CASE A difficult withdrawal

Three days after he stops drinking alcohol, Mr. G, age 49, presents to a detoxification center with his wife, who drove him there because she was concerned about his condition. She says her husband had been drinking alcohol every night for as long as she can remember. Despite numerous admissions to rehabilitation centers, Mr. G usually would resume drinking soon after he was discharged. Three days ago, Mr. G’s wife had told him she “could not take it anymore,” so he got rid of all his alcohol and stopped drinking. Mr. G’s wife felt he was doing fine the first day, but his condition increasingly worsened the second and third days. The triage nurse who attempts to interview Mr. G finds him tremulous, vomiting, and sweating. She notices that he seems preoccupied with pulling at his shirt, appearing to pick at things that are not there.

HISTORY Untreated depression, other comorbidities

Mr. G’s wife says he has never been psychiatrically hospitalized or exhibited suicidal behavior. Mr. G previously received care from a psychiatrist, who diagnosed him with major depressive disorder (MDD) and prescribed an antidepressant, though his wife cannot recall which specific medication. She shares it has been “a long time” since Mr. G has taken the antidepressant and the last time he received treatment for his MDD was 5 years ago. Mr. G’s wife says her husband had once abstained from alcohol use for >6 months following one of his stints at a rehabilitation center. She is not able to share many other details about Mr. G’s previous stays at rehabilitation centers, but says he always had “a rough time.”

She says Mr. G had been drinking an average of 10 drinks each night, usually within 4 hours. He has no history of nicotine or illicit substance use and has held a corporate job for the last 18 years. Several years ago, a physician had diagnosed Mr. G with hypertension and high cholesterol, but he did not follow up for treatment. Mr. G’s wife also recalls a physician told her husband he had a fatty liver. His family history includes heart disease and cancer.

[polldaddy:12041618]

The author’s observations

The treatment team observed several elements of alcohol withdrawal and classified Mr. G as a priority patient. If the team had completed the Clinical Institute Withdrawal Assessment for Alcohol–Revised scale (CIWA-Ar) (Table 1¹), Mr. G would score ≥10. While the protocol for initiating treatment for patients experiencing alcohol withdrawal varies by institution, patients with moderate to severe scores on the CIWA-Ar when experiencing withdrawal typically are managed with pharmacotherapy to address their symptoms.¹ Given the timeline of his last drink as reported by his wife, Mr. G is on the brink of experiencing a cascade of symptoms concerning for delirium tremens (DTs).²Table 2² provides a timeline and symptoms related to alcohol withdrawal. To prevent further exacerbation of symptoms, which could lead to DTs, Mr. G’s treatment team will likely initiate a benzodiazepine, using either scheduled or symptom-driven dosing.³

Two neurotransmitters that play a role in DTs are glutamate (excitatory) and GABA (inhibitory). In a normal state, the competing actions of these neurotransmitters balance each other. Acute alcohol intake causes a shift in the excitatory and inhibitory levels, with more inhibition taking place, thus causing disequilibrium. If chronic alcohol use continues, the amount of GABA inhibition reduction is related to downregulation of receptors.^2,4 Excitation increases by way of upregulation of the N-methyl-D-aspartate receptors.^2,4,5 The goal is to achieve equilibrium of the neurotransmitters, even though the balance is different from when alcohol was not present.^2,4

If alcohol is suddenly removed following chronic use, there is unchecked glutamate excitation related to a blunted GABA state. This added increase in the excitation of glutamate leads to withdrawal symptoms.^2,4Table 3^2,4,5 depicts the neuro­transmitter equilibrium of GABA and glutamate relative to alcohol use.

EVALUATION Bleeding gums and bruising

The treatment team admits Mr. G to the triage bay and contacts the addiction psychiatrist. The physician orders laboratory tests to assess nutritional deficits and electrolyte abnormalities. Mr. G is also placed on routine assessments with symptom-triggered therapy. An assessment reveals bleeding gums and bruises, which are believed to be a result of thrombocytopenia (low blood platelet count).

[polldaddy:12041627]

Continue to: The author's observations

Though regular clinical assessment of PEth varies, it is considered to have high sensitivity and specificity to detect alcohol use.⁶ When ethanol is present, the phospholipase D enzyme acts upon phosphatidylcholine, forming a direct biomarker, PEth, on the surface of the red blood cell.^6,7 PEth’s half-life ranges from 4.5 to 12 days,⁶ and it can be detected in blood for 3 to 4 weeks after alcohol ingestion.^6,7 A PEth value <20 ng/mL indicates light or no alcohol consumption; 20 to 199 ng/mL indicates significant consumption; and >200 ng/mL indicates heavy consumption.⁷ Since Mr. G has a history of chronic alcohol use, his PEth level is expected to be >200 ng/mL.

AST/ALT and MCV are indirect biomarkers, meaning the tests are not alcohol-specific and the role of alcohol is instead observed by the damage to the body with excessive use over time.⁷ The expected AST:ALT ratio is 2:1. This is related to 3 mechanisms. The first is a decrease in ALT usually relative to B6 deficiency in individuals with alcohol use disorder (AUD). Another mechanism is related to alcohol’s propensity to affect mitochondria, which is a source for AST. Additionally, AST is also found in higher proportions in the kidneys, heart, and muscles.⁸

An MCV <100 fL would be within the normal range (80 to 100 fL) for red blood cells. While the reasons for an enlarged red blood cell (or macrocyte) are extensive, alcohol can be a factor once other causes are excluded. Additional laboratory tests and a peripheral blood smear test can help in this investigation.Alcohol disrupts the complete maturation of red blood cells.^9,10 If the cause of the macrocyte is alcohol-related and alcohol use is terminated, those enlarged cells can resolve in an average of 3 months.⁹

Vitamin B1 levels >200 nmol/L would be within normal range (74 to 222 nmol/L). Mr. G’s chronic alcohol use would likely cause him to be vitamin B1–deficient. The deficiency is usually related to diet, malabsorption, and the cells’ impaired ability to utilize vitamin B1. A consequence of vitamin B1 deficiency is Wernicke-Korsakoff syndrome.¹¹

Due to his chronic alcohol use, Mr. G’s magnesium stores most likely would be below normal range (1.7 to 2.2 mg/dL). Acting as a diuretic, alcohol depletes magnesium and other electrolytes. The intracellular shift that occurs to balance the deficit causes the body to use its normal stores of magnesium, which leads to further magnesium depletion. Other common causes include nutritional deficiency and decreased gastrointestinal absorption.¹² The bleeding the physician suspected was a result of drinking likely occurred through direct and indirect mechanisms that affect platelets.^9,13 Platelets can show improvement 1 week after drinking cessation. Some evidence suggests the risk of seizure or DTs increases significantly with a platelet count <119,000 µL per unit of blood.¹³

Continue to: TREATMENT Pharmacotherapy for alcohol use disorder

TREATMENT Pharmacotherapy for alcohol use disorder

As Mr. G’s condition starts to stabilize, he discusses treatment options for AUD with his physician. At the end of the discussion, Mr. G expresses an interest in starting a medication. The doctor reviews his laboratory results and available treatment options.

[polldaddy:12041630]

The author’s observations

Of the 3 FDA-approved medications for treating AUD (disulfiram, acamprosate, and naltrexone), naltrexone has been shown to decrease heavy drinking days^5,14 and comes in oral and injectable forms. Reducing drinking is achieved by reducing the rewarding effects of alcohol^5,14 and alcohol cravings.⁵ Disulfiram often has poor adherence, and like acamprosate it may be more helpful for maintenance of abstinence.Neither topiramate nor gabapentin are FDA-approved for AUD but may be used for their affects on GABA.⁵ Gabapentin may also help patients experiencing alcohol withdrawal syndrome.^5,15 Mr. G did not have any concomitant medications or comorbid medical conditions, but these factors as well as any renal or hepatic dysfunction must be considered before initiating any medications.

OUTCOME Improved well-being

Mr. G’s treatment team initiates oral naltrexone 50 mg/d, which he tolerates well without complications. He stops drinking entirely and expresses an interest in transitioning to an injectable form of naltrexone in the future. In addition to taking medication, Mr. G wants to participate in psychotherapy. Mr. G thanks his team for the care he received in the hospital, telling them, “You all saved my life.” As he discusses his past issues with alcohol, Mr. G asks his physician how he could get involved to make changes to reduce excessive alcohol consumption in his community (Box^5,15-21).

Box

Bottom Line

Patients experiencing alcohol withdrawal can present with several layers of complexity. Failure to achieve acute stabilization may be life-threatening. After providing critical care, promptly start alcohol use disorder treatment for patients who expresses a desire to change.

Related Resources

• American Society of Addiction Medicine. The ASAM Clinical Practice Guideline on Alcohol Withdrawal Management. https://www.asam.org/quality-care/clinical-guidelines/alcohol-withdrawal-management-guideline
• American Psychiatric Association. The American Psychiatric Association Practice Guideline for the Pharmacological Treatment of Patients With Alcohol Use Disorder. American Psychiatric Association Publishing; 2018.

Drug Brand Names

Acamprosate • Campral
Disulfiram • Antabuse
Gabapentin • Neurontin
Naltrexone (injection) • Vivitrol
Naltrexone (oral) • ReVia
Topiramate • Topamax

CASE A difficult withdrawal

Three days after he stops drinking alcohol, Mr. G, age 49, presents to a detoxification center with his wife, who drove him there because she was concerned about his condition. She says her husband had been drinking alcohol every night for as long as she can remember. Despite numerous admissions to rehabilitation centers, Mr. G usually would resume drinking soon after he was discharged. Three days ago, Mr. G’s wife had told him she “could not take it anymore,” so he got rid of all his alcohol and stopped drinking. Mr. G’s wife felt he was doing fine the first day, but his condition increasingly worsened the second and third days. The triage nurse who attempts to interview Mr. G finds him tremulous, vomiting, and sweating. She notices that he seems preoccupied with pulling at his shirt, appearing to pick at things that are not there.

HISTORY Untreated depression, other comorbidities

Mr. G’s wife says he has never been psychiatrically hospitalized or exhibited suicidal behavior. Mr. G previously received care from a psychiatrist, who diagnosed him with major depressive disorder (MDD) and prescribed an antidepressant, though his wife cannot recall which specific medication. She shares it has been “a long time” since Mr. G has taken the antidepressant and the last time he received treatment for his MDD was 5 years ago. Mr. G’s wife says her husband had once abstained from alcohol use for >6 months following one of his stints at a rehabilitation center. She is not able to share many other details about Mr. G’s previous stays at rehabilitation centers, but says he always had “a rough time.”

She says Mr. G had been drinking an average of 10 drinks each night, usually within 4 hours. He has no history of nicotine or illicit substance use and has held a corporate job for the last 18 years. Several years ago, a physician had diagnosed Mr. G with hypertension and high cholesterol, but he did not follow up for treatment. Mr. G’s wife also recalls a physician told her husband he had a fatty liver. His family history includes heart disease and cancer.

[polldaddy:12041618]

The author’s observations

The treatment team observed several elements of alcohol withdrawal and classified Mr. G as a priority patient. If the team had completed the Clinical Institute Withdrawal Assessment for Alcohol–Revised scale (CIWA-Ar) (Table 1¹), Mr. G would score ≥10. While the protocol for initiating treatment for patients experiencing alcohol withdrawal varies by institution, patients with moderate to severe scores on the CIWA-Ar when experiencing withdrawal typically are managed with pharmacotherapy to address their symptoms.¹ Given the timeline of his last drink as reported by his wife, Mr. G is on the brink of experiencing a cascade of symptoms concerning for delirium tremens (DTs).²Table 2² provides a timeline and symptoms related to alcohol withdrawal. To prevent further exacerbation of symptoms, which could lead to DTs, Mr. G’s treatment team will likely initiate a benzodiazepine, using either scheduled or symptom-driven dosing.³

Two neurotransmitters that play a role in DTs are glutamate (excitatory) and GABA (inhibitory). In a normal state, the competing actions of these neurotransmitters balance each other. Acute alcohol intake causes a shift in the excitatory and inhibitory levels, with more inhibition taking place, thus causing disequilibrium. If chronic alcohol use continues, the amount of GABA inhibition reduction is related to downregulation of receptors.^2,4 Excitation increases by way of upregulation of the N-methyl-D-aspartate receptors.^2,4,5 The goal is to achieve equilibrium of the neurotransmitters, even though the balance is different from when alcohol was not present.^2,4

If alcohol is suddenly removed following chronic use, there is unchecked glutamate excitation related to a blunted GABA state. This added increase in the excitation of glutamate leads to withdrawal symptoms.^2,4Table 3^2,4,5 depicts the neuro­transmitter equilibrium of GABA and glutamate relative to alcohol use.

EVALUATION Bleeding gums and bruising

The treatment team admits Mr. G to the triage bay and contacts the addiction psychiatrist. The physician orders laboratory tests to assess nutritional deficits and electrolyte abnormalities. Mr. G is also placed on routine assessments with symptom-triggered therapy. An assessment reveals bleeding gums and bruises, which are believed to be a result of thrombocytopenia (low blood platelet count).

[polldaddy:12041627]

Continue to: The author's observations

Though regular clinical assessment of PEth varies, it is considered to have high sensitivity and specificity to detect alcohol use.⁶ When ethanol is present, the phospholipase D enzyme acts upon phosphatidylcholine, forming a direct biomarker, PEth, on the surface of the red blood cell.^6,7 PEth’s half-life ranges from 4.5 to 12 days,⁶ and it can be detected in blood for 3 to 4 weeks after alcohol ingestion.^6,7 A PEth value <20 ng/mL indicates light or no alcohol consumption; 20 to 199 ng/mL indicates significant consumption; and >200 ng/mL indicates heavy consumption.⁷ Since Mr. G has a history of chronic alcohol use, his PEth level is expected to be >200 ng/mL.

AST/ALT and MCV are indirect biomarkers, meaning the tests are not alcohol-specific and the role of alcohol is instead observed by the damage to the body with excessive use over time.⁷ The expected AST:ALT ratio is 2:1. This is related to 3 mechanisms. The first is a decrease in ALT usually relative to B6 deficiency in individuals with alcohol use disorder (AUD). Another mechanism is related to alcohol’s propensity to affect mitochondria, which is a source for AST. Additionally, AST is also found in higher proportions in the kidneys, heart, and muscles.⁸

An MCV <100 fL would be within the normal range (80 to 100 fL) for red blood cells. While the reasons for an enlarged red blood cell (or macrocyte) are extensive, alcohol can be a factor once other causes are excluded. Additional laboratory tests and a peripheral blood smear test can help in this investigation.Alcohol disrupts the complete maturation of red blood cells.^9,10 If the cause of the macrocyte is alcohol-related and alcohol use is terminated, those enlarged cells can resolve in an average of 3 months.⁹

Vitamin B1 levels >200 nmol/L would be within normal range (74 to 222 nmol/L). Mr. G’s chronic alcohol use would likely cause him to be vitamin B1–deficient. The deficiency is usually related to diet, malabsorption, and the cells’ impaired ability to utilize vitamin B1. A consequence of vitamin B1 deficiency is Wernicke-Korsakoff syndrome.¹¹

Due to his chronic alcohol use, Mr. G’s magnesium stores most likely would be below normal range (1.7 to 2.2 mg/dL). Acting as a diuretic, alcohol depletes magnesium and other electrolytes. The intracellular shift that occurs to balance the deficit causes the body to use its normal stores of magnesium, which leads to further magnesium depletion. Other common causes include nutritional deficiency and decreased gastrointestinal absorption.¹² The bleeding the physician suspected was a result of drinking likely occurred through direct and indirect mechanisms that affect platelets.^9,13 Platelets can show improvement 1 week after drinking cessation. Some evidence suggests the risk of seizure or DTs increases significantly with a platelet count <119,000 µL per unit of blood.¹³

Continue to: TREATMENT Pharmacotherapy for alcohol use disorder

TREATMENT Pharmacotherapy for alcohol use disorder

As Mr. G’s condition starts to stabilize, he discusses treatment options for AUD with his physician. At the end of the discussion, Mr. G expresses an interest in starting a medication. The doctor reviews his laboratory results and available treatment options.

[polldaddy:12041630]

The author’s observations

Of the 3 FDA-approved medications for treating AUD (disulfiram, acamprosate, and naltrexone), naltrexone has been shown to decrease heavy drinking days^5,14 and comes in oral and injectable forms. Reducing drinking is achieved by reducing the rewarding effects of alcohol^5,14 and alcohol cravings.⁵ Disulfiram often has poor adherence, and like acamprosate it may be more helpful for maintenance of abstinence.Neither topiramate nor gabapentin are FDA-approved for AUD but may be used for their affects on GABA.⁵ Gabapentin may also help patients experiencing alcohol withdrawal syndrome.^5,15 Mr. G did not have any concomitant medications or comorbid medical conditions, but these factors as well as any renal or hepatic dysfunction must be considered before initiating any medications.

OUTCOME Improved well-being

Mr. G’s treatment team initiates oral naltrexone 50 mg/d, which he tolerates well without complications. He stops drinking entirely and expresses an interest in transitioning to an injectable form of naltrexone in the future. In addition to taking medication, Mr. G wants to participate in psychotherapy. Mr. G thanks his team for the care he received in the hospital, telling them, “You all saved my life.” As he discusses his past issues with alcohol, Mr. G asks his physician how he could get involved to make changes to reduce excessive alcohol consumption in his community (Box^5,15-21).

Box

Bottom Line

Patients experiencing alcohol withdrawal can present with several layers of complexity. Failure to achieve acute stabilization may be life-threatening. After providing critical care, promptly start alcohol use disorder treatment for patients who expresses a desire to change.

Related Resources

• American Society of Addiction Medicine. The ASAM Clinical Practice Guideline on Alcohol Withdrawal Management. https://www.asam.org/quality-care/clinical-guidelines/alcohol-withdrawal-management-guideline
• American Psychiatric Association. The American Psychiatric Association Practice Guideline for the Pharmacological Treatment of Patients With Alcohol Use Disorder. American Psychiatric Association Publishing; 2018.

Drug Brand Names

Acamprosate • Campral
Disulfiram • Antabuse
Gabapentin • Neurontin
Naltrexone (injection) • Vivitrol
Naltrexone (oral) • ReVia
Topiramate • Topamax

CASE A difficult withdrawal

Three days after he stops drinking alcohol, Mr. G, age 49, presents to a detoxification center with his wife, who drove him there because she was concerned about his condition. She says her husband had been drinking alcohol every night for as long as she can remember. Despite numerous admissions to rehabilitation centers, Mr. G usually would resume drinking soon after he was discharged. Three days ago, Mr. G’s wife had told him she “could not take it anymore,” so he got rid of all his alcohol and stopped drinking. Mr. G’s wife felt he was doing fine the first day, but his condition increasingly worsened the second and third days. The triage nurse who attempts to interview Mr. G finds him tremulous, vomiting, and sweating. She notices that he seems preoccupied with pulling at his shirt, appearing to pick at things that are not there.

HISTORY Untreated depression, other comorbidities

Mr. G’s wife says he has never been psychiatrically hospitalized or exhibited suicidal behavior. Mr. G previously received care from a psychiatrist, who diagnosed him with major depressive disorder (MDD) and prescribed an antidepressant, though his wife cannot recall which specific medication. She shares it has been “a long time” since Mr. G has taken the antidepressant and the last time he received treatment for his MDD was 5 years ago. Mr. G’s wife says her husband had once abstained from alcohol use for >6 months following one of his stints at a rehabilitation center. She is not able to share many other details about Mr. G’s previous stays at rehabilitation centers, but says he always had “a rough time.”

She says Mr. G had been drinking an average of 10 drinks each night, usually within 4 hours. He has no history of nicotine or illicit substance use and has held a corporate job for the last 18 years. Several years ago, a physician had diagnosed Mr. G with hypertension and high cholesterol, but he did not follow up for treatment. Mr. G’s wife also recalls a physician told her husband he had a fatty liver. His family history includes heart disease and cancer.

[polldaddy:12041618]

The author’s observations

The treatment team observed several elements of alcohol withdrawal and classified Mr. G as a priority patient. If the team had completed the Clinical Institute Withdrawal Assessment for Alcohol–Revised scale (CIWA-Ar) (Table 1¹), Mr. G would score ≥10. While the protocol for initiating treatment for patients experiencing alcohol withdrawal varies by institution, patients with moderate to severe scores on the CIWA-Ar when experiencing withdrawal typically are managed with pharmacotherapy to address their symptoms.¹ Given the timeline of his last drink as reported by his wife, Mr. G is on the brink of experiencing a cascade of symptoms concerning for delirium tremens (DTs).²Table 2² provides a timeline and symptoms related to alcohol withdrawal. To prevent further exacerbation of symptoms, which could lead to DTs, Mr. G’s treatment team will likely initiate a benzodiazepine, using either scheduled or symptom-driven dosing.³

Two neurotransmitters that play a role in DTs are glutamate (excitatory) and GABA (inhibitory). In a normal state, the competing actions of these neurotransmitters balance each other. Acute alcohol intake causes a shift in the excitatory and inhibitory levels, with more inhibition taking place, thus causing disequilibrium. If chronic alcohol use continues, the amount of GABA inhibition reduction is related to downregulation of receptors.^2,4 Excitation increases by way of upregulation of the N-methyl-D-aspartate receptors.^2,4,5 The goal is to achieve equilibrium of the neurotransmitters, even though the balance is different from when alcohol was not present.^2,4

If alcohol is suddenly removed following chronic use, there is unchecked glutamate excitation related to a blunted GABA state. This added increase in the excitation of glutamate leads to withdrawal symptoms.^2,4Table 3^2,4,5 depicts the neuro­transmitter equilibrium of GABA and glutamate relative to alcohol use.

EVALUATION Bleeding gums and bruising

The treatment team admits Mr. G to the triage bay and contacts the addiction psychiatrist. The physician orders laboratory tests to assess nutritional deficits and electrolyte abnormalities. Mr. G is also placed on routine assessments with symptom-triggered therapy. An assessment reveals bleeding gums and bruises, which are believed to be a result of thrombocytopenia (low blood platelet count).

[polldaddy:12041627]

Continue to: The author's observations

Though regular clinical assessment of PEth varies, it is considered to have high sensitivity and specificity to detect alcohol use.⁶ When ethanol is present, the phospholipase D enzyme acts upon phosphatidylcholine, forming a direct biomarker, PEth, on the surface of the red blood cell.^6,7 PEth’s half-life ranges from 4.5 to 12 days,⁶ and it can be detected in blood for 3 to 4 weeks after alcohol ingestion.^6,7 A PEth value <20 ng/mL indicates light or no alcohol consumption; 20 to 199 ng/mL indicates significant consumption; and >200 ng/mL indicates heavy consumption.⁷ Since Mr. G has a history of chronic alcohol use, his PEth level is expected to be >200 ng/mL.

AST/ALT and MCV are indirect biomarkers, meaning the tests are not alcohol-specific and the role of alcohol is instead observed by the damage to the body with excessive use over time.⁷ The expected AST:ALT ratio is 2:1. This is related to 3 mechanisms. The first is a decrease in ALT usually relative to B6 deficiency in individuals with alcohol use disorder (AUD). Another mechanism is related to alcohol’s propensity to affect mitochondria, which is a source for AST. Additionally, AST is also found in higher proportions in the kidneys, heart, and muscles.⁸

An MCV <100 fL would be within the normal range (80 to 100 fL) for red blood cells. While the reasons for an enlarged red blood cell (or macrocyte) are extensive, alcohol can be a factor once other causes are excluded. Additional laboratory tests and a peripheral blood smear test can help in this investigation.Alcohol disrupts the complete maturation of red blood cells.^9,10 If the cause of the macrocyte is alcohol-related and alcohol use is terminated, those enlarged cells can resolve in an average of 3 months.⁹

Vitamin B1 levels >200 nmol/L would be within normal range (74 to 222 nmol/L). Mr. G’s chronic alcohol use would likely cause him to be vitamin B1–deficient. The deficiency is usually related to diet, malabsorption, and the cells’ impaired ability to utilize vitamin B1. A consequence of vitamin B1 deficiency is Wernicke-Korsakoff syndrome.¹¹

Due to his chronic alcohol use, Mr. G’s magnesium stores most likely would be below normal range (1.7 to 2.2 mg/dL). Acting as a diuretic, alcohol depletes magnesium and other electrolytes. The intracellular shift that occurs to balance the deficit causes the body to use its normal stores of magnesium, which leads to further magnesium depletion. Other common causes include nutritional deficiency and decreased gastrointestinal absorption.¹² The bleeding the physician suspected was a result of drinking likely occurred through direct and indirect mechanisms that affect platelets.^9,13 Platelets can show improvement 1 week after drinking cessation. Some evidence suggests the risk of seizure or DTs increases significantly with a platelet count <119,000 µL per unit of blood.¹³

Continue to: TREATMENT Pharmacotherapy for alcohol use disorder

TREATMENT Pharmacotherapy for alcohol use disorder

As Mr. G’s condition starts to stabilize, he discusses treatment options for AUD with his physician. At the end of the discussion, Mr. G expresses an interest in starting a medication. The doctor reviews his laboratory results and available treatment options.

[polldaddy:12041630]

The author’s observations

Of the 3 FDA-approved medications for treating AUD (disulfiram, acamprosate, and naltrexone), naltrexone has been shown to decrease heavy drinking days^5,14 and comes in oral and injectable forms. Reducing drinking is achieved by reducing the rewarding effects of alcohol^5,14 and alcohol cravings.⁵ Disulfiram often has poor adherence, and like acamprosate it may be more helpful for maintenance of abstinence.Neither topiramate nor gabapentin are FDA-approved for AUD but may be used for their affects on GABA.⁵ Gabapentin may also help patients experiencing alcohol withdrawal syndrome.^5,15 Mr. G did not have any concomitant medications or comorbid medical conditions, but these factors as well as any renal or hepatic dysfunction must be considered before initiating any medications.

OUTCOME Improved well-being

Mr. G’s treatment team initiates oral naltrexone 50 mg/d, which he tolerates well without complications. He stops drinking entirely and expresses an interest in transitioning to an injectable form of naltrexone in the future. In addition to taking medication, Mr. G wants to participate in psychotherapy. Mr. G thanks his team for the care he received in the hospital, telling them, “You all saved my life.” As he discusses his past issues with alcohol, Mr. G asks his physician how he could get involved to make changes to reduce excessive alcohol consumption in his community (Box^5,15-21).

Box

Bottom Line

Patients experiencing alcohol withdrawal can present with several layers of complexity. Failure to achieve acute stabilization may be life-threatening. After providing critical care, promptly start alcohol use disorder treatment for patients who expresses a desire to change.

Related Resources

• American Society of Addiction Medicine. The ASAM Clinical Practice Guideline on Alcohol Withdrawal Management. https://www.asam.org/quality-care/clinical-guidelines/alcohol-withdrawal-management-guideline
• American Psychiatric Association. The American Psychiatric Association Practice Guideline for the Pharmacological Treatment of Patients With Alcohol Use Disorder. American Psychiatric Association Publishing; 2018.

Drug Brand Names

Acamprosate • Campral
Disulfiram • Antabuse
Gabapentin • Neurontin
Naltrexone (injection) • Vivitrol
Naltrexone (oral) • ReVia
Topiramate • Topamax

In a sea of blonde hair and blue eyes, my black hair and brown eyes stood out. At the time, I was a medical student and one of the few people of color rotating through the inpatient child psychiatric unit. While I was aware I looked “different,” I discovered that my young patients had an unbridled curiosity about such differences. Common questions I received included “Where are you from? Why are your eyes so small? Is it because you eat rice?” Their questions were never of malicious intent, but rather due to my patient’s unfamiliarity with the Asian-American community and with Black, Indigenous, and people of color (BIPOC) communities in general.

Therefore, it came as no surprise that my BIPOC patients could keenly detect similarities. I could see their eyes widen, a spark of recognition, surprise, or even perhaps relief, when they saw my dark hair or the color of my skin. For members of minority racial/ethnic groups in a predominantly White society, there is a special kinship with other underrepresented BIPOC individuals. We are a community; our shared experiences of discrimination and disadvantages bind us together.

Perhaps it was because of our similarities that my BIPOC patients felt comfortable sharing their most intimate secrets: struggling with social anxiety due to language barriers in school, feeling anxious about balancing their familial expectations vs being “American,” or wishing they were dead due to the color of their skin. It hurt to hear this from my patients. My BIPOC patients’ narratives shared a common theme of fear. Fear that others wouldn’t understand their experiences. Fear that no one would understand their pain. When I reflect upon my own experiences with racism, from microaggressions to outright threats, I am reminded of my own fears, loneliness, and pain. It is these experiences that fuel every BIPOC medical student, resident, and physician to provide culturally sensitive care to patients and promote greater mental health for the BIPOC community.

Why diversity matters

Diversity is important in health care. Our patients come from various backgrounds and cultural experiences. A 2019 survey recruited participants who self-identified with >1 race or as a member of an interracial family relationship, to evaluate their preferences in clinicians.¹ Through thematic evaluation of participants’ responses, researchers noted that participants expressed a preference for clinicians who identified as a person of color.¹ Participants desired clinicians who were culturally sensitive, who could connect and empathize with their experiences as people of color.¹ Ultimately, by having a diverse array of clinicians, health care systems ensure that medical professionals can make important connections with patients due to shared experiences.

I remember talking to a mother about her daughter’s suicide attempt. During our conversation, the mother began to shake her head. “She doesn’t have depression,” she exclaimed. “She needs to snap out of it.” As I listened to her, I was reminded of my own grandmother.

My grandmother struggled with depression throughout her life, yet she was adamant she was “fine.” For my grandmother, her insistence that she did not have depression was rooted in shame. In our community, depression was not viewed as a disease, but rather a moral failing. My patient’s mother shared a similar attitude towards depression, believing her daughter was struggling due to her lack of willpower.

As the only person of color on the treatment team, I understood the importance of helping others on the team to also understand the mother’s perspective—doing so changed the dynamics of the relationship between the team and the family. Rather than having an antagonistic view of the mother who seemed to be callous of her daughter’s needs, the team viewed her differently; she was now understood as a mother who was overwhelmed and lacked an understanding of the disease. This changed the treatment team’s focus. The first step was to educate the family about depression, before providing therapeutic and medication treatments.

To fully understand the patient, the physician must place the story in the correct context, recognizing how the intersectionality of race, sexuality, socioeconomic status, and culture impact mental health. I am now a resident, and as a physician, my primary goal is to be an advocate for patients. To improve patient care, we must continue to find ways to improve diversity in the field of psychiatry. One crucial way is for clinicians to share their stories and be vulnerable with our colleagues, as our patients are with us. Through sharing our personal narratives, we further honor and encourage greater diversity.

In a sea of blonde hair and blue eyes, my black hair and brown eyes stood out. At the time, I was a medical student and one of the few people of color rotating through the inpatient child psychiatric unit. While I was aware I looked “different,” I discovered that my young patients had an unbridled curiosity about such differences. Common questions I received included “Where are you from? Why are your eyes so small? Is it because you eat rice?” Their questions were never of malicious intent, but rather due to my patient’s unfamiliarity with the Asian-American community and with Black, Indigenous, and people of color (BIPOC) communities in general.

Therefore, it came as no surprise that my BIPOC patients could keenly detect similarities. I could see their eyes widen, a spark of recognition, surprise, or even perhaps relief, when they saw my dark hair or the color of my skin. For members of minority racial/ethnic groups in a predominantly White society, there is a special kinship with other underrepresented BIPOC individuals. We are a community; our shared experiences of discrimination and disadvantages bind us together.

Perhaps it was because of our similarities that my BIPOC patients felt comfortable sharing their most intimate secrets: struggling with social anxiety due to language barriers in school, feeling anxious about balancing their familial expectations vs being “American,” or wishing they were dead due to the color of their skin. It hurt to hear this from my patients. My BIPOC patients’ narratives shared a common theme of fear. Fear that others wouldn’t understand their experiences. Fear that no one would understand their pain. When I reflect upon my own experiences with racism, from microaggressions to outright threats, I am reminded of my own fears, loneliness, and pain. It is these experiences that fuel every BIPOC medical student, resident, and physician to provide culturally sensitive care to patients and promote greater mental health for the BIPOC community.

Why diversity matters

Diversity is important in health care. Our patients come from various backgrounds and cultural experiences. A 2019 survey recruited participants who self-identified with >1 race or as a member of an interracial family relationship, to evaluate their preferences in clinicians.¹ Through thematic evaluation of participants’ responses, researchers noted that participants expressed a preference for clinicians who identified as a person of color.¹ Participants desired clinicians who were culturally sensitive, who could connect and empathize with their experiences as people of color.¹ Ultimately, by having a diverse array of clinicians, health care systems ensure that medical professionals can make important connections with patients due to shared experiences.

I remember talking to a mother about her daughter’s suicide attempt. During our conversation, the mother began to shake her head. “She doesn’t have depression,” she exclaimed. “She needs to snap out of it.” As I listened to her, I was reminded of my own grandmother.

My grandmother struggled with depression throughout her life, yet she was adamant she was “fine.” For my grandmother, her insistence that she did not have depression was rooted in shame. In our community, depression was not viewed as a disease, but rather a moral failing. My patient’s mother shared a similar attitude towards depression, believing her daughter was struggling due to her lack of willpower.

As the only person of color on the treatment team, I understood the importance of helping others on the team to also understand the mother’s perspective—doing so changed the dynamics of the relationship between the team and the family. Rather than having an antagonistic view of the mother who seemed to be callous of her daughter’s needs, the team viewed her differently; she was now understood as a mother who was overwhelmed and lacked an understanding of the disease. This changed the treatment team’s focus. The first step was to educate the family about depression, before providing therapeutic and medication treatments.

To fully understand the patient, the physician must place the story in the correct context, recognizing how the intersectionality of race, sexuality, socioeconomic status, and culture impact mental health. I am now a resident, and as a physician, my primary goal is to be an advocate for patients. To improve patient care, we must continue to find ways to improve diversity in the field of psychiatry. One crucial way is for clinicians to share their stories and be vulnerable with our colleagues, as our patients are with us. Through sharing our personal narratives, we further honor and encourage greater diversity.

In a sea of blonde hair and blue eyes, my black hair and brown eyes stood out. At the time, I was a medical student and one of the few people of color rotating through the inpatient child psychiatric unit. While I was aware I looked “different,” I discovered that my young patients had an unbridled curiosity about such differences. Common questions I received included “Where are you from? Why are your eyes so small? Is it because you eat rice?” Their questions were never of malicious intent, but rather due to my patient’s unfamiliarity with the Asian-American community and with Black, Indigenous, and people of color (BIPOC) communities in general.

Therefore, it came as no surprise that my BIPOC patients could keenly detect similarities. I could see their eyes widen, a spark of recognition, surprise, or even perhaps relief, when they saw my dark hair or the color of my skin. For members of minority racial/ethnic groups in a predominantly White society, there is a special kinship with other underrepresented BIPOC individuals. We are a community; our shared experiences of discrimination and disadvantages bind us together.

Perhaps it was because of our similarities that my BIPOC patients felt comfortable sharing their most intimate secrets: struggling with social anxiety due to language barriers in school, feeling anxious about balancing their familial expectations vs being “American,” or wishing they were dead due to the color of their skin. It hurt to hear this from my patients. My BIPOC patients’ narratives shared a common theme of fear. Fear that others wouldn’t understand their experiences. Fear that no one would understand their pain. When I reflect upon my own experiences with racism, from microaggressions to outright threats, I am reminded of my own fears, loneliness, and pain. It is these experiences that fuel every BIPOC medical student, resident, and physician to provide culturally sensitive care to patients and promote greater mental health for the BIPOC community.

Why diversity matters

Diversity is important in health care. Our patients come from various backgrounds and cultural experiences. A 2019 survey recruited participants who self-identified with >1 race or as a member of an interracial family relationship, to evaluate their preferences in clinicians.¹ Through thematic evaluation of participants’ responses, researchers noted that participants expressed a preference for clinicians who identified as a person of color.¹ Participants desired clinicians who were culturally sensitive, who could connect and empathize with their experiences as people of color.¹ Ultimately, by having a diverse array of clinicians, health care systems ensure that medical professionals can make important connections with patients due to shared experiences.

I remember talking to a mother about her daughter’s suicide attempt. During our conversation, the mother began to shake her head. “She doesn’t have depression,” she exclaimed. “She needs to snap out of it.” As I listened to her, I was reminded of my own grandmother.

My grandmother struggled with depression throughout her life, yet she was adamant she was “fine.” For my grandmother, her insistence that she did not have depression was rooted in shame. In our community, depression was not viewed as a disease, but rather a moral failing. My patient’s mother shared a similar attitude towards depression, believing her daughter was struggling due to her lack of willpower.

As the only person of color on the treatment team, I understood the importance of helping others on the team to also understand the mother’s perspective—doing so changed the dynamics of the relationship between the team and the family. Rather than having an antagonistic view of the mother who seemed to be callous of her daughter’s needs, the team viewed her differently; she was now understood as a mother who was overwhelmed and lacked an understanding of the disease. This changed the treatment team’s focus. The first step was to educate the family about depression, before providing therapeutic and medication treatments.

To fully understand the patient, the physician must place the story in the correct context, recognizing how the intersectionality of race, sexuality, socioeconomic status, and culture impact mental health. I am now a resident, and as a physician, my primary goal is to be an advocate for patients. To improve patient care, we must continue to find ways to improve diversity in the field of psychiatry. One crucial way is for clinicians to share their stories and be vulnerable with our colleagues, as our patients are with us. Through sharing our personal narratives, we further honor and encourage greater diversity.

Clonidine is a centrally acting alpha-2 agonist originally developed for treating hypertension. It is believed to work by stimulating alpha-2 receptors in various areas of the brain. It is nonselective, binding alpha-2A, -2B, and -2C receptors, and mediates inattentiveness, hyperactivity, impulsivity, sedation, and hypotension.¹ Clonidine is available as immediate-release (IR), extended-release, and patch formulations, with typical doses ranging from 0.1 to 0.4 mg/d. The most common adverse effects are anticholinergic, such as sedation, dry mouth, and constipation. Since clonidine is effective at lowering blood pressure, the main safety concern is the possibility of rebound hypertension if abruptly stopped, which necessitates a short taper period.¹

In child and adolescent psychiatry, the only FDA-approved use of clonidine is for treating attention-deficit/hyperactivity disorder (ADHD). Yet this medication has been increasingly used off-label for several common psychiatric ailments in pediatric patients. In this article, we discuss potential uses of clonidine in child and adolescent psychiatry; except for ADHD, all uses we describe are off-label.

ADHD. Clonidine is effective both as a monotherapy and as an adjunctive therapy to stimulants for pediatric ADHD. When used alone, clonidine is better suited for patients who have hyperactivity as their primary concern, whereas stimulants may be better suited for patients with inattentive subtypes. It also can help reduce sleep disturbances associated with the use of stimulants, especially insomnia.¹

Tics/Tourette syndrome. Clonidine is a first-line treatment for tics in Tourette syndrome, demonstrating high efficacy with limited or no adverse effects. Furthermore, ADHD is the most common comorbid condition in patients with dystonic tics, which makes clonidine useful for simultaneously treating both conditions.²

Insomnia. Currently, there are no FDA-approved medications for treating sleep disorders in children and adolescents. However, clonidine is among the most used medications for childhood sleep difficulties, second only to antihistamines. The IR formulation is often preferred for this indication due to increased sedation.³

Posttraumatic stress disorder (PTSD). Research has shown clonidine can help reduce hyperarousal symptoms, address sleep difficulties, and reduce PTSD trauma nightmares, anxiety, and irritability.⁴

Substance detoxification. Clonidine successfully suppresses opiate withdrawal signs and symptoms by reducing sympathetic overactivity. It can help with alcohol withdrawal and smoking cessation.²

Antipsychotic-induced akathisia. Controlled trials have shown that clonidine significantly reduces akathisia associated with the use of antipsychotics.²

Sialorrhea. Due to its anticholinergic effects, clonidine can effectively reduce antipsychotic-induced hypersalivation.²

Behavioral disturbances. Due to its sedative and anti-impulsive properties, clonidine can be used to address broadly defined behavioral issues, including anxiety-related behaviors, aggression, and agitation, although there is a lack of proven efficacy.^1,2,4

Clonidine is a centrally acting alpha-2 agonist originally developed for treating hypertension. It is believed to work by stimulating alpha-2 receptors in various areas of the brain. It is nonselective, binding alpha-2A, -2B, and -2C receptors, and mediates inattentiveness, hyperactivity, impulsivity, sedation, and hypotension.¹ Clonidine is available as immediate-release (IR), extended-release, and patch formulations, with typical doses ranging from 0.1 to 0.4 mg/d. The most common adverse effects are anticholinergic, such as sedation, dry mouth, and constipation. Since clonidine is effective at lowering blood pressure, the main safety concern is the possibility of rebound hypertension if abruptly stopped, which necessitates a short taper period.¹

In child and adolescent psychiatry, the only FDA-approved use of clonidine is for treating attention-deficit/hyperactivity disorder (ADHD). Yet this medication has been increasingly used off-label for several common psychiatric ailments in pediatric patients. In this article, we discuss potential uses of clonidine in child and adolescent psychiatry; except for ADHD, all uses we describe are off-label.

ADHD. Clonidine is effective both as a monotherapy and as an adjunctive therapy to stimulants for pediatric ADHD. When used alone, clonidine is better suited for patients who have hyperactivity as their primary concern, whereas stimulants may be better suited for patients with inattentive subtypes. It also can help reduce sleep disturbances associated with the use of stimulants, especially insomnia.¹

Tics/Tourette syndrome. Clonidine is a first-line treatment for tics in Tourette syndrome, demonstrating high efficacy with limited or no adverse effects. Furthermore, ADHD is the most common comorbid condition in patients with dystonic tics, which makes clonidine useful for simultaneously treating both conditions.²

Insomnia. Currently, there are no FDA-approved medications for treating sleep disorders in children and adolescents. However, clonidine is among the most used medications for childhood sleep difficulties, second only to antihistamines. The IR formulation is often preferred for this indication due to increased sedation.³

Posttraumatic stress disorder (PTSD). Research has shown clonidine can help reduce hyperarousal symptoms, address sleep difficulties, and reduce PTSD trauma nightmares, anxiety, and irritability.⁴

Substance detoxification. Clonidine successfully suppresses opiate withdrawal signs and symptoms by reducing sympathetic overactivity. It can help with alcohol withdrawal and smoking cessation.²

Antipsychotic-induced akathisia. Controlled trials have shown that clonidine significantly reduces akathisia associated with the use of antipsychotics.²

Sialorrhea. Due to its anticholinergic effects, clonidine can effectively reduce antipsychotic-induced hypersalivation.²

Behavioral disturbances. Due to its sedative and anti-impulsive properties, clonidine can be used to address broadly defined behavioral issues, including anxiety-related behaviors, aggression, and agitation, although there is a lack of proven efficacy.^1,2,4

Clonidine is a centrally acting alpha-2 agonist originally developed for treating hypertension. It is believed to work by stimulating alpha-2 receptors in various areas of the brain. It is nonselective, binding alpha-2A, -2B, and -2C receptors, and mediates inattentiveness, hyperactivity, impulsivity, sedation, and hypotension.¹ Clonidine is available as immediate-release (IR), extended-release, and patch formulations, with typical doses ranging from 0.1 to 0.4 mg/d. The most common adverse effects are anticholinergic, such as sedation, dry mouth, and constipation. Since clonidine is effective at lowering blood pressure, the main safety concern is the possibility of rebound hypertension if abruptly stopped, which necessitates a short taper period.¹

In child and adolescent psychiatry, the only FDA-approved use of clonidine is for treating attention-deficit/hyperactivity disorder (ADHD). Yet this medication has been increasingly used off-label for several common psychiatric ailments in pediatric patients. In this article, we discuss potential uses of clonidine in child and adolescent psychiatry; except for ADHD, all uses we describe are off-label.

ADHD. Clonidine is effective both as a monotherapy and as an adjunctive therapy to stimulants for pediatric ADHD. When used alone, clonidine is better suited for patients who have hyperactivity as their primary concern, whereas stimulants may be better suited for patients with inattentive subtypes. It also can help reduce sleep disturbances associated with the use of stimulants, especially insomnia.¹

Tics/Tourette syndrome. Clonidine is a first-line treatment for tics in Tourette syndrome, demonstrating high efficacy with limited or no adverse effects. Furthermore, ADHD is the most common comorbid condition in patients with dystonic tics, which makes clonidine useful for simultaneously treating both conditions.²

Insomnia. Currently, there are no FDA-approved medications for treating sleep disorders in children and adolescents. However, clonidine is among the most used medications for childhood sleep difficulties, second only to antihistamines. The IR formulation is often preferred for this indication due to increased sedation.³

Posttraumatic stress disorder (PTSD). Research has shown clonidine can help reduce hyperarousal symptoms, address sleep difficulties, and reduce PTSD trauma nightmares, anxiety, and irritability.⁴

Substance detoxification. Clonidine successfully suppresses opiate withdrawal signs and symptoms by reducing sympathetic overactivity. It can help with alcohol withdrawal and smoking cessation.²

Antipsychotic-induced akathisia. Controlled trials have shown that clonidine significantly reduces akathisia associated with the use of antipsychotics.²

Sialorrhea. Due to its anticholinergic effects, clonidine can effectively reduce antipsychotic-induced hypersalivation.²

Behavioral disturbances. Due to its sedative and anti-impulsive properties, clonidine can be used to address broadly defined behavioral issues, including anxiety-related behaviors, aggression, and agitation, although there is a lack of proven efficacy.^1,2,4

Intranasal esketamine is an FDA-approved ketamine molecule indicated for use together with an oral antidepressant for treatment-resistant depression (TRD) in patients age ≥18 who have had an inadequate response to ≥2 antidepressants, and for depressive symptoms in adults with major depressive disorder with suicidal thoughts or actions.¹ Since March 2019, we’ve been treating patients with intranasal esketamine. Based on our experiences, here is a summary of what we have learned.

REMS is required. Due to the potential risks resulting from sedation and dissociation caused by esketamine and the risk of abuse and misuse, esketamine is available only through a Risk Evaluation and Mitigation Strategy (REMS) program. The program links your office Drug Enforcement Administration number to the address where this schedule III medication will be stored and given to the patient for self-administration. Requirements and other details about the REMS are available at www.spravatorems.com.

Treatment. Start with the online REMS patient enrollment/consent form. Contra­indications include having a history of aneurysmal vascular disease, intracerebral hemorrhage, or allergy to ketamine/esketamine. Adjunctive treatment with esketamine plus sertraline, escitalopram, venlafaxine, or duloxetine are comparably effective.¹ We have found that adding magnesium to block glutamate action at N-methyl-D-aspartate (NMDA) receptors, bupropion, and the oral NMDA receptor antagonist dextromethorphan may amplify and prolong esketamine’s therapeutic effects. Titrate to a maximum tolerated dose of 3 devices (84 mg total), 5 minutes apart. Administer esketamine twice weekly for 4 weeks, then weekly for the next 4 weeks (for TRD), and continue weekly or twice monthly.¹ Open-label clinical trial data over 4 years support continuing treatment for relapse prevention, and have not reported the long-term cognitive impairment or ulcerative/interstitial cystitis associated with frequent, chronic ketamine use.² TRD clinical trials have shown a response rate (>50% reduction in baseline Montgomery-Åsberg Depression Rating Scale score) of 70% by the end of Week 4, emerging at 4 hours, independent of dissociation.³

Iatrogenic effects rarely lead to dropout. The first session is critical to allay anticipatory anxiety. Sedation, blood pressure increase, and dissociation are common but transient adverse effects that typically peak at 40 minutes and resolve by 90 minutes. Record blood pressure on a REMS monitoring form before treatment, at 40 minutes, and at 2 hours. Avoid administering sedative or prohypertensive medications together with esketamine.¹ Dissociation is more common in patients with a history of trauma. Combine music, guided image­ry, or psychotherapy to harness this for therapeutic benefit. Sleepiness can last 4 hours; make sure the patient has arranged for a ride home, as they cannot drive until the next day. Verify normal blood pressure before starting treatment. Clonidine or labetalol for hypertension/severe dissociation and ondansetron or prochlorperazine for nausea are rarely needed. Advise patients to use the bathroom before treatment and keep a trash can nearby for vomiting. Other transient adverse effects found in TRD clinical trials that occurred >5% and twice that of placebo were dizziness, vertigo, numbness, and feeling drunk.¹

Reimbursement for treatment with esketamine is available through most insurances, including copay cards, rebates, deductible support, and free assistance programs. Coverage is either through pharmacy benefit, assignment of medical benefit (pharmacy handles the medical benefit), or medical benefit with remuneration above wholesale price.

Zeitgeist shift. Emergency departments are backlogged and patients languish waiting to feel the effects of oral antidepressants. Intranasal esketamine could help alleviate this situation by producing a more immediate response. We also have observed improvements in comorbid posttraumatic stress disorder and in cognitive deficits of dementia, possibly due to rapidly enhanced neuroplasticity, neurogenesis, and astrocyte functioning, which NMDA receptor antagonism, AMPA activation, and downstream mediators (eg, brain-derived neurotrophic factor) may promote.⁴

Intranasal esketamine is an FDA-approved ketamine molecule indicated for use together with an oral antidepressant for treatment-resistant depression (TRD) in patients age ≥18 who have had an inadequate response to ≥2 antidepressants, and for depressive symptoms in adults with major depressive disorder with suicidal thoughts or actions.¹ Since March 2019, we’ve been treating patients with intranasal esketamine. Based on our experiences, here is a summary of what we have learned.

REMS is required. Due to the potential risks resulting from sedation and dissociation caused by esketamine and the risk of abuse and misuse, esketamine is available only through a Risk Evaluation and Mitigation Strategy (REMS) program. The program links your office Drug Enforcement Administration number to the address where this schedule III medication will be stored and given to the patient for self-administration. Requirements and other details about the REMS are available at www.spravatorems.com.

Treatment. Start with the online REMS patient enrollment/consent form. Contra­indications include having a history of aneurysmal vascular disease, intracerebral hemorrhage, or allergy to ketamine/esketamine. Adjunctive treatment with esketamine plus sertraline, escitalopram, venlafaxine, or duloxetine are comparably effective.¹ We have found that adding magnesium to block glutamate action at N-methyl-D-aspartate (NMDA) receptors, bupropion, and the oral NMDA receptor antagonist dextromethorphan may amplify and prolong esketamine’s therapeutic effects. Titrate to a maximum tolerated dose of 3 devices (84 mg total), 5 minutes apart. Administer esketamine twice weekly for 4 weeks, then weekly for the next 4 weeks (for TRD), and continue weekly or twice monthly.¹ Open-label clinical trial data over 4 years support continuing treatment for relapse prevention, and have not reported the long-term cognitive impairment or ulcerative/interstitial cystitis associated with frequent, chronic ketamine use.² TRD clinical trials have shown a response rate (>50% reduction in baseline Montgomery-Åsberg Depression Rating Scale score) of 70% by the end of Week 4, emerging at 4 hours, independent of dissociation.³

Iatrogenic effects rarely lead to dropout. The first session is critical to allay anticipatory anxiety. Sedation, blood pressure increase, and dissociation are common but transient adverse effects that typically peak at 40 minutes and resolve by 90 minutes. Record blood pressure on a REMS monitoring form before treatment, at 40 minutes, and at 2 hours. Avoid administering sedative or prohypertensive medications together with esketamine.¹ Dissociation is more common in patients with a history of trauma. Combine music, guided image­ry, or psychotherapy to harness this for therapeutic benefit. Sleepiness can last 4 hours; make sure the patient has arranged for a ride home, as they cannot drive until the next day. Verify normal blood pressure before starting treatment. Clonidine or labetalol for hypertension/severe dissociation and ondansetron or prochlorperazine for nausea are rarely needed. Advise patients to use the bathroom before treatment and keep a trash can nearby for vomiting. Other transient adverse effects found in TRD clinical trials that occurred >5% and twice that of placebo were dizziness, vertigo, numbness, and feeling drunk.¹

Reimbursement for treatment with esketamine is available through most insurances, including copay cards, rebates, deductible support, and free assistance programs. Coverage is either through pharmacy benefit, assignment of medical benefit (pharmacy handles the medical benefit), or medical benefit with remuneration above wholesale price.

Zeitgeist shift. Emergency departments are backlogged and patients languish waiting to feel the effects of oral antidepressants. Intranasal esketamine could help alleviate this situation by producing a more immediate response. We also have observed improvements in comorbid posttraumatic stress disorder and in cognitive deficits of dementia, possibly due to rapidly enhanced neuroplasticity, neurogenesis, and astrocyte functioning, which NMDA receptor antagonism, AMPA activation, and downstream mediators (eg, brain-derived neurotrophic factor) may promote.⁴

Intranasal esketamine is an FDA-approved ketamine molecule indicated for use together with an oral antidepressant for treatment-resistant depression (TRD) in patients age ≥18 who have had an inadequate response to ≥2 antidepressants, and for depressive symptoms in adults with major depressive disorder with suicidal thoughts or actions.¹ Since March 2019, we’ve been treating patients with intranasal esketamine. Based on our experiences, here is a summary of what we have learned.

REMS is required. Due to the potential risks resulting from sedation and dissociation caused by esketamine and the risk of abuse and misuse, esketamine is available only through a Risk Evaluation and Mitigation Strategy (REMS) program. The program links your office Drug Enforcement Administration number to the address where this schedule III medication will be stored and given to the patient for self-administration. Requirements and other details about the REMS are available at www.spravatorems.com.

Treatment. Start with the online REMS patient enrollment/consent form. Contra­indications include having a history of aneurysmal vascular disease, intracerebral hemorrhage, or allergy to ketamine/esketamine. Adjunctive treatment with esketamine plus sertraline, escitalopram, venlafaxine, or duloxetine are comparably effective.¹ We have found that adding magnesium to block glutamate action at N-methyl-D-aspartate (NMDA) receptors, bupropion, and the oral NMDA receptor antagonist dextromethorphan may amplify and prolong esketamine’s therapeutic effects. Titrate to a maximum tolerated dose of 3 devices (84 mg total), 5 minutes apart. Administer esketamine twice weekly for 4 weeks, then weekly for the next 4 weeks (for TRD), and continue weekly or twice monthly.¹ Open-label clinical trial data over 4 years support continuing treatment for relapse prevention, and have not reported the long-term cognitive impairment or ulcerative/interstitial cystitis associated with frequent, chronic ketamine use.² TRD clinical trials have shown a response rate (>50% reduction in baseline Montgomery-Åsberg Depression Rating Scale score) of 70% by the end of Week 4, emerging at 4 hours, independent of dissociation.³

Iatrogenic effects rarely lead to dropout. The first session is critical to allay anticipatory anxiety. Sedation, blood pressure increase, and dissociation are common but transient adverse effects that typically peak at 40 minutes and resolve by 90 minutes. Record blood pressure on a REMS monitoring form before treatment, at 40 minutes, and at 2 hours. Avoid administering sedative or prohypertensive medications together with esketamine.¹ Dissociation is more common in patients with a history of trauma. Combine music, guided image­ry, or psychotherapy to harness this for therapeutic benefit. Sleepiness can last 4 hours; make sure the patient has arranged for a ride home, as they cannot drive until the next day. Verify normal blood pressure before starting treatment. Clonidine or labetalol for hypertension/severe dissociation and ondansetron or prochlorperazine for nausea are rarely needed. Advise patients to use the bathroom before treatment and keep a trash can nearby for vomiting. Other transient adverse effects found in TRD clinical trials that occurred >5% and twice that of placebo were dizziness, vertigo, numbness, and feeling drunk.¹

Reimbursement for treatment with esketamine is available through most insurances, including copay cards, rebates, deductible support, and free assistance programs. Coverage is either through pharmacy benefit, assignment of medical benefit (pharmacy handles the medical benefit), or medical benefit with remuneration above wholesale price.

Zeitgeist shift. Emergency departments are backlogged and patients languish waiting to feel the effects of oral antidepressants. Intranasal esketamine could help alleviate this situation by producing a more immediate response. We also have observed improvements in comorbid posttraumatic stress disorder and in cognitive deficits of dementia, possibly due to rapidly enhanced neuroplasticity, neurogenesis, and astrocyte functioning, which NMDA receptor antagonism, AMPA activation, and downstream mediators (eg, brain-derived neurotrophic factor) may promote.⁴

I enjoyed reading the optimistic outlook for psychiatry outlined in your SWOT analysis (“Contemporary psychiatry: A SWOT analysis,” Current Psychiatry, January 2023, p. 16-19,27, doi:10.12788/cp.0320). I agree with the challenges ahead, including the challenge of keeping up with the explosion of knowledge in relation to the brain, emotions, and the complex interactions of genetics, environment, and biology. I’m excited by the movements in psychopharmacology, which hold promises for new, more effective, less toxic treatments for some of our most challenging disorders.

I think, though, you misplaced an opportunity as a threat in your assessment that the increase in the amount of advanced practice psychiatric nurses (PMHAPRNs) presents a threat to psychiatry. The presence of an increased number of PMHAPRNs provides access to a larger number of people needing treatment by qualified, skilled mental health professionals and an opportunity for psychiatrists to participate in highly effective teams of psychiatric clinicians. This workforce-building is of particular importance during our current clinician shortage, especially within psychiatry. Most research has shown that advanced practice nurses’ quality of care is competitive with that of physicians with similar experience, and that patient satisfaction is high. Advanced practice nurses are more likely than physicians to provide care in underserved populations and in rural communities. We are educated to practice independently within our scope, to standards established by our professional organizations as well as American Psychiatric Association (APA) clinical guidelines. I hope you will reconsider your view of your PMHAPRN colleagues as a threat and see them as a positive contribution to your chosen field of psychiatry, like the APA has shown in their choice of including a PMHAPRN as a clinical expert team member on the SMI Adviser initiative.

Stella Logan, APRN, PMHCNS-BC, PMHNP-BC
Austin, Texas

Dr. Nasrallah responds

Thank you for your letter regarding my SWOT article. It was originally written for the newsletter of the Ohio Psychiatric Physicians Association, comprised of 1,000 psychiatrists. To them, nurse practitioners (NPs) are regarded as a threat because some mental health care systems have been laying off psychiatrists and hiring NPs to lower costs. This obviously is perceived as a threat. I do agree with you that well-qualified NPs are providing needed mental health services in underserved areas (eg, inner cities and rural areas), where it is very difficult to recruit psychiatrists due to the severe shortage nationally.

Henry A. Nasrallah, MD, DLFAPA
Editor-in-Chief

Continue to: More on the transdiagnostic model

I just had the pleasure of reading your February 2023 editorial (“Depression and schizophrenia: Many biological and clinical similarities,” Current Psychiatry, February 2023, p. 3-5, doi:10.12788/cp.0331) and it was truly wonderful. For years it has seemed to me that the somewhat unnatural divisions in psychiatry with respect to diagnosis were a necessary evil, for numerous reasons. It seems the tide is turning, however, and for those of us who have always afforded a primacy to treating a patient’s symptoms rather than a diagnosis in a book, it seems the research is at last supporting that approach. Your points about insurance companies and the mendacity and cupidity that underlies their policies are very well stated. Thank you for another excellent, timely, and eloquent editorial!

David Krassner, MD
Phoenix, Arizona

I completely agree with your promotion of a unified transdiagnostic model. All of this makes sense on the continuum of consciousness—restricted consciousness represents fear, whereas wide consciousness represents complete connectivity (love in the spiritual sense). Therefore, a threat not resolved can lead to defeat and an unresolved painful defeat can lead to a psychotic projection. Is it no surprise, then, that a medication such as quetiapine can treat the whole continuum from anxiety at low doses to psychosis at high doses?

Mike Primc, MD
Chardon, Ohio

I enjoyed reading the optimistic outlook for psychiatry outlined in your SWOT analysis (“Contemporary psychiatry: A SWOT analysis,” Current Psychiatry, January 2023, p. 16-19,27, doi:10.12788/cp.0320). I agree with the challenges ahead, including the challenge of keeping up with the explosion of knowledge in relation to the brain, emotions, and the complex interactions of genetics, environment, and biology. I’m excited by the movements in psychopharmacology, which hold promises for new, more effective, less toxic treatments for some of our most challenging disorders.

I think, though, you misplaced an opportunity as a threat in your assessment that the increase in the amount of advanced practice psychiatric nurses (PMHAPRNs) presents a threat to psychiatry. The presence of an increased number of PMHAPRNs provides access to a larger number of people needing treatment by qualified, skilled mental health professionals and an opportunity for psychiatrists to participate in highly effective teams of psychiatric clinicians. This workforce-building is of particular importance during our current clinician shortage, especially within psychiatry. Most research has shown that advanced practice nurses’ quality of care is competitive with that of physicians with similar experience, and that patient satisfaction is high. Advanced practice nurses are more likely than physicians to provide care in underserved populations and in rural communities. We are educated to practice independently within our scope, to standards established by our professional organizations as well as American Psychiatric Association (APA) clinical guidelines. I hope you will reconsider your view of your PMHAPRN colleagues as a threat and see them as a positive contribution to your chosen field of psychiatry, like the APA has shown in their choice of including a PMHAPRN as a clinical expert team member on the SMI Adviser initiative.

Stella Logan, APRN, PMHCNS-BC, PMHNP-BC
Austin, Texas

Dr. Nasrallah responds

Thank you for your letter regarding my SWOT article. It was originally written for the newsletter of the Ohio Psychiatric Physicians Association, comprised of 1,000 psychiatrists. To them, nurse practitioners (NPs) are regarded as a threat because some mental health care systems have been laying off psychiatrists and hiring NPs to lower costs. This obviously is perceived as a threat. I do agree with you that well-qualified NPs are providing needed mental health services in underserved areas (eg, inner cities and rural areas), where it is very difficult to recruit psychiatrists due to the severe shortage nationally.

Henry A. Nasrallah, MD, DLFAPA
Editor-in-Chief

Continue to: More on the transdiagnostic model

I just had the pleasure of reading your February 2023 editorial (“Depression and schizophrenia: Many biological and clinical similarities,” Current Psychiatry, February 2023, p. 3-5, doi:10.12788/cp.0331) and it was truly wonderful. For years it has seemed to me that the somewhat unnatural divisions in psychiatry with respect to diagnosis were a necessary evil, for numerous reasons. It seems the tide is turning, however, and for those of us who have always afforded a primacy to treating a patient’s symptoms rather than a diagnosis in a book, it seems the research is at last supporting that approach. Your points about insurance companies and the mendacity and cupidity that underlies their policies are very well stated. Thank you for another excellent, timely, and eloquent editorial!

David Krassner, MD
Phoenix, Arizona

I completely agree with your promotion of a unified transdiagnostic model. All of this makes sense on the continuum of consciousness—restricted consciousness represents fear, whereas wide consciousness represents complete connectivity (love in the spiritual sense). Therefore, a threat not resolved can lead to defeat and an unresolved painful defeat can lead to a psychotic projection. Is it no surprise, then, that a medication such as quetiapine can treat the whole continuum from anxiety at low doses to psychosis at high doses?

Mike Primc, MD
Chardon, Ohio

I enjoyed reading the optimistic outlook for psychiatry outlined in your SWOT analysis (“Contemporary psychiatry: A SWOT analysis,” Current Psychiatry, January 2023, p. 16-19,27, doi:10.12788/cp.0320). I agree with the challenges ahead, including the challenge of keeping up with the explosion of knowledge in relation to the brain, emotions, and the complex interactions of genetics, environment, and biology. I’m excited by the movements in psychopharmacology, which hold promises for new, more effective, less toxic treatments for some of our most challenging disorders.

I think, though, you misplaced an opportunity as a threat in your assessment that the increase in the amount of advanced practice psychiatric nurses (PMHAPRNs) presents a threat to psychiatry. The presence of an increased number of PMHAPRNs provides access to a larger number of people needing treatment by qualified, skilled mental health professionals and an opportunity for psychiatrists to participate in highly effective teams of psychiatric clinicians. This workforce-building is of particular importance during our current clinician shortage, especially within psychiatry. Most research has shown that advanced practice nurses’ quality of care is competitive with that of physicians with similar experience, and that patient satisfaction is high. Advanced practice nurses are more likely than physicians to provide care in underserved populations and in rural communities. We are educated to practice independently within our scope, to standards established by our professional organizations as well as American Psychiatric Association (APA) clinical guidelines. I hope you will reconsider your view of your PMHAPRN colleagues as a threat and see them as a positive contribution to your chosen field of psychiatry, like the APA has shown in their choice of including a PMHAPRN as a clinical expert team member on the SMI Adviser initiative.

Stella Logan, APRN, PMHCNS-BC, PMHNP-BC
Austin, Texas

Dr. Nasrallah responds

Thank you for your letter regarding my SWOT article. It was originally written for the newsletter of the Ohio Psychiatric Physicians Association, comprised of 1,000 psychiatrists. To them, nurse practitioners (NPs) are regarded as a threat because some mental health care systems have been laying off psychiatrists and hiring NPs to lower costs. This obviously is perceived as a threat. I do agree with you that well-qualified NPs are providing needed mental health services in underserved areas (eg, inner cities and rural areas), where it is very difficult to recruit psychiatrists due to the severe shortage nationally.

Henry A. Nasrallah, MD, DLFAPA
Editor-in-Chief

Continue to: More on the transdiagnostic model

I just had the pleasure of reading your February 2023 editorial (“Depression and schizophrenia: Many biological and clinical similarities,” Current Psychiatry, February 2023, p. 3-5, doi:10.12788/cp.0331) and it was truly wonderful. For years it has seemed to me that the somewhat unnatural divisions in psychiatry with respect to diagnosis were a necessary evil, for numerous reasons. It seems the tide is turning, however, and for those of us who have always afforded a primacy to treating a patient’s symptoms rather than a diagnosis in a book, it seems the research is at last supporting that approach. Your points about insurance companies and the mendacity and cupidity that underlies their policies are very well stated. Thank you for another excellent, timely, and eloquent editorial!

David Krassner, MD
Phoenix, Arizona

I completely agree with your promotion of a unified transdiagnostic model. All of this makes sense on the continuum of consciousness—restricted consciousness represents fear, whereas wide consciousness represents complete connectivity (love in the spiritual sense). Therefore, a threat not resolved can lead to defeat and an unresolved painful defeat can lead to a psychotic projection. Is it no surprise, then, that a medication such as quetiapine can treat the whole continuum from anxiety at low doses to psychosis at high doses?

Mike Primc, MD
Chardon, Ohio

Total fertility rate and fertility care: Demographic shifts and changing demands

Vollset SE, Goren E, Yuan C-W, et al. Fertility, mortality, migration, and population scenarios for 195 countries and territories from 2017 to 2100: a forecasting analysis for the Global Burden of Disease Study. Lancet. 2020;396:1285-1306.

The total fertility rate (TFR) globally is decreasing rapidly, and in the United States it is now 1.8 births per woman, well below the required replacement rate of 2.1 that maintains the population.¹ These reduced TFRs result in significant demographic shifts that affect the economy, workforce, society, health care needs, environment, and geopolitical standing of every country. These changes also will shift demands for the volume and type of services delivered by women’s health care clinicians.

In addition to the TFR, mortality rates and migration rates play essential roles in determining a country’s population.² Anticipation and planning for these population and health care service changes by each country’s government, business, professionals, and other stakeholders are imperative to manage their impact and optimize quality of life.

Illustration: Kimberly Martens for OBG Management

US standings in projected population and economic growth

The US population is predicted to peak at 364 million in 2062 and decrease to 336 million in 2100, at which time it will be the fourth largest country in the world, according to a forecasting analysis by Vollset and colleagues.¹ China is expected to become the biggest economy in the world in 2035, but this is predicted to change because of its decreasing population so that by 2098 the United States will again be the country with the largest economy (FIGURE 1).¹

For the United States to maintain its economic and geopolitical standing, it is important to have policies that promote families. Other countries, especially in northern Europe, have implemented such policies. These include education of the population,economic incentives to create families, extended day care, and favorable tax policies.³ They also include increased access to family-forming fertility care. Such policies in Denmark have resulted in approximately 10% of all children being born from assisted reproductive technology (ART), compared with about 1.5% in the United States. Other countries have similar policies and success in increasing the number of children born from ART.

In the United States, the American Society for Reproductive Medicine (ASRM), RESOLVE: the National Infertility Association, the American Medical Women’s Association (AMWA), and others are promoting the need for increased access to fertility care and family-forming resources, primarily through family-forming benefits provided by companies.⁴ Such benefits are critical since the primary reason most people do not undergo fertility care is a lack of affordability. Only 1 person in 4 in the United States who needs fertility care receives treatment. Increased access would result in more babies being born to help address the reduced TFR.

Educational access, contraceptive goals, and access to fertility care

Continued trends in women’s educational attainment and access to contraception will hasten declines in the fertility rate and slow population growth (TABLE).¹ These educational and contraceptive goals also must be pursued so that every person can achieve their individual reproductive life goals of having a family if and when they want to have a family. In addition to helping address the decreasing TFR, there is a fundamental right to found a family, as stated in the United Nations charter. It is a matter of social justice and equity that everyone who wants to have a family can access reproductive care on a nondiscriminatory basis when needed.

While the need for more and better insurance coverage for infertility has been well documented for many years, the decreasing TFR in the United States is an additional compelling reason that government, business, and other stakeholders should continue to increase access to fertility benefits and care. Women’s health care clinicians are encouraged to support these initiatives that also improve quality of life, equity, and social justice.

Continue to: A new comprehensive ovulatory disorders classification system developed by FIGO...

Munro MG, Balen AH, Cho S, et al; FIGO Committee on Menstrual Disorders and Related Health Impacts, and FIGO Committee on Reproductive Medicine, Endocrinology, and Infertility. The FIGO ovulatory disorders classification system. Fertil Steril. 2022;118:768-786.

Ovulatory disorders are well-recognized and common causes of infertility and abnormal uterine bleeding (AUB). Ovulatory disorders occur on a spectrum, with the most severe form being anovulation, and comprise a heterogeneous group that has been classically categorized based on an initial monograph published by the World Health Organization (WHO) in 1973. That classification was based on gonadotropin levels and categorized these disorders into 3 groups: 1) hypogonadotropic (such as hypothalamic amenorrhea), 2) eugonadotropic (such as polycystic ovary syndrome [PCOS]), and 3) hypergonadotropic (such as primary ovarian insufficiency). This initial classification was the subject of several subsequent iterations and modifications over the past 50 years; for example, at one point, ovulatory disorder caused by hyperprolactinemia was added as a separate fourth category. However, due to advances in endocrine assays, imaging technology, and genetics, our understanding of ovulatory disorders has expanded remarkably over the past several decades.

Previous FIGO classifications

Considering the emergent complexity of these disorders and the limitations of the original WHO classification to capture these subtleties adequately, the International Federation of Gynecology and Obstetrics (FIGO) recently developed and published a new classification system for ovulatory disorders.⁵ This new system was designed using a meticulously followed Delphi process with inputs from a diverse group of national and international professional organizations, subspecialty societies, specialty journals, recognized experts in the field, and lay individuals interested in the subject matter.

Of note, FIGO had previously published classification systems for nongestational normal and abnormal uterine bleeding in the reproductive years (FIGO AUB System 1),as well as a subsequent classification system that described potential causes of AUB symptoms (FIGO AUB System 2), with the 9 categories arranged under the acronym PALM-COEIN (Polyp, Adenomyosis, Leiomyoma, Malignancy–Coagulopathy, Ovulatory dysfunction, Endometrial disorders, Iatrogenic, and Not otherwise classified). This new FIGO classification of ovulatory disorders can be viewed as a continuation of the previous initiatives and aims to further categorize the subgroup of AUB-O (AUB with ovulatory disorders). However, it is important to recognize that while most ovulatory disorders manifest with the symptoms of AUB, the absence of AUB symptoms does not necessarily preclude ovulatory disorders.

New system uses a 3-tier approach

The new FIGO classification system for ovulatory disorders has adopted a 3-tier system.

The first tier is based on the anatomic components of the hypothalamic-pituitary-ovarian (HPO) axis and is referred to with the acronym HyPO, for Hypothalamic-Pituitary-Ovarian. Recognizing that PCOS refers to a distinct spectrum of conditions that share a variable combination of signs and symptoms caused to varying degrees by different pathophysiologic mechanisms that involve inherent ovarian follicular dysfunction, neuroendocrine dysfunction, insulin resistance, and androgen excess, it is categorized in a separate class of its own in the first tier, referred to with the letter P.

Adding PCOS to the anatomical categories referred to by HyPO, the first tier is overall referred to with the acronym HyPO-P (FIGURE 2).⁵

The second tier of stratification provides further etiologic details for any of the primary 3 anatomic classifications of hypothalamic, pituitary, and ovarian. These etiologies are arranged in 10 distinct groups under the mnemonic GAIN-FIT-PIE, which stands for Genetic, Autoimmune, Iatrogenic, Neoplasm; Functional, Infectious/inflammatory, Trauma and vascular; and Physiological, Idiopathic, Endocrine.

The third tier of the system refers to the specific clinical diagnosis. For example, an individual with Kallmann syndrome would be categorized as having type I (hypothalamic), Genetic, Kallmann syndrome, and an individual with PCOS would be categorized simply as having type IV, PCOS.

Continue to: Live birth rate with conventional IVF shown noninferior to that with PGT-A...

Yan J, Qin Y, Zhao H, et al. Live birth with or without preimplantation genetic testing for aneuploidy. N Engl J Med. 2021;385:2047-2058.

Preimplantation genetic testing for aneuploidy (PGT-A) is increasingly used in many in vitro fertilization (IVF) cycles in the United States. Based on data from the Centers for Disease Control and Prevention, 43.8% of embryo transfers in the United States in 2019 included at least 1 PGT-A–tested embryo.⁶ Despite this widespread use, however, there are still no robust clinical data for PGT-A’s efficacy and safety, and the guidelines published by the ASRM do not recommend its routine use in all IVF cycles.⁷ In the past 2 to 3 years, several large studies have raised questions about the reported benefit of this technology.^8,9

Details of the trial

In a multicenter, controlled, noninferiority trial conducted by Yan and colleagues, 1,212 subfertile women were randomly assigned to either conventional IVF with embryo selection based on morphology or embryo selection based on PGT-A with next-generation sequencing. Inclusion criteria were the diagnosis of subfertility, undergoing their first IVF cycle, female age of 20 to 37, and the availability of 3 or more good-quality blastocysts.

On day 5 of embryo culture, patients with 3 or more blastocysts were randomly assigned in a 1:1 ratio to either the PGT-A group or conventional IVF. All embryos were then frozen, and patients subsequently underwent frozen embryo transfer of a single blastocyst, selected based on either morphology or euploid result by PGT-A. If the initial transfer did not result in a live birth, and there were remaining transferable embryos (either a euploid embryo in the PGT-A group or a morphologically transferable embryo in the conventional IVF group), patients underwent successive frozen embryo transfers until either there was a live birth or no more embryos were available for transfer.

The study’s primary outcome was the cumulative live birth rate per randomly assigned patient that resulted from up to 3 frozen embryo transfer cycles within 1 year. There were 606 patients randomly assigned to the PGT-A group and 606 randomly assigned to the conventional IVF group.

In the PGT-A group, 468 women (77.2%) had live births; in the conventional IVF group, 496 women (81.8%) had live births. Women in the PGT-A group had a lower incidence of pregnancy loss compared with the conventional IVF group: 8.7% versus 12.6% (absolute difference of -3.9%; 95% confidence interval [CI], -7.5 to -0.2). There was no difference in obstetric and neonatal outcomes between the 2 groups. The authors concluded that among women with 3 or more good-quality blastocysts, conventional IVF resulted in a cumulative live birth rate that was noninferior to that of the PGT-A group.

Some benefit shown with PGT-A

Although the study by Yan and colleagues did not show any benefit, and even a possible reduction, with regard to cumulative live birth rate for PGT-A, it did show a 4% reduction in clinical pregnancy loss when PGT-A was used. Furthermore, the study design has been criticized for performing PGT-A on only 3 blastocysts in the PGT-A group. It is quite conceivable that the PGT-A group would have had more euploid embryos available for transfer if the study design had included all the available embryos instead of only 3. On the other hand, one could argue that if the authors had extended the study to include all the available embryos, the conventional group would have also had more embryos for transfer and, therefore, more chances for pregnancy and live birth.

It is also important to recognize that only patients who had at least 3 embryos available for biopsy were included in this study, and therefore the results of this study cannot be extended to patients with fewer embryos, such as those with diminished ovarian reserve.

In summary, based on this study’s results, we may conclude that for the good-prognosis patients in the age group of 20 to 37 who have at least 3 embryos available for biopsy, PGT-A may reduce the miscarriage rate by about 4%, but this benefit comes at the expense of about a 4% reduction in the cumulative live birth rate. ●

Total fertility rate and fertility care: Demographic shifts and changing demands

Vollset SE, Goren E, Yuan C-W, et al. Fertility, mortality, migration, and population scenarios for 195 countries and territories from 2017 to 2100: a forecasting analysis for the Global Burden of Disease Study. Lancet. 2020;396:1285-1306.

The total fertility rate (TFR) globally is decreasing rapidly, and in the United States it is now 1.8 births per woman, well below the required replacement rate of 2.1 that maintains the population.¹ These reduced TFRs result in significant demographic shifts that affect the economy, workforce, society, health care needs, environment, and geopolitical standing of every country. These changes also will shift demands for the volume and type of services delivered by women’s health care clinicians.

In addition to the TFR, mortality rates and migration rates play essential roles in determining a country’s population.² Anticipation and planning for these population and health care service changes by each country’s government, business, professionals, and other stakeholders are imperative to manage their impact and optimize quality of life.

Illustration: Kimberly Martens for OBG Management

US standings in projected population and economic growth

The US population is predicted to peak at 364 million in 2062 and decrease to 336 million in 2100, at which time it will be the fourth largest country in the world, according to a forecasting analysis by Vollset and colleagues.¹ China is expected to become the biggest economy in the world in 2035, but this is predicted to change because of its decreasing population so that by 2098 the United States will again be the country with the largest economy (FIGURE 1).¹

For the United States to maintain its economic and geopolitical standing, it is important to have policies that promote families. Other countries, especially in northern Europe, have implemented such policies. These include education of the population,economic incentives to create families, extended day care, and favorable tax policies.³ They also include increased access to family-forming fertility care. Such policies in Denmark have resulted in approximately 10% of all children being born from assisted reproductive technology (ART), compared with about 1.5% in the United States. Other countries have similar policies and success in increasing the number of children born from ART.

In the United States, the American Society for Reproductive Medicine (ASRM), RESOLVE: the National Infertility Association, the American Medical Women’s Association (AMWA), and others are promoting the need for increased access to fertility care and family-forming resources, primarily through family-forming benefits provided by companies.⁴ Such benefits are critical since the primary reason most people do not undergo fertility care is a lack of affordability. Only 1 person in 4 in the United States who needs fertility care receives treatment. Increased access would result in more babies being born to help address the reduced TFR.

Educational access, contraceptive goals, and access to fertility care

Continued trends in women’s educational attainment and access to contraception will hasten declines in the fertility rate and slow population growth (TABLE).¹ These educational and contraceptive goals also must be pursued so that every person can achieve their individual reproductive life goals of having a family if and when they want to have a family. In addition to helping address the decreasing TFR, there is a fundamental right to found a family, as stated in the United Nations charter. It is a matter of social justice and equity that everyone who wants to have a family can access reproductive care on a nondiscriminatory basis when needed.

While the need for more and better insurance coverage for infertility has been well documented for many years, the decreasing TFR in the United States is an additional compelling reason that government, business, and other stakeholders should continue to increase access to fertility benefits and care. Women’s health care clinicians are encouraged to support these initiatives that also improve quality of life, equity, and social justice.

Continue to: A new comprehensive ovulatory disorders classification system developed by FIGO...

Munro MG, Balen AH, Cho S, et al; FIGO Committee on Menstrual Disorders and Related Health Impacts, and FIGO Committee on Reproductive Medicine, Endocrinology, and Infertility. The FIGO ovulatory disorders classification system. Fertil Steril. 2022;118:768-786.

Ovulatory disorders are well-recognized and common causes of infertility and abnormal uterine bleeding (AUB). Ovulatory disorders occur on a spectrum, with the most severe form being anovulation, and comprise a heterogeneous group that has been classically categorized based on an initial monograph published by the World Health Organization (WHO) in 1973. That classification was based on gonadotropin levels and categorized these disorders into 3 groups: 1) hypogonadotropic (such as hypothalamic amenorrhea), 2) eugonadotropic (such as polycystic ovary syndrome [PCOS]), and 3) hypergonadotropic (such as primary ovarian insufficiency). This initial classification was the subject of several subsequent iterations and modifications over the past 50 years; for example, at one point, ovulatory disorder caused by hyperprolactinemia was added as a separate fourth category. However, due to advances in endocrine assays, imaging technology, and genetics, our understanding of ovulatory disorders has expanded remarkably over the past several decades.

Previous FIGO classifications

Considering the emergent complexity of these disorders and the limitations of the original WHO classification to capture these subtleties adequately, the International Federation of Gynecology and Obstetrics (FIGO) recently developed and published a new classification system for ovulatory disorders.⁵ This new system was designed using a meticulously followed Delphi process with inputs from a diverse group of national and international professional organizations, subspecialty societies, specialty journals, recognized experts in the field, and lay individuals interested in the subject matter.

Of note, FIGO had previously published classification systems for nongestational normal and abnormal uterine bleeding in the reproductive years (FIGO AUB System 1),as well as a subsequent classification system that described potential causes of AUB symptoms (FIGO AUB System 2), with the 9 categories arranged under the acronym PALM-COEIN (Polyp, Adenomyosis, Leiomyoma, Malignancy–Coagulopathy, Ovulatory dysfunction, Endometrial disorders, Iatrogenic, and Not otherwise classified). This new FIGO classification of ovulatory disorders can be viewed as a continuation of the previous initiatives and aims to further categorize the subgroup of AUB-O (AUB with ovulatory disorders). However, it is important to recognize that while most ovulatory disorders manifest with the symptoms of AUB, the absence of AUB symptoms does not necessarily preclude ovulatory disorders.

New system uses a 3-tier approach

The new FIGO classification system for ovulatory disorders has adopted a 3-tier system.

The first tier is based on the anatomic components of the hypothalamic-pituitary-ovarian (HPO) axis and is referred to with the acronym HyPO, for Hypothalamic-Pituitary-Ovarian. Recognizing that PCOS refers to a distinct spectrum of conditions that share a variable combination of signs and symptoms caused to varying degrees by different pathophysiologic mechanisms that involve inherent ovarian follicular dysfunction, neuroendocrine dysfunction, insulin resistance, and androgen excess, it is categorized in a separate class of its own in the first tier, referred to with the letter P.

Adding PCOS to the anatomical categories referred to by HyPO, the first tier is overall referred to with the acronym HyPO-P (FIGURE 2).⁵

The second tier of stratification provides further etiologic details for any of the primary 3 anatomic classifications of hypothalamic, pituitary, and ovarian. These etiologies are arranged in 10 distinct groups under the mnemonic GAIN-FIT-PIE, which stands for Genetic, Autoimmune, Iatrogenic, Neoplasm; Functional, Infectious/inflammatory, Trauma and vascular; and Physiological, Idiopathic, Endocrine.

The third tier of the system refers to the specific clinical diagnosis. For example, an individual with Kallmann syndrome would be categorized as having type I (hypothalamic), Genetic, Kallmann syndrome, and an individual with PCOS would be categorized simply as having type IV, PCOS.

Continue to: Live birth rate with conventional IVF shown noninferior to that with PGT-A...

Yan J, Qin Y, Zhao H, et al. Live birth with or without preimplantation genetic testing for aneuploidy. N Engl J Med. 2021;385:2047-2058.

Preimplantation genetic testing for aneuploidy (PGT-A) is increasingly used in many in vitro fertilization (IVF) cycles in the United States. Based on data from the Centers for Disease Control and Prevention, 43.8% of embryo transfers in the United States in 2019 included at least 1 PGT-A–tested embryo.⁶ Despite this widespread use, however, there are still no robust clinical data for PGT-A’s efficacy and safety, and the guidelines published by the ASRM do not recommend its routine use in all IVF cycles.⁷ In the past 2 to 3 years, several large studies have raised questions about the reported benefit of this technology.^8,9

Details of the trial

In a multicenter, controlled, noninferiority trial conducted by Yan and colleagues, 1,212 subfertile women were randomly assigned to either conventional IVF with embryo selection based on morphology or embryo selection based on PGT-A with next-generation sequencing. Inclusion criteria were the diagnosis of subfertility, undergoing their first IVF cycle, female age of 20 to 37, and the availability of 3 or more good-quality blastocysts.

On day 5 of embryo culture, patients with 3 or more blastocysts were randomly assigned in a 1:1 ratio to either the PGT-A group or conventional IVF. All embryos were then frozen, and patients subsequently underwent frozen embryo transfer of a single blastocyst, selected based on either morphology or euploid result by PGT-A. If the initial transfer did not result in a live birth, and there were remaining transferable embryos (either a euploid embryo in the PGT-A group or a morphologically transferable embryo in the conventional IVF group), patients underwent successive frozen embryo transfers until either there was a live birth or no more embryos were available for transfer.

The study’s primary outcome was the cumulative live birth rate per randomly assigned patient that resulted from up to 3 frozen embryo transfer cycles within 1 year. There were 606 patients randomly assigned to the PGT-A group and 606 randomly assigned to the conventional IVF group.

In the PGT-A group, 468 women (77.2%) had live births; in the conventional IVF group, 496 women (81.8%) had live births. Women in the PGT-A group had a lower incidence of pregnancy loss compared with the conventional IVF group: 8.7% versus 12.6% (absolute difference of -3.9%; 95% confidence interval [CI], -7.5 to -0.2). There was no difference in obstetric and neonatal outcomes between the 2 groups. The authors concluded that among women with 3 or more good-quality blastocysts, conventional IVF resulted in a cumulative live birth rate that was noninferior to that of the PGT-A group.

Some benefit shown with PGT-A

Although the study by Yan and colleagues did not show any benefit, and even a possible reduction, with regard to cumulative live birth rate for PGT-A, it did show a 4% reduction in clinical pregnancy loss when PGT-A was used. Furthermore, the study design has been criticized for performing PGT-A on only 3 blastocysts in the PGT-A group. It is quite conceivable that the PGT-A group would have had more euploid embryos available for transfer if the study design had included all the available embryos instead of only 3. On the other hand, one could argue that if the authors had extended the study to include all the available embryos, the conventional group would have also had more embryos for transfer and, therefore, more chances for pregnancy and live birth.

It is also important to recognize that only patients who had at least 3 embryos available for biopsy were included in this study, and therefore the results of this study cannot be extended to patients with fewer embryos, such as those with diminished ovarian reserve.

In summary, based on this study’s results, we may conclude that for the good-prognosis patients in the age group of 20 to 37 who have at least 3 embryos available for biopsy, PGT-A may reduce the miscarriage rate by about 4%, but this benefit comes at the expense of about a 4% reduction in the cumulative live birth rate. ●

Total fertility rate and fertility care: Demographic shifts and changing demands

Vollset SE, Goren E, Yuan C-W, et al. Fertility, mortality, migration, and population scenarios for 195 countries and territories from 2017 to 2100: a forecasting analysis for the Global Burden of Disease Study. Lancet. 2020;396:1285-1306.

The total fertility rate (TFR) globally is decreasing rapidly, and in the United States it is now 1.8 births per woman, well below the required replacement rate of 2.1 that maintains the population.¹ These reduced TFRs result in significant demographic shifts that affect the economy, workforce, society, health care needs, environment, and geopolitical standing of every country. These changes also will shift demands for the volume and type of services delivered by women’s health care clinicians.

In addition to the TFR, mortality rates and migration rates play essential roles in determining a country’s population.² Anticipation and planning for these population and health care service changes by each country’s government, business, professionals, and other stakeholders are imperative to manage their impact and optimize quality of life.

Illustration: Kimberly Martens for OBG Management

US standings in projected population and economic growth

The US population is predicted to peak at 364 million in 2062 and decrease to 336 million in 2100, at which time it will be the fourth largest country in the world, according to a forecasting analysis by Vollset and colleagues.¹ China is expected to become the biggest economy in the world in 2035, but this is predicted to change because of its decreasing population so that by 2098 the United States will again be the country with the largest economy (FIGURE 1).¹

For the United States to maintain its economic and geopolitical standing, it is important to have policies that promote families. Other countries, especially in northern Europe, have implemented such policies. These include education of the population,economic incentives to create families, extended day care, and favorable tax policies.³ They also include increased access to family-forming fertility care. Such policies in Denmark have resulted in approximately 10% of all children being born from assisted reproductive technology (ART), compared with about 1.5% in the United States. Other countries have similar policies and success in increasing the number of children born from ART.

In the United States, the American Society for Reproductive Medicine (ASRM), RESOLVE: the National Infertility Association, the American Medical Women’s Association (AMWA), and others are promoting the need for increased access to fertility care and family-forming resources, primarily through family-forming benefits provided by companies.⁴ Such benefits are critical since the primary reason most people do not undergo fertility care is a lack of affordability. Only 1 person in 4 in the United States who needs fertility care receives treatment. Increased access would result in more babies being born to help address the reduced TFR.

Educational access, contraceptive goals, and access to fertility care

Continued trends in women’s educational attainment and access to contraception will hasten declines in the fertility rate and slow population growth (TABLE).¹ These educational and contraceptive goals also must be pursued so that every person can achieve their individual reproductive life goals of having a family if and when they want to have a family. In addition to helping address the decreasing TFR, there is a fundamental right to found a family, as stated in the United Nations charter. It is a matter of social justice and equity that everyone who wants to have a family can access reproductive care on a nondiscriminatory basis when needed.

While the need for more and better insurance coverage for infertility has been well documented for many years, the decreasing TFR in the United States is an additional compelling reason that government, business, and other stakeholders should continue to increase access to fertility benefits and care. Women’s health care clinicians are encouraged to support these initiatives that also improve quality of life, equity, and social justice.

Continue to: A new comprehensive ovulatory disorders classification system developed by FIGO...

Munro MG, Balen AH, Cho S, et al; FIGO Committee on Menstrual Disorders and Related Health Impacts, and FIGO Committee on Reproductive Medicine, Endocrinology, and Infertility. The FIGO ovulatory disorders classification system. Fertil Steril. 2022;118:768-786.

Ovulatory disorders are well-recognized and common causes of infertility and abnormal uterine bleeding (AUB). Ovulatory disorders occur on a spectrum, with the most severe form being anovulation, and comprise a heterogeneous group that has been classically categorized based on an initial monograph published by the World Health Organization (WHO) in 1973. That classification was based on gonadotropin levels and categorized these disorders into 3 groups: 1) hypogonadotropic (such as hypothalamic amenorrhea), 2) eugonadotropic (such as polycystic ovary syndrome [PCOS]), and 3) hypergonadotropic (such as primary ovarian insufficiency). This initial classification was the subject of several subsequent iterations and modifications over the past 50 years; for example, at one point, ovulatory disorder caused by hyperprolactinemia was added as a separate fourth category. However, due to advances in endocrine assays, imaging technology, and genetics, our understanding of ovulatory disorders has expanded remarkably over the past several decades.

Previous FIGO classifications

Considering the emergent complexity of these disorders and the limitations of the original WHO classification to capture these subtleties adequately, the International Federation of Gynecology and Obstetrics (FIGO) recently developed and published a new classification system for ovulatory disorders.⁵ This new system was designed using a meticulously followed Delphi process with inputs from a diverse group of national and international professional organizations, subspecialty societies, specialty journals, recognized experts in the field, and lay individuals interested in the subject matter.

Of note, FIGO had previously published classification systems for nongestational normal and abnormal uterine bleeding in the reproductive years (FIGO AUB System 1),as well as a subsequent classification system that described potential causes of AUB symptoms (FIGO AUB System 2), with the 9 categories arranged under the acronym PALM-COEIN (Polyp, Adenomyosis, Leiomyoma, Malignancy–Coagulopathy, Ovulatory dysfunction, Endometrial disorders, Iatrogenic, and Not otherwise classified). This new FIGO classification of ovulatory disorders can be viewed as a continuation of the previous initiatives and aims to further categorize the subgroup of AUB-O (AUB with ovulatory disorders). However, it is important to recognize that while most ovulatory disorders manifest with the symptoms of AUB, the absence of AUB symptoms does not necessarily preclude ovulatory disorders.

New system uses a 3-tier approach

The new FIGO classification system for ovulatory disorders has adopted a 3-tier system.

The first tier is based on the anatomic components of the hypothalamic-pituitary-ovarian (HPO) axis and is referred to with the acronym HyPO, for Hypothalamic-Pituitary-Ovarian. Recognizing that PCOS refers to a distinct spectrum of conditions that share a variable combination of signs and symptoms caused to varying degrees by different pathophysiologic mechanisms that involve inherent ovarian follicular dysfunction, neuroendocrine dysfunction, insulin resistance, and androgen excess, it is categorized in a separate class of its own in the first tier, referred to with the letter P.

Adding PCOS to the anatomical categories referred to by HyPO, the first tier is overall referred to with the acronym HyPO-P (FIGURE 2).⁵

The second tier of stratification provides further etiologic details for any of the primary 3 anatomic classifications of hypothalamic, pituitary, and ovarian. These etiologies are arranged in 10 distinct groups under the mnemonic GAIN-FIT-PIE, which stands for Genetic, Autoimmune, Iatrogenic, Neoplasm; Functional, Infectious/inflammatory, Trauma and vascular; and Physiological, Idiopathic, Endocrine.

The third tier of the system refers to the specific clinical diagnosis. For example, an individual with Kallmann syndrome would be categorized as having type I (hypothalamic), Genetic, Kallmann syndrome, and an individual with PCOS would be categorized simply as having type IV, PCOS.

Continue to: Live birth rate with conventional IVF shown noninferior to that with PGT-A...

Yan J, Qin Y, Zhao H, et al. Live birth with or without preimplantation genetic testing for aneuploidy. N Engl J Med. 2021;385:2047-2058.

Preimplantation genetic testing for aneuploidy (PGT-A) is increasingly used in many in vitro fertilization (IVF) cycles in the United States. Based on data from the Centers for Disease Control and Prevention, 43.8% of embryo transfers in the United States in 2019 included at least 1 PGT-A–tested embryo.⁶ Despite this widespread use, however, there are still no robust clinical data for PGT-A’s efficacy and safety, and the guidelines published by the ASRM do not recommend its routine use in all IVF cycles.⁷ In the past 2 to 3 years, several large studies have raised questions about the reported benefit of this technology.^8,9

Details of the trial

In a multicenter, controlled, noninferiority trial conducted by Yan and colleagues, 1,212 subfertile women were randomly assigned to either conventional IVF with embryo selection based on morphology or embryo selection based on PGT-A with next-generation sequencing. Inclusion criteria were the diagnosis of subfertility, undergoing their first IVF cycle, female age of 20 to 37, and the availability of 3 or more good-quality blastocysts.

On day 5 of embryo culture, patients with 3 or more blastocysts were randomly assigned in a 1:1 ratio to either the PGT-A group or conventional IVF. All embryos were then frozen, and patients subsequently underwent frozen embryo transfer of a single blastocyst, selected based on either morphology or euploid result by PGT-A. If the initial transfer did not result in a live birth, and there were remaining transferable embryos (either a euploid embryo in the PGT-A group or a morphologically transferable embryo in the conventional IVF group), patients underwent successive frozen embryo transfers until either there was a live birth or no more embryos were available for transfer.

The study’s primary outcome was the cumulative live birth rate per randomly assigned patient that resulted from up to 3 frozen embryo transfer cycles within 1 year. There were 606 patients randomly assigned to the PGT-A group and 606 randomly assigned to the conventional IVF group.

In the PGT-A group, 468 women (77.2%) had live births; in the conventional IVF group, 496 women (81.8%) had live births. Women in the PGT-A group had a lower incidence of pregnancy loss compared with the conventional IVF group: 8.7% versus 12.6% (absolute difference of -3.9%; 95% confidence interval [CI], -7.5 to -0.2). There was no difference in obstetric and neonatal outcomes between the 2 groups. The authors concluded that among women with 3 or more good-quality blastocysts, conventional IVF resulted in a cumulative live birth rate that was noninferior to that of the PGT-A group.

Some benefit shown with PGT-A

Although the study by Yan and colleagues did not show any benefit, and even a possible reduction, with regard to cumulative live birth rate for PGT-A, it did show a 4% reduction in clinical pregnancy loss when PGT-A was used. Furthermore, the study design has been criticized for performing PGT-A on only 3 blastocysts in the PGT-A group. It is quite conceivable that the PGT-A group would have had more euploid embryos available for transfer if the study design had included all the available embryos instead of only 3. On the other hand, one could argue that if the authors had extended the study to include all the available embryos, the conventional group would have also had more embryos for transfer and, therefore, more chances for pregnancy and live birth.

It is also important to recognize that only patients who had at least 3 embryos available for biopsy were included in this study, and therefore the results of this study cannot be extended to patients with fewer embryos, such as those with diminished ovarian reserve.

In summary, based on this study’s results, we may conclude that for the good-prognosis patients in the age group of 20 to 37 who have at least 3 embryos available for biopsy, PGT-A may reduce the miscarriage rate by about 4%, but this benefit comes at the expense of about a 4% reduction in the cumulative live birth rate. ●

Due to an increasing incidence of colon cancer among men and women aged 45 and younger, in 2018 the American Cancer Society, and in 2021 the US Preventive Services Task Force, recommended that screening for colon cancer begin at age 45 rather than age 50. More than half of the US population reports being up to date with these screening guidelines.

Source: Barbieri R. Colorectal cancer screening, 2021: An update. OBG Manag. 2021;33:9-11, 15. doi: 10.12788/obgm.0119.

Due to an increasing incidence of colon cancer among men and women aged 45 and younger, in 2018 the American Cancer Society, and in 2021 the US Preventive Services Task Force, recommended that screening for colon cancer begin at age 45 rather than age 50. More than half of the US population reports being up to date with these screening guidelines.

Source: Barbieri R. Colorectal cancer screening, 2021: An update. OBG Manag. 2021;33:9-11, 15. doi: 10.12788/obgm.0119.

Due to an increasing incidence of colon cancer among men and women aged 45 and younger, in 2018 the American Cancer Society, and in 2021 the US Preventive Services Task Force, recommended that screening for colon cancer begin at age 45 rather than age 50. More than half of the US population reports being up to date with these screening guidelines.

Source: Barbieri R. Colorectal cancer screening, 2021: An update. OBG Manag. 2021;33:9-11, 15. doi: 10.12788/obgm.0119.

Medical library access

During most of my clinical career I had an affiliation with a local medical school as a “Clinical Instructor” and then “Assistant Clinical Professor.” In addition to teaching medical students and residents from that institution that rotated through my hospital, it also gave me certain privileges, the most important of which was access to that institution’s electronic medical library. Using that access, even as an “LMD,” I have been able to contribute to the medical literature on subjects of interest to me and to others in my specialty. 

Recently, now as an older clinician, I gave up my hospital privileges, although I continue my office practice. Giving up my hospital privileges meant that I no longer qualified as a faculty member—and therefore lost online access to the medical library. Still wishing to continue my medical writing, I have attempted to attain access to the medical literature by special request to that library, by contacting my state medical society, by contacting my national specialty organization, by contacting the department chair at the institution to which I had been affiliated, and by calling the Dean of the medical school to which my hospital was affiliated. Although meaning well, none was able to get me access to an online medical library. Thus, I am greatly hampered in my attempts to do research and to continue to write further papers on those areas in which I have previously published. 

Is there no remedy for this? Should all clinicians who “age out” of institutional affiliations no longer be able to pursue research interests? And what about community physicians who have no academic affiliations? Can they not access the latest information they need to practice evidence-based, up-to-date medicine? 

It makes no sense to me that access to the latest and most current aspects of medical care should be withheld from any clinician. For every clinician not to have access to such medical knowledge does a disservice to all those practicing medicine who wish to keep up to date and to all patients of American clinicians whose providers are prevented from practicing the best, evidence-based care.

Henry Lerner, MD

Boston, Massachusetts

Medical library access

During most of my clinical career I had an affiliation with a local medical school as a “Clinical Instructor” and then “Assistant Clinical Professor.” In addition to teaching medical students and residents from that institution that rotated through my hospital, it also gave me certain privileges, the most important of which was access to that institution’s electronic medical library. Using that access, even as an “LMD,” I have been able to contribute to the medical literature on subjects of interest to me and to others in my specialty. 

Recently, now as an older clinician, I gave up my hospital privileges, although I continue my office practice. Giving up my hospital privileges meant that I no longer qualified as a faculty member—and therefore lost online access to the medical library. Still wishing to continue my medical writing, I have attempted to attain access to the medical literature by special request to that library, by contacting my state medical society, by contacting my national specialty organization, by contacting the department chair at the institution to which I had been affiliated, and by calling the Dean of the medical school to which my hospital was affiliated. Although meaning well, none was able to get me access to an online medical library. Thus, I am greatly hampered in my attempts to do research and to continue to write further papers on those areas in which I have previously published. 

Is there no remedy for this? Should all clinicians who “age out” of institutional affiliations no longer be able to pursue research interests? And what about community physicians who have no academic affiliations? Can they not access the latest information they need to practice evidence-based, up-to-date medicine? 

It makes no sense to me that access to the latest and most current aspects of medical care should be withheld from any clinician. For every clinician not to have access to such medical knowledge does a disservice to all those practicing medicine who wish to keep up to date and to all patients of American clinicians whose providers are prevented from practicing the best, evidence-based care.

Henry Lerner, MD

Boston, Massachusetts

Medical library access

During most of my clinical career I had an affiliation with a local medical school as a “Clinical Instructor” and then “Assistant Clinical Professor.” In addition to teaching medical students and residents from that institution that rotated through my hospital, it also gave me certain privileges, the most important of which was access to that institution’s electronic medical library. Using that access, even as an “LMD,” I have been able to contribute to the medical literature on subjects of interest to me and to others in my specialty. 

Recently, now as an older clinician, I gave up my hospital privileges, although I continue my office practice. Giving up my hospital privileges meant that I no longer qualified as a faculty member—and therefore lost online access to the medical library. Still wishing to continue my medical writing, I have attempted to attain access to the medical literature by special request to that library, by contacting my state medical society, by contacting my national specialty organization, by contacting the department chair at the institution to which I had been affiliated, and by calling the Dean of the medical school to which my hospital was affiliated. Although meaning well, none was able to get me access to an online medical library. Thus, I am greatly hampered in my attempts to do research and to continue to write further papers on those areas in which I have previously published. 

Is there no remedy for this? Should all clinicians who “age out” of institutional affiliations no longer be able to pursue research interests? And what about community physicians who have no academic affiliations? Can they not access the latest information they need to practice evidence-based, up-to-date medicine? 

It makes no sense to me that access to the latest and most current aspects of medical care should be withheld from any clinician. For every clinician not to have access to such medical knowledge does a disservice to all those practicing medicine who wish to keep up to date and to all patients of American clinicians whose providers are prevented from practicing the best, evidence-based care.

Henry Lerner, MD

Boston, Massachusetts

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Riding alongside known STIs, this historically elusive microbe may have often been the underlying cause of a variety of symptoms. In this supplement to OBG Management Dr. Kyle Bukowski discusses how to meet the challenge presented by this not-so-new microbe while helping foster regular STI testing, and encourage patients to seek care when symptoms occur.

Click Here to Read the Supplement

Riding alongside known STIs, this historically elusive microbe may have often been the underlying cause of a variety of symptoms. In this supplement to OBG Management Dr. Kyle Bukowski discusses how to meet the challenge presented by this not-so-new microbe while helping foster regular STI testing, and encourage patients to seek care when symptoms occur.

Click Here to Read the Supplement

Riding alongside known STIs, this historically elusive microbe may have often been the underlying cause of a variety of symptoms. In this supplement to OBG Management Dr. Kyle Bukowski discusses how to meet the challenge presented by this not-so-new microbe while helping foster regular STI testing, and encourage patients to seek care when symptoms occur.

Click Here to Read the Supplement