mammalian life is dependent on a continuous supply of molecular oxygen. Molecular oxygen is carried to cells by noncovalent binding to the iron moiety in the hemoglobin of red blood cells. It is utilized within cells by noncovalent binding to the iron moiety in various microsomal and mitochondrial proteins, including myoglobin and cytochromes. Consequently, to efficiently utilize molecular oxygen all mammalian life is dependent on an adequate supply of iron. Surprisingly, in an era of high technology precision medicine, many pregnant women are iron deficient, anemic, and not receiving adequate iron supplementation.

Iron deficiency is prevalent in women and pregnant women

Women often become iron deficient because of pregnancy or heavy menstrual bleeding. During pregnancy, maternal iron is provided to supply the needs of the fetus and placenta. Additional iron is needed to expand maternal red blood cell volume and replace iron lost due to bleeding at delivery. In the National Health and Nutrition Examination Survey (NHANES) of 1988–1994, 11% of women aged 16 to 49 years were iron deficient. By contrast, less than 1% of men aged 16 to 49 years were iron deficient.¹

In a NHANES study from 1999–2006, risk factors for iron deficiency included multiparity, current pregnancy, and regular menstrual cycles. Use of hormonal contraception reduced the rate of iron deficiency.² Using the same data, the prevalences of iron deficiency during the first, second, and third trimesters of pregnancy were reported to be 7%, 14%, and 30%, respectively.³ In addition to pregnancy and menstrual bleeding there are many other medical problems that may contribute to iron deficiency, including Helicobacter pylori (H pylori) infection, gastritis, celiac disease, and bariatric surgery.

Iron deficiency anemia may be associated with adverse pregnancy outcomes

In a retrospective study of 75,660 singleton pregnancies, 7,977 women were diagnosed with iron deficiency anemia when they were admitted for delivery. Compared with pregnant women without iron deficiency, the presence of iron deficiency increased the risk of:

• blood transfusion (odds ratio [OR], 5.48; 95% confidence interval [CI], 4.57–6.58)
• preterm delivery (OR, 1.54; 95% CI, 1.36–1.76)
• cesarean delivery (OR, 1.30; 95% CI, 1.13–1.49)
• 5-minute Apgar score <7 (OR, 2.21; 95% CI, 1.84–2.64)
• intensive care unit (ICU) admission (OR, 1.28; 95% CI, 1.20–1.39).⁴

In a systematic review and meta-analysis of 26 studies, maternal anemia (mostly iron deficiency anemia) was associated with a higher risk of low birth weight (relative risk [RR], 1.31; 95% CI, 1.13–1.51), preterm birth (RR, 1.63; 95% CI, 1.33–2.01), perinatal mortality (RR, 1.51; 95% CI, 1.30–1.76), and neonatal mortality (RR, 2.72; 95% CI, 1.19–6.25).⁵

In a clinical trial, pregnant women were randomly assigned to receive folic acid alone; folic acid plus iron supplements; or 15 vitamins and minerals, including folic acid and iron. At delivery, women in the iron-folic acid and the 15 vitamin and minerals groups had higher hemoglobin concentrations than the folic acid monotherapy group. Among 4,697 live births, women in the iron-folic acid group had significantly fewer preterm births (<34 weeks’ gestation) than the folic acid group (RR, 0.50; 95% CI, 0.27–0.94; P = .031).⁶ Data from additional randomized trials are needed to further clarify the effect of iron supplementation on obstetric outcomes.

Related article:
Treating polycystic ovary syndrome: Start using dual medical therapy

The diagnosis of iron deficiency is optimized by measuring serum ferritin

Serum ferritin measurement is an excellent test of iron deficiency. We recommend that all pregnant women have serum ferritin measured at the first prenatal visit and at the beginning of the third trimester to assess maternal iron stores. In pregnancy, the Centers for Disease Control and Prevention and the World Health Organization define anemia as a hemoglobin level of less than 11 g/dL or hematocrit less than 33% in the first and third trimesters. If a pregnant woman is not anemic, a serum ferritin level less than 15 ng/mL indicates iron deficiency.⁷ Some experts believe that in pregnant women who are not anemic, a serum ferritin level between 15 and 30 ng/mL may also indicate iron deficiency.⁸ If the pregnant woman is anemic and does not have another cause of the anemia, a serum ferritin level less than 40 ng/mL is indicative of iron deficiency.⁷

Ferritin is an acute phase reactant and levels may be falsely elevated due to chronic or acute inflammation, liver disease, renal failure, metabolic syndrome, or malignancy. Some women with iron deficiency due to bariatric surgery or malabsorption also have vitamin B12 and, less commonly, folate deficiency, which can contribute to the development of anemia (see “Diagnosis of anemia, iron deficiency, and iron deficiency anemia in pregnancy.”) Clinicians are often advised that a mean corpuscular volume demonstrating microcytosis is the “best test” to assess a patient for iron deficiency. However, reduced iron availability and low ferritin precede microcytosis. Hence microcytosis is a lagging measure and iron deficiency is diagnosed at an earlier stage by ferritin.

Dietary iron

Iron in food is present in heme (meat, poultry, fish) and non-heme forms (grains, plant food, supplements). Heme iron is better absorbed than non-heme iron. Foods rich in non-heme iron include spinach, lentils, prune juice, dried prunes, and fortified cereals. Absorption of non-heme iron can be increased by vitamin C or vitamin C–rich foods (broccoli, bell peppers, cantaloupe, grapefruit, oranges, strawberries, and tomatoes). Absorption of non-heme iron is reduced by consumption of dairy products, coffee, tea, and chocolate.

Oral iron treatment

Oral iron is an effective treatment for iron deficiency^9,10 and is inexpensive, safe, and widely available. The CDC recommends that all pregnant women take a 30 mg/day iron supplement, unless they have hemochromatosis.¹¹ For women with a low ferritin level and anemia, iron supplementation should be increased to 30 to 120 mg daily.¹¹ Not all prenatal vitamins contain iron; those that do typically contain 17 to 28 mg of elemental iron per dose.

Many pregnant women taking oral iron, especially at doses greater than 30 mg daily, have gastrointestinal side effects, which cause them to discontinue the iron therapy.¹² Taking iron supplementation on an intermittent basis may help to reduce gastrointestinal side effects and improve iron stores.¹³

In the past, a standard approach to the treatment of iron deficiency anemia was oral ferrous sulfate 325 mg (65 mg elemental iron) spaced in 3 doses each day for a total daily dose of 195 mg elemental iron. However, recent absorption studies concluded that maximal absorption of iron occurs with a dose in the range of 40 to 80 mg of elemental iron daily. Greater doses do not result in more iron absorption and are associated with more side effects.^14,15 (See “Start using alternate-day oral iron dosing, and stop using daily iron dosing.”)

Oral iron should not be taken in close approximation to the consumption of milk, cereals, tea, coffee, eggs, or calcium supplements. The absorption of oral iron is enhanced by the consumption of orange juice or 250 mg of vitamin C. Gastrointestinal side effects include nausea, flatulence, constipation, diarrhea, epigastric distress, and vomiting. If gastrointestinal side effects occur, interventions that might improve tolerability include: reduce the dose of iron or administer intermittently or use a low dose of oral iron, where dosing can be more easily titrated.

We re-check ferritin and hemoglobin levels 2 to 4 weeks after initiation of oral iron therapy and expect to see a hemoglobin rise of 1 g/dL if the therapy is effective.

Intravenous iron treatment

For women with iron deficiency anemia who cannot tolerate oral iron or in whom oral iron treatment has not resolved their anemia, intravenous (IV) iron treatment may be an optimal approach. Women in the third trimester of pregnancy with iron deficiency anemia have very little time to consume sufficient quantities of oral iron in food and supplements to restore their deficiency and reverse their anemia. Consequently, treatment with IV iron may be especially appropriate for women with iron deficiency anemia in the third trimester of pregnancy. Prior gastric surgery, including gastric bypass, results in reduced gastric acid production and causes severe impairment of intestinal absorption of iron. Patients with malabsorption syndromes, including celiac disease, also may have limited absorption of oral iron. These populations of pregnant women may particularly benefit from the use of IV iron. In pregnant women IV iron has fewer gastrointestinal side effects than oral iron.¹⁶

Many severely iron deficient patients need 1,000 mg of iron to resolve their deficit. In order to avoid giving multiple standard doses (200 mg per infusion, with 5 infusions over many days), some centers have explored the use of 1 large dose of IV iron (1,000 mg of low molecular weight iron dextran administered over 1 hour) (INFeD, Watson Pharma).^17–19 This is not a regimen that is specifically approved by the US Food and Drug Administration. An alternative regimen is to administer 750 mg of ferrous carboxymaltose (Injectafer, Luitpold Pharmaceuticals) over 15 minutes, which is an FDA-approved regimen.¹⁸ Many hematologists prefer to administer multiple smaller doses of iron. For example, in our practice, pregnant women are commonly treated with IV iron sucrose (300 mg) every 2 weeks for 3 doses. To increase access of pregnant women to IV iron treatment, obstetricians need to work with hematologists and infusion centers to create collaborative protocols to expeditiously treat women in the third trimester.

There is an epidemic of iron deficiency in pregnant women in the United States. In an era of high technology medicine, it is surprising that iron deficiency remains an unsolved obstetric problem in our country.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

For all those who say that the surgeon in the trenches doesn’t have a voice in the world of organized surgery, I have a story or two for you.

About 10 or more years ago, I was at a lovely old hotel in Cooperstown, N.Y., listening to a group of elder rural surgery colleagues hold forth about feeling ignored by the American College of Surgeons and how we should all band together to form a new society of rural surgeons. Like most crowds, they were getting pretty worked up. They were pretty sure such a revolution would solve our problems and we would quit being the Rodney Dangerfields of surgery (not getting any respect, as the great comic used to say).

Dr. Hughes is clinical professor in the department of surgery and director of medical education at the Kansas University School of Medicine, Salina Campus, and Co-Editor of ACS Surgery News.

For all those who say that the surgeon in the trenches doesn’t have a voice in the world of organized surgery, I have a story or two for you.

About 10 or more years ago, I was at a lovely old hotel in Cooperstown, N.Y., listening to a group of elder rural surgery colleagues hold forth about feeling ignored by the American College of Surgeons and how we should all band together to form a new society of rural surgeons. Like most crowds, they were getting pretty worked up. They were pretty sure such a revolution would solve our problems and we would quit being the Rodney Dangerfields of surgery (not getting any respect, as the great comic used to say).

Dr. Hughes is clinical professor in the department of surgery and director of medical education at the Kansas University School of Medicine, Salina Campus, and Co-Editor of ACS Surgery News.

For all those who say that the surgeon in the trenches doesn’t have a voice in the world of organized surgery, I have a story or two for you.

About 10 or more years ago, I was at a lovely old hotel in Cooperstown, N.Y., listening to a group of elder rural surgery colleagues hold forth about feeling ignored by the American College of Surgeons and how we should all band together to form a new society of rural surgeons. Like most crowds, they were getting pretty worked up. They were pretty sure such a revolution would solve our problems and we would quit being the Rodney Dangerfields of surgery (not getting any respect, as the great comic used to say).

Dr. Hughes is clinical professor in the department of surgery and director of medical education at the Kansas University School of Medicine, Salina Campus, and Co-Editor of ACS Surgery News.

Clinical experience and observational studies made us aware that African American patients responded differently to some treatments than the white male patients in the clinical trials. This awareness led to some interesting biologic hypotheses and, over the past 13 years, has led to trials focused on the treatment of heart failure and hypertension in African Americans. But a full biologic understanding of the apparent racial differences in clinical response to specific therapies has for the most part remained elusive.

Contributing to this understanding gap was that we historically did not fully appreciate the differences according to race (and likely sex) in the clinical progression of diseases such as hypertension, heart failure, and, as discussed in this issue of the Journal by Dr. Joseph V. Nally, Jr., chronic kidney disease. African Americans with congestive heart failure seem to fare worse than their white counterparts with the same disease. Given the strong link between heart failure and chronic kidney disease and the crosstalk between the heart and kidneys, it is no surprise that African Americans with chronic kidney disease progress to end-stage renal disease at a higher rate than whites. Yet, as Dr. Nally points out, once on dialysis, African Americans live longer—an intriguing observation that came from analysis of large databases devoted to the study of patients with chronic kidney disease.

As a patient’s self-defined racial identity may not be biologically accurate, using molecular genetic techniques to delve more deeply into the characteristics of patients in these chronic kidney disease registries is starting to yield fascinating results—and even more questions. Links between APOL1 gene polymorphisms and the occurrence of renal disease and the survival of transplanted kidneys is assuredly just the start of a journey of genomic discovery and understanding.

Readers will note the short editor’s note at the start of Dr. Nally’s article, indicating that it was based on a Medicine Grand Rounds lecture at Cleveland Clinic, the 14th annual Lawrence “Chris” Crain Memorial Lecture. In 1997, Chris became the first African American chief resident in internal medicine at Cleveland Clinic, and I had the pleasure of interacting with him while he was in that role. Chris was a natural leader. He was soft-spoken, curious, and passionate about delivering and understanding the basics of high-quality clinical care.

After his residency, with Byron Hoogwerf as the internal medicine program director, Chris trained with Joe Nally as his program director in nephrology, and further developed his interest in renal and cardiovascular disease in African Americans. He moved to Atlanta, where he died far too prematurely in July 2003. That year, in conjunction with Chris’s mother, wife, extended family, and other faculty, Drs. Hoogwerf and Nally established the Lawrence “Chris” Crain Memorial Lectureship, devoted to Chris’s passion of furthering our understanding and our ability to deliver optimal care to African American patients with cardiovascular and renal disease.

I am pleased to share this lecture with you.

Clinical experience and observational studies made us aware that African American patients responded differently to some treatments than the white male patients in the clinical trials. This awareness led to some interesting biologic hypotheses and, over the past 13 years, has led to trials focused on the treatment of heart failure and hypertension in African Americans. But a full biologic understanding of the apparent racial differences in clinical response to specific therapies has for the most part remained elusive.

Contributing to this understanding gap was that we historically did not fully appreciate the differences according to race (and likely sex) in the clinical progression of diseases such as hypertension, heart failure, and, as discussed in this issue of the Journal by Dr. Joseph V. Nally, Jr., chronic kidney disease. African Americans with congestive heart failure seem to fare worse than their white counterparts with the same disease. Given the strong link between heart failure and chronic kidney disease and the crosstalk between the heart and kidneys, it is no surprise that African Americans with chronic kidney disease progress to end-stage renal disease at a higher rate than whites. Yet, as Dr. Nally points out, once on dialysis, African Americans live longer—an intriguing observation that came from analysis of large databases devoted to the study of patients with chronic kidney disease.

As a patient’s self-defined racial identity may not be biologically accurate, using molecular genetic techniques to delve more deeply into the characteristics of patients in these chronic kidney disease registries is starting to yield fascinating results—and even more questions. Links between APOL1 gene polymorphisms and the occurrence of renal disease and the survival of transplanted kidneys is assuredly just the start of a journey of genomic discovery and understanding.

Readers will note the short editor’s note at the start of Dr. Nally’s article, indicating that it was based on a Medicine Grand Rounds lecture at Cleveland Clinic, the 14th annual Lawrence “Chris” Crain Memorial Lecture. In 1997, Chris became the first African American chief resident in internal medicine at Cleveland Clinic, and I had the pleasure of interacting with him while he was in that role. Chris was a natural leader. He was soft-spoken, curious, and passionate about delivering and understanding the basics of high-quality clinical care.

After his residency, with Byron Hoogwerf as the internal medicine program director, Chris trained with Joe Nally as his program director in nephrology, and further developed his interest in renal and cardiovascular disease in African Americans. He moved to Atlanta, where he died far too prematurely in July 2003. That year, in conjunction with Chris’s mother, wife, extended family, and other faculty, Drs. Hoogwerf and Nally established the Lawrence “Chris” Crain Memorial Lectureship, devoted to Chris’s passion of furthering our understanding and our ability to deliver optimal care to African American patients with cardiovascular and renal disease.

I am pleased to share this lecture with you.

Clinical experience and observational studies made us aware that African American patients responded differently to some treatments than the white male patients in the clinical trials. This awareness led to some interesting biologic hypotheses and, over the past 13 years, has led to trials focused on the treatment of heart failure and hypertension in African Americans. But a full biologic understanding of the apparent racial differences in clinical response to specific therapies has for the most part remained elusive.

Contributing to this understanding gap was that we historically did not fully appreciate the differences according to race (and likely sex) in the clinical progression of diseases such as hypertension, heart failure, and, as discussed in this issue of the Journal by Dr. Joseph V. Nally, Jr., chronic kidney disease. African Americans with congestive heart failure seem to fare worse than their white counterparts with the same disease. Given the strong link between heart failure and chronic kidney disease and the crosstalk between the heart and kidneys, it is no surprise that African Americans with chronic kidney disease progress to end-stage renal disease at a higher rate than whites. Yet, as Dr. Nally points out, once on dialysis, African Americans live longer—an intriguing observation that came from analysis of large databases devoted to the study of patients with chronic kidney disease.

As a patient’s self-defined racial identity may not be biologically accurate, using molecular genetic techniques to delve more deeply into the characteristics of patients in these chronic kidney disease registries is starting to yield fascinating results—and even more questions. Links between APOL1 gene polymorphisms and the occurrence of renal disease and the survival of transplanted kidneys is assuredly just the start of a journey of genomic discovery and understanding.

Readers will note the short editor’s note at the start of Dr. Nally’s article, indicating that it was based on a Medicine Grand Rounds lecture at Cleveland Clinic, the 14th annual Lawrence “Chris” Crain Memorial Lecture. In 1997, Chris became the first African American chief resident in internal medicine at Cleveland Clinic, and I had the pleasure of interacting with him while he was in that role. Chris was a natural leader. He was soft-spoken, curious, and passionate about delivering and understanding the basics of high-quality clinical care.

After his residency, with Byron Hoogwerf as the internal medicine program director, Chris trained with Joe Nally as his program director in nephrology, and further developed his interest in renal and cardiovascular disease in African Americans. He moved to Atlanta, where he died far too prematurely in July 2003. That year, in conjunction with Chris’s mother, wife, extended family, and other faculty, Drs. Hoogwerf and Nally established the Lawrence “Chris” Crain Memorial Lectureship, devoted to Chris’s passion of furthering our understanding and our ability to deliver optimal care to African American patients with cardiovascular and renal disease.

I am pleased to share this lecture with you.

There are many rewards for full-time academic psychiatrists such as myself, including didactic teaching, clinical supervision, and 1:1 mentorship of freshly minted medical school graduates, transforming them into accomplished clinical psychiatrists. The technical and personal growth of psychiatric residents over 4 years of post-MD training can be amazing and very gratifying to witness.

But the road to clinical competence often is littered with mistakes. It is the duty of the clinical supervisor to convert every error into a learning opportunity to hone the skills of a future psychiatrist. Over time, fewer mistakes occur, not only because of maturity and seasoning, but also because psychiatric residents learn how to thoughtfully deliberate about their clinical decision-making to select the best treatment option for their patients.

Yet, even with exemplary training, the rigors and constraints of clinical practice inevitably lead to some unforced errors, mostly minor but sometimes consequential. Even experienced practitioners are not immune from making a mistake in the hustle and bustle of daily work (exacerbated by the time-consuming pressures of electronic health record documentation). No one is infallible, but everyone must avoid making the same mistake twice, even if mounting demands lead to “shortcuts” that may not necessarily put the patient at risk but could lead to suboptimal outcomes. But once in a while, a serious complication may ensue.

Here are some common errors of omission or commission that even competent practitioners may make in a busy clinical practice.

Rushing to a diagnosis. To arrive at a primary psychiatric diagnosis, all potential secondary causes must be ruled out. This includes systematic screening for possible drug-induced psychopathology related not only to drugs of abuse, but also to prescription medications, some of which can have serious iatrogenic effects, including depression, anxiety, mania, psychosis, or cognitive dulling. The other important cause to rule out is the possibility of a general medical condition triggering psychiatric symptoms, which requires targeted questioning about medical history, a review of organ systems, and ordering key laboratory tests.

Skipping a baseline cognitive assessment. Cognitive impairment, especially memory and executive function, is now well recognized as an important component of major psychiatric disorders, including schizophrenia, bipolar disorder, major depressive disorder, anxiety, and attention-deficit/hyperactivity disorder. A standardized cognitive battery can provide a valuable profile of brain functions. Knowing the patient’s cognitive strengths and weaknesses before initiating pharmacotherapy is essential to assess the positive or negative impact of the medications. It also can help with patients’ vocational rehabilitation, matching them with jobs compatible with their cognitive strengths.

Inaccurate differential diagnosis. Is it borderline personality or bipolar disorder? Is it schizophrenia or psychotic bipolar disorder? Is it unipolar or bipolar depression? Is it a conversion reaction or a genuine medical condition? The answers to such questions are critical, because inaccurate diagnosis can lead to a lack of improvement and prolonged suffering for patients or adverse effects that could be avoided.

Using a high dose of a medication immediately for a first-episode psychiatric disorder. One of the least patient-friendly medical decisions is to start a first-episode patient on a high dose of a medication on day 1. Gradual titration can circumvent intolerable adverse effects and help establish the lowest effective dose. Patient acceptance and adherence are far more likely if the patient’s brain is not “abruptly medicated.”

Using combination therapy right away. There are a few psychiatric conditions for which combination therapy is FDA-approved and regarded as “rational polypharmacy.” However, it always makes sense to start with 1 (primary) medication and assess its efficacy, tolerability, and safety before adding an adjunctive agent. Some patients may improve substantially with monotherapy, which is always preferable. Using drug combinations as the initial intervention can be problematic, especially if they are not evidence-based and off-label.

Selecting an obesogenic drug as first-line. Many psychotropics, such as antipsychotics, antidepressants, or mood stabilizers, often come as a class of several agents. Clinicians can select any member of the same class (such as selective serotonin reuptake inhibitors [SSRIs] or atypical antipsychotics) because they are all FDA-approved for efficacy. However, the major difference among what often are called “me too” drugs is the adverse effects profile. For many psychotropic medications, significant weight gain is one of the worst medical adverse effects, because it often leads to metabolic dysregulation (hyperglycemia, dyslipidemia, and hypertension) and increases the risk of cardiovascular disease. Many psychiatric patients become obese and have great difficulty losing weight, especially if they are sedentary and have poor eating habits.

Using benzodiazepines as a first-line treatment for anxiety. Although certainly efficacious, and rapidly so, benzodiazepines must be avoided as a first-line treatment for anxiety. The addiction potential is significant, and patients with anxiety will subsequently not respond adequately to standard anxiolytic pharmacotherapy, such as an SSRI, because the anxiolytic effect of these other medications is gradual and not as rapid or potent. Some primary care providers (PCPs) resort to using strong benzodiazepines (such as alprazolam) as first-line, and then refer the patient to a psychiatrist, who finds it quite challenging to steer the patient to an evidence-based option that is less harmful for long-term management. The residents and I have encountered such situations often, sometimes leading to complex interactions with patients who demand renewal of a high dose of a benzodiazepine that had been prescribed to them by a different clinician.

Low utilization of some efficacious agents. It is surprising how some useful pharmacotherapeutic strategies are not employed as often as they should be. This includes lithium for a manic episode; a long-acting injectable antipsychotic in the early phase of schizophrenia; clozapine for patients who failed to respond to a couple of antipsychotics or have chronic suicidal tendencies; lurasidone or quetiapine for bipolar depression (the only FDA-approved medications for this condition); or monoamine oxidase inhibitors for treatment-resistant depression. These drugs can be useful, although some require ongoing blood-level measurements and monitoring for efficacy and adverse effects.

Not recognizing tardive dyskinesia (TD) earlier. TD is one of the most serious neurologic complications of dopamine-receptor working agents (antipsychotics). FDA-approved treatments finally arrived in 2017, but the recognition of the abnormal oro-bucco-lingual or facial choreiform movements remain low (and the use of the Abnormal Involuntary Movement Scale to screen for TD has faded since second-generation antipsychotics were introduced). It is essential to identify this adverse effect early and treat it promptly to avoid its worsening and potential irreversibility.

Other errors of omission or commission include:

• Not collaborating actively with the patient’s PCP to integrate the medical care to improve the patient’s overall health, not just mental health. Collaborative care improves clinical outcomes for most patients.
• Not using available pharmacogenetics testing to provide the patient with “personalized medicine,” such as establishing if they are poor or rapid metabolizers of certain cytochrome hepatic enzymes or checking whether they are less likely to respond to antidepressant medications.
• “Lowering expectations” for patients with severe psychiatric disorders, giving them the message (verbally or nonverbally) that their condition is “hopeless” and that recovery is beyond their reach. Giving hope and trying hard to find better treatment options are the foundation of good medical practice, especially for the sickest patients.

Psychiatrists always aim to do the right thing for their patients, even when the pressures of clinical practice are intense and palpable. But sometimes, an inadvertent slip may occur in the form of an error of omission or commission. These unforced errors are rarely dangerous, but they have the potential to delay response, increase the disease burden, or complicate the illness course. Compassion may be in generous supply, but it’s not enough: We must strive to make our patient-centered, evidence-based clinical practice an error-free zone.

There are many rewards for full-time academic psychiatrists such as myself, including didactic teaching, clinical supervision, and 1:1 mentorship of freshly minted medical school graduates, transforming them into accomplished clinical psychiatrists. The technical and personal growth of psychiatric residents over 4 years of post-MD training can be amazing and very gratifying to witness.

But the road to clinical competence often is littered with mistakes. It is the duty of the clinical supervisor to convert every error into a learning opportunity to hone the skills of a future psychiatrist. Over time, fewer mistakes occur, not only because of maturity and seasoning, but also because psychiatric residents learn how to thoughtfully deliberate about their clinical decision-making to select the best treatment option for their patients.

Yet, even with exemplary training, the rigors and constraints of clinical practice inevitably lead to some unforced errors, mostly minor but sometimes consequential. Even experienced practitioners are not immune from making a mistake in the hustle and bustle of daily work (exacerbated by the time-consuming pressures of electronic health record documentation). No one is infallible, but everyone must avoid making the same mistake twice, even if mounting demands lead to “shortcuts” that may not necessarily put the patient at risk but could lead to suboptimal outcomes. But once in a while, a serious complication may ensue.

Here are some common errors of omission or commission that even competent practitioners may make in a busy clinical practice.

Rushing to a diagnosis. To arrive at a primary psychiatric diagnosis, all potential secondary causes must be ruled out. This includes systematic screening for possible drug-induced psychopathology related not only to drugs of abuse, but also to prescription medications, some of which can have serious iatrogenic effects, including depression, anxiety, mania, psychosis, or cognitive dulling. The other important cause to rule out is the possibility of a general medical condition triggering psychiatric symptoms, which requires targeted questioning about medical history, a review of organ systems, and ordering key laboratory tests.

Skipping a baseline cognitive assessment. Cognitive impairment, especially memory and executive function, is now well recognized as an important component of major psychiatric disorders, including schizophrenia, bipolar disorder, major depressive disorder, anxiety, and attention-deficit/hyperactivity disorder. A standardized cognitive battery can provide a valuable profile of brain functions. Knowing the patient’s cognitive strengths and weaknesses before initiating pharmacotherapy is essential to assess the positive or negative impact of the medications. It also can help with patients’ vocational rehabilitation, matching them with jobs compatible with their cognitive strengths.

Inaccurate differential diagnosis. Is it borderline personality or bipolar disorder? Is it schizophrenia or psychotic bipolar disorder? Is it unipolar or bipolar depression? Is it a conversion reaction or a genuine medical condition? The answers to such questions are critical, because inaccurate diagnosis can lead to a lack of improvement and prolonged suffering for patients or adverse effects that could be avoided.

Using a high dose of a medication immediately for a first-episode psychiatric disorder. One of the least patient-friendly medical decisions is to start a first-episode patient on a high dose of a medication on day 1. Gradual titration can circumvent intolerable adverse effects and help establish the lowest effective dose. Patient acceptance and adherence are far more likely if the patient’s brain is not “abruptly medicated.”

Using combination therapy right away. There are a few psychiatric conditions for which combination therapy is FDA-approved and regarded as “rational polypharmacy.” However, it always makes sense to start with 1 (primary) medication and assess its efficacy, tolerability, and safety before adding an adjunctive agent. Some patients may improve substantially with monotherapy, which is always preferable. Using drug combinations as the initial intervention can be problematic, especially if they are not evidence-based and off-label.

Selecting an obesogenic drug as first-line. Many psychotropics, such as antipsychotics, antidepressants, or mood stabilizers, often come as a class of several agents. Clinicians can select any member of the same class (such as selective serotonin reuptake inhibitors [SSRIs] or atypical antipsychotics) because they are all FDA-approved for efficacy. However, the major difference among what often are called “me too” drugs is the adverse effects profile. For many psychotropic medications, significant weight gain is one of the worst medical adverse effects, because it often leads to metabolic dysregulation (hyperglycemia, dyslipidemia, and hypertension) and increases the risk of cardiovascular disease. Many psychiatric patients become obese and have great difficulty losing weight, especially if they are sedentary and have poor eating habits.

Using benzodiazepines as a first-line treatment for anxiety. Although certainly efficacious, and rapidly so, benzodiazepines must be avoided as a first-line treatment for anxiety. The addiction potential is significant, and patients with anxiety will subsequently not respond adequately to standard anxiolytic pharmacotherapy, such as an SSRI, because the anxiolytic effect of these other medications is gradual and not as rapid or potent. Some primary care providers (PCPs) resort to using strong benzodiazepines (such as alprazolam) as first-line, and then refer the patient to a psychiatrist, who finds it quite challenging to steer the patient to an evidence-based option that is less harmful for long-term management. The residents and I have encountered such situations often, sometimes leading to complex interactions with patients who demand renewal of a high dose of a benzodiazepine that had been prescribed to them by a different clinician.

Low utilization of some efficacious agents. It is surprising how some useful pharmacotherapeutic strategies are not employed as often as they should be. This includes lithium for a manic episode; a long-acting injectable antipsychotic in the early phase of schizophrenia; clozapine for patients who failed to respond to a couple of antipsychotics or have chronic suicidal tendencies; lurasidone or quetiapine for bipolar depression (the only FDA-approved medications for this condition); or monoamine oxidase inhibitors for treatment-resistant depression. These drugs can be useful, although some require ongoing blood-level measurements and monitoring for efficacy and adverse effects.

Not recognizing tardive dyskinesia (TD) earlier. TD is one of the most serious neurologic complications of dopamine-receptor working agents (antipsychotics). FDA-approved treatments finally arrived in 2017, but the recognition of the abnormal oro-bucco-lingual or facial choreiform movements remain low (and the use of the Abnormal Involuntary Movement Scale to screen for TD has faded since second-generation antipsychotics were introduced). It is essential to identify this adverse effect early and treat it promptly to avoid its worsening and potential irreversibility.

Other errors of omission or commission include:

• Not collaborating actively with the patient’s PCP to integrate the medical care to improve the patient’s overall health, not just mental health. Collaborative care improves clinical outcomes for most patients.
• Not using available pharmacogenetics testing to provide the patient with “personalized medicine,” such as establishing if they are poor or rapid metabolizers of certain cytochrome hepatic enzymes or checking whether they are less likely to respond to antidepressant medications.
• “Lowering expectations” for patients with severe psychiatric disorders, giving them the message (verbally or nonverbally) that their condition is “hopeless” and that recovery is beyond their reach. Giving hope and trying hard to find better treatment options are the foundation of good medical practice, especially for the sickest patients.

Psychiatrists always aim to do the right thing for their patients, even when the pressures of clinical practice are intense and palpable. But sometimes, an inadvertent slip may occur in the form of an error of omission or commission. These unforced errors are rarely dangerous, but they have the potential to delay response, increase the disease burden, or complicate the illness course. Compassion may be in generous supply, but it’s not enough: We must strive to make our patient-centered, evidence-based clinical practice an error-free zone.

There are many rewards for full-time academic psychiatrists such as myself, including didactic teaching, clinical supervision, and 1:1 mentorship of freshly minted medical school graduates, transforming them into accomplished clinical psychiatrists. The technical and personal growth of psychiatric residents over 4 years of post-MD training can be amazing and very gratifying to witness.

But the road to clinical competence often is littered with mistakes. It is the duty of the clinical supervisor to convert every error into a learning opportunity to hone the skills of a future psychiatrist. Over time, fewer mistakes occur, not only because of maturity and seasoning, but also because psychiatric residents learn how to thoughtfully deliberate about their clinical decision-making to select the best treatment option for their patients.

Yet, even with exemplary training, the rigors and constraints of clinical practice inevitably lead to some unforced errors, mostly minor but sometimes consequential. Even experienced practitioners are not immune from making a mistake in the hustle and bustle of daily work (exacerbated by the time-consuming pressures of electronic health record documentation). No one is infallible, but everyone must avoid making the same mistake twice, even if mounting demands lead to “shortcuts” that may not necessarily put the patient at risk but could lead to suboptimal outcomes. But once in a while, a serious complication may ensue.

Here are some common errors of omission or commission that even competent practitioners may make in a busy clinical practice.

Rushing to a diagnosis. To arrive at a primary psychiatric diagnosis, all potential secondary causes must be ruled out. This includes systematic screening for possible drug-induced psychopathology related not only to drugs of abuse, but also to prescription medications, some of which can have serious iatrogenic effects, including depression, anxiety, mania, psychosis, or cognitive dulling. The other important cause to rule out is the possibility of a general medical condition triggering psychiatric symptoms, which requires targeted questioning about medical history, a review of organ systems, and ordering key laboratory tests.

Skipping a baseline cognitive assessment. Cognitive impairment, especially memory and executive function, is now well recognized as an important component of major psychiatric disorders, including schizophrenia, bipolar disorder, major depressive disorder, anxiety, and attention-deficit/hyperactivity disorder. A standardized cognitive battery can provide a valuable profile of brain functions. Knowing the patient’s cognitive strengths and weaknesses before initiating pharmacotherapy is essential to assess the positive or negative impact of the medications. It also can help with patients’ vocational rehabilitation, matching them with jobs compatible with their cognitive strengths.

Inaccurate differential diagnosis. Is it borderline personality or bipolar disorder? Is it schizophrenia or psychotic bipolar disorder? Is it unipolar or bipolar depression? Is it a conversion reaction or a genuine medical condition? The answers to such questions are critical, because inaccurate diagnosis can lead to a lack of improvement and prolonged suffering for patients or adverse effects that could be avoided.

Using a high dose of a medication immediately for a first-episode psychiatric disorder. One of the least patient-friendly medical decisions is to start a first-episode patient on a high dose of a medication on day 1. Gradual titration can circumvent intolerable adverse effects and help establish the lowest effective dose. Patient acceptance and adherence are far more likely if the patient’s brain is not “abruptly medicated.”

Using combination therapy right away. There are a few psychiatric conditions for which combination therapy is FDA-approved and regarded as “rational polypharmacy.” However, it always makes sense to start with 1 (primary) medication and assess its efficacy, tolerability, and safety before adding an adjunctive agent. Some patients may improve substantially with monotherapy, which is always preferable. Using drug combinations as the initial intervention can be problematic, especially if they are not evidence-based and off-label.

Selecting an obesogenic drug as first-line. Many psychotropics, such as antipsychotics, antidepressants, or mood stabilizers, often come as a class of several agents. Clinicians can select any member of the same class (such as selective serotonin reuptake inhibitors [SSRIs] or atypical antipsychotics) because they are all FDA-approved for efficacy. However, the major difference among what often are called “me too” drugs is the adverse effects profile. For many psychotropic medications, significant weight gain is one of the worst medical adverse effects, because it often leads to metabolic dysregulation (hyperglycemia, dyslipidemia, and hypertension) and increases the risk of cardiovascular disease. Many psychiatric patients become obese and have great difficulty losing weight, especially if they are sedentary and have poor eating habits.

Using benzodiazepines as a first-line treatment for anxiety. Although certainly efficacious, and rapidly so, benzodiazepines must be avoided as a first-line treatment for anxiety. The addiction potential is significant, and patients with anxiety will subsequently not respond adequately to standard anxiolytic pharmacotherapy, such as an SSRI, because the anxiolytic effect of these other medications is gradual and not as rapid or potent. Some primary care providers (PCPs) resort to using strong benzodiazepines (such as alprazolam) as first-line, and then refer the patient to a psychiatrist, who finds it quite challenging to steer the patient to an evidence-based option that is less harmful for long-term management. The residents and I have encountered such situations often, sometimes leading to complex interactions with patients who demand renewal of a high dose of a benzodiazepine that had been prescribed to them by a different clinician.

Low utilization of some efficacious agents. It is surprising how some useful pharmacotherapeutic strategies are not employed as often as they should be. This includes lithium for a manic episode; a long-acting injectable antipsychotic in the early phase of schizophrenia; clozapine for patients who failed to respond to a couple of antipsychotics or have chronic suicidal tendencies; lurasidone or quetiapine for bipolar depression (the only FDA-approved medications for this condition); or monoamine oxidase inhibitors for treatment-resistant depression. These drugs can be useful, although some require ongoing blood-level measurements and monitoring for efficacy and adverse effects.

Not recognizing tardive dyskinesia (TD) earlier. TD is one of the most serious neurologic complications of dopamine-receptor working agents (antipsychotics). FDA-approved treatments finally arrived in 2017, but the recognition of the abnormal oro-bucco-lingual or facial choreiform movements remain low (and the use of the Abnormal Involuntary Movement Scale to screen for TD has faded since second-generation antipsychotics were introduced). It is essential to identify this adverse effect early and treat it promptly to avoid its worsening and potential irreversibility.

Other errors of omission or commission include:

• Not collaborating actively with the patient’s PCP to integrate the medical care to improve the patient’s overall health, not just mental health. Collaborative care improves clinical outcomes for most patients.
• Not using available pharmacogenetics testing to provide the patient with “personalized medicine,” such as establishing if they are poor or rapid metabolizers of certain cytochrome hepatic enzymes or checking whether they are less likely to respond to antidepressant medications.
• “Lowering expectations” for patients with severe psychiatric disorders, giving them the message (verbally or nonverbally) that their condition is “hopeless” and that recovery is beyond their reach. Giving hope and trying hard to find better treatment options are the foundation of good medical practice, especially for the sickest patients.

Psychiatrists always aim to do the right thing for their patients, even when the pressures of clinical practice are intense and palpable. But sometimes, an inadvertent slip may occur in the form of an error of omission or commission. These unforced errors are rarely dangerous, but they have the potential to delay response, increase the disease burden, or complicate the illness course. Compassion may be in generous supply, but it’s not enough: We must strive to make our patient-centered, evidence-based clinical practice an error-free zone.