Key clinical point: Administration of gonadotropin-releasing hormone analogs (GnRHa) with chemotherapy reduced the risk for premature ovarian insufficiency (POI) in premenopausal women with breast cancer.

Major finding: At 12 months after chemotherapy, POI was reported by 10.3% vs 44.5% of patients in the GnRHa + chemotherapy vs chemotherapy-only group (odds ratio, 0.23; P < .001). No serious adverse events were reported.

Study details: Findings are from a phase 3 superiority trial including 330 premenopausal women with stages I-III operable breast cancer who were randomly assigned to GnRHa (3.6 mg of goserelin or 3.75 mg of leuprorelin) + chemotherapy or chemotherapy alone.

Disclosures: This study was funded by the Science and Technology Commission, Shanghai, and Zhejiang Medical Association. Dr. Zong reported receiving grants from the Science and Technology Commission of Shanghai Municipality.

Source: Zong X et al. JAMA Oncol. 2021 Dec 30. doi: 10.1001/jamaoncol.2021.6214.

Key clinical point: Administration of gonadotropin-releasing hormone analogs (GnRHa) with chemotherapy reduced the risk for premature ovarian insufficiency (POI) in premenopausal women with breast cancer.

Major finding: At 12 months after chemotherapy, POI was reported by 10.3% vs 44.5% of patients in the GnRHa + chemotherapy vs chemotherapy-only group (odds ratio, 0.23; P < .001). No serious adverse events were reported.

Study details: Findings are from a phase 3 superiority trial including 330 premenopausal women with stages I-III operable breast cancer who were randomly assigned to GnRHa (3.6 mg of goserelin or 3.75 mg of leuprorelin) + chemotherapy or chemotherapy alone.

Disclosures: This study was funded by the Science and Technology Commission, Shanghai, and Zhejiang Medical Association. Dr. Zong reported receiving grants from the Science and Technology Commission of Shanghai Municipality.

Source: Zong X et al. JAMA Oncol. 2021 Dec 30. doi: 10.1001/jamaoncol.2021.6214.

Key clinical point: Administration of gonadotropin-releasing hormone analogs (GnRHa) with chemotherapy reduced the risk for premature ovarian insufficiency (POI) in premenopausal women with breast cancer.

Major finding: At 12 months after chemotherapy, POI was reported by 10.3% vs 44.5% of patients in the GnRHa + chemotherapy vs chemotherapy-only group (odds ratio, 0.23; P < .001). No serious adverse events were reported.

Study details: Findings are from a phase 3 superiority trial including 330 premenopausal women with stages I-III operable breast cancer who were randomly assigned to GnRHa (3.6 mg of goserelin or 3.75 mg of leuprorelin) + chemotherapy or chemotherapy alone.

Disclosures: This study was funded by the Science and Technology Commission, Shanghai, and Zhejiang Medical Association. Dr. Zong reported receiving grants from the Science and Technology Commission of Shanghai Municipality.

Source: Zong X et al. JAMA Oncol. 2021 Dec 30. doi: 10.1001/jamaoncol.2021.6214.

Key clinical point: Residual cancer burden (RCB) after neoadjuvant chemotherapy was prognostic for event-free survival (EFS) in each hormone receptor (HR) and human epidermal growth factor receptor 2 (HER2) subtype of breast cancer.

Major finding: RCB was prognostic for EFS with the hazard ratio associated with each unit increase in RCB being 1.69 (P < .0001) for the overall population and ranging from 1.52 in HR-positive/HER2-negative group to 2.09 in HR-negative/HER2-positive group (P < .0001 for all subtypes).

Study details: Findings are pooled analysis of 4 trials and 8 clinical cohorts, including 5,161 adult patients with primary stage I-III breast cancer treated with neoadjuvant chemotherapy followed by surgery.

Disclosures: This study was funded by the National Cancer Institute, USA. Some of the authors declared serving as a consultant, data and safety monitoring advisor, and/or receiving grants, funding, personal fees, travel support, and honoraria from several sources.

Source: Yau C et al. Lancet Oncol. 2021 Dec 10. doi: 10.1016/S1470-2045(21)00589-1.

Key clinical point: Residual cancer burden (RCB) after neoadjuvant chemotherapy was prognostic for event-free survival (EFS) in each hormone receptor (HR) and human epidermal growth factor receptor 2 (HER2) subtype of breast cancer.

Major finding: RCB was prognostic for EFS with the hazard ratio associated with each unit increase in RCB being 1.69 (P < .0001) for the overall population and ranging from 1.52 in HR-positive/HER2-negative group to 2.09 in HR-negative/HER2-positive group (P < .0001 for all subtypes).

Study details: Findings are pooled analysis of 4 trials and 8 clinical cohorts, including 5,161 adult patients with primary stage I-III breast cancer treated with neoadjuvant chemotherapy followed by surgery.

Disclosures: This study was funded by the National Cancer Institute, USA. Some of the authors declared serving as a consultant, data and safety monitoring advisor, and/or receiving grants, funding, personal fees, travel support, and honoraria from several sources.

Source: Yau C et al. Lancet Oncol. 2021 Dec 10. doi: 10.1016/S1470-2045(21)00589-1.

Key clinical point: Residual cancer burden (RCB) after neoadjuvant chemotherapy was prognostic for event-free survival (EFS) in each hormone receptor (HR) and human epidermal growth factor receptor 2 (HER2) subtype of breast cancer.

Major finding: RCB was prognostic for EFS with the hazard ratio associated with each unit increase in RCB being 1.69 (P < .0001) for the overall population and ranging from 1.52 in HR-positive/HER2-negative group to 2.09 in HR-negative/HER2-positive group (P < .0001 for all subtypes).

Study details: Findings are pooled analysis of 4 trials and 8 clinical cohorts, including 5,161 adult patients with primary stage I-III breast cancer treated with neoadjuvant chemotherapy followed by surgery.

Disclosures: This study was funded by the National Cancer Institute, USA. Some of the authors declared serving as a consultant, data and safety monitoring advisor, and/or receiving grants, funding, personal fees, travel support, and honoraria from several sources.

Source: Yau C et al. Lancet Oncol. 2021 Dec 10. doi: 10.1016/S1470-2045(21)00589-1.

A genetic risk factor could explain why some people lose their senses of smell and taste when they get infected with COVID-19, according to a new study published in the journal Nature Genetics

The finding could eventually help the 1.6 million people in the United States who still can’t smell or have had a change in their ability to smell more than 6 months after getting the coronavirus. The exact cause related to COVID-19 is still unknown, but researchers believe it could be because of damage in a part of the nose called the olfactory epithelium.

“How we get from infection to smell loss remains unclear,” Justin Turner, MD, an associate professor of otolaryngology at Vanderbilt University, Nashville, Tenn., told NBC News. Dr. Turner was not part of the research team.

“Early data suggest that supporting cells of the olfactory epithelium are the ones mostly being infected by the virus, and presumably this leads to the death of the neurons themselves,” he said. “But we don’t really, really know why and when that happens, and why it seems to preferentially happen in certain individuals.”

Researchers at 23andMe, a genomics and biotechnology company, did the study as part of a larger COVID-19 project, which includes people in the United States and the United Kingdom. They analyzed data from nearly 70,000 people who took online surveys after receiving a positive coronavirus test. Among those, 68% reported a loss of smell or taste as a symptom.

The study team compared the genetic differences between those who lost their sense of smell and taste and those who didn’t. They found that a location near two olfactory genes – UGT2A1 and UGT2A2 – is associated with COVID-19 loss of smell and taste. The genetic risk factor makes it 11% more likely for a person with COVID-19 to lose their sense of smell or taste.

The research team also found that women were 11% more likely than men to report a loss of smell and taste. About 73% of those who reported a loss of smell and taste were ages 26-35.

The researchers aren’t sure how the genes are involved, though they suspect that infected cells could lead to smell loss. Typically, the genes are expressed in tissue inside the nose involved with smell and play a role in processing things that have an odor. To use the findings, researchers need to learn more about the genes, how they are expressed, and what their functions are, NBC News reported.

The findings could help lead to treatments. Other research has shown that the loss of taste and smell is related to a “failure to protect the sensory cells of the nose and tongue from viral infection,” Danielle Reed, PhD, associate director of the Monell Chemical Senses Center in Philadelphia, told NBC News. She was not part of the research team but studies person-to-person differences in the loss of these senses because of COVID-19.

“This study suggests a different direction,” she said. “The pathways that break down the chemicals that cause taste and smell in the first place might be over or underactive, reducing or distorting the ability to taste and smell.”

A version of this article first appeared on WebMD.com.

A genetic risk factor could explain why some people lose their senses of smell and taste when they get infected with COVID-19, according to a new study published in the journal Nature Genetics

The finding could eventually help the 1.6 million people in the United States who still can’t smell or have had a change in their ability to smell more than 6 months after getting the coronavirus. The exact cause related to COVID-19 is still unknown, but researchers believe it could be because of damage in a part of the nose called the olfactory epithelium.

“How we get from infection to smell loss remains unclear,” Justin Turner, MD, an associate professor of otolaryngology at Vanderbilt University, Nashville, Tenn., told NBC News. Dr. Turner was not part of the research team.

“Early data suggest that supporting cells of the olfactory epithelium are the ones mostly being infected by the virus, and presumably this leads to the death of the neurons themselves,” he said. “But we don’t really, really know why and when that happens, and why it seems to preferentially happen in certain individuals.”

Researchers at 23andMe, a genomics and biotechnology company, did the study as part of a larger COVID-19 project, which includes people in the United States and the United Kingdom. They analyzed data from nearly 70,000 people who took online surveys after receiving a positive coronavirus test. Among those, 68% reported a loss of smell or taste as a symptom.

The study team compared the genetic differences between those who lost their sense of smell and taste and those who didn’t. They found that a location near two olfactory genes – UGT2A1 and UGT2A2 – is associated with COVID-19 loss of smell and taste. The genetic risk factor makes it 11% more likely for a person with COVID-19 to lose their sense of smell or taste.

The research team also found that women were 11% more likely than men to report a loss of smell and taste. About 73% of those who reported a loss of smell and taste were ages 26-35.

The researchers aren’t sure how the genes are involved, though they suspect that infected cells could lead to smell loss. Typically, the genes are expressed in tissue inside the nose involved with smell and play a role in processing things that have an odor. To use the findings, researchers need to learn more about the genes, how they are expressed, and what their functions are, NBC News reported.

The findings could help lead to treatments. Other research has shown that the loss of taste and smell is related to a “failure to protect the sensory cells of the nose and tongue from viral infection,” Danielle Reed, PhD, associate director of the Monell Chemical Senses Center in Philadelphia, told NBC News. She was not part of the research team but studies person-to-person differences in the loss of these senses because of COVID-19.

“This study suggests a different direction,” she said. “The pathways that break down the chemicals that cause taste and smell in the first place might be over or underactive, reducing or distorting the ability to taste and smell.”

A version of this article first appeared on WebMD.com.

A genetic risk factor could explain why some people lose their senses of smell and taste when they get infected with COVID-19, according to a new study published in the journal Nature Genetics

The finding could eventually help the 1.6 million people in the United States who still can’t smell or have had a change in their ability to smell more than 6 months after getting the coronavirus. The exact cause related to COVID-19 is still unknown, but researchers believe it could be because of damage in a part of the nose called the olfactory epithelium.

“How we get from infection to smell loss remains unclear,” Justin Turner, MD, an associate professor of otolaryngology at Vanderbilt University, Nashville, Tenn., told NBC News. Dr. Turner was not part of the research team.

“Early data suggest that supporting cells of the olfactory epithelium are the ones mostly being infected by the virus, and presumably this leads to the death of the neurons themselves,” he said. “But we don’t really, really know why and when that happens, and why it seems to preferentially happen in certain individuals.”

Researchers at 23andMe, a genomics and biotechnology company, did the study as part of a larger COVID-19 project, which includes people in the United States and the United Kingdom. They analyzed data from nearly 70,000 people who took online surveys after receiving a positive coronavirus test. Among those, 68% reported a loss of smell or taste as a symptom.

The study team compared the genetic differences between those who lost their sense of smell and taste and those who didn’t. They found that a location near two olfactory genes – UGT2A1 and UGT2A2 – is associated with COVID-19 loss of smell and taste. The genetic risk factor makes it 11% more likely for a person with COVID-19 to lose their sense of smell or taste.

The research team also found that women were 11% more likely than men to report a loss of smell and taste. About 73% of those who reported a loss of smell and taste were ages 26-35.

The researchers aren’t sure how the genes are involved, though they suspect that infected cells could lead to smell loss. Typically, the genes are expressed in tissue inside the nose involved with smell and play a role in processing things that have an odor. To use the findings, researchers need to learn more about the genes, how they are expressed, and what their functions are, NBC News reported.

The findings could help lead to treatments. Other research has shown that the loss of taste and smell is related to a “failure to protect the sensory cells of the nose and tongue from viral infection,” Danielle Reed, PhD, associate director of the Monell Chemical Senses Center in Philadelphia, told NBC News. She was not part of the research team but studies person-to-person differences in the loss of these senses because of COVID-19.

“This study suggests a different direction,” she said. “The pathways that break down the chemicals that cause taste and smell in the first place might be over or underactive, reducing or distorting the ability to taste and smell.”

A version of this article first appeared on WebMD.com.

A fourth shot of the COVID-19 vaccine boosts antibodies but doesn’t provide enough protection to prevent infections from the Omicron variant, according to new research at an Israeli hospital.

The preliminary results, released on Jan. 17, challenge the idea of giving a second booster dose to slow the spread of the coronavirus, according to USA Today.

“Despite increased antibody levels, the fourth vaccine only offers a partial defense against the virus,” Gili Regev-Yochay, MD, director of the hospital’s infection prevention and control units, told reporters.

“The vaccines, which were more effective against previous variants, offer less protection versus Omicron,” she said.

In a clinical trial, 274 medical workers at Sheba Medical Center near Tel Aviv received a fourth vaccine dose in December – 154 got the Pfizer vaccine and 120 got the Moderna vaccine – after previously getting three Pfizer shots.

Both groups received a boost in antibodies that was “slightly higher” than after the third shot, Dr. Regev-Yochay said. But when compared with a control group that didn’t receive the fourth dose, the extra boost didn’t prevent the spread of Omicron.

“We see many infected with Omicron who received the fourth dose,” Dr. Regev-Yochay said. “Granted, a bit less than in the control group, but still a lot of infections.”

Some public health officials in Israel say the campaign for fourth doses is still worthwhile, according to The Times of Israel. The vaccine still works well against the Alpha and Delta variants, Dr. Regev-Yochay said, and a fourth shot should go to older adults and those who face higher risks for severe COVID-19.

Hours after releasing the preliminary results, Sheba Medical Center published a statement calling for “continuing the vaccination drive for risk groups at this time, even though the vaccine doesn’t provide optimal protection against getting infected with the variant.” News outlets reported that the hospital was pressured into issuing the statement after Israel’s Health Ministry didn’t like the release of the early study results, The Times of Israel reported.

The second booster “returns the level of antibodies to what it was at the beginning of the third booster,” Nachman Ash, MD, director of Israel’s Health Ministry, told Channel 13 TV in Israel, according to The Associated Press.

“That has great importance, especially among the older population,” he said.

As of Sunday, more than 500,000 people in Israel had received fourth doses since the country began offering them last month to medical workers, immunocompromised patients, and people ages 60 years and older, the AP reported. At the same time, the country has faced a recent coronavirus surge that has led to record-breaking numbers of cases and rising hospitalizations.

On Tuesday, the Israeli government said it would shorten the mandatory quarantine period from 7 days to 5 days, the AP reported.

“This decision will enable us to continue safeguarding public health on the one hand and to keep the economy going at this time on the other, even though it is difficult, so that we can get through this wave safely,” Prime Minister Naftali Bennett said.

A version of this article first appeared on WebMD.com.

A fourth shot of the COVID-19 vaccine boosts antibodies but doesn’t provide enough protection to prevent infections from the Omicron variant, according to new research at an Israeli hospital.

The preliminary results, released on Jan. 17, challenge the idea of giving a second booster dose to slow the spread of the coronavirus, according to USA Today.

“Despite increased antibody levels, the fourth vaccine only offers a partial defense against the virus,” Gili Regev-Yochay, MD, director of the hospital’s infection prevention and control units, told reporters.

“The vaccines, which were more effective against previous variants, offer less protection versus Omicron,” she said.

In a clinical trial, 274 medical workers at Sheba Medical Center near Tel Aviv received a fourth vaccine dose in December – 154 got the Pfizer vaccine and 120 got the Moderna vaccine – after previously getting three Pfizer shots.

Both groups received a boost in antibodies that was “slightly higher” than after the third shot, Dr. Regev-Yochay said. But when compared with a control group that didn’t receive the fourth dose, the extra boost didn’t prevent the spread of Omicron.

“We see many infected with Omicron who received the fourth dose,” Dr. Regev-Yochay said. “Granted, a bit less than in the control group, but still a lot of infections.”

Some public health officials in Israel say the campaign for fourth doses is still worthwhile, according to The Times of Israel. The vaccine still works well against the Alpha and Delta variants, Dr. Regev-Yochay said, and a fourth shot should go to older adults and those who face higher risks for severe COVID-19.

Hours after releasing the preliminary results, Sheba Medical Center published a statement calling for “continuing the vaccination drive for risk groups at this time, even though the vaccine doesn’t provide optimal protection against getting infected with the variant.” News outlets reported that the hospital was pressured into issuing the statement after Israel’s Health Ministry didn’t like the release of the early study results, The Times of Israel reported.

The second booster “returns the level of antibodies to what it was at the beginning of the third booster,” Nachman Ash, MD, director of Israel’s Health Ministry, told Channel 13 TV in Israel, according to The Associated Press.

“That has great importance, especially among the older population,” he said.

As of Sunday, more than 500,000 people in Israel had received fourth doses since the country began offering them last month to medical workers, immunocompromised patients, and people ages 60 years and older, the AP reported. At the same time, the country has faced a recent coronavirus surge that has led to record-breaking numbers of cases and rising hospitalizations.

On Tuesday, the Israeli government said it would shorten the mandatory quarantine period from 7 days to 5 days, the AP reported.

“This decision will enable us to continue safeguarding public health on the one hand and to keep the economy going at this time on the other, even though it is difficult, so that we can get through this wave safely,” Prime Minister Naftali Bennett said.

A version of this article first appeared on WebMD.com.

A fourth shot of the COVID-19 vaccine boosts antibodies but doesn’t provide enough protection to prevent infections from the Omicron variant, according to new research at an Israeli hospital.

The preliminary results, released on Jan. 17, challenge the idea of giving a second booster dose to slow the spread of the coronavirus, according to USA Today.

“Despite increased antibody levels, the fourth vaccine only offers a partial defense against the virus,” Gili Regev-Yochay, MD, director of the hospital’s infection prevention and control units, told reporters.

“The vaccines, which were more effective against previous variants, offer less protection versus Omicron,” she said.

In a clinical trial, 274 medical workers at Sheba Medical Center near Tel Aviv received a fourth vaccine dose in December – 154 got the Pfizer vaccine and 120 got the Moderna vaccine – after previously getting three Pfizer shots.

Both groups received a boost in antibodies that was “slightly higher” than after the third shot, Dr. Regev-Yochay said. But when compared with a control group that didn’t receive the fourth dose, the extra boost didn’t prevent the spread of Omicron.

“We see many infected with Omicron who received the fourth dose,” Dr. Regev-Yochay said. “Granted, a bit less than in the control group, but still a lot of infections.”

Some public health officials in Israel say the campaign for fourth doses is still worthwhile, according to The Times of Israel. The vaccine still works well against the Alpha and Delta variants, Dr. Regev-Yochay said, and a fourth shot should go to older adults and those who face higher risks for severe COVID-19.

Hours after releasing the preliminary results, Sheba Medical Center published a statement calling for “continuing the vaccination drive for risk groups at this time, even though the vaccine doesn’t provide optimal protection against getting infected with the variant.” News outlets reported that the hospital was pressured into issuing the statement after Israel’s Health Ministry didn’t like the release of the early study results, The Times of Israel reported.

The second booster “returns the level of antibodies to what it was at the beginning of the third booster,” Nachman Ash, MD, director of Israel’s Health Ministry, told Channel 13 TV in Israel, according to The Associated Press.

“That has great importance, especially among the older population,” he said.

As of Sunday, more than 500,000 people in Israel had received fourth doses since the country began offering them last month to medical workers, immunocompromised patients, and people ages 60 years and older, the AP reported. At the same time, the country has faced a recent coronavirus surge that has led to record-breaking numbers of cases and rising hospitalizations.

On Tuesday, the Israeli government said it would shorten the mandatory quarantine period from 7 days to 5 days, the AP reported.

“This decision will enable us to continue safeguarding public health on the one hand and to keep the economy going at this time on the other, even though it is difficult, so that we can get through this wave safely,” Prime Minister Naftali Bennett said.

A version of this article first appeared on WebMD.com.

The Diagnosis: Coma Blisters

Histologic examination revealed pauci-inflammatory subepidermal blisters with swelling of eccrine cells, signaling impending gland necrosis (Figure). Direct immunofluorescence testing on perilesional skin was negative. These findings would be inconsistent for diagnoses of edema blisters (most commonly seen in patients with an acute exacerbation of chronic lower extremity edema), friction blisters (intraepidermal blisters seen on histopathology), and bullous pemphigoid (linear IgG and/or C3 staining along the basement membrane zone on direct immunofluorescence testing is characteristic). Although eccrine gland alterations have been seen in toxic epidermal necrolysis,¹ the mucous membranes are involved in more than 90% of cases, making the diagnosis less likely. Furthermore, interface changes including prominent keratinocyte necrosis were not seen on histology.

Given the localized nature of the lesions in our patient and negative direct immunofluorescence studies, a diagnosis of coma blisters was made. Gentle wound care practices to the areas of denuded skin were implemented with complete resolution. The patient’s condition gradually improved, and she was extubated and discharged home.

Coma blisters are self-limited bullous lesions that have been reported in comatose patients as early as 1812 when Napoleon’s surgeon first noticed cutaneous blisters in comatose French soldiers being treated for carbon monoxide intoxication.² Since then, barbiturate overdose has remained the most common association, but coma blisters have occurred in the absence of specific drug exposures. Clinically, erythematous or violaceous plaques typically appear within 24 hours of drug ingestion, and progression to large tense bullae usually occurs within 48 to 72 hours of unconsciousness.³ They characteristically occur in pressure-dependent areas, but reports have shown lesions in non–pressure-dependent areas, including the penis and mouth.^1,4 Spontaneous resolution within 1 to 2 weeks is typical.⁵

The underlying pathogenesis remains controversial, as multiple mechanisms have been suggested, but clear causal evidence is lacking. The original proposition that direct effects of drug toxicity caused the cutaneous observations was later refuted after similar bullous lesions with eccrine gland necrosis were reported in comatose patients with neurologic conditions.⁶ It is largely accepted that pressure-induced local ischemia—proportional to the duration and amount of pressure—leads to tissue injury and is critical to the pathogenesis. During periods of ischemia, the most metabolically active tissues will undergo necrosis first; however, in eccrine glands, the earliest and most severe damage does not seem to occur in the most metabolically active cells.⁷ Additionally, this would not provide a viable explanation for coma blisters with eccrine gland necrosis developing in variable non–pressuredependent areas.

Moreover, drug- and non–drug-induced coma blisters can appear identically, but specific histopathologic differences have been reported. The most notable markers of non–drug-induced coma blisters are the absence of an inflammatory infiltrate in the epidermis and the presence of thrombosis in dermal vessels.⁸ Demonstration of necrotic changes in the secretory portion of the eccrine gland is considered the histopathologic hallmark for drug-induced coma blisters, but other findings can include subepidermal or intraepidermal bullae; perivascular infiltrates; and focal necrosis of the epidermis, dermis, subcutis, or epidermal appendages.⁶ Arteriolar wall necrosis and dermal inflammatory infiltrates also have been observed.⁷

Benzodiazepines have been widely prescribed and abused since their development, and overdose is much more common today than with barbiturates.⁹ Coma blisters rarely have been documented in the setting of isolated benzodiazepine overdose, and of the few cases, only one report implicated lorazepam as the causative agent.^4,7 The characteristic finding of eccrine gland necrosis consistently was seen in our patient. This case not only emphasizes the need for greater awareness of the association between benzodiazepine overdose and coma blisters but also the importance of clinical context when considering diagnoses. It is essential to note that coma blisters themselves are nonspecific, and the diagnosis of drug-induced coma blisters warrants confirmatory toxicologic analysis.

The Diagnosis: Coma Blisters

Histologic examination revealed pauci-inflammatory subepidermal blisters with swelling of eccrine cells, signaling impending gland necrosis (Figure). Direct immunofluorescence testing on perilesional skin was negative. These findings would be inconsistent for diagnoses of edema blisters (most commonly seen in patients with an acute exacerbation of chronic lower extremity edema), friction blisters (intraepidermal blisters seen on histopathology), and bullous pemphigoid (linear IgG and/or C3 staining along the basement membrane zone on direct immunofluorescence testing is characteristic). Although eccrine gland alterations have been seen in toxic epidermal necrolysis,¹ the mucous membranes are involved in more than 90% of cases, making the diagnosis less likely. Furthermore, interface changes including prominent keratinocyte necrosis were not seen on histology.

Given the localized nature of the lesions in our patient and negative direct immunofluorescence studies, a diagnosis of coma blisters was made. Gentle wound care practices to the areas of denuded skin were implemented with complete resolution. The patient’s condition gradually improved, and she was extubated and discharged home.

Coma blisters are self-limited bullous lesions that have been reported in comatose patients as early as 1812 when Napoleon’s surgeon first noticed cutaneous blisters in comatose French soldiers being treated for carbon monoxide intoxication.² Since then, barbiturate overdose has remained the most common association, but coma blisters have occurred in the absence of specific drug exposures. Clinically, erythematous or violaceous plaques typically appear within 24 hours of drug ingestion, and progression to large tense bullae usually occurs within 48 to 72 hours of unconsciousness.³ They characteristically occur in pressure-dependent areas, but reports have shown lesions in non–pressure-dependent areas, including the penis and mouth.^1,4 Spontaneous resolution within 1 to 2 weeks is typical.⁵

The underlying pathogenesis remains controversial, as multiple mechanisms have been suggested, but clear causal evidence is lacking. The original proposition that direct effects of drug toxicity caused the cutaneous observations was later refuted after similar bullous lesions with eccrine gland necrosis were reported in comatose patients with neurologic conditions.⁶ It is largely accepted that pressure-induced local ischemia—proportional to the duration and amount of pressure—leads to tissue injury and is critical to the pathogenesis. During periods of ischemia, the most metabolically active tissues will undergo necrosis first; however, in eccrine glands, the earliest and most severe damage does not seem to occur in the most metabolically active cells.⁷ Additionally, this would not provide a viable explanation for coma blisters with eccrine gland necrosis developing in variable non–pressuredependent areas.

Moreover, drug- and non–drug-induced coma blisters can appear identically, but specific histopathologic differences have been reported. The most notable markers of non–drug-induced coma blisters are the absence of an inflammatory infiltrate in the epidermis and the presence of thrombosis in dermal vessels.⁸ Demonstration of necrotic changes in the secretory portion of the eccrine gland is considered the histopathologic hallmark for drug-induced coma blisters, but other findings can include subepidermal or intraepidermal bullae; perivascular infiltrates; and focal necrosis of the epidermis, dermis, subcutis, or epidermal appendages.⁶ Arteriolar wall necrosis and dermal inflammatory infiltrates also have been observed.⁷

Benzodiazepines have been widely prescribed and abused since their development, and overdose is much more common today than with barbiturates.⁹ Coma blisters rarely have been documented in the setting of isolated benzodiazepine overdose, and of the few cases, only one report implicated lorazepam as the causative agent.^4,7 The characteristic finding of eccrine gland necrosis consistently was seen in our patient. This case not only emphasizes the need for greater awareness of the association between benzodiazepine overdose and coma blisters but also the importance of clinical context when considering diagnoses. It is essential to note that coma blisters themselves are nonspecific, and the diagnosis of drug-induced coma blisters warrants confirmatory toxicologic analysis.

The Diagnosis: Coma Blisters

Histologic examination revealed pauci-inflammatory subepidermal blisters with swelling of eccrine cells, signaling impending gland necrosis (Figure). Direct immunofluorescence testing on perilesional skin was negative. These findings would be inconsistent for diagnoses of edema blisters (most commonly seen in patients with an acute exacerbation of chronic lower extremity edema), friction blisters (intraepidermal blisters seen on histopathology), and bullous pemphigoid (linear IgG and/or C3 staining along the basement membrane zone on direct immunofluorescence testing is characteristic). Although eccrine gland alterations have been seen in toxic epidermal necrolysis,¹ the mucous membranes are involved in more than 90% of cases, making the diagnosis less likely. Furthermore, interface changes including prominent keratinocyte necrosis were not seen on histology.

Given the localized nature of the lesions in our patient and negative direct immunofluorescence studies, a diagnosis of coma blisters was made. Gentle wound care practices to the areas of denuded skin were implemented with complete resolution. The patient’s condition gradually improved, and she was extubated and discharged home.

Coma blisters are self-limited bullous lesions that have been reported in comatose patients as early as 1812 when Napoleon’s surgeon first noticed cutaneous blisters in comatose French soldiers being treated for carbon monoxide intoxication.² Since then, barbiturate overdose has remained the most common association, but coma blisters have occurred in the absence of specific drug exposures. Clinically, erythematous or violaceous plaques typically appear within 24 hours of drug ingestion, and progression to large tense bullae usually occurs within 48 to 72 hours of unconsciousness.³ They characteristically occur in pressure-dependent areas, but reports have shown lesions in non–pressure-dependent areas, including the penis and mouth.^1,4 Spontaneous resolution within 1 to 2 weeks is typical.⁵

The underlying pathogenesis remains controversial, as multiple mechanisms have been suggested, but clear causal evidence is lacking. The original proposition that direct effects of drug toxicity caused the cutaneous observations was later refuted after similar bullous lesions with eccrine gland necrosis were reported in comatose patients with neurologic conditions.⁶ It is largely accepted that pressure-induced local ischemia—proportional to the duration and amount of pressure—leads to tissue injury and is critical to the pathogenesis. During periods of ischemia, the most metabolically active tissues will undergo necrosis first; however, in eccrine glands, the earliest and most severe damage does not seem to occur in the most metabolically active cells.⁷ Additionally, this would not provide a viable explanation for coma blisters with eccrine gland necrosis developing in variable non–pressuredependent areas.

Moreover, drug- and non–drug-induced coma blisters can appear identically, but specific histopathologic differences have been reported. The most notable markers of non–drug-induced coma blisters are the absence of an inflammatory infiltrate in the epidermis and the presence of thrombosis in dermal vessels.⁸ Demonstration of necrotic changes in the secretory portion of the eccrine gland is considered the histopathologic hallmark for drug-induced coma blisters, but other findings can include subepidermal or intraepidermal bullae; perivascular infiltrates; and focal necrosis of the epidermis, dermis, subcutis, or epidermal appendages.⁶ Arteriolar wall necrosis and dermal inflammatory infiltrates also have been observed.⁷

Benzodiazepines have been widely prescribed and abused since their development, and overdose is much more common today than with barbiturates.⁹ Coma blisters rarely have been documented in the setting of isolated benzodiazepine overdose, and of the few cases, only one report implicated lorazepam as the causative agent.^4,7 The characteristic finding of eccrine gland necrosis consistently was seen in our patient. This case not only emphasizes the need for greater awareness of the association between benzodiazepine overdose and coma blisters but also the importance of clinical context when considering diagnoses. It is essential to note that coma blisters themselves are nonspecific, and the diagnosis of drug-induced coma blisters warrants confirmatory toxicologic analysis.

On the basis of the patient's history and clinical presentation, the likely diagnosis is ketosis-prone diabetes (KPD) type 2. KPD is widely thought of as an atypical diabetes syndrome, though some groups consider it to be a common clinical presentation in newly diagnosed patients with type 2 diabetes (T2D) rather than a subtype of disease. The condition is more prevalent in males and among Black and Hispanic populations.

Definitive diagnosis of the type of diabetes can present a clinical challenge during acute presentation. Although the majority of diabetic ketoacidosis (DKA) episodes occur in patients previously diagnosed with type 1 diabetes, an estimated 34% occur in patients with T2D. For patients who are obese or have a family history of diabetes, there should be a high index of suspicion for new-onset DKA in type 2 diabetes.

Patients with KPD typically present in a state of ketoacidosis with a brief but acute history of hyperglycemic symptoms. Hyperglycemia, elevated anion gap acidosis, and ketonemia form the expected constellation of DKA symptoms. A key consideration in the differential diagnosis is hyperosmolar hyperglycemic state (HHS). Patients with HHS are much more likely to have altered mental status than are patients with DKA. Metabolic acidosis and ketonemia are absent or mild, and anion gap is either normal or slightly elevated. In HHS, extreme elevations of glucose are seen, with a lack of significant ketoacidosis. Glucose levels tend to be higher in HHS than in DKA; they are almost always > 600 mg/dL, and levels > 1000 mg/dL are not uncommon. In DKA, glucose levels are still markedly high — generally 500-800 mg/dL but rarely exceeding 900 mg/dL. Patients with DKA also usually present with an A1c > 10% and a blood pH < 7.30. 

Treatment for KPD is initially acute, beginning with aggressive intravenous fluid and insulin therapy A. Once this state resolves, insulin requirements typically decrease for patients with T2D, and they are able to maintain adequate glycemic control with an oral therapy regimen.

Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia  Medical School; EVMS Medical Group, Norfolk, Virginia.

Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.

On the basis of the patient's history and clinical presentation, the likely diagnosis is ketosis-prone diabetes (KPD) type 2. KPD is widely thought of as an atypical diabetes syndrome, though some groups consider it to be a common clinical presentation in newly diagnosed patients with type 2 diabetes (T2D) rather than a subtype of disease. The condition is more prevalent in males and among Black and Hispanic populations.

Definitive diagnosis of the type of diabetes can present a clinical challenge during acute presentation. Although the majority of diabetic ketoacidosis (DKA) episodes occur in patients previously diagnosed with type 1 diabetes, an estimated 34% occur in patients with T2D. For patients who are obese or have a family history of diabetes, there should be a high index of suspicion for new-onset DKA in type 2 diabetes.

Patients with KPD typically present in a state of ketoacidosis with a brief but acute history of hyperglycemic symptoms. Hyperglycemia, elevated anion gap acidosis, and ketonemia form the expected constellation of DKA symptoms. A key consideration in the differential diagnosis is hyperosmolar hyperglycemic state (HHS). Patients with HHS are much more likely to have altered mental status than are patients with DKA. Metabolic acidosis and ketonemia are absent or mild, and anion gap is either normal or slightly elevated. In HHS, extreme elevations of glucose are seen, with a lack of significant ketoacidosis. Glucose levels tend to be higher in HHS than in DKA; they are almost always > 600 mg/dL, and levels > 1000 mg/dL are not uncommon. In DKA, glucose levels are still markedly high — generally 500-800 mg/dL but rarely exceeding 900 mg/dL. Patients with DKA also usually present with an A1c > 10% and a blood pH < 7.30. 

Treatment for KPD is initially acute, beginning with aggressive intravenous fluid and insulin therapy A. Once this state resolves, insulin requirements typically decrease for patients with T2D, and they are able to maintain adequate glycemic control with an oral therapy regimen.

Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia  Medical School; EVMS Medical Group, Norfolk, Virginia.

Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.

On the basis of the patient's history and clinical presentation, the likely diagnosis is ketosis-prone diabetes (KPD) type 2. KPD is widely thought of as an atypical diabetes syndrome, though some groups consider it to be a common clinical presentation in newly diagnosed patients with type 2 diabetes (T2D) rather than a subtype of disease. The condition is more prevalent in males and among Black and Hispanic populations.

Definitive diagnosis of the type of diabetes can present a clinical challenge during acute presentation. Although the majority of diabetic ketoacidosis (DKA) episodes occur in patients previously diagnosed with type 1 diabetes, an estimated 34% occur in patients with T2D. For patients who are obese or have a family history of diabetes, there should be a high index of suspicion for new-onset DKA in type 2 diabetes.

Patients with KPD typically present in a state of ketoacidosis with a brief but acute history of hyperglycemic symptoms. Hyperglycemia, elevated anion gap acidosis, and ketonemia form the expected constellation of DKA symptoms. A key consideration in the differential diagnosis is hyperosmolar hyperglycemic state (HHS). Patients with HHS are much more likely to have altered mental status than are patients with DKA. Metabolic acidosis and ketonemia are absent or mild, and anion gap is either normal or slightly elevated. In HHS, extreme elevations of glucose are seen, with a lack of significant ketoacidosis. Glucose levels tend to be higher in HHS than in DKA; they are almost always > 600 mg/dL, and levels > 1000 mg/dL are not uncommon. In DKA, glucose levels are still markedly high — generally 500-800 mg/dL but rarely exceeding 900 mg/dL. Patients with DKA also usually present with an A1c > 10% and a blood pH < 7.30. 

Treatment for KPD is initially acute, beginning with aggressive intravenous fluid and insulin therapy A. Once this state resolves, insulin requirements typically decrease for patients with T2D, and they are able to maintain adequate glycemic control with an oral therapy regimen.

Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia  Medical School; EVMS Medical Group, Norfolk, Virginia.

Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.

Obstetrical practice saw updates in 2021 to 3 major areas of pregnancy management: preterm birth prevention, antepartum fetal surveillance, and the use of antenatal corticosteroids.

Updated guidance on predicting and preventing spontaneous PTB

American College of Obstetricians and Gynecologists’ Committee on Practice Bulletins–Obstetrics. Prediction and prevention of spontaneous preterm birth: ACOG practice bulletin, number 234. Obstet Gynecol. 2021;138:e65-e90.

Preterm birth (PTB) continues to pose a challenge in clinical obstetrics, with the most recently reported rate of 10.2% in the United States.¹ This accounts for almost 75% of perinatal mortality and more than half of neonatal morbidity, in which effects last well past the neonatal period. PTB is classified as spontaneous (following preterm labor, preterm prelabor rupture of membranes, or cervical insufficiency) or iatrogenic (indicated due to maternal and/or fetal complications).

Assessing risk for PTB

The single strongest predictor of subsequent PTB is a history of spontaneous PTB. Recurrence risk is further increased by the number of prior PTBs and the gestational age at prior PTB. Identification of and intervention for a short cervix has been shown to prolong gestation. Transvaginal ultrasonography of the cervix is the most accurate method for evaluating cervical length (CL). Specific examination criteria exist to ensure that CL measurements are reproducible and reliable.² A short CL is generally defined as a measurement of less than 25 mm between 16 and 24 weeks’ gestation.

Screening strategies

The American College of Obstetricians and Gynecologists (ACOG), with an endorsement from the Society for Maternal-Fetal Medicine (SMFM), recommends cervical evaluation during the anatomy ultrasound exam between 18 0/7 and 22 6/7 weeks’ gestation in all pregnant patients regardless of prior PTB.³ If transabdominal imaging is concerning for a shortened cervix, transvaginal ultrasonography should be performed to assess the CL.

Serial transvaginal CL measurements are recommended between 16 0/7 and 24 0/7 weeks’ gestation for patients with a current singleton pregnancy and history of a spontaneous PTB, but not for patients with a history of iatrogenic or indicated PTB.

Interventions: Mind your p’s and c’s

Interventions to reduce the risk of spontaneous PTB depend on whether the current pregnancy is a singleton, twins, or higher-order multiples; CL measurement; and history of spontaneous PTB. Preconception optimization of underlying medical conditions also is important to reduce the risk of recurrent indicated PTB.

Continue to: Progesterone...

Progesterone

Vaginal administration. Several trials have shown that vaginal progesterone can be used to reduce the risk of spontaneous PTB in asymptomatic patients with a singleton pregnancy, incidental finding of a short cervix (<25 mm), and no history of spontaneous PTB. This is a change from the prior recommendation of CL of less than 20 mm. In the setting of a twin pregnancy, regardless of CL, data do not definitively support the use of vaginal progesterone.

Intramuscular administration.^4,5 The popularity of intramuscular progesterone has waxed and waned. At present, ACOG recommends that all patients with a singleton pregnancy and history of spontaneous PTB be offered progesterone beginning at 16 0/7 weeks’ gestation following a shared decision-making process that includes the limited data of efficacy noted in existing studies.

In a twin pregnancy with no history of spontaneous PTB, the use of intramuscular progesterone has been shown to potentially increase the risk of PTB and admission to the neonatal intensive care unit. As such, intramuscular progesterone in the setting of a twin gestation without a history of spontaneous PTB is not recommended. When a prior spontaneous PTB has occurred, there may be some benefit to intramuscular progesterone in twin gestations.

Cerclage

Ultrasound indicated. In a singleton pregnancy with an incidental finding of short cervix (<25 mm) and no history of PTB, the use of cerclage is of uncertain benefit. Effectiveness may be seen if the cervix is less than 10 mm. Ultrasound-indicated cerclage should be considered in a singleton pregnancy with a CL less than 25 mm and a history of spontaneous PTB.

Possibly one of the most controversial topics is ultrasound-indicated cerclage placement in twin gestation. As with many situations in obstetrics, data regarding ultrasound-indicated cerclage in twin gestation is based on small retrospective studies fraught with bias. Results from these studies range from no benefit, to potential benefit, to even possible increased risk of PTB. Since data are limited, as we await more evidence, it is recommended that the clinician and patient use shared decision making to decide on cerclage placement in a twin gestation.

Exam indicated. In a singleton pregnancy with a dilated cervix on digital or speculum exam between 16 0/7 to 23 6/7 weeks’ gestation, a physical exam–indicated cerclage should be offered. Exam-indicated cerclage also may reduce the incidence of PTB in twin gestations with cervical dilation between 16 0/7 and 23 6/7 weeks’ gestation. Indomethacin tocolysis and perioperative antibiotics should be considered when an exam-indicated cerclage is placed.

As the limits of viability are continually pushed earlier, more in-depth conversation is needed with patients who are considering an exam-indicated cerclage. The nuances of periviability and the likelihood that an exam-indicated cerclage will commit a pregnancy to a periviable or extremely preterm birth should be discussed in detail using a shared decision making model.

Regardless of whether the cerclage is ultrasound or exam indicated, once it is placed there is no utility in additional CL ultrasound monitoring.

Pessary

Vaginal pessaries for prevention of PTB have not gained popularity in the United States as they have in other countries. Trials are being conducted to determine the utility of vaginal pessary, but current data have not proven its effectiveness in preventing PTB in the setting of singleton pregnancy, short cervix, and no history of spontaneous PTB. So for now, pessary is not recommended. The same can be said for use in the twin gestation.

Which patients may benefit from antepartum fetal surveillance and when to initiate it

American College of Obstetricians and Gynecologists’ Committee on Obstetrics Practice, Society for Maternal-Fetal Medicine. Indications for outpatient antenatal surveillance: ACOG committee opinion, number 828. Obstet Gynecol. 2021;137:e177-e197.

American College of Obstetricians and Gynecologists’ Committee on Practice Bulletins—Obstetrics. Antepartum fetal surveillance: ACOG practice bulletin, number 229. Obstet Gynecol. 2021;137:e116-e127.

The ultimate purpose of antenatal fetal surveillance is to prevent stillbirth. However, stillbirth has multiple etiologies, not all of which are preventable with testing. In June 2021, ACOG released a new Committee Opinion containing guidelines for fetal surveillance, including suggested gestational age at initiation and frequency of testing, for the most common high-risk conditions. ACOG also released an update to the Practice Bulletin on antepartum fetal surveillance; additions include randomized controlled trial level data on the utility of fetal kick counts (FKCs) and recommendations that align with the new Committee Opinion.

Data for the efficacy of antepartum fetal surveillance are lacking, mainly due to the difficulty of performing prospective studies in stillbirth. The existing evidence is subject to intervention bias, as deliveries increase in tested patients, and recommendations rely heavily on expert consensus and nonrandomized studies. Antenatal testing is also time, cost, and labor intensive, with the risk of intervention for a false-positive result. Despite these limitations, obstetrical practices routinely perform antenatal fetal surveillance.

The new guidelines: The why, when, and how often

Why. Antepartum fetal surveillance is suggested for conditions that have a risk of stillbirth greater than 0.8 per 1,000 (that is, the false-negative rate of a biophysical profile or a modified biophysical profile) and the relative risk or odds ratio is greater than 2.0 for stillbirth compared with unaffected pregnancies.

When. For most conditions, ACOG recommends initiation of testing at 32 weeks or later, with notable earlier exceptions for some of the highest-risk patients. For certain conditions, such as fetal growth restriction and hypertensive disorders of pregnancy, the recommendation is to start “at diagnosis,” with the corollary “or at a gestational age when delivery would be considered because of abnormal results.” Shared decision making with the patient about pregnancy goals therefore is required, particularly in cases of fetal anomalies, genetic conditions, or at very early gestational ages.

How often. The recommended frequency of testing is at least weekly. Testing frequency should be increased to twice-weekly outpatient or daily inpatient for the most complicated pregnancies (for example, fetal growth restriction with abnormal umbilical artery Doppler studies, preeclampsia with severe features).

Once or twice weekly is an option for many conditions, which gives the clinician the opportunity to assess clinical stability as well as the patient’s input in terms of logistics and anxiety.

Patients with multiple conditions may fall into the “individualized” category, as do patients with suboptimal control of conditions (for example, diabetes, hypertension) that may affect the fetus as the pregnancy progresses.

New diagnoses included for surveillance

Several diagnoses not previously included now qualify for antepartum fetal surveillance under the new guidelines, most notably:

• history of obstetrical complications in the immediate preceding pregnancy

—history of prior fetal growth restriction requiring preterm delivery

—history of prior preeclampsia requiring delivery

• alcohol use of 5 or more drinks per day
• in vitro fertilization
• abnormal serum markers

—pregnancy-associated plasma protein A (PAPP-A) in the fifth or lower percentile or 0.4 multiples of the median (MoM)

—second trimester inhibin A of 2 or greater MoM

• prepregnancy body mass index (BMI)

—this is divided into 2 categories for timing of initiation of testing:

1.  37 weeks for BMI of 35 to 39.9 kg/m²
2.  34 weeks for BMI of or greater than 40 kg/m².

Fetal kick counts

The major change to the updated Practice Bulletin on antenatal surveillance is the inclusion of data on FKCs, a simple modality of fetal surveillance that does not require a clinical visit. For FKCs, a meta-analysis of more than 450,000 patients did not demonstrate a difference in perinatal death between the FKC intervention group (0.54%) and the control group (0.59%). Of note, there were small but statistically significant increases in the rates of induction of labor, cesarean delivery, and preterm delivery in the FKC intervention group. Therefore, this update does not recommend a formal program of FKCs for all patients.

Continue to: Use of antenatal corticosteroids now may be considered at 22 weeks’ gestation...

Use of antenatal corticosteroids now may be considered at 22 weeks’ gestation

American College of Obstetricians and Gynecologists. Use of antenatal corticosteroids at 22 weeks of gestation: ACOG practice advisory. September 2021. https://www .acog.org/clinical/clinical-guidance/practice-advisory /articles/2021/09/use-of-antenatal-corticosteroids-at -22-weeks-of-gestation. Accessed December 11, 2021.

In September 2021, ACOG and SMFM released a Practice Advisory updating the current recommendations for the administration of antenatal corticosteroids in the periviable period (22 to 25 6/7 weeks’ gestation). Whereas the prior lower limit of gestational age for consideration of steroids was 23 weeks, the new recommendation now extends this consideration down to 22 weeks.

The cited data include a meta-analysis of more than 2,200 patients in which the survival rate of infants born between 22 and 22 6/7 weeks who were exposed to antenatal steroids was 39% compared with 19.5% in the unexposed group. Another study of more than 1,000 patients demonstrated a statistically significant increase in overall survival in patients treated with antenatal steroids plus life support compared with life support only (38.5% vs 17.7%). Survival without major morbidity in this study, although increased from 1% to 4.4%, was still low.

Recommendation carries caveats

Given this information, the Practice Advisory offers a 2C level recommendation (weak recommendation, low quality of evidence) for antenatal steroids at 22 to 22 6/7 weeks’ gestation if neonatal resuscitation is planned, acknowledging the limitations and potential bias of the available data.

The Practice Advisory emphasizes the importance of counseling and patient involvement in the decision making. This requires a multidisciplinary collaboration among the neonatology and obstetrical teams, flexibility in the plan after birth depending on the infant’s condition, and redirection of care if appropriate. Estimated fetal weight, the presence of multiple gestations, fetal biologic sex, and any anomalies are also important in helping families make an informed decision for their particular pregnancy. As described in the Obstetric Care Consensus on periviable birth,⁶ it is important to remember that considerations and recommendations are not the same as requirements, and redirection of care to comfort and family memory making is not the same as withholding care.

The rest of the recommendations for the administration of antenatal steroids remain the same: Antenatal steroids are not recommended at less than 22 weeks due to lack of evidence of benefit, and they continue to be recommended at 24 weeks and beyond. ●

Obstetrical practice saw updates in 2021 to 3 major areas of pregnancy management: preterm birth prevention, antepartum fetal surveillance, and the use of antenatal corticosteroids.

Updated guidance on predicting and preventing spontaneous PTB

American College of Obstetricians and Gynecologists’ Committee on Practice Bulletins–Obstetrics. Prediction and prevention of spontaneous preterm birth: ACOG practice bulletin, number 234. Obstet Gynecol. 2021;138:e65-e90.

Preterm birth (PTB) continues to pose a challenge in clinical obstetrics, with the most recently reported rate of 10.2% in the United States.¹ This accounts for almost 75% of perinatal mortality and more than half of neonatal morbidity, in which effects last well past the neonatal period. PTB is classified as spontaneous (following preterm labor, preterm prelabor rupture of membranes, or cervical insufficiency) or iatrogenic (indicated due to maternal and/or fetal complications).

Assessing risk for PTB

The single strongest predictor of subsequent PTB is a history of spontaneous PTB. Recurrence risk is further increased by the number of prior PTBs and the gestational age at prior PTB. Identification of and intervention for a short cervix has been shown to prolong gestation. Transvaginal ultrasonography of the cervix is the most accurate method for evaluating cervical length (CL). Specific examination criteria exist to ensure that CL measurements are reproducible and reliable.² A short CL is generally defined as a measurement of less than 25 mm between 16 and 24 weeks’ gestation.

Screening strategies

The American College of Obstetricians and Gynecologists (ACOG), with an endorsement from the Society for Maternal-Fetal Medicine (SMFM), recommends cervical evaluation during the anatomy ultrasound exam between 18 0/7 and 22 6/7 weeks’ gestation in all pregnant patients regardless of prior PTB.³ If transabdominal imaging is concerning for a shortened cervix, transvaginal ultrasonography should be performed to assess the CL.

Serial transvaginal CL measurements are recommended between 16 0/7 and 24 0/7 weeks’ gestation for patients with a current singleton pregnancy and history of a spontaneous PTB, but not for patients with a history of iatrogenic or indicated PTB.

Interventions: Mind your p’s and c’s

Interventions to reduce the risk of spontaneous PTB depend on whether the current pregnancy is a singleton, twins, or higher-order multiples; CL measurement; and history of spontaneous PTB. Preconception optimization of underlying medical conditions also is important to reduce the risk of recurrent indicated PTB.

Continue to: Progesterone...

Progesterone

Vaginal administration. Several trials have shown that vaginal progesterone can be used to reduce the risk of spontaneous PTB in asymptomatic patients with a singleton pregnancy, incidental finding of a short cervix (<25 mm), and no history of spontaneous PTB. This is a change from the prior recommendation of CL of less than 20 mm. In the setting of a twin pregnancy, regardless of CL, data do not definitively support the use of vaginal progesterone.

Intramuscular administration.^4,5 The popularity of intramuscular progesterone has waxed and waned. At present, ACOG recommends that all patients with a singleton pregnancy and history of spontaneous PTB be offered progesterone beginning at 16 0/7 weeks’ gestation following a shared decision-making process that includes the limited data of efficacy noted in existing studies.

In a twin pregnancy with no history of spontaneous PTB, the use of intramuscular progesterone has been shown to potentially increase the risk of PTB and admission to the neonatal intensive care unit. As such, intramuscular progesterone in the setting of a twin gestation without a history of spontaneous PTB is not recommended. When a prior spontaneous PTB has occurred, there may be some benefit to intramuscular progesterone in twin gestations.

Cerclage

Ultrasound indicated. In a singleton pregnancy with an incidental finding of short cervix (<25 mm) and no history of PTB, the use of cerclage is of uncertain benefit. Effectiveness may be seen if the cervix is less than 10 mm. Ultrasound-indicated cerclage should be considered in a singleton pregnancy with a CL less than 25 mm and a history of spontaneous PTB.

Possibly one of the most controversial topics is ultrasound-indicated cerclage placement in twin gestation. As with many situations in obstetrics, data regarding ultrasound-indicated cerclage in twin gestation is based on small retrospective studies fraught with bias. Results from these studies range from no benefit, to potential benefit, to even possible increased risk of PTB. Since data are limited, as we await more evidence, it is recommended that the clinician and patient use shared decision making to decide on cerclage placement in a twin gestation.

Exam indicated. In a singleton pregnancy with a dilated cervix on digital or speculum exam between 16 0/7 to 23 6/7 weeks’ gestation, a physical exam–indicated cerclage should be offered. Exam-indicated cerclage also may reduce the incidence of PTB in twin gestations with cervical dilation between 16 0/7 and 23 6/7 weeks’ gestation. Indomethacin tocolysis and perioperative antibiotics should be considered when an exam-indicated cerclage is placed.

As the limits of viability are continually pushed earlier, more in-depth conversation is needed with patients who are considering an exam-indicated cerclage. The nuances of periviability and the likelihood that an exam-indicated cerclage will commit a pregnancy to a periviable or extremely preterm birth should be discussed in detail using a shared decision making model.

Regardless of whether the cerclage is ultrasound or exam indicated, once it is placed there is no utility in additional CL ultrasound monitoring.

Pessary

Vaginal pessaries for prevention of PTB have not gained popularity in the United States as they have in other countries. Trials are being conducted to determine the utility of vaginal pessary, but current data have not proven its effectiveness in preventing PTB in the setting of singleton pregnancy, short cervix, and no history of spontaneous PTB. So for now, pessary is not recommended. The same can be said for use in the twin gestation.

Which patients may benefit from antepartum fetal surveillance and when to initiate it

American College of Obstetricians and Gynecologists’ Committee on Obstetrics Practice, Society for Maternal-Fetal Medicine. Indications for outpatient antenatal surveillance: ACOG committee opinion, number 828. Obstet Gynecol. 2021;137:e177-e197.

American College of Obstetricians and Gynecologists’ Committee on Practice Bulletins—Obstetrics. Antepartum fetal surveillance: ACOG practice bulletin, number 229. Obstet Gynecol. 2021;137:e116-e127.

The ultimate purpose of antenatal fetal surveillance is to prevent stillbirth. However, stillbirth has multiple etiologies, not all of which are preventable with testing. In June 2021, ACOG released a new Committee Opinion containing guidelines for fetal surveillance, including suggested gestational age at initiation and frequency of testing, for the most common high-risk conditions. ACOG also released an update to the Practice Bulletin on antepartum fetal surveillance; additions include randomized controlled trial level data on the utility of fetal kick counts (FKCs) and recommendations that align with the new Committee Opinion.

Data for the efficacy of antepartum fetal surveillance are lacking, mainly due to the difficulty of performing prospective studies in stillbirth. The existing evidence is subject to intervention bias, as deliveries increase in tested patients, and recommendations rely heavily on expert consensus and nonrandomized studies. Antenatal testing is also time, cost, and labor intensive, with the risk of intervention for a false-positive result. Despite these limitations, obstetrical practices routinely perform antenatal fetal surveillance.

The new guidelines: The why, when, and how often

Why. Antepartum fetal surveillance is suggested for conditions that have a risk of stillbirth greater than 0.8 per 1,000 (that is, the false-negative rate of a biophysical profile or a modified biophysical profile) and the relative risk or odds ratio is greater than 2.0 for stillbirth compared with unaffected pregnancies.

When. For most conditions, ACOG recommends initiation of testing at 32 weeks or later, with notable earlier exceptions for some of the highest-risk patients. For certain conditions, such as fetal growth restriction and hypertensive disorders of pregnancy, the recommendation is to start “at diagnosis,” with the corollary “or at a gestational age when delivery would be considered because of abnormal results.” Shared decision making with the patient about pregnancy goals therefore is required, particularly in cases of fetal anomalies, genetic conditions, or at very early gestational ages.

How often. The recommended frequency of testing is at least weekly. Testing frequency should be increased to twice-weekly outpatient or daily inpatient for the most complicated pregnancies (for example, fetal growth restriction with abnormal umbilical artery Doppler studies, preeclampsia with severe features).

Once or twice weekly is an option for many conditions, which gives the clinician the opportunity to assess clinical stability as well as the patient’s input in terms of logistics and anxiety.

Patients with multiple conditions may fall into the “individualized” category, as do patients with suboptimal control of conditions (for example, diabetes, hypertension) that may affect the fetus as the pregnancy progresses.

New diagnoses included for surveillance

Several diagnoses not previously included now qualify for antepartum fetal surveillance under the new guidelines, most notably:

• history of obstetrical complications in the immediate preceding pregnancy

—history of prior fetal growth restriction requiring preterm delivery

—history of prior preeclampsia requiring delivery

• alcohol use of 5 or more drinks per day
• in vitro fertilization
• abnormal serum markers

—pregnancy-associated plasma protein A (PAPP-A) in the fifth or lower percentile or 0.4 multiples of the median (MoM)

—second trimester inhibin A of 2 or greater MoM

• prepregnancy body mass index (BMI)

—this is divided into 2 categories for timing of initiation of testing:

1.  37 weeks for BMI of 35 to 39.9 kg/m²
2.  34 weeks for BMI of or greater than 40 kg/m².

Fetal kick counts

The major change to the updated Practice Bulletin on antenatal surveillance is the inclusion of data on FKCs, a simple modality of fetal surveillance that does not require a clinical visit. For FKCs, a meta-analysis of more than 450,000 patients did not demonstrate a difference in perinatal death between the FKC intervention group (0.54%) and the control group (0.59%). Of note, there were small but statistically significant increases in the rates of induction of labor, cesarean delivery, and preterm delivery in the FKC intervention group. Therefore, this update does not recommend a formal program of FKCs for all patients.

Continue to: Use of antenatal corticosteroids now may be considered at 22 weeks’ gestation...

Use of antenatal corticosteroids now may be considered at 22 weeks’ gestation

American College of Obstetricians and Gynecologists. Use of antenatal corticosteroids at 22 weeks of gestation: ACOG practice advisory. September 2021. https://www .acog.org/clinical/clinical-guidance/practice-advisory /articles/2021/09/use-of-antenatal-corticosteroids-at -22-weeks-of-gestation. Accessed December 11, 2021.

In September 2021, ACOG and SMFM released a Practice Advisory updating the current recommendations for the administration of antenatal corticosteroids in the periviable period (22 to 25 6/7 weeks’ gestation). Whereas the prior lower limit of gestational age for consideration of steroids was 23 weeks, the new recommendation now extends this consideration down to 22 weeks.

The cited data include a meta-analysis of more than 2,200 patients in which the survival rate of infants born between 22 and 22 6/7 weeks who were exposed to antenatal steroids was 39% compared with 19.5% in the unexposed group. Another study of more than 1,000 patients demonstrated a statistically significant increase in overall survival in patients treated with antenatal steroids plus life support compared with life support only (38.5% vs 17.7%). Survival without major morbidity in this study, although increased from 1% to 4.4%, was still low.

Recommendation carries caveats

Given this information, the Practice Advisory offers a 2C level recommendation (weak recommendation, low quality of evidence) for antenatal steroids at 22 to 22 6/7 weeks’ gestation if neonatal resuscitation is planned, acknowledging the limitations and potential bias of the available data.

The Practice Advisory emphasizes the importance of counseling and patient involvement in the decision making. This requires a multidisciplinary collaboration among the neonatology and obstetrical teams, flexibility in the plan after birth depending on the infant’s condition, and redirection of care if appropriate. Estimated fetal weight, the presence of multiple gestations, fetal biologic sex, and any anomalies are also important in helping families make an informed decision for their particular pregnancy. As described in the Obstetric Care Consensus on periviable birth,⁶ it is important to remember that considerations and recommendations are not the same as requirements, and redirection of care to comfort and family memory making is not the same as withholding care.

The rest of the recommendations for the administration of antenatal steroids remain the same: Antenatal steroids are not recommended at less than 22 weeks due to lack of evidence of benefit, and they continue to be recommended at 24 weeks and beyond. ●

Obstetrical practice saw updates in 2021 to 3 major areas of pregnancy management: preterm birth prevention, antepartum fetal surveillance, and the use of antenatal corticosteroids.

Updated guidance on predicting and preventing spontaneous PTB

American College of Obstetricians and Gynecologists’ Committee on Practice Bulletins–Obstetrics. Prediction and prevention of spontaneous preterm birth: ACOG practice bulletin, number 234. Obstet Gynecol. 2021;138:e65-e90.

Preterm birth (PTB) continues to pose a challenge in clinical obstetrics, with the most recently reported rate of 10.2% in the United States.¹ This accounts for almost 75% of perinatal mortality and more than half of neonatal morbidity, in which effects last well past the neonatal period. PTB is classified as spontaneous (following preterm labor, preterm prelabor rupture of membranes, or cervical insufficiency) or iatrogenic (indicated due to maternal and/or fetal complications).

Assessing risk for PTB

The single strongest predictor of subsequent PTB is a history of spontaneous PTB. Recurrence risk is further increased by the number of prior PTBs and the gestational age at prior PTB. Identification of and intervention for a short cervix has been shown to prolong gestation. Transvaginal ultrasonography of the cervix is the most accurate method for evaluating cervical length (CL). Specific examination criteria exist to ensure that CL measurements are reproducible and reliable.² A short CL is generally defined as a measurement of less than 25 mm between 16 and 24 weeks’ gestation.

Screening strategies

The American College of Obstetricians and Gynecologists (ACOG), with an endorsement from the Society for Maternal-Fetal Medicine (SMFM), recommends cervical evaluation during the anatomy ultrasound exam between 18 0/7 and 22 6/7 weeks’ gestation in all pregnant patients regardless of prior PTB.³ If transabdominal imaging is concerning for a shortened cervix, transvaginal ultrasonography should be performed to assess the CL.

Serial transvaginal CL measurements are recommended between 16 0/7 and 24 0/7 weeks’ gestation for patients with a current singleton pregnancy and history of a spontaneous PTB, but not for patients with a history of iatrogenic or indicated PTB.

Interventions: Mind your p’s and c’s

Interventions to reduce the risk of spontaneous PTB depend on whether the current pregnancy is a singleton, twins, or higher-order multiples; CL measurement; and history of spontaneous PTB. Preconception optimization of underlying medical conditions also is important to reduce the risk of recurrent indicated PTB.

Continue to: Progesterone...

Progesterone

Vaginal administration. Several trials have shown that vaginal progesterone can be used to reduce the risk of spontaneous PTB in asymptomatic patients with a singleton pregnancy, incidental finding of a short cervix (<25 mm), and no history of spontaneous PTB. This is a change from the prior recommendation of CL of less than 20 mm. In the setting of a twin pregnancy, regardless of CL, data do not definitively support the use of vaginal progesterone.

Intramuscular administration.^4,5 The popularity of intramuscular progesterone has waxed and waned. At present, ACOG recommends that all patients with a singleton pregnancy and history of spontaneous PTB be offered progesterone beginning at 16 0/7 weeks’ gestation following a shared decision-making process that includes the limited data of efficacy noted in existing studies.

In a twin pregnancy with no history of spontaneous PTB, the use of intramuscular progesterone has been shown to potentially increase the risk of PTB and admission to the neonatal intensive care unit. As such, intramuscular progesterone in the setting of a twin gestation without a history of spontaneous PTB is not recommended. When a prior spontaneous PTB has occurred, there may be some benefit to intramuscular progesterone in twin gestations.

Cerclage

Ultrasound indicated. In a singleton pregnancy with an incidental finding of short cervix (<25 mm) and no history of PTB, the use of cerclage is of uncertain benefit. Effectiveness may be seen if the cervix is less than 10 mm. Ultrasound-indicated cerclage should be considered in a singleton pregnancy with a CL less than 25 mm and a history of spontaneous PTB.

Possibly one of the most controversial topics is ultrasound-indicated cerclage placement in twin gestation. As with many situations in obstetrics, data regarding ultrasound-indicated cerclage in twin gestation is based on small retrospective studies fraught with bias. Results from these studies range from no benefit, to potential benefit, to even possible increased risk of PTB. Since data are limited, as we await more evidence, it is recommended that the clinician and patient use shared decision making to decide on cerclage placement in a twin gestation.

Exam indicated. In a singleton pregnancy with a dilated cervix on digital or speculum exam between 16 0/7 to 23 6/7 weeks’ gestation, a physical exam–indicated cerclage should be offered. Exam-indicated cerclage also may reduce the incidence of PTB in twin gestations with cervical dilation between 16 0/7 and 23 6/7 weeks’ gestation. Indomethacin tocolysis and perioperative antibiotics should be considered when an exam-indicated cerclage is placed.

As the limits of viability are continually pushed earlier, more in-depth conversation is needed with patients who are considering an exam-indicated cerclage. The nuances of periviability and the likelihood that an exam-indicated cerclage will commit a pregnancy to a periviable or extremely preterm birth should be discussed in detail using a shared decision making model.

Regardless of whether the cerclage is ultrasound or exam indicated, once it is placed there is no utility in additional CL ultrasound monitoring.

Pessary

Vaginal pessaries for prevention of PTB have not gained popularity in the United States as they have in other countries. Trials are being conducted to determine the utility of vaginal pessary, but current data have not proven its effectiveness in preventing PTB in the setting of singleton pregnancy, short cervix, and no history of spontaneous PTB. So for now, pessary is not recommended. The same can be said for use in the twin gestation.

Which patients may benefit from antepartum fetal surveillance and when to initiate it

American College of Obstetricians and Gynecologists’ Committee on Obstetrics Practice, Society for Maternal-Fetal Medicine. Indications for outpatient antenatal surveillance: ACOG committee opinion, number 828. Obstet Gynecol. 2021;137:e177-e197.

American College of Obstetricians and Gynecologists’ Committee on Practice Bulletins—Obstetrics. Antepartum fetal surveillance: ACOG practice bulletin, number 229. Obstet Gynecol. 2021;137:e116-e127.

The ultimate purpose of antenatal fetal surveillance is to prevent stillbirth. However, stillbirth has multiple etiologies, not all of which are preventable with testing. In June 2021, ACOG released a new Committee Opinion containing guidelines for fetal surveillance, including suggested gestational age at initiation and frequency of testing, for the most common high-risk conditions. ACOG also released an update to the Practice Bulletin on antepartum fetal surveillance; additions include randomized controlled trial level data on the utility of fetal kick counts (FKCs) and recommendations that align with the new Committee Opinion.

Data for the efficacy of antepartum fetal surveillance are lacking, mainly due to the difficulty of performing prospective studies in stillbirth. The existing evidence is subject to intervention bias, as deliveries increase in tested patients, and recommendations rely heavily on expert consensus and nonrandomized studies. Antenatal testing is also time, cost, and labor intensive, with the risk of intervention for a false-positive result. Despite these limitations, obstetrical practices routinely perform antenatal fetal surveillance.

The new guidelines: The why, when, and how often

Why. Antepartum fetal surveillance is suggested for conditions that have a risk of stillbirth greater than 0.8 per 1,000 (that is, the false-negative rate of a biophysical profile or a modified biophysical profile) and the relative risk or odds ratio is greater than 2.0 for stillbirth compared with unaffected pregnancies.

When. For most conditions, ACOG recommends initiation of testing at 32 weeks or later, with notable earlier exceptions for some of the highest-risk patients. For certain conditions, such as fetal growth restriction and hypertensive disorders of pregnancy, the recommendation is to start “at diagnosis,” with the corollary “or at a gestational age when delivery would be considered because of abnormal results.” Shared decision making with the patient about pregnancy goals therefore is required, particularly in cases of fetal anomalies, genetic conditions, or at very early gestational ages.

How often. The recommended frequency of testing is at least weekly. Testing frequency should be increased to twice-weekly outpatient or daily inpatient for the most complicated pregnancies (for example, fetal growth restriction with abnormal umbilical artery Doppler studies, preeclampsia with severe features).

Once or twice weekly is an option for many conditions, which gives the clinician the opportunity to assess clinical stability as well as the patient’s input in terms of logistics and anxiety.

Patients with multiple conditions may fall into the “individualized” category, as do patients with suboptimal control of conditions (for example, diabetes, hypertension) that may affect the fetus as the pregnancy progresses.

New diagnoses included for surveillance

Several diagnoses not previously included now qualify for antepartum fetal surveillance under the new guidelines, most notably:

• history of obstetrical complications in the immediate preceding pregnancy

—history of prior fetal growth restriction requiring preterm delivery

—history of prior preeclampsia requiring delivery

• alcohol use of 5 or more drinks per day
• in vitro fertilization
• abnormal serum markers

—pregnancy-associated plasma protein A (PAPP-A) in the fifth or lower percentile or 0.4 multiples of the median (MoM)

—second trimester inhibin A of 2 or greater MoM

• prepregnancy body mass index (BMI)

—this is divided into 2 categories for timing of initiation of testing:

1.  37 weeks for BMI of 35 to 39.9 kg/m²
2.  34 weeks for BMI of or greater than 40 kg/m².

Fetal kick counts

The major change to the updated Practice Bulletin on antenatal surveillance is the inclusion of data on FKCs, a simple modality of fetal surveillance that does not require a clinical visit. For FKCs, a meta-analysis of more than 450,000 patients did not demonstrate a difference in perinatal death between the FKC intervention group (0.54%) and the control group (0.59%). Of note, there were small but statistically significant increases in the rates of induction of labor, cesarean delivery, and preterm delivery in the FKC intervention group. Therefore, this update does not recommend a formal program of FKCs for all patients.

Continue to: Use of antenatal corticosteroids now may be considered at 22 weeks’ gestation...

Use of antenatal corticosteroids now may be considered at 22 weeks’ gestation

American College of Obstetricians and Gynecologists. Use of antenatal corticosteroids at 22 weeks of gestation: ACOG practice advisory. September 2021. https://www .acog.org/clinical/clinical-guidance/practice-advisory /articles/2021/09/use-of-antenatal-corticosteroids-at -22-weeks-of-gestation. Accessed December 11, 2021.

In September 2021, ACOG and SMFM released a Practice Advisory updating the current recommendations for the administration of antenatal corticosteroids in the periviable period (22 to 25 6/7 weeks’ gestation). Whereas the prior lower limit of gestational age for consideration of steroids was 23 weeks, the new recommendation now extends this consideration down to 22 weeks.

The cited data include a meta-analysis of more than 2,200 patients in which the survival rate of infants born between 22 and 22 6/7 weeks who were exposed to antenatal steroids was 39% compared with 19.5% in the unexposed group. Another study of more than 1,000 patients demonstrated a statistically significant increase in overall survival in patients treated with antenatal steroids plus life support compared with life support only (38.5% vs 17.7%). Survival without major morbidity in this study, although increased from 1% to 4.4%, was still low.

Recommendation carries caveats

Given this information, the Practice Advisory offers a 2C level recommendation (weak recommendation, low quality of evidence) for antenatal steroids at 22 to 22 6/7 weeks’ gestation if neonatal resuscitation is planned, acknowledging the limitations and potential bias of the available data.

The Practice Advisory emphasizes the importance of counseling and patient involvement in the decision making. This requires a multidisciplinary collaboration among the neonatology and obstetrical teams, flexibility in the plan after birth depending on the infant’s condition, and redirection of care if appropriate. Estimated fetal weight, the presence of multiple gestations, fetal biologic sex, and any anomalies are also important in helping families make an informed decision for their particular pregnancy. As described in the Obstetric Care Consensus on periviable birth,⁶ it is important to remember that considerations and recommendations are not the same as requirements, and redirection of care to comfort and family memory making is not the same as withholding care.

The rest of the recommendations for the administration of antenatal steroids remain the same: Antenatal steroids are not recommended at less than 22 weeks due to lack of evidence of benefit, and they continue to be recommended at 24 weeks and beyond. ●

There’s another doctor with whom I’ve referred patients, back and forth, for the last 20 years. I think he’s good at his job and assume he feels the same way about me. We aren’t social friends, but chat briefly when we run into each other at the hospital, or store, or local restaurants.

Last week I was at the hospital to read EEGs, and happened to see him in the doctor’s parking lot. We wished each other a happy new year, talked briefly about a few mutual patients, and then went our separate ways.

As he pulled out, I noticed his car had a bumper sticker for a cause I strongly disagree with. I mean, 180 degrees opposed.

Suddenly, I didn’t want to ever refer to him again. Why should I support him? He’s the enemy.

Why should I help him out by referring patients?

But then I had to stop. Isn’t this 2022? Aren’t we supposed to be in a civilized world? This isn’t my tribe versus your tribe, my cave versus your cave. The closest we’re supposed to come to direct conflict with others is the “us versus them” world of professional and college sports.

I hope.

Aren’t I supposed to be better than this? Isn’t learning to coexist the whole point of the playground as a kid (besides burning off energy and giving the teacher a break)? Isn’t the idea behind civilization to get along with each other, accept our differences as “agreeing to disagree,” and work together? Like Hamilton and Jefferson, or Ronald Reagan and Tip O’Neill?

Refusing to work with another competent physician because I disagree with their personal, religious, or political beliefs is just plain stupid.

Politicians and pundits try to convince us that people who disagree with us are the enemy, but that’s horse hockey. The truth is that the majority of people out there, regardless of personal beliefs, are decent, hardworking, and just trying to support their families like I am mine.

Later that week I had a patient who clearly needed the other doctor’s expertise, and I gave her his name and phone number. She asked if I’d send my own family to him, and I said, unequivocally, “yes” (actually I have).

Because, at the end of the day, we’re all people, along on the same ride. To not send a patient to him wouldn’t be in their best interest, which is what I’m supposed to be watching out for.

Not only that, but if I don’t refer just because I disagree with him as a person, then I’ve become the problem and not the solution.

Because I, and everyone else, have to try to be better than that.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

There’s another doctor with whom I’ve referred patients, back and forth, for the last 20 years. I think he’s good at his job and assume he feels the same way about me. We aren’t social friends, but chat briefly when we run into each other at the hospital, or store, or local restaurants.

Last week I was at the hospital to read EEGs, and happened to see him in the doctor’s parking lot. We wished each other a happy new year, talked briefly about a few mutual patients, and then went our separate ways.

As he pulled out, I noticed his car had a bumper sticker for a cause I strongly disagree with. I mean, 180 degrees opposed.

Suddenly, I didn’t want to ever refer to him again. Why should I support him? He’s the enemy.

Why should I help him out by referring patients?

But then I had to stop. Isn’t this 2022? Aren’t we supposed to be in a civilized world? This isn’t my tribe versus your tribe, my cave versus your cave. The closest we’re supposed to come to direct conflict with others is the “us versus them” world of professional and college sports.

I hope.

Aren’t I supposed to be better than this? Isn’t learning to coexist the whole point of the playground as a kid (besides burning off energy and giving the teacher a break)? Isn’t the idea behind civilization to get along with each other, accept our differences as “agreeing to disagree,” and work together? Like Hamilton and Jefferson, or Ronald Reagan and Tip O’Neill?

Refusing to work with another competent physician because I disagree with their personal, religious, or political beliefs is just plain stupid.

Politicians and pundits try to convince us that people who disagree with us are the enemy, but that’s horse hockey. The truth is that the majority of people out there, regardless of personal beliefs, are decent, hardworking, and just trying to support their families like I am mine.

Later that week I had a patient who clearly needed the other doctor’s expertise, and I gave her his name and phone number. She asked if I’d send my own family to him, and I said, unequivocally, “yes” (actually I have).

Because, at the end of the day, we’re all people, along on the same ride. To not send a patient to him wouldn’t be in their best interest, which is what I’m supposed to be watching out for.

Not only that, but if I don’t refer just because I disagree with him as a person, then I’ve become the problem and not the solution.

Because I, and everyone else, have to try to be better than that.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

There’s another doctor with whom I’ve referred patients, back and forth, for the last 20 years. I think he’s good at his job and assume he feels the same way about me. We aren’t social friends, but chat briefly when we run into each other at the hospital, or store, or local restaurants.

Last week I was at the hospital to read EEGs, and happened to see him in the doctor’s parking lot. We wished each other a happy new year, talked briefly about a few mutual patients, and then went our separate ways.

As he pulled out, I noticed his car had a bumper sticker for a cause I strongly disagree with. I mean, 180 degrees opposed.

Suddenly, I didn’t want to ever refer to him again. Why should I support him? He’s the enemy.

Why should I help him out by referring patients?

But then I had to stop. Isn’t this 2022? Aren’t we supposed to be in a civilized world? This isn’t my tribe versus your tribe, my cave versus your cave. The closest we’re supposed to come to direct conflict with others is the “us versus them” world of professional and college sports.

I hope.

Aren’t I supposed to be better than this? Isn’t learning to coexist the whole point of the playground as a kid (besides burning off energy and giving the teacher a break)? Isn’t the idea behind civilization to get along with each other, accept our differences as “agreeing to disagree,” and work together? Like Hamilton and Jefferson, or Ronald Reagan and Tip O’Neill?

Refusing to work with another competent physician because I disagree with their personal, religious, or political beliefs is just plain stupid.

Politicians and pundits try to convince us that people who disagree with us are the enemy, but that’s horse hockey. The truth is that the majority of people out there, regardless of personal beliefs, are decent, hardworking, and just trying to support their families like I am mine.

Later that week I had a patient who clearly needed the other doctor’s expertise, and I gave her his name and phone number. She asked if I’d send my own family to him, and I said, unequivocally, “yes” (actually I have).

Because, at the end of the day, we’re all people, along on the same ride. To not send a patient to him wouldn’t be in their best interest, which is what I’m supposed to be watching out for.

Not only that, but if I don’t refer just because I disagree with him as a person, then I’ve become the problem and not the solution.

Because I, and everyone else, have to try to be better than that.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

The Group for the Advancement of Psychiatry’s Committee on the Family published an updated curriculum in October 2021 on family-oriented care. The first curriculum, published in 2006, was nominated as the American Association of Directors of Psychiatric Residency Training model curriculum for family-oriented care. The updated curriculum, produced by the GAP family committee and guests, is shorter and more focused.

The following is a summary of the introduction and the highlights.
 

Introduction

Use of family systems–based techniques in the diagnosis and care of patients is a key evidence-based tool for psychiatric disorders. However, it is not a current Accreditation Council for Graduate Medical Education Training training requirement, and it is possible to complete psychiatry residency without exposure to this key framework.

Here, we highlight the importance of considering patients through a “family systems” lens and the incorporation of multiple individuals from an individual patient’s identified system in their care.

Current medicine curricula emphasize patient autonomy, one of the core pillars of ethics. Autonomy is the cornerstone of the everyday practice within medicine of communicating all risks, benefits, and alternatives of a proposed treatment to a patient making decisions about desired paths forward. This prevents paternalistic care in which the doctor “knows best” and makes decisions for the patient. Unfortunately, the emphasis of this pillar has morphed over time into the idea that the individual patient is the only person to whom this information should be provided or from whom information should be obtained.

Extensive research proves conclusively that family support, education, and psychoeducation improve both patient and family functioning in medical and psychiatric illness. When clinicians focus solely on the identified patient, they miss the ability to obtain key information that might influence diagnosis and treatment as well as overlook the opportunity to use the structure and support system around a patient to strengthen their care and improve treatment outcomes.

The network and family dynamics around a patient can be critical to providing accurate information on medication adherence and symptoms, supporting recovery, and handling emergencies. Markedly improved patient outcomes occur when family members are seen as allies and offered support, assessment, and psychoeducation. In fact, the American Psychiatric Association’s Practice Guidelines on the treatment of schizophrenia (2020), major depressive disorder (2010), and bipolar disorder (2002) include the expectation that patients’ family members will be involved in the assessment and treatment of patients. Yet, training in how to incorporate these practices is often minimal or nonexistent during residency.

A family systems orientation is distinguished by its view of the family as a transactional system. Stressful events and problems of an individual member affect the whole family as a functional unit, with ripple effects for all members and their relationships. In turn, the family response – how the family handles problems – contributes significantly to positive adaptation or to individual and relational dysfunction. Thus, individual problems are assessed and addressed in the context of the family, with attention to socioeconomic and other environmental stressors.

A family systems approach is distinguished less by who is in the room and more by the clinician’s attention to relationship systems in assessment and treatment planning. We need to consider how family members may contribute to – and be affected by – problem situations. Most importantly, regardless of the source of difficulties, we involve key family members who can contribute to needed changes. Interventions are aimed at modifying dysfunctional patterns, tapping family resources, and strengthening both individual and family functioning.

A family systemic lens is useful for working with all types of families, for example: refugee families, thinking through child adoption processes, working with families with specific social disadvantages, etc. Incorporating issues of race, gender, and sexual orientation is important in this work, as is working with larger systems such as schools, workplaces, and health care settings.

As opposed to previous viewpoints that family therapy is the only “family” skill to be taught during residency, the GAP committee proposes that psychiatric residents should be trained in skills of family inclusion, support, and psychoeducation, and that these skills should be taught throughout the residency. Our goal is to have residents be able to consider any case through a family systems lens, to understand how patients’ illnesses and their family systems have bidirectional effects on each other, to perform a basic assessment of family system functioning, and to use this information in diagnostic and treatment planning.
 

Training goals

Systems-based thinking will enable trainees to:

1. Ally with family members to work with the patient to comply with goals of care (for example, taking medications, complying with lifestyle changes, and maintaining sobriety).

• Teachers focus on engagement, joining with families.

2. Help patients understand the influences of their families in their own lives, such as intergenerational transmission of trauma and resilience.

• Teachers focus on the creation of a genogram, and the location of the individual within their family system.

3. Understand that mental health includes the creation and maintenance of healthy relationships.

• Teachers focus on assessing a willingness to listen to others’ points of view and the cocreation of a shared reality and belief system: a belief that relationships can change over time and how to create new family narratives.

4. Understand the impact of illness on the family unit and the impact of the family unit on illness.

• Teachers focus on the concept of a family system, clarifying the roles within the family, including caregiving responsibilities.

5. Assess the family for strengths and weaknesses.

• Teachers focus on how families maintain a healthy emotional climate, allocate roles, decide on rules, problem-solving abilities, and so on.

6. Gather information from multiple informants in the same room.

• Teachers focus on using communication techniques to elicit, guide, and redirect information from multiple individuals of a system with varying perspectives in the same room. Teachers help students understand that there are multiple realities in families and learn how to maintain multidirectional partiality.

Knowledge, skills, and attitudes across all treatment settings

Knowledge: Beginning level

• Healthy family functioning at the various phases of the family life cycle. Systems concepts are applicable to families, multidisciplinary teams in clinical settings, and medical/government organizations. However, family systems are distinguished by deep attachment bonds, specific generational hierarchy, goals of emotional safety and, for many families, child rearing.
• Systemic thinking, unlike a linear cause and effect model, examines the feedback loops by which multiple persons or groups arrive at a specific way of functioning.
• Understanding boundaries, subsystems, and feedback loops is critical to understanding interpersonal connections. Understand how the family affects and is affected by psychiatric and medical illnesses. Impact of interpersonal stress on biological systems. The role of expressed emotion (EE) in psychiatric illness. EE describes the level of criticism, hostility, and emotional overinvolvement in families. It has been studied extensively across the health care spectrum, and cultural variance is significant.
• The components of family psychoeducation, and its associated research in improving patient and family outcomes.

Knowledge: Advanced level

• Principles of adaptive and maladaptive relational functioning in family life and family organization, communication, problem solving, and emotional regulation. Role of family strengths, resilience in reducing vulnerability.
• Couple and family development over the life cycle.
• Understanding multigenerational patterns.
• How age, gender, class, culture, and spirituality affect family life.
• The variety of family forms (for example, single parent, stepfamilies, same-sex parents).
• Special issues in couples and families, including loss, divorce and remarriage, immigration, illness, secrets, affairs, violence, alcohol and substance abuse, sexuality, including LGBTQi. Relationship of families to larger systems, for example, schools, work, health care systems, government agencies.

Skills

• Family-interviewing skills, especially managing high levels of emotion and making room for multiple points of view.
• Promoting resilience, hope, and strength.
• Basic psychoeducation techniques, which includes providing a therapeutic space for emotional processing, providing information about the illness, skills such as better communication, problem-solving, and relapse drill and support.
• Collaborative treatment planning with family members and other helping professionals. Treatment planning should include all members of the system: patient, family members, and members of the treatment team. Good planning establishes a role for family members, helps define criteria for managing emergencies, looks for areas of strength and resilience and provides clear and realistic goals for treatment.
• Knowledge of, and referral to, local and national resources, both in the community and online.

Attitudes

• Appreciate the multiple points of view in a family.
• Interest in family members as people with their own needs and history.
• Including family members as a resource in recovery.
• Understand caregiver burden and rewards and that stress extends to all family members.

Training techniques

Most learning takes place at the level of patient, supervisor, and resident. It is critical that the resident sees faculty members dealing with patients in observed or shared family sessions, and /or sees videos made by faculty or professionally made videos. Attitudes are best learned by modeling.

Areas of focus can include time management, addressing the fear that family sessions may get out of control, and the influence of the residents’ own life experiences and background including potential generational or cultural differences on their assessment and interactions with patient family dynamics. In skill development, our goal is efficient interviewing, history taking, and support in controlling sessions.

It is difficult to specify which techniques are most useful in didactic sessions as each presenter will have a different skill set for engaging the class. The techniques that work best are the ones most comfortable to the presenter. Any technique that gets emotions involved, such as role play, sculpting, discussing movie clips, bringing in family members to discuss their experiences, or self-exploration, will generate the most powerful learning. If time permits, exploration of the resident’s own family, including a genogram, is an exceptionally helpful technique, especially if accompanied by asking the residents to interview their own families.
 

Adult didactic curriculum

The curriculum represents basic concepts. We have vignettes by the authors, if needed, but it is best if the class, including the supervisor, uses vignettes from their own experiences. Material for use in class is in references, but the class is urged to draw on their own experiences as this supports strength-based teaching. The following are key topics and concepts for each of the training years.
 

Basic concepts for PGY1 and PGY2

1. Where are you in the family and individual life cycles? What are your experiences with psychiatric illness in family/friends? Open discussion about how individual and family life cycles interact. Draw genograms of s/o in the class or with the supervisor.

2. Healthy family functioning and family resilience. Recommend asking residents to talk to their parents/elders about their lives and family life cycle when they were your age. Open discussion about what makes a healthy resilient family.

3. How do I connect with the family rather than just one person? How do you learn to hold multiple perspectives? How do I try not to take sides/multidirectional partiality? How do I see each person in a positive way? How do I focus on family strengths, rather than focusing on someone behaving badly (which is really hard because it is overlearned in individual therapy).

4. What are the common factors used across all therapies, both individual and family? When is it best to use an individual relational approach versus a family systemic approach?

5. How do I decide if a family needs support or education or family therapy?

6. Psychoeducation: Research, current use and cultural adaptations.

7. Attachment styles and couples therapy.

8. What is the evidence base behind our work?

System practice for PGY 3 and 4

These seminars follow the basic seminars. The focus is on clarification of what systems thinking means. Systems thinking or relational thinking is to be differentiated from systems-based practice. These lectures require knowledge of systemic practice. If there are no local experts, residency programs can reach out to national experts at the Association of Family Psychiatrists, for help with virtual/remote or in-person teaching.

Here is a list of other topics that should be covered:

• Relational formulation, nested subsystems, boundaries, history of these concepts, contributions to the development of family therapy.
• How to define and identify common systems concepts, such as circular patterns, feedback loops, and triangulation. Teach circular questioning. Framing. This concept is the family systems equivalent of insight. How to intervene to effect communication change and behavior change?
• Working at interfaces: community, legal, government, agencies, and so on, and other treaters, consultation. Include systemic and individual racism.
• Understanding the complexity of intimacy.
• Emergency situations. When to report regarding abuse. Dealing with family trauma.
• Varieties of family therapy; assumptions and major concepts.

*The new curriculum was written by The GAP Committee on the Family: Ellen Berman, MD; John Rolland, MD, MPH; John Sargent, MD; and me, and with guests Chayanin Foongsathaporn, MD; Sarah Nguyen, MD, MPH; Neha Sharma, DO; and Jodi Zik, MD. For the full curriculum, which includes residency milestones, site-specific training goals, references, and case studies, please access the Association of Family Psychiatry’s website: www.familypsychiatrists.org.Dr. Heru is professor of psychiatry at the University of Colorado Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). She has no conflicts of interest to disclose. Contact Dr. Heru at [email protected].


 

The Group for the Advancement of Psychiatry’s Committee on the Family published an updated curriculum in October 2021 on family-oriented care. The first curriculum, published in 2006, was nominated as the American Association of Directors of Psychiatric Residency Training model curriculum for family-oriented care. The updated curriculum, produced by the GAP family committee and guests, is shorter and more focused.

The following is a summary of the introduction and the highlights.
 

Introduction

Use of family systems–based techniques in the diagnosis and care of patients is a key evidence-based tool for psychiatric disorders. However, it is not a current Accreditation Council for Graduate Medical Education Training training requirement, and it is possible to complete psychiatry residency without exposure to this key framework.

Here, we highlight the importance of considering patients through a “family systems” lens and the incorporation of multiple individuals from an individual patient’s identified system in their care.

Current medicine curricula emphasize patient autonomy, one of the core pillars of ethics. Autonomy is the cornerstone of the everyday practice within medicine of communicating all risks, benefits, and alternatives of a proposed treatment to a patient making decisions about desired paths forward. This prevents paternalistic care in which the doctor “knows best” and makes decisions for the patient. Unfortunately, the emphasis of this pillar has morphed over time into the idea that the individual patient is the only person to whom this information should be provided or from whom information should be obtained.

Extensive research proves conclusively that family support, education, and psychoeducation improve both patient and family functioning in medical and psychiatric illness. When clinicians focus solely on the identified patient, they miss the ability to obtain key information that might influence diagnosis and treatment as well as overlook the opportunity to use the structure and support system around a patient to strengthen their care and improve treatment outcomes.

The network and family dynamics around a patient can be critical to providing accurate information on medication adherence and symptoms, supporting recovery, and handling emergencies. Markedly improved patient outcomes occur when family members are seen as allies and offered support, assessment, and psychoeducation. In fact, the American Psychiatric Association’s Practice Guidelines on the treatment of schizophrenia (2020), major depressive disorder (2010), and bipolar disorder (2002) include the expectation that patients’ family members will be involved in the assessment and treatment of patients. Yet, training in how to incorporate these practices is often minimal or nonexistent during residency.

A family systems orientation is distinguished by its view of the family as a transactional system. Stressful events and problems of an individual member affect the whole family as a functional unit, with ripple effects for all members and their relationships. In turn, the family response – how the family handles problems – contributes significantly to positive adaptation or to individual and relational dysfunction. Thus, individual problems are assessed and addressed in the context of the family, with attention to socioeconomic and other environmental stressors.

A family systems approach is distinguished less by who is in the room and more by the clinician’s attention to relationship systems in assessment and treatment planning. We need to consider how family members may contribute to – and be affected by – problem situations. Most importantly, regardless of the source of difficulties, we involve key family members who can contribute to needed changes. Interventions are aimed at modifying dysfunctional patterns, tapping family resources, and strengthening both individual and family functioning.

A family systemic lens is useful for working with all types of families, for example: refugee families, thinking through child adoption processes, working with families with specific social disadvantages, etc. Incorporating issues of race, gender, and sexual orientation is important in this work, as is working with larger systems such as schools, workplaces, and health care settings.

As opposed to previous viewpoints that family therapy is the only “family” skill to be taught during residency, the GAP committee proposes that psychiatric residents should be trained in skills of family inclusion, support, and psychoeducation, and that these skills should be taught throughout the residency. Our goal is to have residents be able to consider any case through a family systems lens, to understand how patients’ illnesses and their family systems have bidirectional effects on each other, to perform a basic assessment of family system functioning, and to use this information in diagnostic and treatment planning.
 

Training goals

Systems-based thinking will enable trainees to:

1. Ally with family members to work with the patient to comply with goals of care (for example, taking medications, complying with lifestyle changes, and maintaining sobriety).

• Teachers focus on engagement, joining with families.

2. Help patients understand the influences of their families in their own lives, such as intergenerational transmission of trauma and resilience.

• Teachers focus on the creation of a genogram, and the location of the individual within their family system.

3. Understand that mental health includes the creation and maintenance of healthy relationships.

• Teachers focus on assessing a willingness to listen to others’ points of view and the cocreation of a shared reality and belief system: a belief that relationships can change over time and how to create new family narratives.

4. Understand the impact of illness on the family unit and the impact of the family unit on illness.

• Teachers focus on the concept of a family system, clarifying the roles within the family, including caregiving responsibilities.

5. Assess the family for strengths and weaknesses.

• Teachers focus on how families maintain a healthy emotional climate, allocate roles, decide on rules, problem-solving abilities, and so on.

6. Gather information from multiple informants in the same room.

• Teachers focus on using communication techniques to elicit, guide, and redirect information from multiple individuals of a system with varying perspectives in the same room. Teachers help students understand that there are multiple realities in families and learn how to maintain multidirectional partiality.

Knowledge, skills, and attitudes across all treatment settings

Knowledge: Beginning level

• Healthy family functioning at the various phases of the family life cycle. Systems concepts are applicable to families, multidisciplinary teams in clinical settings, and medical/government organizations. However, family systems are distinguished by deep attachment bonds, specific generational hierarchy, goals of emotional safety and, for many families, child rearing.
• Systemic thinking, unlike a linear cause and effect model, examines the feedback loops by which multiple persons or groups arrive at a specific way of functioning.
• Understanding boundaries, subsystems, and feedback loops is critical to understanding interpersonal connections. Understand how the family affects and is affected by psychiatric and medical illnesses. Impact of interpersonal stress on biological systems. The role of expressed emotion (EE) in psychiatric illness. EE describes the level of criticism, hostility, and emotional overinvolvement in families. It has been studied extensively across the health care spectrum, and cultural variance is significant.
• The components of family psychoeducation, and its associated research in improving patient and family outcomes.

Knowledge: Advanced level

• Principles of adaptive and maladaptive relational functioning in family life and family organization, communication, problem solving, and emotional regulation. Role of family strengths, resilience in reducing vulnerability.
• Couple and family development over the life cycle.
• Understanding multigenerational patterns.
• How age, gender, class, culture, and spirituality affect family life.
• The variety of family forms (for example, single parent, stepfamilies, same-sex parents).
• Special issues in couples and families, including loss, divorce and remarriage, immigration, illness, secrets, affairs, violence, alcohol and substance abuse, sexuality, including LGBTQi. Relationship of families to larger systems, for example, schools, work, health care systems, government agencies.

Skills

• Family-interviewing skills, especially managing high levels of emotion and making room for multiple points of view.
• Promoting resilience, hope, and strength.
• Basic psychoeducation techniques, which includes providing a therapeutic space for emotional processing, providing information about the illness, skills such as better communication, problem-solving, and relapse drill and support.
• Collaborative treatment planning with family members and other helping professionals. Treatment planning should include all members of the system: patient, family members, and members of the treatment team. Good planning establishes a role for family members, helps define criteria for managing emergencies, looks for areas of strength and resilience and provides clear and realistic goals for treatment.
• Knowledge of, and referral to, local and national resources, both in the community and online.

Attitudes

• Appreciate the multiple points of view in a family.
• Interest in family members as people with their own needs and history.
• Including family members as a resource in recovery.
• Understand caregiver burden and rewards and that stress extends to all family members.

Training techniques

Most learning takes place at the level of patient, supervisor, and resident. It is critical that the resident sees faculty members dealing with patients in observed or shared family sessions, and /or sees videos made by faculty or professionally made videos. Attitudes are best learned by modeling.

Areas of focus can include time management, addressing the fear that family sessions may get out of control, and the influence of the residents’ own life experiences and background including potential generational or cultural differences on their assessment and interactions with patient family dynamics. In skill development, our goal is efficient interviewing, history taking, and support in controlling sessions.

It is difficult to specify which techniques are most useful in didactic sessions as each presenter will have a different skill set for engaging the class. The techniques that work best are the ones most comfortable to the presenter. Any technique that gets emotions involved, such as role play, sculpting, discussing movie clips, bringing in family members to discuss their experiences, or self-exploration, will generate the most powerful learning. If time permits, exploration of the resident’s own family, including a genogram, is an exceptionally helpful technique, especially if accompanied by asking the residents to interview their own families.
 

Adult didactic curriculum

The curriculum represents basic concepts. We have vignettes by the authors, if needed, but it is best if the class, including the supervisor, uses vignettes from their own experiences. Material for use in class is in references, but the class is urged to draw on their own experiences as this supports strength-based teaching. The following are key topics and concepts for each of the training years.
 

Basic concepts for PGY1 and PGY2

1. Where are you in the family and individual life cycles? What are your experiences with psychiatric illness in family/friends? Open discussion about how individual and family life cycles interact. Draw genograms of s/o in the class or with the supervisor.

2. Healthy family functioning and family resilience. Recommend asking residents to talk to their parents/elders about their lives and family life cycle when they were your age. Open discussion about what makes a healthy resilient family.

3. How do I connect with the family rather than just one person? How do you learn to hold multiple perspectives? How do I try not to take sides/multidirectional partiality? How do I see each person in a positive way? How do I focus on family strengths, rather than focusing on someone behaving badly (which is really hard because it is overlearned in individual therapy).

4. What are the common factors used across all therapies, both individual and family? When is it best to use an individual relational approach versus a family systemic approach?

5. How do I decide if a family needs support or education or family therapy?

6. Psychoeducation: Research, current use and cultural adaptations.

7. Attachment styles and couples therapy.

8. What is the evidence base behind our work?

System practice for PGY 3 and 4

These seminars follow the basic seminars. The focus is on clarification of what systems thinking means. Systems thinking or relational thinking is to be differentiated from systems-based practice. These lectures require knowledge of systemic practice. If there are no local experts, residency programs can reach out to national experts at the Association of Family Psychiatrists, for help with virtual/remote or in-person teaching.

Here is a list of other topics that should be covered:

• Relational formulation, nested subsystems, boundaries, history of these concepts, contributions to the development of family therapy.
• How to define and identify common systems concepts, such as circular patterns, feedback loops, and triangulation. Teach circular questioning. Framing. This concept is the family systems equivalent of insight. How to intervene to effect communication change and behavior change?
• Working at interfaces: community, legal, government, agencies, and so on, and other treaters, consultation. Include systemic and individual racism.
• Understanding the complexity of intimacy.
• Emergency situations. When to report regarding abuse. Dealing with family trauma.
• Varieties of family therapy; assumptions and major concepts.

*The new curriculum was written by The GAP Committee on the Family: Ellen Berman, MD; John Rolland, MD, MPH; John Sargent, MD; and me, and with guests Chayanin Foongsathaporn, MD; Sarah Nguyen, MD, MPH; Neha Sharma, DO; and Jodi Zik, MD. For the full curriculum, which includes residency milestones, site-specific training goals, references, and case studies, please access the Association of Family Psychiatry’s website: www.familypsychiatrists.org.Dr. Heru is professor of psychiatry at the University of Colorado Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). She has no conflicts of interest to disclose. Contact Dr. Heru at [email protected].


 

The Group for the Advancement of Psychiatry’s Committee on the Family published an updated curriculum in October 2021 on family-oriented care. The first curriculum, published in 2006, was nominated as the American Association of Directors of Psychiatric Residency Training model curriculum for family-oriented care. The updated curriculum, produced by the GAP family committee and guests, is shorter and more focused.

The following is a summary of the introduction and the highlights.
 

Introduction

Use of family systems–based techniques in the diagnosis and care of patients is a key evidence-based tool for psychiatric disorders. However, it is not a current Accreditation Council for Graduate Medical Education Training training requirement, and it is possible to complete psychiatry residency without exposure to this key framework.

Here, we highlight the importance of considering patients through a “family systems” lens and the incorporation of multiple individuals from an individual patient’s identified system in their care.

Current medicine curricula emphasize patient autonomy, one of the core pillars of ethics. Autonomy is the cornerstone of the everyday practice within medicine of communicating all risks, benefits, and alternatives of a proposed treatment to a patient making decisions about desired paths forward. This prevents paternalistic care in which the doctor “knows best” and makes decisions for the patient. Unfortunately, the emphasis of this pillar has morphed over time into the idea that the individual patient is the only person to whom this information should be provided or from whom information should be obtained.

Extensive research proves conclusively that family support, education, and psychoeducation improve both patient and family functioning in medical and psychiatric illness. When clinicians focus solely on the identified patient, they miss the ability to obtain key information that might influence diagnosis and treatment as well as overlook the opportunity to use the structure and support system around a patient to strengthen their care and improve treatment outcomes.

The network and family dynamics around a patient can be critical to providing accurate information on medication adherence and symptoms, supporting recovery, and handling emergencies. Markedly improved patient outcomes occur when family members are seen as allies and offered support, assessment, and psychoeducation. In fact, the American Psychiatric Association’s Practice Guidelines on the treatment of schizophrenia (2020), major depressive disorder (2010), and bipolar disorder (2002) include the expectation that patients’ family members will be involved in the assessment and treatment of patients. Yet, training in how to incorporate these practices is often minimal or nonexistent during residency.

A family systems orientation is distinguished by its view of the family as a transactional system. Stressful events and problems of an individual member affect the whole family as a functional unit, with ripple effects for all members and their relationships. In turn, the family response – how the family handles problems – contributes significantly to positive adaptation or to individual and relational dysfunction. Thus, individual problems are assessed and addressed in the context of the family, with attention to socioeconomic and other environmental stressors.

A family systems approach is distinguished less by who is in the room and more by the clinician’s attention to relationship systems in assessment and treatment planning. We need to consider how family members may contribute to – and be affected by – problem situations. Most importantly, regardless of the source of difficulties, we involve key family members who can contribute to needed changes. Interventions are aimed at modifying dysfunctional patterns, tapping family resources, and strengthening both individual and family functioning.

A family systemic lens is useful for working with all types of families, for example: refugee families, thinking through child adoption processes, working with families with specific social disadvantages, etc. Incorporating issues of race, gender, and sexual orientation is important in this work, as is working with larger systems such as schools, workplaces, and health care settings.

As opposed to previous viewpoints that family therapy is the only “family” skill to be taught during residency, the GAP committee proposes that psychiatric residents should be trained in skills of family inclusion, support, and psychoeducation, and that these skills should be taught throughout the residency. Our goal is to have residents be able to consider any case through a family systems lens, to understand how patients’ illnesses and their family systems have bidirectional effects on each other, to perform a basic assessment of family system functioning, and to use this information in diagnostic and treatment planning.
 

Training goals

Systems-based thinking will enable trainees to:

1. Ally with family members to work with the patient to comply with goals of care (for example, taking medications, complying with lifestyle changes, and maintaining sobriety).

• Teachers focus on engagement, joining with families.

2. Help patients understand the influences of their families in their own lives, such as intergenerational transmission of trauma and resilience.

• Teachers focus on the creation of a genogram, and the location of the individual within their family system.

3. Understand that mental health includes the creation and maintenance of healthy relationships.

• Teachers focus on assessing a willingness to listen to others’ points of view and the cocreation of a shared reality and belief system: a belief that relationships can change over time and how to create new family narratives.

4. Understand the impact of illness on the family unit and the impact of the family unit on illness.

• Teachers focus on the concept of a family system, clarifying the roles within the family, including caregiving responsibilities.

5. Assess the family for strengths and weaknesses.

• Teachers focus on how families maintain a healthy emotional climate, allocate roles, decide on rules, problem-solving abilities, and so on.

6. Gather information from multiple informants in the same room.

• Teachers focus on using communication techniques to elicit, guide, and redirect information from multiple individuals of a system with varying perspectives in the same room. Teachers help students understand that there are multiple realities in families and learn how to maintain multidirectional partiality.

Knowledge, skills, and attitudes across all treatment settings

Knowledge: Beginning level

• Healthy family functioning at the various phases of the family life cycle. Systems concepts are applicable to families, multidisciplinary teams in clinical settings, and medical/government organizations. However, family systems are distinguished by deep attachment bonds, specific generational hierarchy, goals of emotional safety and, for many families, child rearing.
• Systemic thinking, unlike a linear cause and effect model, examines the feedback loops by which multiple persons or groups arrive at a specific way of functioning.
• Understanding boundaries, subsystems, and feedback loops is critical to understanding interpersonal connections. Understand how the family affects and is affected by psychiatric and medical illnesses. Impact of interpersonal stress on biological systems. The role of expressed emotion (EE) in psychiatric illness. EE describes the level of criticism, hostility, and emotional overinvolvement in families. It has been studied extensively across the health care spectrum, and cultural variance is significant.
• The components of family psychoeducation, and its associated research in improving patient and family outcomes.

Knowledge: Advanced level

• Principles of adaptive and maladaptive relational functioning in family life and family organization, communication, problem solving, and emotional regulation. Role of family strengths, resilience in reducing vulnerability.
• Couple and family development over the life cycle.
• Understanding multigenerational patterns.
• How age, gender, class, culture, and spirituality affect family life.
• The variety of family forms (for example, single parent, stepfamilies, same-sex parents).
• Special issues in couples and families, including loss, divorce and remarriage, immigration, illness, secrets, affairs, violence, alcohol and substance abuse, sexuality, including LGBTQi. Relationship of families to larger systems, for example, schools, work, health care systems, government agencies.

Skills

• Family-interviewing skills, especially managing high levels of emotion and making room for multiple points of view.
• Promoting resilience, hope, and strength.
• Basic psychoeducation techniques, which includes providing a therapeutic space for emotional processing, providing information about the illness, skills such as better communication, problem-solving, and relapse drill and support.
• Collaborative treatment planning with family members and other helping professionals. Treatment planning should include all members of the system: patient, family members, and members of the treatment team. Good planning establishes a role for family members, helps define criteria for managing emergencies, looks for areas of strength and resilience and provides clear and realistic goals for treatment.
• Knowledge of, and referral to, local and national resources, both in the community and online.

Attitudes

• Appreciate the multiple points of view in a family.
• Interest in family members as people with their own needs and history.
• Including family members as a resource in recovery.
• Understand caregiver burden and rewards and that stress extends to all family members.

Training techniques

Most learning takes place at the level of patient, supervisor, and resident. It is critical that the resident sees faculty members dealing with patients in observed or shared family sessions, and /or sees videos made by faculty or professionally made videos. Attitudes are best learned by modeling.

Areas of focus can include time management, addressing the fear that family sessions may get out of control, and the influence of the residents’ own life experiences and background including potential generational or cultural differences on their assessment and interactions with patient family dynamics. In skill development, our goal is efficient interviewing, history taking, and support in controlling sessions.

It is difficult to specify which techniques are most useful in didactic sessions as each presenter will have a different skill set for engaging the class. The techniques that work best are the ones most comfortable to the presenter. Any technique that gets emotions involved, such as role play, sculpting, discussing movie clips, bringing in family members to discuss their experiences, or self-exploration, will generate the most powerful learning. If time permits, exploration of the resident’s own family, including a genogram, is an exceptionally helpful technique, especially if accompanied by asking the residents to interview their own families.
 

Adult didactic curriculum

The curriculum represents basic concepts. We have vignettes by the authors, if needed, but it is best if the class, including the supervisor, uses vignettes from their own experiences. Material for use in class is in references, but the class is urged to draw on their own experiences as this supports strength-based teaching. The following are key topics and concepts for each of the training years.
 

Basic concepts for PGY1 and PGY2

1. Where are you in the family and individual life cycles? What are your experiences with psychiatric illness in family/friends? Open discussion about how individual and family life cycles interact. Draw genograms of s/o in the class or with the supervisor.

2. Healthy family functioning and family resilience. Recommend asking residents to talk to their parents/elders about their lives and family life cycle when they were your age. Open discussion about what makes a healthy resilient family.

3. How do I connect with the family rather than just one person? How do you learn to hold multiple perspectives? How do I try not to take sides/multidirectional partiality? How do I see each person in a positive way? How do I focus on family strengths, rather than focusing on someone behaving badly (which is really hard because it is overlearned in individual therapy).

4. What are the common factors used across all therapies, both individual and family? When is it best to use an individual relational approach versus a family systemic approach?

5. How do I decide if a family needs support or education or family therapy?

6. Psychoeducation: Research, current use and cultural adaptations.

7. Attachment styles and couples therapy.

8. What is the evidence base behind our work?

System practice for PGY 3 and 4

These seminars follow the basic seminars. The focus is on clarification of what systems thinking means. Systems thinking or relational thinking is to be differentiated from systems-based practice. These lectures require knowledge of systemic practice. If there are no local experts, residency programs can reach out to national experts at the Association of Family Psychiatrists, for help with virtual/remote or in-person teaching.

Here is a list of other topics that should be covered:

• Relational formulation, nested subsystems, boundaries, history of these concepts, contributions to the development of family therapy.
• How to define and identify common systems concepts, such as circular patterns, feedback loops, and triangulation. Teach circular questioning. Framing. This concept is the family systems equivalent of insight. How to intervene to effect communication change and behavior change?
• Working at interfaces: community, legal, government, agencies, and so on, and other treaters, consultation. Include systemic and individual racism.
• Understanding the complexity of intimacy.
• Emergency situations. When to report regarding abuse. Dealing with family trauma.
• Varieties of family therapy; assumptions and major concepts.

*The new curriculum was written by The GAP Committee on the Family: Ellen Berman, MD; John Rolland, MD, MPH; John Sargent, MD; and me, and with guests Chayanin Foongsathaporn, MD; Sarah Nguyen, MD, MPH; Neha Sharma, DO; and Jodi Zik, MD. For the full curriculum, which includes residency milestones, site-specific training goals, references, and case studies, please access the Association of Family Psychiatry’s website: www.familypsychiatrists.org.Dr. Heru is professor of psychiatry at the University of Colorado Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). She has no conflicts of interest to disclose. Contact Dr. Heru at [email protected].


 

Vinogradova Y, Dening T, Hippisley-Cox J, et al. Use of menopausal hormone therapy and risk of dementia: nested case-control studies using QResearch and CPRD databases. BMJ. 2021;374:n2182. doi: 10.1136/bmj.n2182.

Much interest has surrounded whether the use of menopausal HT impacts future risk of cognitive decline. Recently, Vinogradova and colleagues conducted an observational study using data from 2 large primary care databases, QResearch and the Clinical Practice Research Datalink (CPRD), in the United Kingdom.¹ The investigators conducted case-control studies that included women aged 55 and older diagnosed with dementia and up to 5 controls without dementia. Only cases and controls with at least 10 years of medical records prior to the index date (that is, the time of dementia diagnosis in cases) were included. Since early symptoms of dementia prior to diagnosis may cause sleep problems and dysphoria (which also may be symptoms of menopause), HT prescriptions during the 3 years prior to the index date were excluded.

Details of the study

Among 16,291 cases and 68,726 controls, the women’s mean age was approximately 83 years. Cases were identified by using codes for dementia from patients’ clinical records or records of prescriptions for drugs used to treat dementia.

More than half the women were being treated for hypertension, and 14% of women in both groups had used HT. Women were considered users of estrogen-only therapy if they had no prescriptions containing a progestogen after their first prescription for systemic estrogen as the start of exposure to HT. Those with any subsequent prescription containing a progestogen were classified as combined HT users.

Results. In an analysis adjusted for all available potential confounders—including lifestyle factors, ethnicity, family history of dementia, early menopause, oophorectomy/ hysterectomy, comorbidities, and use of other relevant drugs—the use of HT was not associated with risk of dementia.

A reduced risk of dementia was noted among women who had been taking estrogen-only HT for 10 years or more (odds ratio [OR], 0.85; 95% confidence interval [CI], 0.76–0.94). An elevated risk of Alzheimer disease was noted among women who had used estrogen-progestin HT for 5 to 9 years (OR, 1.19; CI, 1.06–1.33).¹

Study strengths and limitations

The authors pointed out that this study’s main strengths were that it had a very large sample size representative of the general population and that its design permitted capture of all known cases as well as precision recording for prescribed drugs. On the other hand, the study is limited by the possible lack of data for some older women before the index date; that is, menopause in this latter group started before their registration or before these data were gathered electronically by their practice. ●

Vinogradova Y, Dening T, Hippisley-Cox J, et al. Use of menopausal hormone therapy and risk of dementia: nested case-control studies using QResearch and CPRD databases. BMJ. 2021;374:n2182. doi: 10.1136/bmj.n2182.

Much interest has surrounded whether the use of menopausal HT impacts future risk of cognitive decline. Recently, Vinogradova and colleagues conducted an observational study using data from 2 large primary care databases, QResearch and the Clinical Practice Research Datalink (CPRD), in the United Kingdom.¹ The investigators conducted case-control studies that included women aged 55 and older diagnosed with dementia and up to 5 controls without dementia. Only cases and controls with at least 10 years of medical records prior to the index date (that is, the time of dementia diagnosis in cases) were included. Since early symptoms of dementia prior to diagnosis may cause sleep problems and dysphoria (which also may be symptoms of menopause), HT prescriptions during the 3 years prior to the index date were excluded.

Details of the study

Among 16,291 cases and 68,726 controls, the women’s mean age was approximately 83 years. Cases were identified by using codes for dementia from patients’ clinical records or records of prescriptions for drugs used to treat dementia.

More than half the women were being treated for hypertension, and 14% of women in both groups had used HT. Women were considered users of estrogen-only therapy if they had no prescriptions containing a progestogen after their first prescription for systemic estrogen as the start of exposure to HT. Those with any subsequent prescription containing a progestogen were classified as combined HT users.

Results. In an analysis adjusted for all available potential confounders—including lifestyle factors, ethnicity, family history of dementia, early menopause, oophorectomy/ hysterectomy, comorbidities, and use of other relevant drugs—the use of HT was not associated with risk of dementia.

A reduced risk of dementia was noted among women who had been taking estrogen-only HT for 10 years or more (odds ratio [OR], 0.85; 95% confidence interval [CI], 0.76–0.94). An elevated risk of Alzheimer disease was noted among women who had used estrogen-progestin HT for 5 to 9 years (OR, 1.19; CI, 1.06–1.33).¹

Study strengths and limitations

The authors pointed out that this study’s main strengths were that it had a very large sample size representative of the general population and that its design permitted capture of all known cases as well as precision recording for prescribed drugs. On the other hand, the study is limited by the possible lack of data for some older women before the index date; that is, menopause in this latter group started before their registration or before these data were gathered electronically by their practice. ●

Vinogradova Y, Dening T, Hippisley-Cox J, et al. Use of menopausal hormone therapy and risk of dementia: nested case-control studies using QResearch and CPRD databases. BMJ. 2021;374:n2182. doi: 10.1136/bmj.n2182.

Much interest has surrounded whether the use of menopausal HT impacts future risk of cognitive decline. Recently, Vinogradova and colleagues conducted an observational study using data from 2 large primary care databases, QResearch and the Clinical Practice Research Datalink (CPRD), in the United Kingdom.¹ The investigators conducted case-control studies that included women aged 55 and older diagnosed with dementia and up to 5 controls without dementia. Only cases and controls with at least 10 years of medical records prior to the index date (that is, the time of dementia diagnosis in cases) were included. Since early symptoms of dementia prior to diagnosis may cause sleep problems and dysphoria (which also may be symptoms of menopause), HT prescriptions during the 3 years prior to the index date were excluded.

Details of the study

Among 16,291 cases and 68,726 controls, the women’s mean age was approximately 83 years. Cases were identified by using codes for dementia from patients’ clinical records or records of prescriptions for drugs used to treat dementia.

More than half the women were being treated for hypertension, and 14% of women in both groups had used HT. Women were considered users of estrogen-only therapy if they had no prescriptions containing a progestogen after their first prescription for systemic estrogen as the start of exposure to HT. Those with any subsequent prescription containing a progestogen were classified as combined HT users.

Results. In an analysis adjusted for all available potential confounders—including lifestyle factors, ethnicity, family history of dementia, early menopause, oophorectomy/ hysterectomy, comorbidities, and use of other relevant drugs—the use of HT was not associated with risk of dementia.

A reduced risk of dementia was noted among women who had been taking estrogen-only HT for 10 years or more (odds ratio [OR], 0.85; 95% confidence interval [CI], 0.76–0.94). An elevated risk of Alzheimer disease was noted among women who had used estrogen-progestin HT for 5 to 9 years (OR, 1.19; CI, 1.06–1.33).¹

Study strengths and limitations

The authors pointed out that this study’s main strengths were that it had a very large sample size representative of the general population and that its design permitted capture of all known cases as well as precision recording for prescribed drugs. On the other hand, the study is limited by the possible lack of data for some older women before the index date; that is, menopause in this latter group started before their registration or before these data were gathered electronically by their practice. ●