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Expert gives tips on less-discussed dermatologic diseases

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While less frequently seen dermatologic diseases do not get a “ton of attention” in expert talks and discussions, even one to two patients presenting with these conditions a month warrants continuing education, according to Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington.

These semi-forsaken diseases are important not to miss and can “also be quite challenging when we think about their management,” he said at the ODAC Dermatology, Aesthetic & Surgical Conference.

Dr. Adam Friedman

Dr. Friedman, also director of the GW dermatology residency program, reviewed several of these diseases – along with tips for management – during a session at the meeting.

Granuloma annulare (GA). This condition, Dr. Friedman said, can have “a lot of faces” – with a localized, general, perforating, subcutaneous, micropapular, or patchy appearance. It does not always have the classic ring pattern for which it is best known, he said. And in patients with darker skin tones, it is characterized by more of a brown or black color, rather than the pink-red color.

Dr. Friedman said that despite a kind of “Pavlovian response” linking GA with diabetes, this link might not be as strong as the field has come to believe, since the studies on which this belief was based included a patient population with narrow demographics. “Maybe GA and type 1 diabetes aren’t necessarily connected,” he said.

Dyslipidemia, on the other hand, has a strong connection with GA, he said. The disease is also linked to thyroid disease and is linked with malignancy, especially in older patients with generalized or atypical presentations of GA, he said.

Spontaneous resolution of the disease is seen within 2 years for 50% to 75% of patients, so “no treatment may be the best treatment,” but antimalarials can be effective, Dr. Friedman said. “I use antimalarials frequently in my practice,” he said. “The key is, they take time to work (4-5 months),” which should be explained to patients.

Antibiotics, he said, can be “somewhat effective,” but in the case of doxycycline at least, the disease can resolve within weeks but then may return when treatment is stopped.

There is some evidence to support using biologics and more recently, Janus kinase (JAK) inhibitors, off-label, to treat GA. Efficacy has been seen with the tumor necrosis factor (TNF) blocker infliximab and with the JAK inhibitor tofacitinib, he said.

 Lichen planus (LP). This is another common disease that can go off-script with its presentation. The disease is often described with the “six P’s” indicating the following characteristics: pruritic, polygonal, planar or flat-topped, purple papules, and plaques. But LP “didn’t read the textbook,” Dr. Friedman said.

“The clinical presentation of lichen planus can be quite broad,” he said. “The P’s aren’t always followed as there are a variety of colors and configurations which can be witnessed.”

With LP, there is a clear association with dyslipidemia and diabetes, so “asking the right questions is going to be important” when talking to the patient. There is also a higher risk of autoimmune diseases, especially of the thyroid type, associated with LP, he said.

No treatment has been Food and Drug Administration approved for LP, but some are expected in the future, he said.

For now, he emphasized creativity in the management of patients with LP. “I love oral retinoids for this,” he said. Antimalarials and methotrexate are also options.

In one case Dr. Friedman saw, nothing seemed to work: light therapy for a year; metronidazole; isotretinoin; halobetasol/tazarotene lotion; and the TNF-blocker adalimumab either weren’t effective or resulted in complications in the patient.

Knowing the recent implication of the interleukin (IL)-17 pathway in the pathophysiology of LP, he then tried the anti-IL17 antibody secukinumab. “This patient had a pretty robust response to treatment,” Dr. Friedman said. “He was very excited. The problem, as always, is access, especially for off-label therapies.”

Tumid lupus erythematosus. This disease is characterized by erythematous, edematous, nonscarring plaques on sun-exposed sites. For treatment, Dr. Friedman said antimalarials can be up to 90% effective, sometimes with rapid resolution of the lesions.

“You want to dose below that 5 mg per kg of true body weight to limit the small potential for ocular toxicity over time,” he said. And, he emphasized, “always combine treatment with good sun-protective measures.”

Dr. Friedman reported financial relationships with Sanova, Pfizer, Novartis, and other companies.

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While less frequently seen dermatologic diseases do not get a “ton of attention” in expert talks and discussions, even one to two patients presenting with these conditions a month warrants continuing education, according to Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington.

These semi-forsaken diseases are important not to miss and can “also be quite challenging when we think about their management,” he said at the ODAC Dermatology, Aesthetic & Surgical Conference.

Dr. Adam Friedman

Dr. Friedman, also director of the GW dermatology residency program, reviewed several of these diseases – along with tips for management – during a session at the meeting.

Granuloma annulare (GA). This condition, Dr. Friedman said, can have “a lot of faces” – with a localized, general, perforating, subcutaneous, micropapular, or patchy appearance. It does not always have the classic ring pattern for which it is best known, he said. And in patients with darker skin tones, it is characterized by more of a brown or black color, rather than the pink-red color.

Dr. Friedman said that despite a kind of “Pavlovian response” linking GA with diabetes, this link might not be as strong as the field has come to believe, since the studies on which this belief was based included a patient population with narrow demographics. “Maybe GA and type 1 diabetes aren’t necessarily connected,” he said.

Dyslipidemia, on the other hand, has a strong connection with GA, he said. The disease is also linked to thyroid disease and is linked with malignancy, especially in older patients with generalized or atypical presentations of GA, he said.

Spontaneous resolution of the disease is seen within 2 years for 50% to 75% of patients, so “no treatment may be the best treatment,” but antimalarials can be effective, Dr. Friedman said. “I use antimalarials frequently in my practice,” he said. “The key is, they take time to work (4-5 months),” which should be explained to patients.

Antibiotics, he said, can be “somewhat effective,” but in the case of doxycycline at least, the disease can resolve within weeks but then may return when treatment is stopped.

There is some evidence to support using biologics and more recently, Janus kinase (JAK) inhibitors, off-label, to treat GA. Efficacy has been seen with the tumor necrosis factor (TNF) blocker infliximab and with the JAK inhibitor tofacitinib, he said.

 Lichen planus (LP). This is another common disease that can go off-script with its presentation. The disease is often described with the “six P’s” indicating the following characteristics: pruritic, polygonal, planar or flat-topped, purple papules, and plaques. But LP “didn’t read the textbook,” Dr. Friedman said.

“The clinical presentation of lichen planus can be quite broad,” he said. “The P’s aren’t always followed as there are a variety of colors and configurations which can be witnessed.”

With LP, there is a clear association with dyslipidemia and diabetes, so “asking the right questions is going to be important” when talking to the patient. There is also a higher risk of autoimmune diseases, especially of the thyroid type, associated with LP, he said.

No treatment has been Food and Drug Administration approved for LP, but some are expected in the future, he said.

For now, he emphasized creativity in the management of patients with LP. “I love oral retinoids for this,” he said. Antimalarials and methotrexate are also options.

In one case Dr. Friedman saw, nothing seemed to work: light therapy for a year; metronidazole; isotretinoin; halobetasol/tazarotene lotion; and the TNF-blocker adalimumab either weren’t effective or resulted in complications in the patient.

Knowing the recent implication of the interleukin (IL)-17 pathway in the pathophysiology of LP, he then tried the anti-IL17 antibody secukinumab. “This patient had a pretty robust response to treatment,” Dr. Friedman said. “He was very excited. The problem, as always, is access, especially for off-label therapies.”

Tumid lupus erythematosus. This disease is characterized by erythematous, edematous, nonscarring plaques on sun-exposed sites. For treatment, Dr. Friedman said antimalarials can be up to 90% effective, sometimes with rapid resolution of the lesions.

“You want to dose below that 5 mg per kg of true body weight to limit the small potential for ocular toxicity over time,” he said. And, he emphasized, “always combine treatment with good sun-protective measures.”

Dr. Friedman reported financial relationships with Sanova, Pfizer, Novartis, and other companies.

While less frequently seen dermatologic diseases do not get a “ton of attention” in expert talks and discussions, even one to two patients presenting with these conditions a month warrants continuing education, according to Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington.

These semi-forsaken diseases are important not to miss and can “also be quite challenging when we think about their management,” he said at the ODAC Dermatology, Aesthetic & Surgical Conference.

Dr. Adam Friedman

Dr. Friedman, also director of the GW dermatology residency program, reviewed several of these diseases – along with tips for management – during a session at the meeting.

Granuloma annulare (GA). This condition, Dr. Friedman said, can have “a lot of faces” – with a localized, general, perforating, subcutaneous, micropapular, or patchy appearance. It does not always have the classic ring pattern for which it is best known, he said. And in patients with darker skin tones, it is characterized by more of a brown or black color, rather than the pink-red color.

Dr. Friedman said that despite a kind of “Pavlovian response” linking GA with diabetes, this link might not be as strong as the field has come to believe, since the studies on which this belief was based included a patient population with narrow demographics. “Maybe GA and type 1 diabetes aren’t necessarily connected,” he said.

Dyslipidemia, on the other hand, has a strong connection with GA, he said. The disease is also linked to thyroid disease and is linked with malignancy, especially in older patients with generalized or atypical presentations of GA, he said.

Spontaneous resolution of the disease is seen within 2 years for 50% to 75% of patients, so “no treatment may be the best treatment,” but antimalarials can be effective, Dr. Friedman said. “I use antimalarials frequently in my practice,” he said. “The key is, they take time to work (4-5 months),” which should be explained to patients.

Antibiotics, he said, can be “somewhat effective,” but in the case of doxycycline at least, the disease can resolve within weeks but then may return when treatment is stopped.

There is some evidence to support using biologics and more recently, Janus kinase (JAK) inhibitors, off-label, to treat GA. Efficacy has been seen with the tumor necrosis factor (TNF) blocker infliximab and with the JAK inhibitor tofacitinib, he said.

 Lichen planus (LP). This is another common disease that can go off-script with its presentation. The disease is often described with the “six P’s” indicating the following characteristics: pruritic, polygonal, planar or flat-topped, purple papules, and plaques. But LP “didn’t read the textbook,” Dr. Friedman said.

“The clinical presentation of lichen planus can be quite broad,” he said. “The P’s aren’t always followed as there are a variety of colors and configurations which can be witnessed.”

With LP, there is a clear association with dyslipidemia and diabetes, so “asking the right questions is going to be important” when talking to the patient. There is also a higher risk of autoimmune diseases, especially of the thyroid type, associated with LP, he said.

No treatment has been Food and Drug Administration approved for LP, but some are expected in the future, he said.

For now, he emphasized creativity in the management of patients with LP. “I love oral retinoids for this,” he said. Antimalarials and methotrexate are also options.

In one case Dr. Friedman saw, nothing seemed to work: light therapy for a year; metronidazole; isotretinoin; halobetasol/tazarotene lotion; and the TNF-blocker adalimumab either weren’t effective or resulted in complications in the patient.

Knowing the recent implication of the interleukin (IL)-17 pathway in the pathophysiology of LP, he then tried the anti-IL17 antibody secukinumab. “This patient had a pretty robust response to treatment,” Dr. Friedman said. “He was very excited. The problem, as always, is access, especially for off-label therapies.”

Tumid lupus erythematosus. This disease is characterized by erythematous, edematous, nonscarring plaques on sun-exposed sites. For treatment, Dr. Friedman said antimalarials can be up to 90% effective, sometimes with rapid resolution of the lesions.

“You want to dose below that 5 mg per kg of true body weight to limit the small potential for ocular toxicity over time,” he said. And, he emphasized, “always combine treatment with good sun-protective measures.”

Dr. Friedman reported financial relationships with Sanova, Pfizer, Novartis, and other companies.

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Expert offers insights on pediatric dermatology emergencies

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ORLANDO – Three weeks after a course of trimethoprim/sulfamethoxazole (Bactrim), a young female patient developed facial edema that involved “dusky erythematous papules” that were itchy. The eruption spread away from the head and her transaminase levels were “dramatic,” in the 700s, said Kalyani S. Marathe, MD, MPH, associate professor of dermatology and pediatrics at the University of Cincinnati.

Dr. Marathe, director of the division of dermatology at Cincinnati Children’s Hospital, reviewed this case in a presentation on pediatric dermatologic emergencies at the ODAC Dermatology, Aesthetic & Surgery Conference, pointing out potential pitfalls and important aspects that might require swift action.

Dr. Kalyani S. Marathe

The patient was diagnosed with drug reaction with eosinophilia and systemic symptoms (DRESS).

Facial involvement is common in pediatric cases of DRESS, but edema of the face is less common in children than adults, Dr. Marathe said.

Antiepileptic medications are the most common cause of DRESS, followed by antibiotics – most often, vancomycin and trimethoprim/sulfamethoxazole, she said. But sometimes the trigger is not clear, she noted, recalling a vexing case she once saw in which IV contrast was eventually identified as the cause.

When DRESS is suspected, she said, lab work should be done during the acute eruption and after resolution. This should include CBC, liver function tests, creatinine, and urinalysis, and human herpesvirus 6 (HHV-6) and thyroid testing.

Treatment typically includes supportive care, unless symptoms are systemic, or if there is impending liver failure, when steroids, cyclosporine, or IVIG can be used.

Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN): Mortality rates when these diseases overlap is 4%, Dr. Marathe said. Clues to diagnosing this other medication-induced condition include involvement of the palms and the soles of the feet; presence of the Nikolsky sign in which the top layers of the skin slip away from the lower layers when rubbed; mucosal involvement, which often precedes cutaneous involvement; and these symptoms occurring within the first 8 weeks of taking a medication, which are most commonly antibiotics and anti-epileptics.

Dr. Marathe underscored how important it is to get ophthalmology involved right away, because of the risk of vision loss. Amniotic membrane transfer to the eye at the time of diagnosis has been found to produce dramatically better outcomes, she said. The membrane has anti-inflammatory and antiscarring properties and can promote wound healing on the surface of the eye.

“I would recommend getting your ophthalmology team on board early because they have to advocate for these patients,” she said.

Corticosteroids and IVIG can improve ocular outcomes, but cyclosporine is associated with better mortality outcomes, she said. Emerging data on etanercept has also led to more use of that drug, she said.



Erythema multiforme (EM): unlike urticaria, multiforme EM can have mucosal involvement, Dr. Marathe said. Clinicians should look for three zones of color: A central duskiness, a rim of pallor, and a ring of erythema.

EM is triggered by a virus, which is usually herpes simplex virus (HSV). But she added that HSV is not always found. “So, there are certainly other triggers out there that we just haven’t identified,” she said.

If HSV is suspected, oral acyclovir is effective, she noted.

Other cases might not be as straightforward. Dr. Marathe said that during her fellowship, she saw a patient with EM that was controlled only by IVIG, so it was administered every 3 months. In that case, the trigger was never found.

Multisystem inflammatory syndrome in children (MIS-C): This syndrome can follow COVID-19 infection, and usually presents with 3-5 days of fever after COVID has resolved. It can include gastrointestinal, cardiorespiratory, and neurocognitive symptoms.

The skin presentation is mainly a morbilliform pattern, but clinicians might also see conjunctival involvement, mucosal involvement, and “COVID toes,” painful red or purple lesions on the toes.

Treatment is usually IVIG and systemic corticosteroids, with the treatment course depending on the severity.

MIS-C was initially thought to be Kawasaki’s disease, another autoinflammatory disorder, which is related but distinct, Dr. Marathe said.

Patients with MIS-C “are usually going to have COVID-positive antibodies,” she said. But since almost everybody may have COVID antibodies, “it’s not usually a helpful test for you now. But early on, that’s what we used as helpful indicator.”

Dr. Marathe reported no relevant financial relationships.

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ORLANDO – Three weeks after a course of trimethoprim/sulfamethoxazole (Bactrim), a young female patient developed facial edema that involved “dusky erythematous papules” that were itchy. The eruption spread away from the head and her transaminase levels were “dramatic,” in the 700s, said Kalyani S. Marathe, MD, MPH, associate professor of dermatology and pediatrics at the University of Cincinnati.

Dr. Marathe, director of the division of dermatology at Cincinnati Children’s Hospital, reviewed this case in a presentation on pediatric dermatologic emergencies at the ODAC Dermatology, Aesthetic & Surgery Conference, pointing out potential pitfalls and important aspects that might require swift action.

Dr. Kalyani S. Marathe

The patient was diagnosed with drug reaction with eosinophilia and systemic symptoms (DRESS).

Facial involvement is common in pediatric cases of DRESS, but edema of the face is less common in children than adults, Dr. Marathe said.

Antiepileptic medications are the most common cause of DRESS, followed by antibiotics – most often, vancomycin and trimethoprim/sulfamethoxazole, she said. But sometimes the trigger is not clear, she noted, recalling a vexing case she once saw in which IV contrast was eventually identified as the cause.

When DRESS is suspected, she said, lab work should be done during the acute eruption and after resolution. This should include CBC, liver function tests, creatinine, and urinalysis, and human herpesvirus 6 (HHV-6) and thyroid testing.

Treatment typically includes supportive care, unless symptoms are systemic, or if there is impending liver failure, when steroids, cyclosporine, or IVIG can be used.

Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN): Mortality rates when these diseases overlap is 4%, Dr. Marathe said. Clues to diagnosing this other medication-induced condition include involvement of the palms and the soles of the feet; presence of the Nikolsky sign in which the top layers of the skin slip away from the lower layers when rubbed; mucosal involvement, which often precedes cutaneous involvement; and these symptoms occurring within the first 8 weeks of taking a medication, which are most commonly antibiotics and anti-epileptics.

Dr. Marathe underscored how important it is to get ophthalmology involved right away, because of the risk of vision loss. Amniotic membrane transfer to the eye at the time of diagnosis has been found to produce dramatically better outcomes, she said. The membrane has anti-inflammatory and antiscarring properties and can promote wound healing on the surface of the eye.

“I would recommend getting your ophthalmology team on board early because they have to advocate for these patients,” she said.

Corticosteroids and IVIG can improve ocular outcomes, but cyclosporine is associated with better mortality outcomes, she said. Emerging data on etanercept has also led to more use of that drug, she said.



Erythema multiforme (EM): unlike urticaria, multiforme EM can have mucosal involvement, Dr. Marathe said. Clinicians should look for three zones of color: A central duskiness, a rim of pallor, and a ring of erythema.

EM is triggered by a virus, which is usually herpes simplex virus (HSV). But she added that HSV is not always found. “So, there are certainly other triggers out there that we just haven’t identified,” she said.

If HSV is suspected, oral acyclovir is effective, she noted.

Other cases might not be as straightforward. Dr. Marathe said that during her fellowship, she saw a patient with EM that was controlled only by IVIG, so it was administered every 3 months. In that case, the trigger was never found.

Multisystem inflammatory syndrome in children (MIS-C): This syndrome can follow COVID-19 infection, and usually presents with 3-5 days of fever after COVID has resolved. It can include gastrointestinal, cardiorespiratory, and neurocognitive symptoms.

The skin presentation is mainly a morbilliform pattern, but clinicians might also see conjunctival involvement, mucosal involvement, and “COVID toes,” painful red or purple lesions on the toes.

Treatment is usually IVIG and systemic corticosteroids, with the treatment course depending on the severity.

MIS-C was initially thought to be Kawasaki’s disease, another autoinflammatory disorder, which is related but distinct, Dr. Marathe said.

Patients with MIS-C “are usually going to have COVID-positive antibodies,” she said. But since almost everybody may have COVID antibodies, “it’s not usually a helpful test for you now. But early on, that’s what we used as helpful indicator.”

Dr. Marathe reported no relevant financial relationships.

ORLANDO – Three weeks after a course of trimethoprim/sulfamethoxazole (Bactrim), a young female patient developed facial edema that involved “dusky erythematous papules” that were itchy. The eruption spread away from the head and her transaminase levels were “dramatic,” in the 700s, said Kalyani S. Marathe, MD, MPH, associate professor of dermatology and pediatrics at the University of Cincinnati.

Dr. Marathe, director of the division of dermatology at Cincinnati Children’s Hospital, reviewed this case in a presentation on pediatric dermatologic emergencies at the ODAC Dermatology, Aesthetic & Surgery Conference, pointing out potential pitfalls and important aspects that might require swift action.

Dr. Kalyani S. Marathe

The patient was diagnosed with drug reaction with eosinophilia and systemic symptoms (DRESS).

Facial involvement is common in pediatric cases of DRESS, but edema of the face is less common in children than adults, Dr. Marathe said.

Antiepileptic medications are the most common cause of DRESS, followed by antibiotics – most often, vancomycin and trimethoprim/sulfamethoxazole, she said. But sometimes the trigger is not clear, she noted, recalling a vexing case she once saw in which IV contrast was eventually identified as the cause.

When DRESS is suspected, she said, lab work should be done during the acute eruption and after resolution. This should include CBC, liver function tests, creatinine, and urinalysis, and human herpesvirus 6 (HHV-6) and thyroid testing.

Treatment typically includes supportive care, unless symptoms are systemic, or if there is impending liver failure, when steroids, cyclosporine, or IVIG can be used.

Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN): Mortality rates when these diseases overlap is 4%, Dr. Marathe said. Clues to diagnosing this other medication-induced condition include involvement of the palms and the soles of the feet; presence of the Nikolsky sign in which the top layers of the skin slip away from the lower layers when rubbed; mucosal involvement, which often precedes cutaneous involvement; and these symptoms occurring within the first 8 weeks of taking a medication, which are most commonly antibiotics and anti-epileptics.

Dr. Marathe underscored how important it is to get ophthalmology involved right away, because of the risk of vision loss. Amniotic membrane transfer to the eye at the time of diagnosis has been found to produce dramatically better outcomes, she said. The membrane has anti-inflammatory and antiscarring properties and can promote wound healing on the surface of the eye.

“I would recommend getting your ophthalmology team on board early because they have to advocate for these patients,” she said.

Corticosteroids and IVIG can improve ocular outcomes, but cyclosporine is associated with better mortality outcomes, she said. Emerging data on etanercept has also led to more use of that drug, she said.



Erythema multiforme (EM): unlike urticaria, multiforme EM can have mucosal involvement, Dr. Marathe said. Clinicians should look for three zones of color: A central duskiness, a rim of pallor, and a ring of erythema.

EM is triggered by a virus, which is usually herpes simplex virus (HSV). But she added that HSV is not always found. “So, there are certainly other triggers out there that we just haven’t identified,” she said.

If HSV is suspected, oral acyclovir is effective, she noted.

Other cases might not be as straightforward. Dr. Marathe said that during her fellowship, she saw a patient with EM that was controlled only by IVIG, so it was administered every 3 months. In that case, the trigger was never found.

Multisystem inflammatory syndrome in children (MIS-C): This syndrome can follow COVID-19 infection, and usually presents with 3-5 days of fever after COVID has resolved. It can include gastrointestinal, cardiorespiratory, and neurocognitive symptoms.

The skin presentation is mainly a morbilliform pattern, but clinicians might also see conjunctival involvement, mucosal involvement, and “COVID toes,” painful red or purple lesions on the toes.

Treatment is usually IVIG and systemic corticosteroids, with the treatment course depending on the severity.

MIS-C was initially thought to be Kawasaki’s disease, another autoinflammatory disorder, which is related but distinct, Dr. Marathe said.

Patients with MIS-C “are usually going to have COVID-positive antibodies,” she said. But since almost everybody may have COVID antibodies, “it’s not usually a helpful test for you now. But early on, that’s what we used as helpful indicator.”

Dr. Marathe reported no relevant financial relationships.

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First Humira biosimilar launches in U.S.

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The first biosimilar for Humira, adalimumab-atto (Amjevita), is now available in the United States, according to an announcement on Jan. 31 by the manufacturer, Amgen. At least seven other U.S. Food and Drug Administration–approved Humira biosimilars are expected to become available later in 2023.

Amjevita was approved by the FDA in September 2016 for multiple inflammatory diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn’s disease, ulcerative colitis, and plaque psoriasis. The delayed launch was part of a global settlement with Humira’s manufacturer, AbbVie.

Humira (adalimumab) has been available since 2002 and is consistently one of the top-selling drugs in the United States. A single 40-mg Amjevita pen device will be available at two prices: a list price (wholesale acquisition cost) of $1,557.59, 55% below the current Humira list price, and a list price of $3,288.24, 5% below the current Humira list price, according to Amgen.

“Amgen’s goal is to provide broad access for patients by offering two options to health plans and pharmacy benefit managers,” the company said in the press release.

Patients are less likely to benefit from the more significant discount, said Marta Wosinska, PhD, a health care economist at the Brookings Institute in Washington, DC. It's expected that insurance companies will use the higher list price for Amjevita, she said, as this higher price will also likely have higher rebates. Rebates are payments to health insurance payers provided by drug manufacturers to promote use of an expensive drug. Some pharmacy benefit managers have already said that they plan to charge patients the same amount for Humira as its biosimilars, Dr. Wosinska said.

"For an existing patient, there's really no incentive for them to switch," she said in an interview.

So far only one insurance company, Kaiser Permanente, has plans to switch patients over to biosimilars, according to the health policy podcast Tradeoffs, and the insurer will stop covering Humira by the end of this year.

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

*This story was updated 2/1/2023.

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The first biosimilar for Humira, adalimumab-atto (Amjevita), is now available in the United States, according to an announcement on Jan. 31 by the manufacturer, Amgen. At least seven other U.S. Food and Drug Administration–approved Humira biosimilars are expected to become available later in 2023.

Amjevita was approved by the FDA in September 2016 for multiple inflammatory diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn’s disease, ulcerative colitis, and plaque psoriasis. The delayed launch was part of a global settlement with Humira’s manufacturer, AbbVie.

Humira (adalimumab) has been available since 2002 and is consistently one of the top-selling drugs in the United States. A single 40-mg Amjevita pen device will be available at two prices: a list price (wholesale acquisition cost) of $1,557.59, 55% below the current Humira list price, and a list price of $3,288.24, 5% below the current Humira list price, according to Amgen.

“Amgen’s goal is to provide broad access for patients by offering two options to health plans and pharmacy benefit managers,” the company said in the press release.

Patients are less likely to benefit from the more significant discount, said Marta Wosinska, PhD, a health care economist at the Brookings Institute in Washington, DC. It's expected that insurance companies will use the higher list price for Amjevita, she said, as this higher price will also likely have higher rebates. Rebates are payments to health insurance payers provided by drug manufacturers to promote use of an expensive drug. Some pharmacy benefit managers have already said that they plan to charge patients the same amount for Humira as its biosimilars, Dr. Wosinska said.

"For an existing patient, there's really no incentive for them to switch," she said in an interview.

So far only one insurance company, Kaiser Permanente, has plans to switch patients over to biosimilars, according to the health policy podcast Tradeoffs, and the insurer will stop covering Humira by the end of this year.

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

*This story was updated 2/1/2023.

The first biosimilar for Humira, adalimumab-atto (Amjevita), is now available in the United States, according to an announcement on Jan. 31 by the manufacturer, Amgen. At least seven other U.S. Food and Drug Administration–approved Humira biosimilars are expected to become available later in 2023.

Amjevita was approved by the FDA in September 2016 for multiple inflammatory diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn’s disease, ulcerative colitis, and plaque psoriasis. The delayed launch was part of a global settlement with Humira’s manufacturer, AbbVie.

Humira (adalimumab) has been available since 2002 and is consistently one of the top-selling drugs in the United States. A single 40-mg Amjevita pen device will be available at two prices: a list price (wholesale acquisition cost) of $1,557.59, 55% below the current Humira list price, and a list price of $3,288.24, 5% below the current Humira list price, according to Amgen.

“Amgen’s goal is to provide broad access for patients by offering two options to health plans and pharmacy benefit managers,” the company said in the press release.

Patients are less likely to benefit from the more significant discount, said Marta Wosinska, PhD, a health care economist at the Brookings Institute in Washington, DC. It's expected that insurance companies will use the higher list price for Amjevita, she said, as this higher price will also likely have higher rebates. Rebates are payments to health insurance payers provided by drug manufacturers to promote use of an expensive drug. Some pharmacy benefit managers have already said that they plan to charge patients the same amount for Humira as its biosimilars, Dr. Wosinska said.

"For an existing patient, there's really no incentive for them to switch," she said in an interview.

So far only one insurance company, Kaiser Permanente, has plans to switch patients over to biosimilars, according to the health policy podcast Tradeoffs, and the insurer will stop covering Humira by the end of this year.

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

*This story was updated 2/1/2023.

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The Ins and Outs of Transferring Residency Programs

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The Ins and Outs of Transferring Residency Programs

Transferring from one residency program to another is rare but not unheard of. According to the most recent Accreditation Council for Graduate Medical Education Data Resource Book, there were 1020 residents who transferred residency programs in the 2020-2021 academic year.1 With a total of 126,759 active residents in specialty programs, the percentage of transferring residents was less than 1%. The specialties with the highest number of transferring residents included psychiatry, general surgery, internal medicine, and family medicine. In dermatology programs, there were only 2 resident transfers during the 2019-2020 academic year and 6 transfers in the 2020-2021 academic year.1,2 A resident contemplating transferring training programs must carefully consider the advantages and disadvantages before undertaking the uncertain transfer process, but transferring residency programs can be achieved successfully with planning and luck.

Deciding to Transfer

The decision to transfer residency programs may be a difficult one that is wrought with anxiety. There are many reasons why a trainee may wish to pursue transferring training programs. A transfer to another geographic area may be necessary for personal or family reasons, such as to reunite with a spouse and children or to care for a sick family member. A resident may find their program to be a poor fit and may wish to train in a different educational environment. Occasionally, a program can lose its accreditation, and its residents will be tasked with finding a new position elsewhere. A trainee also may realize that the specialty they matched into initially does not align with their true passions. It is important for the potential transfer applicant to be levelheaded about their decision. Residency is a demanding period for every trainee; switching programs may not be the best solution for every problem and should only be considered if essential.

Transfer Timing

A trainee may have thoughts of leaving a program soon after starting residency or perhaps even before starting if their National Resident Matching Program (NRMP) Match result was a disappointment; however, there are certain rules related to transfer timing. The NRMP Match represents a binding commitment for both the applicant and program. If for any reason an applicant will not honor the binding commitment, the NRMP requires the applicant to initiate a waiver review, which can be requested for unanticipated serious and extreme hardship, change of specialty, or ineligibility. According to the NRMP rules and regulations, applicants cannot apply for, discuss, interview for, or accept a position in another program until a waiver has been granted.3 Waivers based on change of specialty must be requested by mid-January prior to the start of training, which means most applicants who match to positions that begin in the same year of the Match do not qualify for change of specialty waivers. However, those who matched to an advanced position and are doing a preliminary year position may consider this option if they have a change of heart during their internship. The NRMP may consider a 1-year deferral to delay training if mutually agreed upon by both the matched applicant and the program.3 The binding commitment is in place for the first 45 days of training, and applicants who resign within 45 days or a program that tries to solicit the transfer of a resident prior to that date could be in violation of the Match and can face consequences such as being barred from entering the matching process in future cycles. Of the 1020 transfers that occurred among residents in specialty programs during the 2020-2021 academic year, 354 (34.7%) occurred during the first year of the training program; 228 (22.4%) occurred during the second year; 389 (38.1%) occurred during the third year; and 49 (4.8%) occurred in the fourth, fifth, or sixth year of the program.1 Unlike other jobs/occupations in which one can simply give notice, in medical training even if a transfer position is accepted, the transition date between programs must be mutually agreed upon. Often, this may coincide with the start of the new academic year.

The Transfer Process

Transferring residency programs is a substantial undertaking. Unlike the Match, a trainee seeking to transfer programs does so without a standardized application system or structured support through the process; the transfer applicant must be prepared to navigate the transfer process on their own. The first step after making the decision to transfer is for the resident to meet with the program leadership (ie, program director[s], coordinator, designated official) at their home program to discuss the decision—a nerve-wracking but imperative first step. A receiving program may not favor an applicant secretly applying to a new program without the knowledge of their home program and often will require the home program’s blessing to proceed. The receiving program also would want to ensure the applicant is in good standing and not leaving due to misconduct. Once given the go-ahead, the process is largely in the hands of the applicant. The transfer applicant should identify locations or programs of interest and then take initiative to reach out to potential programs. FREIDA (Fellowship and Residency Electronic Interactive Database Access) is the American Medical Association’s residency and fellowship database that allows vacant position listings to be posted online.4 Additionally, the Association of American Medical Colleges’ FindAResident website is a year-round search tool designed to help find open residency and fellowship positions.5 Various specialties also may have program director listserves that communicate vacant positions. On occasion, there are spots in the main NRMP Match that are reserved positions (“R”). These are postgraduate year 2 positions in specialty programs that begin in the year of the Match and are reserved for physicians with prior graduate medical education; these also are known as “Physician Positions.”6 Ultimately, advertisements for vacancies may be few and far between, requiring the resident to send unsolicited emails with curriculum vitae attached to the program directors at programs of interest to inquire about any vacancies and hope for a favorable response. Even if the transfer applicant is qualified, luck that the right spot will be available at the right time may be the deciding factor in transferring programs.

The next step is interviewing for the position. There likely will be fewer candidates interviewing for an open spot but that does not make the process less competitive. The candidate should highlight their strengths and achievements and discuss why the new program would be a great fit both personally and professionally. Even if an applicant is seeking a transfer due to discontent with a prior program, it is best to act graciously and not speak poorly about another training program.

Prior to selection, the candidate may be asked to provide information such as diplomas, US Medical Licensing Examination Step and residency in-service training examination scores, and academic reviews from their current residency program. The interview process may take several weeks as the graduate medical education office often will need to officially approve of an applicant before a formal offer to transfer is extended.

Finally, once an offer is made and accepted, there still is a great amount of paperwork to complete before the transition. The applicant should stay on track with all off-boarding and on-boarding requirements, such as signing a contract, obtaining background checks, and applying for a new license to ensure the switch is not delayed.

 

 

Disadvantages of Transferring Programs

The transfer process is not easy to navigate and can be a source of stress for the applicant. It is natural to fear resentment from colleagues and co-residents. Although transferring programs might be in the best interest of the trainee, it may leave a large gap in the program that they are leaving, which can place a burden on the remaining residents.

There are many adjustments to be made after transferring programs. The transferring resident will again start from scratch, needing to learn the ropes and adapt to the growing pains of being at a new institution. This may require learning a completely new electronic medical record, adapting to a new culture, and in many cases stepping in as a senior resident without fully knowing the ins and outs of the program.

Advantages of Transferring Programs

Successfully transferring programs is something to celebrate. There may be great benefits to transferring to a program that is better suited to the trainee—either personally or professionally. Ameliorating the adversity that led to the decision to transfer such as reuniting a long-distance family or realizing one’s true passion can allow the resident to thrive as a trainee and maximize their potential. Transferring programs can give a resident a more well-rounded training experience, as different programs may have different strengths, patient populations, and practice settings. Working with different faculty members with varied niches and practice styles can create a more comprehensive residency experience.

Final Thoughts

Ultimately, transferring residency programs is not easy but also is not impossible. Successfully switching residency programs can be a rewarding experience providing greater well-being and fulfillment.

References
  1. Accreditation Council for Graduate Medical Education. Data Resource Book, Academic Year 2021-2022. Accreditation Council for Graduate Medical Education. Accessed January 20, 2023. https://www.acgme.org/globalassets/pfassets/publicationsbooks/2021-2022_acgme__databook_document.pdf
  2. Accreditation Council for Graduate Medical Education. Data Resource Book, Academic Year 2020-2021. Accreditation Council for Graduate Medical Education. Accessed January 20, 2023. https://www.acgme.org/globalassets/pfassets/publicationsbooks/2020-2021_acgme_databook_document.pdf
  3. After the Match. National Resident Matching Program website. Accessed January 23, 2023. https://www.nrmp.org/fellowship-applicants/after-the-match/
  4. FREIDA vacant position listings. American Medical Association website. Accessed January 23, 2023. https://freida.ama-assn.org/vacant-position
  5. FindAResident. Association of American Medical Colleges website. Accessed January 23, 2023. https://students-residents.aamc.org/findaresident/findaresident
  6. What are the types of program positions in the main residency match? National Resident Matching Program website. Published August 5, 2021. Accessed January 23, 2023. https://www.nrmp.org/help/item/what-types-of-programs-participate-in-the-main-residency-match/
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Correspondence: Samantha R. Pop, MD, 1 Worlds Fair Dr, 2nd Floor, Ste 2400, Somerset, NJ 08873 ([email protected]).

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Transferring from one residency program to another is rare but not unheard of. According to the most recent Accreditation Council for Graduate Medical Education Data Resource Book, there were 1020 residents who transferred residency programs in the 2020-2021 academic year.1 With a total of 126,759 active residents in specialty programs, the percentage of transferring residents was less than 1%. The specialties with the highest number of transferring residents included psychiatry, general surgery, internal medicine, and family medicine. In dermatology programs, there were only 2 resident transfers during the 2019-2020 academic year and 6 transfers in the 2020-2021 academic year.1,2 A resident contemplating transferring training programs must carefully consider the advantages and disadvantages before undertaking the uncertain transfer process, but transferring residency programs can be achieved successfully with planning and luck.

Deciding to Transfer

The decision to transfer residency programs may be a difficult one that is wrought with anxiety. There are many reasons why a trainee may wish to pursue transferring training programs. A transfer to another geographic area may be necessary for personal or family reasons, such as to reunite with a spouse and children or to care for a sick family member. A resident may find their program to be a poor fit and may wish to train in a different educational environment. Occasionally, a program can lose its accreditation, and its residents will be tasked with finding a new position elsewhere. A trainee also may realize that the specialty they matched into initially does not align with their true passions. It is important for the potential transfer applicant to be levelheaded about their decision. Residency is a demanding period for every trainee; switching programs may not be the best solution for every problem and should only be considered if essential.

Transfer Timing

A trainee may have thoughts of leaving a program soon after starting residency or perhaps even before starting if their National Resident Matching Program (NRMP) Match result was a disappointment; however, there are certain rules related to transfer timing. The NRMP Match represents a binding commitment for both the applicant and program. If for any reason an applicant will not honor the binding commitment, the NRMP requires the applicant to initiate a waiver review, which can be requested for unanticipated serious and extreme hardship, change of specialty, or ineligibility. According to the NRMP rules and regulations, applicants cannot apply for, discuss, interview for, or accept a position in another program until a waiver has been granted.3 Waivers based on change of specialty must be requested by mid-January prior to the start of training, which means most applicants who match to positions that begin in the same year of the Match do not qualify for change of specialty waivers. However, those who matched to an advanced position and are doing a preliminary year position may consider this option if they have a change of heart during their internship. The NRMP may consider a 1-year deferral to delay training if mutually agreed upon by both the matched applicant and the program.3 The binding commitment is in place for the first 45 days of training, and applicants who resign within 45 days or a program that tries to solicit the transfer of a resident prior to that date could be in violation of the Match and can face consequences such as being barred from entering the matching process in future cycles. Of the 1020 transfers that occurred among residents in specialty programs during the 2020-2021 academic year, 354 (34.7%) occurred during the first year of the training program; 228 (22.4%) occurred during the second year; 389 (38.1%) occurred during the third year; and 49 (4.8%) occurred in the fourth, fifth, or sixth year of the program.1 Unlike other jobs/occupations in which one can simply give notice, in medical training even if a transfer position is accepted, the transition date between programs must be mutually agreed upon. Often, this may coincide with the start of the new academic year.

The Transfer Process

Transferring residency programs is a substantial undertaking. Unlike the Match, a trainee seeking to transfer programs does so without a standardized application system or structured support through the process; the transfer applicant must be prepared to navigate the transfer process on their own. The first step after making the decision to transfer is for the resident to meet with the program leadership (ie, program director[s], coordinator, designated official) at their home program to discuss the decision—a nerve-wracking but imperative first step. A receiving program may not favor an applicant secretly applying to a new program without the knowledge of their home program and often will require the home program’s blessing to proceed. The receiving program also would want to ensure the applicant is in good standing and not leaving due to misconduct. Once given the go-ahead, the process is largely in the hands of the applicant. The transfer applicant should identify locations or programs of interest and then take initiative to reach out to potential programs. FREIDA (Fellowship and Residency Electronic Interactive Database Access) is the American Medical Association’s residency and fellowship database that allows vacant position listings to be posted online.4 Additionally, the Association of American Medical Colleges’ FindAResident website is a year-round search tool designed to help find open residency and fellowship positions.5 Various specialties also may have program director listserves that communicate vacant positions. On occasion, there are spots in the main NRMP Match that are reserved positions (“R”). These are postgraduate year 2 positions in specialty programs that begin in the year of the Match and are reserved for physicians with prior graduate medical education; these also are known as “Physician Positions.”6 Ultimately, advertisements for vacancies may be few and far between, requiring the resident to send unsolicited emails with curriculum vitae attached to the program directors at programs of interest to inquire about any vacancies and hope for a favorable response. Even if the transfer applicant is qualified, luck that the right spot will be available at the right time may be the deciding factor in transferring programs.

The next step is interviewing for the position. There likely will be fewer candidates interviewing for an open spot but that does not make the process less competitive. The candidate should highlight their strengths and achievements and discuss why the new program would be a great fit both personally and professionally. Even if an applicant is seeking a transfer due to discontent with a prior program, it is best to act graciously and not speak poorly about another training program.

Prior to selection, the candidate may be asked to provide information such as diplomas, US Medical Licensing Examination Step and residency in-service training examination scores, and academic reviews from their current residency program. The interview process may take several weeks as the graduate medical education office often will need to officially approve of an applicant before a formal offer to transfer is extended.

Finally, once an offer is made and accepted, there still is a great amount of paperwork to complete before the transition. The applicant should stay on track with all off-boarding and on-boarding requirements, such as signing a contract, obtaining background checks, and applying for a new license to ensure the switch is not delayed.

 

 

Disadvantages of Transferring Programs

The transfer process is not easy to navigate and can be a source of stress for the applicant. It is natural to fear resentment from colleagues and co-residents. Although transferring programs might be in the best interest of the trainee, it may leave a large gap in the program that they are leaving, which can place a burden on the remaining residents.

There are many adjustments to be made after transferring programs. The transferring resident will again start from scratch, needing to learn the ropes and adapt to the growing pains of being at a new institution. This may require learning a completely new electronic medical record, adapting to a new culture, and in many cases stepping in as a senior resident without fully knowing the ins and outs of the program.

Advantages of Transferring Programs

Successfully transferring programs is something to celebrate. There may be great benefits to transferring to a program that is better suited to the trainee—either personally or professionally. Ameliorating the adversity that led to the decision to transfer such as reuniting a long-distance family or realizing one’s true passion can allow the resident to thrive as a trainee and maximize their potential. Transferring programs can give a resident a more well-rounded training experience, as different programs may have different strengths, patient populations, and practice settings. Working with different faculty members with varied niches and practice styles can create a more comprehensive residency experience.

Final Thoughts

Ultimately, transferring residency programs is not easy but also is not impossible. Successfully switching residency programs can be a rewarding experience providing greater well-being and fulfillment.

Transferring from one residency program to another is rare but not unheard of. According to the most recent Accreditation Council for Graduate Medical Education Data Resource Book, there were 1020 residents who transferred residency programs in the 2020-2021 academic year.1 With a total of 126,759 active residents in specialty programs, the percentage of transferring residents was less than 1%. The specialties with the highest number of transferring residents included psychiatry, general surgery, internal medicine, and family medicine. In dermatology programs, there were only 2 resident transfers during the 2019-2020 academic year and 6 transfers in the 2020-2021 academic year.1,2 A resident contemplating transferring training programs must carefully consider the advantages and disadvantages before undertaking the uncertain transfer process, but transferring residency programs can be achieved successfully with planning and luck.

Deciding to Transfer

The decision to transfer residency programs may be a difficult one that is wrought with anxiety. There are many reasons why a trainee may wish to pursue transferring training programs. A transfer to another geographic area may be necessary for personal or family reasons, such as to reunite with a spouse and children or to care for a sick family member. A resident may find their program to be a poor fit and may wish to train in a different educational environment. Occasionally, a program can lose its accreditation, and its residents will be tasked with finding a new position elsewhere. A trainee also may realize that the specialty they matched into initially does not align with their true passions. It is important for the potential transfer applicant to be levelheaded about their decision. Residency is a demanding period for every trainee; switching programs may not be the best solution for every problem and should only be considered if essential.

Transfer Timing

A trainee may have thoughts of leaving a program soon after starting residency or perhaps even before starting if their National Resident Matching Program (NRMP) Match result was a disappointment; however, there are certain rules related to transfer timing. The NRMP Match represents a binding commitment for both the applicant and program. If for any reason an applicant will not honor the binding commitment, the NRMP requires the applicant to initiate a waiver review, which can be requested for unanticipated serious and extreme hardship, change of specialty, or ineligibility. According to the NRMP rules and regulations, applicants cannot apply for, discuss, interview for, or accept a position in another program until a waiver has been granted.3 Waivers based on change of specialty must be requested by mid-January prior to the start of training, which means most applicants who match to positions that begin in the same year of the Match do not qualify for change of specialty waivers. However, those who matched to an advanced position and are doing a preliminary year position may consider this option if they have a change of heart during their internship. The NRMP may consider a 1-year deferral to delay training if mutually agreed upon by both the matched applicant and the program.3 The binding commitment is in place for the first 45 days of training, and applicants who resign within 45 days or a program that tries to solicit the transfer of a resident prior to that date could be in violation of the Match and can face consequences such as being barred from entering the matching process in future cycles. Of the 1020 transfers that occurred among residents in specialty programs during the 2020-2021 academic year, 354 (34.7%) occurred during the first year of the training program; 228 (22.4%) occurred during the second year; 389 (38.1%) occurred during the third year; and 49 (4.8%) occurred in the fourth, fifth, or sixth year of the program.1 Unlike other jobs/occupations in which one can simply give notice, in medical training even if a transfer position is accepted, the transition date between programs must be mutually agreed upon. Often, this may coincide with the start of the new academic year.

The Transfer Process

Transferring residency programs is a substantial undertaking. Unlike the Match, a trainee seeking to transfer programs does so without a standardized application system or structured support through the process; the transfer applicant must be prepared to navigate the transfer process on their own. The first step after making the decision to transfer is for the resident to meet with the program leadership (ie, program director[s], coordinator, designated official) at their home program to discuss the decision—a nerve-wracking but imperative first step. A receiving program may not favor an applicant secretly applying to a new program without the knowledge of their home program and often will require the home program’s blessing to proceed. The receiving program also would want to ensure the applicant is in good standing and not leaving due to misconduct. Once given the go-ahead, the process is largely in the hands of the applicant. The transfer applicant should identify locations or programs of interest and then take initiative to reach out to potential programs. FREIDA (Fellowship and Residency Electronic Interactive Database Access) is the American Medical Association’s residency and fellowship database that allows vacant position listings to be posted online.4 Additionally, the Association of American Medical Colleges’ FindAResident website is a year-round search tool designed to help find open residency and fellowship positions.5 Various specialties also may have program director listserves that communicate vacant positions. On occasion, there are spots in the main NRMP Match that are reserved positions (“R”). These are postgraduate year 2 positions in specialty programs that begin in the year of the Match and are reserved for physicians with prior graduate medical education; these also are known as “Physician Positions.”6 Ultimately, advertisements for vacancies may be few and far between, requiring the resident to send unsolicited emails with curriculum vitae attached to the program directors at programs of interest to inquire about any vacancies and hope for a favorable response. Even if the transfer applicant is qualified, luck that the right spot will be available at the right time may be the deciding factor in transferring programs.

The next step is interviewing for the position. There likely will be fewer candidates interviewing for an open spot but that does not make the process less competitive. The candidate should highlight their strengths and achievements and discuss why the new program would be a great fit both personally and professionally. Even if an applicant is seeking a transfer due to discontent with a prior program, it is best to act graciously and not speak poorly about another training program.

Prior to selection, the candidate may be asked to provide information such as diplomas, US Medical Licensing Examination Step and residency in-service training examination scores, and academic reviews from their current residency program. The interview process may take several weeks as the graduate medical education office often will need to officially approve of an applicant before a formal offer to transfer is extended.

Finally, once an offer is made and accepted, there still is a great amount of paperwork to complete before the transition. The applicant should stay on track with all off-boarding and on-boarding requirements, such as signing a contract, obtaining background checks, and applying for a new license to ensure the switch is not delayed.

 

 

Disadvantages of Transferring Programs

The transfer process is not easy to navigate and can be a source of stress for the applicant. It is natural to fear resentment from colleagues and co-residents. Although transferring programs might be in the best interest of the trainee, it may leave a large gap in the program that they are leaving, which can place a burden on the remaining residents.

There are many adjustments to be made after transferring programs. The transferring resident will again start from scratch, needing to learn the ropes and adapt to the growing pains of being at a new institution. This may require learning a completely new electronic medical record, adapting to a new culture, and in many cases stepping in as a senior resident without fully knowing the ins and outs of the program.

Advantages of Transferring Programs

Successfully transferring programs is something to celebrate. There may be great benefits to transferring to a program that is better suited to the trainee—either personally or professionally. Ameliorating the adversity that led to the decision to transfer such as reuniting a long-distance family or realizing one’s true passion can allow the resident to thrive as a trainee and maximize their potential. Transferring programs can give a resident a more well-rounded training experience, as different programs may have different strengths, patient populations, and practice settings. Working with different faculty members with varied niches and practice styles can create a more comprehensive residency experience.

Final Thoughts

Ultimately, transferring residency programs is not easy but also is not impossible. Successfully switching residency programs can be a rewarding experience providing greater well-being and fulfillment.

References
  1. Accreditation Council for Graduate Medical Education. Data Resource Book, Academic Year 2021-2022. Accreditation Council for Graduate Medical Education. Accessed January 20, 2023. https://www.acgme.org/globalassets/pfassets/publicationsbooks/2021-2022_acgme__databook_document.pdf
  2. Accreditation Council for Graduate Medical Education. Data Resource Book, Academic Year 2020-2021. Accreditation Council for Graduate Medical Education. Accessed January 20, 2023. https://www.acgme.org/globalassets/pfassets/publicationsbooks/2020-2021_acgme_databook_document.pdf
  3. After the Match. National Resident Matching Program website. Accessed January 23, 2023. https://www.nrmp.org/fellowship-applicants/after-the-match/
  4. FREIDA vacant position listings. American Medical Association website. Accessed January 23, 2023. https://freida.ama-assn.org/vacant-position
  5. FindAResident. Association of American Medical Colleges website. Accessed January 23, 2023. https://students-residents.aamc.org/findaresident/findaresident
  6. What are the types of program positions in the main residency match? National Resident Matching Program website. Published August 5, 2021. Accessed January 23, 2023. https://www.nrmp.org/help/item/what-types-of-programs-participate-in-the-main-residency-match/
References
  1. Accreditation Council for Graduate Medical Education. Data Resource Book, Academic Year 2021-2022. Accreditation Council for Graduate Medical Education. Accessed January 20, 2023. https://www.acgme.org/globalassets/pfassets/publicationsbooks/2021-2022_acgme__databook_document.pdf
  2. Accreditation Council for Graduate Medical Education. Data Resource Book, Academic Year 2020-2021. Accreditation Council for Graduate Medical Education. Accessed January 20, 2023. https://www.acgme.org/globalassets/pfassets/publicationsbooks/2020-2021_acgme_databook_document.pdf
  3. After the Match. National Resident Matching Program website. Accessed January 23, 2023. https://www.nrmp.org/fellowship-applicants/after-the-match/
  4. FREIDA vacant position listings. American Medical Association website. Accessed January 23, 2023. https://freida.ama-assn.org/vacant-position
  5. FindAResident. Association of American Medical Colleges website. Accessed January 23, 2023. https://students-residents.aamc.org/findaresident/findaresident
  6. What are the types of program positions in the main residency match? National Resident Matching Program website. Published August 5, 2021. Accessed January 23, 2023. https://www.nrmp.org/help/item/what-types-of-programs-participate-in-the-main-residency-match/
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Hemorrhagic Lacrimation and Epistaxis: Rare Findings in Acute Hemorrhagic Edema of Infancy

To the Editor:

Hemorrhagic lacrimation and epistaxis are dramatic presentations with a narrow differential diagnosis. It rarely has been reported to present alongside the more typical features of acute hemorrhagic edema of infancy (AHEI), which is a benign self-limited leukocytoclastic vasculitis most often seen in children aged 4 months to 2 years. Extracutaneous involvement rarely is seen in AHEI, though joint, gastrointestinal tract, and renal involvement have been reported.1 Most patients present with edematous, annular, or cockade purpuric vasculitic lesions classically involving the face and distal extremities with relative sparing of the trunk. We present a case of a well-appearing, 10-month-old infant boy with hemorrhagic vasculitic lesions, acral edema, and an associated episode of hemorrhagic lacrimation and epistaxis.

A, Targetoid hemorrhagic and purpuric lesions with scalloped margins of varying sizes involving the distal and proximal left leg
FIGURE 1. A, Targetoid hemorrhagic and purpuric lesions with scalloped margins of varying sizes involving the distal and proximal left leg. B, A targetoid hemorrhagic and purpuric lesion with scalloped margins and a necrotic center surrounded by additional coin-shaped lesions of varying sizes involving the distal and proximal right leg.

A 10-month-old infant boy who was otherwise healthy presented to the emergency department (ED) with an acute-onset, progressively worsening cutaneous eruption of 2 days’ duration. A thorough history revealed that the eruption initially had presented as several small, bright-red papules on the thighs. The eruption subsequently spread to involve the buttocks, legs, and arms (Figures 1 and 2). The parents also noted that the patient had experienced an episode of bloody tears and epistaxis that lasted a few minutes at the pediatrician’s office earlier that morning, a finding that prompted the urgent referral to the ED.

Several coin-shaped hemorrhagic lesions of varying sizes on the left arm.
FIGURE 2. Several coin-shaped hemorrhagic lesions of varying sizes on the left arm.

Dermatology was then consulted. A review of systems was notable for rhinorrhea and diarrhea during the week leading to the eruption. The patient’s parents denied fevers, decreased oral intake, or a recent course of antibiotics. The patient’s medical history was notable only for atopic dermatitis treated with emollients and occasional topical steroids. The parents denied recent travel or vaccinations. Physical examination showed an afebrile, well-appearing infant with multiple nontender, slightly edematous, circular, purpuric papules and plaques scattered on the buttocks and extremities with edema on the dorsal feet. The remainder of the patient’s workup in the ED was notable for mild elevations in C-reactive protein levels (1.4 mg/dL [reference range, 0–1.2 mg/dL]) and an elevated erythrocyte sedimentation rate (22 mm/h [reference range, 2–12 mm/h]). A complete blood cell count; liver function tests; urinalysis; and coagulation studies, including prothrombin, partial thromboplastin time, and international normalized ratio, were unremarkable. Acute hemorrhagic edema of infancy was diagnosed based on the clinical manifestations.

Acute hemorrhagic edema of infancy (also known as Finkelstein disease, medallionlike purpura, Seidemayer syndrome, infantile postinfectious irislike purpura and edema, and purpura en cocarde avec oedeme) is believed to result from an immune complex–related reaction, often in the setting of an upper respiratory tract infection; medications, especially antibiotics; or vaccinations. The condition previously was considered a benign form of Henoch-Schönlein purpura; however, it is now recognized as its own clinical entity. Acute hemorrhagic edema of infancy commonly affects children between the ages of 4 months and 2 years. The incidence peaks in the winter months, and males tend to be more affected than females.1

Acute hemorrhagic edema of infancy is clinically characterized by a triad of large purpuric lesions, low-grade fever, and peripheral acral edema. Edema can develop on the hands, feet, and genitalia. Importantly, facial edema has been noted to precede skin lesions.2 Coin-shaped or targetoid hemorrhagic and purpuric lesions in a cockade or rosette pattern with scalloped margins typically begin on the distal extremities and tend to spread proximally. The lesions are variable in size but have been reported to be as large as 5 cm in diameter. Although joint pain, bloody diarrhea, hematuria, and proteinuria can accompany AHEI, most cases are devoid of systemic symptoms.3 Hemorrhagic lacrimation and epistaxis—both present in our patient—are rare findings with AHEI. It is likely that most providers, including dermatologists, may be unfamiliar with these striking clinical findings. Although the pathophysiology of hemorrhagic lacrimation and epistaxis has not been formally investigated, we postulate that it likely is related to the formation of immune complexes that lead to small vessel vasculitis, underpinning the characteristic findings in AHEI.4,5 This reasoning is supported by the complete resolution of symptoms corresponding with clinical clearance of the cutaneous vasculitis in 2 prior cases4,5 as well as in our patient who did not have a relapse of symptoms following cessation of the cutaneous eruption at a pediatric follow-up appointment 2 weeks later.

Acute hemorrhagic edema of infancy is a clinical diagnosis; however, a skin biopsy can be performed to confirm the clinical suspicion and rule out more serious conditions. Histopathologic examination reveals a leukocytoclastic vasculitis involving the capillaries and postcapillary venules of the upper and mid dermis. Laboratory test results usually are nonspecific but can help distinguish AHEI from more serious diseases. The erythrocyte sedimentation rate and C-reactive protein level may be slightly elevated in infants with AHEI. Urinalysis and stool guaiac tests also can be performed to evaluate for any renal or gastrointestinal involvement.6

The differential diagnosis includes IgA vasculitis, erythema multiforme, acute meningococcemia, urticarial vasculitis, Kawasaki disease, and child abuse. IgA vasculitis often presents with more systemic involvement, with abdominal pain, vomiting, hematemesis, diarrhea, and hematochezia occurring in up to 50% of patients. The cutaneous findings of erythema multiforme classically are confined to the limbs and face, and edema of the extremities typically is not seen. Patients with acute meningococcemia appear toxic with high fevers, malaise, and possible septic shock.5

Acute hemorrhagic edema of infancy is a self-limited condition typically lasting 1 to 3 weeks and requires only supportive care.7 Antibiotics should be given to treat concurrent bacterial infections, and antihistamines and steroids may be useful for symptomatic relief. Importantly, however, systemic corticosteroids do not appear to conclusively alter the disease course.8

Acute hemorrhagic edema of infancy is a rare benign leukocytoclastic vasculitis with a striking presentation often seen following an upper respiratory tract infection or course of antibiotics. Our case demonstrates that on rare occasions, AHEI may be accompanied by hemorrhagic lacrimation and epistaxis—findings that can be quite alarming to both parents and medical providers. Nonetheless, patients and their caretakers should be assured that the condition is self-limited and resolves without permanent sequalae.

References
  1. Emerich PS, Prebianchi PA, Motta LL, et al. Acute hemorrhagic edema of infancy: report of three cases. An Bras Dermatol2011;86:1181-1184.
  2. Avhad G, Ghuge P, Jerajani H. Acute hemorrhagic edema of infancy. Indian Dermatol Online J. 2014;5:356-357.
  3. Krause I, Lazarov A, Rachmel A, et al. Acute haemorrhagic oedema of infancy, a benign variant of leucocytoclastic vasculitis. Acta Paediatr. 1996;85:114-117.
  4. Sneller H, Vega C, Zemel L, et al. Acute hemorrhagic edema of infancy with associated hemorrhagic lacrimation. Pediatr Emerg Care. 2021;37:E70-E72. doi:10.1097/PEC.0000000000001542
  5. Mreish S, Al-Tatari H. Hemorrhagic lacrimation and epistaxis in acute hemorrhagic edema of infancy. Case Rep Pediatr. 2016;2016:9762185. doi:10.1155/2016/9762185
  6. Savino F, Lupica MM, Tarasco V, et al. Acute hemorrhagic edema of infancy: a troubling cutaneous presentation with a self-limiting course. Pediatr Dermatol. 2013;30:E149-E152.
  7. Fiore E, Rizzi M, Ragazzi M, et al. Acute hemorrhagic edema of young children (cockade purpura and edema): a case series and systematic review. J Am Acad Dermatol. 2008;59:684-695.
  8. Fiore E, Rizzi M, Simonetti GD, et al. Acute hemorrhagic edema of young children: a concise narrative review. Eur J Pediatr2011;170:1507-1511.
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Dr. Bambekova is from the University of Texas Health San Antonio, Long School of Medicine. Drs. Cervantes, Reichenberg, and Ruth are from the Department of Dermatology, Dell Medical School at Austin/Dell Children’s Hospital, Austin, Texas.

The authors report no conflict of interest.

Correspondence: Pavela G. Bambekova, MD, 7979 Wurzbach Rd, San Antonio, TX 78229 ([email protected]).

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Dr. Bambekova is from the University of Texas Health San Antonio, Long School of Medicine. Drs. Cervantes, Reichenberg, and Ruth are from the Department of Dermatology, Dell Medical School at Austin/Dell Children’s Hospital, Austin, Texas.

The authors report no conflict of interest.

Correspondence: Pavela G. Bambekova, MD, 7979 Wurzbach Rd, San Antonio, TX 78229 ([email protected]).

Author and Disclosure Information

Dr. Bambekova is from the University of Texas Health San Antonio, Long School of Medicine. Drs. Cervantes, Reichenberg, and Ruth are from the Department of Dermatology, Dell Medical School at Austin/Dell Children’s Hospital, Austin, Texas.

The authors report no conflict of interest.

Correspondence: Pavela G. Bambekova, MD, 7979 Wurzbach Rd, San Antonio, TX 78229 ([email protected]).

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To the Editor:

Hemorrhagic lacrimation and epistaxis are dramatic presentations with a narrow differential diagnosis. It rarely has been reported to present alongside the more typical features of acute hemorrhagic edema of infancy (AHEI), which is a benign self-limited leukocytoclastic vasculitis most often seen in children aged 4 months to 2 years. Extracutaneous involvement rarely is seen in AHEI, though joint, gastrointestinal tract, and renal involvement have been reported.1 Most patients present with edematous, annular, or cockade purpuric vasculitic lesions classically involving the face and distal extremities with relative sparing of the trunk. We present a case of a well-appearing, 10-month-old infant boy with hemorrhagic vasculitic lesions, acral edema, and an associated episode of hemorrhagic lacrimation and epistaxis.

A, Targetoid hemorrhagic and purpuric lesions with scalloped margins of varying sizes involving the distal and proximal left leg
FIGURE 1. A, Targetoid hemorrhagic and purpuric lesions with scalloped margins of varying sizes involving the distal and proximal left leg. B, A targetoid hemorrhagic and purpuric lesion with scalloped margins and a necrotic center surrounded by additional coin-shaped lesions of varying sizes involving the distal and proximal right leg.

A 10-month-old infant boy who was otherwise healthy presented to the emergency department (ED) with an acute-onset, progressively worsening cutaneous eruption of 2 days’ duration. A thorough history revealed that the eruption initially had presented as several small, bright-red papules on the thighs. The eruption subsequently spread to involve the buttocks, legs, and arms (Figures 1 and 2). The parents also noted that the patient had experienced an episode of bloody tears and epistaxis that lasted a few minutes at the pediatrician’s office earlier that morning, a finding that prompted the urgent referral to the ED.

Several coin-shaped hemorrhagic lesions of varying sizes on the left arm.
FIGURE 2. Several coin-shaped hemorrhagic lesions of varying sizes on the left arm.

Dermatology was then consulted. A review of systems was notable for rhinorrhea and diarrhea during the week leading to the eruption. The patient’s parents denied fevers, decreased oral intake, or a recent course of antibiotics. The patient’s medical history was notable only for atopic dermatitis treated with emollients and occasional topical steroids. The parents denied recent travel or vaccinations. Physical examination showed an afebrile, well-appearing infant with multiple nontender, slightly edematous, circular, purpuric papules and plaques scattered on the buttocks and extremities with edema on the dorsal feet. The remainder of the patient’s workup in the ED was notable for mild elevations in C-reactive protein levels (1.4 mg/dL [reference range, 0–1.2 mg/dL]) and an elevated erythrocyte sedimentation rate (22 mm/h [reference range, 2–12 mm/h]). A complete blood cell count; liver function tests; urinalysis; and coagulation studies, including prothrombin, partial thromboplastin time, and international normalized ratio, were unremarkable. Acute hemorrhagic edema of infancy was diagnosed based on the clinical manifestations.

Acute hemorrhagic edema of infancy (also known as Finkelstein disease, medallionlike purpura, Seidemayer syndrome, infantile postinfectious irislike purpura and edema, and purpura en cocarde avec oedeme) is believed to result from an immune complex–related reaction, often in the setting of an upper respiratory tract infection; medications, especially antibiotics; or vaccinations. The condition previously was considered a benign form of Henoch-Schönlein purpura; however, it is now recognized as its own clinical entity. Acute hemorrhagic edema of infancy commonly affects children between the ages of 4 months and 2 years. The incidence peaks in the winter months, and males tend to be more affected than females.1

Acute hemorrhagic edema of infancy is clinically characterized by a triad of large purpuric lesions, low-grade fever, and peripheral acral edema. Edema can develop on the hands, feet, and genitalia. Importantly, facial edema has been noted to precede skin lesions.2 Coin-shaped or targetoid hemorrhagic and purpuric lesions in a cockade or rosette pattern with scalloped margins typically begin on the distal extremities and tend to spread proximally. The lesions are variable in size but have been reported to be as large as 5 cm in diameter. Although joint pain, bloody diarrhea, hematuria, and proteinuria can accompany AHEI, most cases are devoid of systemic symptoms.3 Hemorrhagic lacrimation and epistaxis—both present in our patient—are rare findings with AHEI. It is likely that most providers, including dermatologists, may be unfamiliar with these striking clinical findings. Although the pathophysiology of hemorrhagic lacrimation and epistaxis has not been formally investigated, we postulate that it likely is related to the formation of immune complexes that lead to small vessel vasculitis, underpinning the characteristic findings in AHEI.4,5 This reasoning is supported by the complete resolution of symptoms corresponding with clinical clearance of the cutaneous vasculitis in 2 prior cases4,5 as well as in our patient who did not have a relapse of symptoms following cessation of the cutaneous eruption at a pediatric follow-up appointment 2 weeks later.

Acute hemorrhagic edema of infancy is a clinical diagnosis; however, a skin biopsy can be performed to confirm the clinical suspicion and rule out more serious conditions. Histopathologic examination reveals a leukocytoclastic vasculitis involving the capillaries and postcapillary venules of the upper and mid dermis. Laboratory test results usually are nonspecific but can help distinguish AHEI from more serious diseases. The erythrocyte sedimentation rate and C-reactive protein level may be slightly elevated in infants with AHEI. Urinalysis and stool guaiac tests also can be performed to evaluate for any renal or gastrointestinal involvement.6

The differential diagnosis includes IgA vasculitis, erythema multiforme, acute meningococcemia, urticarial vasculitis, Kawasaki disease, and child abuse. IgA vasculitis often presents with more systemic involvement, with abdominal pain, vomiting, hematemesis, diarrhea, and hematochezia occurring in up to 50% of patients. The cutaneous findings of erythema multiforme classically are confined to the limbs and face, and edema of the extremities typically is not seen. Patients with acute meningococcemia appear toxic with high fevers, malaise, and possible septic shock.5

Acute hemorrhagic edema of infancy is a self-limited condition typically lasting 1 to 3 weeks and requires only supportive care.7 Antibiotics should be given to treat concurrent bacterial infections, and antihistamines and steroids may be useful for symptomatic relief. Importantly, however, systemic corticosteroids do not appear to conclusively alter the disease course.8

Acute hemorrhagic edema of infancy is a rare benign leukocytoclastic vasculitis with a striking presentation often seen following an upper respiratory tract infection or course of antibiotics. Our case demonstrates that on rare occasions, AHEI may be accompanied by hemorrhagic lacrimation and epistaxis—findings that can be quite alarming to both parents and medical providers. Nonetheless, patients and their caretakers should be assured that the condition is self-limited and resolves without permanent sequalae.

To the Editor:

Hemorrhagic lacrimation and epistaxis are dramatic presentations with a narrow differential diagnosis. It rarely has been reported to present alongside the more typical features of acute hemorrhagic edema of infancy (AHEI), which is a benign self-limited leukocytoclastic vasculitis most often seen in children aged 4 months to 2 years. Extracutaneous involvement rarely is seen in AHEI, though joint, gastrointestinal tract, and renal involvement have been reported.1 Most patients present with edematous, annular, or cockade purpuric vasculitic lesions classically involving the face and distal extremities with relative sparing of the trunk. We present a case of a well-appearing, 10-month-old infant boy with hemorrhagic vasculitic lesions, acral edema, and an associated episode of hemorrhagic lacrimation and epistaxis.

A, Targetoid hemorrhagic and purpuric lesions with scalloped margins of varying sizes involving the distal and proximal left leg
FIGURE 1. A, Targetoid hemorrhagic and purpuric lesions with scalloped margins of varying sizes involving the distal and proximal left leg. B, A targetoid hemorrhagic and purpuric lesion with scalloped margins and a necrotic center surrounded by additional coin-shaped lesions of varying sizes involving the distal and proximal right leg.

A 10-month-old infant boy who was otherwise healthy presented to the emergency department (ED) with an acute-onset, progressively worsening cutaneous eruption of 2 days’ duration. A thorough history revealed that the eruption initially had presented as several small, bright-red papules on the thighs. The eruption subsequently spread to involve the buttocks, legs, and arms (Figures 1 and 2). The parents also noted that the patient had experienced an episode of bloody tears and epistaxis that lasted a few minutes at the pediatrician’s office earlier that morning, a finding that prompted the urgent referral to the ED.

Several coin-shaped hemorrhagic lesions of varying sizes on the left arm.
FIGURE 2. Several coin-shaped hemorrhagic lesions of varying sizes on the left arm.

Dermatology was then consulted. A review of systems was notable for rhinorrhea and diarrhea during the week leading to the eruption. The patient’s parents denied fevers, decreased oral intake, or a recent course of antibiotics. The patient’s medical history was notable only for atopic dermatitis treated with emollients and occasional topical steroids. The parents denied recent travel or vaccinations. Physical examination showed an afebrile, well-appearing infant with multiple nontender, slightly edematous, circular, purpuric papules and plaques scattered on the buttocks and extremities with edema on the dorsal feet. The remainder of the patient’s workup in the ED was notable for mild elevations in C-reactive protein levels (1.4 mg/dL [reference range, 0–1.2 mg/dL]) and an elevated erythrocyte sedimentation rate (22 mm/h [reference range, 2–12 mm/h]). A complete blood cell count; liver function tests; urinalysis; and coagulation studies, including prothrombin, partial thromboplastin time, and international normalized ratio, were unremarkable. Acute hemorrhagic edema of infancy was diagnosed based on the clinical manifestations.

Acute hemorrhagic edema of infancy (also known as Finkelstein disease, medallionlike purpura, Seidemayer syndrome, infantile postinfectious irislike purpura and edema, and purpura en cocarde avec oedeme) is believed to result from an immune complex–related reaction, often in the setting of an upper respiratory tract infection; medications, especially antibiotics; or vaccinations. The condition previously was considered a benign form of Henoch-Schönlein purpura; however, it is now recognized as its own clinical entity. Acute hemorrhagic edema of infancy commonly affects children between the ages of 4 months and 2 years. The incidence peaks in the winter months, and males tend to be more affected than females.1

Acute hemorrhagic edema of infancy is clinically characterized by a triad of large purpuric lesions, low-grade fever, and peripheral acral edema. Edema can develop on the hands, feet, and genitalia. Importantly, facial edema has been noted to precede skin lesions.2 Coin-shaped or targetoid hemorrhagic and purpuric lesions in a cockade or rosette pattern with scalloped margins typically begin on the distal extremities and tend to spread proximally. The lesions are variable in size but have been reported to be as large as 5 cm in diameter. Although joint pain, bloody diarrhea, hematuria, and proteinuria can accompany AHEI, most cases are devoid of systemic symptoms.3 Hemorrhagic lacrimation and epistaxis—both present in our patient—are rare findings with AHEI. It is likely that most providers, including dermatologists, may be unfamiliar with these striking clinical findings. Although the pathophysiology of hemorrhagic lacrimation and epistaxis has not been formally investigated, we postulate that it likely is related to the formation of immune complexes that lead to small vessel vasculitis, underpinning the characteristic findings in AHEI.4,5 This reasoning is supported by the complete resolution of symptoms corresponding with clinical clearance of the cutaneous vasculitis in 2 prior cases4,5 as well as in our patient who did not have a relapse of symptoms following cessation of the cutaneous eruption at a pediatric follow-up appointment 2 weeks later.

Acute hemorrhagic edema of infancy is a clinical diagnosis; however, a skin biopsy can be performed to confirm the clinical suspicion and rule out more serious conditions. Histopathologic examination reveals a leukocytoclastic vasculitis involving the capillaries and postcapillary venules of the upper and mid dermis. Laboratory test results usually are nonspecific but can help distinguish AHEI from more serious diseases. The erythrocyte sedimentation rate and C-reactive protein level may be slightly elevated in infants with AHEI. Urinalysis and stool guaiac tests also can be performed to evaluate for any renal or gastrointestinal involvement.6

The differential diagnosis includes IgA vasculitis, erythema multiforme, acute meningococcemia, urticarial vasculitis, Kawasaki disease, and child abuse. IgA vasculitis often presents with more systemic involvement, with abdominal pain, vomiting, hematemesis, diarrhea, and hematochezia occurring in up to 50% of patients. The cutaneous findings of erythema multiforme classically are confined to the limbs and face, and edema of the extremities typically is not seen. Patients with acute meningococcemia appear toxic with high fevers, malaise, and possible septic shock.5

Acute hemorrhagic edema of infancy is a self-limited condition typically lasting 1 to 3 weeks and requires only supportive care.7 Antibiotics should be given to treat concurrent bacterial infections, and antihistamines and steroids may be useful for symptomatic relief. Importantly, however, systemic corticosteroids do not appear to conclusively alter the disease course.8

Acute hemorrhagic edema of infancy is a rare benign leukocytoclastic vasculitis with a striking presentation often seen following an upper respiratory tract infection or course of antibiotics. Our case demonstrates that on rare occasions, AHEI may be accompanied by hemorrhagic lacrimation and epistaxis—findings that can be quite alarming to both parents and medical providers. Nonetheless, patients and their caretakers should be assured that the condition is self-limited and resolves without permanent sequalae.

References
  1. Emerich PS, Prebianchi PA, Motta LL, et al. Acute hemorrhagic edema of infancy: report of three cases. An Bras Dermatol2011;86:1181-1184.
  2. Avhad G, Ghuge P, Jerajani H. Acute hemorrhagic edema of infancy. Indian Dermatol Online J. 2014;5:356-357.
  3. Krause I, Lazarov A, Rachmel A, et al. Acute haemorrhagic oedema of infancy, a benign variant of leucocytoclastic vasculitis. Acta Paediatr. 1996;85:114-117.
  4. Sneller H, Vega C, Zemel L, et al. Acute hemorrhagic edema of infancy with associated hemorrhagic lacrimation. Pediatr Emerg Care. 2021;37:E70-E72. doi:10.1097/PEC.0000000000001542
  5. Mreish S, Al-Tatari H. Hemorrhagic lacrimation and epistaxis in acute hemorrhagic edema of infancy. Case Rep Pediatr. 2016;2016:9762185. doi:10.1155/2016/9762185
  6. Savino F, Lupica MM, Tarasco V, et al. Acute hemorrhagic edema of infancy: a troubling cutaneous presentation with a self-limiting course. Pediatr Dermatol. 2013;30:E149-E152.
  7. Fiore E, Rizzi M, Ragazzi M, et al. Acute hemorrhagic edema of young children (cockade purpura and edema): a case series and systematic review. J Am Acad Dermatol. 2008;59:684-695.
  8. Fiore E, Rizzi M, Simonetti GD, et al. Acute hemorrhagic edema of young children: a concise narrative review. Eur J Pediatr2011;170:1507-1511.
References
  1. Emerich PS, Prebianchi PA, Motta LL, et al. Acute hemorrhagic edema of infancy: report of three cases. An Bras Dermatol2011;86:1181-1184.
  2. Avhad G, Ghuge P, Jerajani H. Acute hemorrhagic edema of infancy. Indian Dermatol Online J. 2014;5:356-357.
  3. Krause I, Lazarov A, Rachmel A, et al. Acute haemorrhagic oedema of infancy, a benign variant of leucocytoclastic vasculitis. Acta Paediatr. 1996;85:114-117.
  4. Sneller H, Vega C, Zemel L, et al. Acute hemorrhagic edema of infancy with associated hemorrhagic lacrimation. Pediatr Emerg Care. 2021;37:E70-E72. doi:10.1097/PEC.0000000000001542
  5. Mreish S, Al-Tatari H. Hemorrhagic lacrimation and epistaxis in acute hemorrhagic edema of infancy. Case Rep Pediatr. 2016;2016:9762185. doi:10.1155/2016/9762185
  6. Savino F, Lupica MM, Tarasco V, et al. Acute hemorrhagic edema of infancy: a troubling cutaneous presentation with a self-limiting course. Pediatr Dermatol. 2013;30:E149-E152.
  7. Fiore E, Rizzi M, Ragazzi M, et al. Acute hemorrhagic edema of young children (cockade purpura and edema): a case series and systematic review. J Am Acad Dermatol. 2008;59:684-695.
  8. Fiore E, Rizzi M, Simonetti GD, et al. Acute hemorrhagic edema of young children: a concise narrative review. Eur J Pediatr2011;170:1507-1511.
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  • Acute hemorrhagic edema of infancy (AHEI) is clinically characterized by a triad of large purpuric lesions, low-grade fever, and peripheral acral edema. Although joint pain, bloody diarrhea, hematuria, and proteinuria can accompany AHEI, most cases are devoid of systemic symptoms.
  • It is a self-limited condition typically lasting 1 to 3 weeks and requires only supportive care.
  • On rare occasions, AHEI may be accompanied by hemorrhagic lacrimation and epistaxis. Patients should be assured that the condition is self-limited and resolves without permanent sequalae.
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Skin of Color Society Scientific Symposium Winners: 2022

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Skin of Color Society Scientific Symposium Winners: 2022

The 18th Annual Skin of Color Society Scientific Symposium was held in March 2022 in Boston, Massachusetts. With a theme of Diversity in Action: Science, Healthcare & Society, researchers gathered to present new findings, share key insights, and discuss the continuing evolution of the field. Three awards were presented from the scientific posters at the symposium.

The Best Poster Presentation Award was presented to Brandyn M. White, BS, for “A Preliminary Analysis of the DDB1 Gene: Genome-Wide Association Studies in African and Admixed African American Populations—Is Our Skin Different?” authored by Brandyn M. White, BS; Chidubem A.V. Okeke, BS; Raveena Khanna, MD; Ginette A. Okoye, MD; Michael C. Campbell, PhD; and Angel S. Byrd, MD, PhD. Their research evaluated the association of variant DNA damage binding protein 1, DDB1, with African populations and highlighted the possible phenotypic variations between African and admixed African American populations. Further, it discussed the advantages of conducting future genome-wide association studies in the Washington metropolitan area to better understand dermatological diseases that disproportionately affect skin of color patients.

The Best Oral Presentation Award was presented to Erica Ogwumike, BA, for “Matching into Dermatology Residency: The Impact of Research Fellowships” authored by Erica Ogwumike, BA; Chine Chime, MS, MPH; and Rebecca Vasquez, MD. The aim of this study was to explore what variables were important for 2 events: taking a research fellowship and matching into dermatology. The authors analyzed Electronic Residency Application Service (ERAS) applications for all medical students applying to the UT Southwestern Dermatology Residency Program in the 2014-2015 cycle. They found that 1 of 5 students participated in a research fellowship prior to applying to dermatology residency, and it was not associated with increased odds of matching. They also discovered that students more likely to take a research fellowship were Latinx, attended a medical school ranked in the Top 25, and were not Alpha Omega Alpha members. Nevertheless, total publications did increase the odds of matching; therefore, the authors concluded that when looking for a research fellowship, applicants should look for one that allows productivity so that this measure can be achieved. Further investigation is needed to substantiate these results, but this study was a starting point to examine the characteristics involved in taking a research fellowship in dermatology. 

Finally, the Crowd Favorite Award was presented to Jennifer Cucalon, BS, for “Non-invasive, In-Vivo RCM Monitoring of Lentigines Treated With Cryotherapy to Establish Minimum Freeze Time in Seconds (Dose) in Skin of Color” authored by Jennifer Cucalon, BS, and Babar K. Rao, MD. This pilot study showed a minimum freezing time of 3 seconds to be effective in removing lentigines in darker skin; increasing the dose to 6 and 9 seconds had no added benefit. The authors also demonstrated reflectance confocal microscopy to be an appropriate, noninvasive, in vivo tool to visualize pigmentary changes and monitor the effectiveness of treatments for various skin conditions.

The 19th Annual Scientific Symposium will take place on March 16, 2023, in New Orleans, Louisiana. The theme will be Where Science, Innovation & Inclusion Meet. For more information, visit https://skinofcolorsociety.org/19th-annual-skin-of-color-society-scientific-symposium/.

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The 18th Annual Skin of Color Society Scientific Symposium was held in March 2022 in Boston, Massachusetts. With a theme of Diversity in Action: Science, Healthcare & Society, researchers gathered to present new findings, share key insights, and discuss the continuing evolution of the field. Three awards were presented from the scientific posters at the symposium.

The Best Poster Presentation Award was presented to Brandyn M. White, BS, for “A Preliminary Analysis of the DDB1 Gene: Genome-Wide Association Studies in African and Admixed African American Populations—Is Our Skin Different?” authored by Brandyn M. White, BS; Chidubem A.V. Okeke, BS; Raveena Khanna, MD; Ginette A. Okoye, MD; Michael C. Campbell, PhD; and Angel S. Byrd, MD, PhD. Their research evaluated the association of variant DNA damage binding protein 1, DDB1, with African populations and highlighted the possible phenotypic variations between African and admixed African American populations. Further, it discussed the advantages of conducting future genome-wide association studies in the Washington metropolitan area to better understand dermatological diseases that disproportionately affect skin of color patients.

The Best Oral Presentation Award was presented to Erica Ogwumike, BA, for “Matching into Dermatology Residency: The Impact of Research Fellowships” authored by Erica Ogwumike, BA; Chine Chime, MS, MPH; and Rebecca Vasquez, MD. The aim of this study was to explore what variables were important for 2 events: taking a research fellowship and matching into dermatology. The authors analyzed Electronic Residency Application Service (ERAS) applications for all medical students applying to the UT Southwestern Dermatology Residency Program in the 2014-2015 cycle. They found that 1 of 5 students participated in a research fellowship prior to applying to dermatology residency, and it was not associated with increased odds of matching. They also discovered that students more likely to take a research fellowship were Latinx, attended a medical school ranked in the Top 25, and were not Alpha Omega Alpha members. Nevertheless, total publications did increase the odds of matching; therefore, the authors concluded that when looking for a research fellowship, applicants should look for one that allows productivity so that this measure can be achieved. Further investigation is needed to substantiate these results, but this study was a starting point to examine the characteristics involved in taking a research fellowship in dermatology. 

Finally, the Crowd Favorite Award was presented to Jennifer Cucalon, BS, for “Non-invasive, In-Vivo RCM Monitoring of Lentigines Treated With Cryotherapy to Establish Minimum Freeze Time in Seconds (Dose) in Skin of Color” authored by Jennifer Cucalon, BS, and Babar K. Rao, MD. This pilot study showed a minimum freezing time of 3 seconds to be effective in removing lentigines in darker skin; increasing the dose to 6 and 9 seconds had no added benefit. The authors also demonstrated reflectance confocal microscopy to be an appropriate, noninvasive, in vivo tool to visualize pigmentary changes and monitor the effectiveness of treatments for various skin conditions.

The 19th Annual Scientific Symposium will take place on March 16, 2023, in New Orleans, Louisiana. The theme will be Where Science, Innovation & Inclusion Meet. For more information, visit https://skinofcolorsociety.org/19th-annual-skin-of-color-society-scientific-symposium/.

The 18th Annual Skin of Color Society Scientific Symposium was held in March 2022 in Boston, Massachusetts. With a theme of Diversity in Action: Science, Healthcare & Society, researchers gathered to present new findings, share key insights, and discuss the continuing evolution of the field. Three awards were presented from the scientific posters at the symposium.

The Best Poster Presentation Award was presented to Brandyn M. White, BS, for “A Preliminary Analysis of the DDB1 Gene: Genome-Wide Association Studies in African and Admixed African American Populations—Is Our Skin Different?” authored by Brandyn M. White, BS; Chidubem A.V. Okeke, BS; Raveena Khanna, MD; Ginette A. Okoye, MD; Michael C. Campbell, PhD; and Angel S. Byrd, MD, PhD. Their research evaluated the association of variant DNA damage binding protein 1, DDB1, with African populations and highlighted the possible phenotypic variations between African and admixed African American populations. Further, it discussed the advantages of conducting future genome-wide association studies in the Washington metropolitan area to better understand dermatological diseases that disproportionately affect skin of color patients.

The Best Oral Presentation Award was presented to Erica Ogwumike, BA, for “Matching into Dermatology Residency: The Impact of Research Fellowships” authored by Erica Ogwumike, BA; Chine Chime, MS, MPH; and Rebecca Vasquez, MD. The aim of this study was to explore what variables were important for 2 events: taking a research fellowship and matching into dermatology. The authors analyzed Electronic Residency Application Service (ERAS) applications for all medical students applying to the UT Southwestern Dermatology Residency Program in the 2014-2015 cycle. They found that 1 of 5 students participated in a research fellowship prior to applying to dermatology residency, and it was not associated with increased odds of matching. They also discovered that students more likely to take a research fellowship were Latinx, attended a medical school ranked in the Top 25, and were not Alpha Omega Alpha members. Nevertheless, total publications did increase the odds of matching; therefore, the authors concluded that when looking for a research fellowship, applicants should look for one that allows productivity so that this measure can be achieved. Further investigation is needed to substantiate these results, but this study was a starting point to examine the characteristics involved in taking a research fellowship in dermatology. 

Finally, the Crowd Favorite Award was presented to Jennifer Cucalon, BS, for “Non-invasive, In-Vivo RCM Monitoring of Lentigines Treated With Cryotherapy to Establish Minimum Freeze Time in Seconds (Dose) in Skin of Color” authored by Jennifer Cucalon, BS, and Babar K. Rao, MD. This pilot study showed a minimum freezing time of 3 seconds to be effective in removing lentigines in darker skin; increasing the dose to 6 and 9 seconds had no added benefit. The authors also demonstrated reflectance confocal microscopy to be an appropriate, noninvasive, in vivo tool to visualize pigmentary changes and monitor the effectiveness of treatments for various skin conditions.

The 19th Annual Scientific Symposium will take place on March 16, 2023, in New Orleans, Louisiana. The theme will be Where Science, Innovation & Inclusion Meet. For more information, visit https://skinofcolorsociety.org/19th-annual-skin-of-color-society-scientific-symposium/.

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Fungal Osler Nodes Indicate Candidal Infective Endocarditis

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Fungal Osler Nodes Indicate Candidal Infective Endocarditis

To the Editor:

A 44-year-old woman presented with a low-grade fever (temperature, 38.0 °C) and painful acral lesions of 1 week’s duration. She had a history of hepatitis C viral infection and intravenous (IV) drug use, as well as polymicrobial infective endocarditis that involved the tricuspid and aortic valves; pathogenic organisms were identified via blood culture as Enterococcus faecalis, Serratia species, Streptococcus viridans, and Candida albicans. The patient had received a mechanical aortic valve and bioprosthetic tricuspid valve replacement 5 months prior with warfarin therapy and had completed a postsurgical 6-week course of high-dose micafungin. She reported that she had developed painful, violaceous, thin papules on the plantar surface of the left foot 2 weeks prior to presentation. Her symptoms improved with a short systemic steroid taper; however, within a week she developed new tender, erythematous, thin papules on the plantar surface of the right foot and the palmar surface of the left hand with associated lower extremity swelling. She denied other symptoms, including fever, chills, neurologic symptoms, shortness of breath, chest pain, nausea, vomiting, hematuria, and hematochezia. Due to worsening cutaneous findings, the patient presented to the emergency department, prompting hospital admission for empiric antibacterial therapy with vancomycin and piperacillin-tazobactam for suspected infectious endocarditis. Dermatology was consulted after 1 day of antibacterial therapy without improvement to determine the etiology of the patient’s skin findings.

Physical examination revealed the patient was afebrile with partially blanching violaceous to purpuric, tender, edematous papules on the left fourth and fifth finger pads, as well as scattered, painful, purpuric patches with stellate borders on the right plantar foot (Figure 1). Laboratory test results revealed mild anemia (hemoglobin, 11.9 g/dL [reference range, 12.0–15.0 g/dL], mild neutrophilia (neutrophils, 8.4×109/L [reference range, 1.9–7.9×109/L], elevated acute-phase reactants (erythrocyte sedimentation rate, 71 mm/h [reference range, 0–20 mm/h]; C-reactive protein, 5.7 mg/dL [reference range, 0.0–0.5 mg/dL]), and positive hepatitis C virus antibody with an undetectable viral load. At the time of dermatologic evaluation, admission blood cultures and transthoracic echocardiogram were negative. Additionally, a transesophageal echocardiogram, limited by artifact from the mechanical aortic valve, was equivocal for valvular pathology. Subsequent ophthalmologic evaluation was negative for lesions associated with endocarditis, such as retinal hemorrhages.

A, Left fourth and fifth distal volar fingers with tender, edematous, purpuric papules. B, Right plantar foot with a purpuric stellate patch; similar lesions were present on the left plantar foot (not pictured).
FIGURE 1. A, Left fourth and fifth distal volar fingers with tender, edematous, purpuric papules. B, Right plantar foot with a purpuric stellate patch; similar lesions were present on the left plantar foot (not pictured).

Punch biopsies of the left fourth finger pad were submitted for histopathologic analysis and tissue cultures. Histopathology demonstrated deep dermal perivascular neutrophilic inflammation with multiple intravascular thrombi, perivascular fibrin, and karyorrhectic debris (Figure 2). Periodic acid–Schiff and Grocott-Gomori methenamine-silver stains revealed fungal spores with rare pseudohyphae within the thrombosed vascular spaces and the perivascular dermis, consistent with fungal septic emboli (Figure 3).

A, A punch biopsy of the left fourth finger pad revealed multiple intravascular microthrombi with edema and a dense perivascular neutrophilic infiltrate (H&E, original magnification ×40). B, Higher power showed a thrombus with surrounding fibrin...
FIGURE 2. A, A punch biopsy of the left fourth finger pad revealed multiple intravascular microthrombi with edema and a dense perivascular neutrophilic infiltrate (H&E, original magnification ×40). B, Higher power showed a thrombus with surrounding fibrin deposition and a dense perivascular neutrophilic infiltrate (H&E, original magnification ×100).

Empiric systemic antifungal coverage composed of IV liposomal amphotericin B and oral flucytosine was initiated, and the patient’s tender acral papules rapidly improved. Within 48 hours of biopsy, skin tissue culture confirmed the presence of C albicans. Four days after the preliminary dermatopathology report, confirmatory blood cultures resulted with pansensitive C albicans. Final tissue and blood cultures were negative for bacteria including mycobacteria. In addition to a 6-week course of IV amphotericin B and flucytosine, repeat surgical intervention was considered, and lifelong suppressive antifungal oral therapy was recommended. Unfortunately, the patient did not present for follow-up. Three months later, she presented to the emergency department with peritonitis; in the operating room, she was found to have ischemia of the entirety of the small and large intestines and died shortly thereafter.

 A, Periodic acid–Schiff stain highlighted fungal spores and pseudohyphae within the thrombosed vascular spaces (original magnification ×100). B, Grocott-Gomori methenamine-silver stain demonstrated fungal spores in the thrombosed vascular space
FIGURE 3. A, Periodic acid–Schiff stain highlighted fungal spores and pseudohyphae within the thrombosed vascular spaces (original magnification ×100). B, Grocott-Gomori methenamine-silver stain demonstrated fungal spores in the thrombosed vascular space (original magnification ×100).

Fungal endocarditis is rare, tending to develop in patient populations with particular risk factors such as immune compromise, structural heart defects or prosthetic valves, and IV drug use. Candida infective endocarditis (CIE) represents less than 2% of infective endocarditis cases and carries a high mortality rate (30%–80%).1-3 Diagnosis may be challenging, as the clinical presentation varies widely. Although some patients may present with classic features of infective endocarditis, including fever, cardiac murmurs, and positive blood cultures, many cases of infective endocarditis present with nonspecific symptoms, raising a broad clinical differential diagnosis. Delay in diagnosis, which is seen in 82% of patients with fungal endocarditis, may be attributed to the slow progression of symptoms, inconclusive cardiac imaging, or negative blood cultures seen in almost one-third of cases.2,3 The feared complication of systemic embolization via infective endocarditis may occur in up to one-half of cases, with the highest rates associated with staphylococcal or fungal pathogens.2 The risk for embolization in fungal endocarditis is independent of the size of the cardiac valve vegetations; accordingly, sequelae of embolic complications may arise despite negative cardiac imaging.4 Embolic complications, which typically are seen within the first 2 to 4 weeks of treatment, may serve as the presenting feature of endocarditis and may even occur after completion of antimicrobial therapy.

Detection of cutaneous manifestations of infective endocarditis, including Janeway lesions, Osler nodes, and splinter hemorrhages, may allow for earlier diagnosis. Despite eponymous recognition, Janeway lesions and Osler nodes are relatively uncommon manifestations of infective endocarditis and may be found in only 5% to 15% of cases.5 Biopsies of suspected Janeway lesions and Osler nodes may allow for recognition of relevant vascular pathology, identification of the causative pathogen, and strong support for the diagnosis of infective endocarditis.4-7

The initial photomicrograph of corresponding Janeway lesion histopathology was published by Kerr in 1955 and revealed dermal microabscesses posited to be secondary to bacterial emboli.8,9 Additional cases through the years have reported overlapping histopathologic features of Janeway lesions and Osler nodes, with the latter often defined by the presence of vasculitis.4 Although there appears to be ongoing debate and overlap between the 2 integumentary findings, a general consensus on differentiation takes into account both the clinical signs and symptoms as well as the histopathologic findings.10,11

 

 

Osler nodes present as tender, violaceous, subcutaneous nodules on the acral surfaces, usually on the pads of the fingers and toes.5 The pathogenesis involves the deposition of immune complexes as a sequela of vascular occlusion by microthrombi classically seen in the late phase of subacute endocarditis. Janeway lesions present as nontender erythematous macules on the acral surfaces and are thought to represent microthrombi with dermal microabscesses, more common in acute endocarditis. Our patient demonstrated features of both Osler nodes and Janeway lesions. Despite the presence of fungal thrombi—a pathophysiology closer to that of Janeway lesions—the clinical presentation of painful acral nodules affecting finger pads and histologic features of vasculitis may be better characterized as Osler nodes. Regardless of pathogenesis, these cutaneous findings serve as a minor clinical criterion in the Duke criteria for the diagnosis of infective endocarditis when present.12

Candida infective endocarditis should be suspected in a patient with a history of valvular disease or prior infective endocarditis with fungemia, unexplained neurologic signs, or manifestations of peripheral embolization despite negative blood cultures.3 Particularly in the setting of negative cardiac imaging, recognition of CIE requires heightened diagnostic acumen and clinicopathologic correlation. Although culture and pathologic examination of valvular vegetations represents the gold standard for diagnosis of CIE, aspiration and culture of easily accessible septic emboli may provide rapid identification of the etiologic pathogen. In 1976, Alpert et al13 identified C albicans from an aspirated Osler node. Postmortem examination revealed extensive involvement of the homograft valve and aortic root with C albicans.13 Many other examples exist in the literature demonstrating matching pathogenic isolates from microbiologic cultures of skin and blood.4,9,14,15 Thadepalli and Francis7 investigated 26 cases of endocarditis in heroin users in which the admitting diagnosis was endocarditis in only 4 cases. The etiologic pathogen was aspirated from secondary sites of localized infections secondary to emboli, including cutaneous lesions in 10 of the cases. Gram stain and culture revealed the causative organism leading to the ultimate diagnosis and management in 17 of 26 patients with endocarditis.7

The incidence of fungal endocarditis is increasing, with a reported 67% of cases caused by nosocomial infection.1 Given the rising incidence of fungal endocarditis and its accompanying diagnostic difficulties, including frequently negative blood cultures and cardiac imaging, clinicians must perform careful skin examinations, employ judicious use of skin biopsy, and carefully correlate clinical and pathologic findings to improve recognition of this disease and guide patient care.

References
  1. Arnold CJ, Johnson M, Bayer AS, et al. Infective endocarditis: an observational cohort study with a focus on therapy. Antimicrob Agents Chemother. 2015;59:2365. doi:10.1128/AAC.04867-14
  2. Chaudhary SC, Sawlani KK, Arora R, et al. Native aortic valve fungal endocarditis. BMJ Case Rep. 2013;2013:bcr2012007144. doi:10.1136/bcr-2012-007144
  3. Ellis ME, Al-Abdely H, Sandridge A, et al. Fungal endocarditis: evidence in the world literature, 1965–1995. Clin Infect Dis. 2001;32:50-62. doi:10.1086/317550
  4. Gil MP, Velasco M, Botella R, et al. Janeway lesions: differential diagnosis with Osler’s nodes. Int J Dermatol. 1993;32:673-674. doi:10.1111/j.1365-4362.1993.tb04025.x
  5. Gomes RT, Tiberto LR, Bello VNM, et al. Dermatologic manifestations of infective endocarditis. An Bras Dermatol. 2016;91:92-94.
  6. Yee JM. Osler’s nodes and the recognition of infective endocarditis: a lesion of diagnostic importance. South Med J. 1987;80:753-757.
  7. Thadepalli H, Francis C. Diagnostic clues in metastatic lesions of endocarditia in addicts. West J Med. 1978;128:1-5.
  8. Kerr A Jr. Subacute Bacterial Endocarditis. Charles C. Thomas; 1955.
  9. Kerr A Jr, Tan JS. Biopsies of the Janeway lesion of infective endocarditis. J Cutan Pathol. 1979;6:124-129. doi:10.1111/j.1600-0560.1979.tb01113.x
  10. Marrie TJ. Osler’s nodes and Janeway lesions. Am J Med. 2008;121:105-106. doi:10.1016/j.amjmed.2007.07.035
  11. Gunson TH, Oliver GF. Osler’s nodes and Janeway lesions. Australas J Dermatol. 2007;48:251-255. doi:10.1111/j.1440-0960.2007.00397.x
  12. Durack DT, Lukes AS, Bright DK, et al. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Am J Med. 1994;96:200-209.
  13. Alpert JS, Krous HF, Dalen JE, et al. Pathogenesis of Osler’s nodes. Ann Intern Med. 1976;85:471-473. doi:10.7326/0003-4819-85-4-471
  14. Cardullo AC, Silvers DN, Grossman ME. Janeway lesions and Osler’s nodes: a review of histopathologic findings. J Am Acad Dermatol. 1990;22:1088-1090. doi:10.1016/0190-9622(90)70157-D
  15. Vinson RP, Chung A, Elston DM, et al. Septic microemboli in a Janeway lesion of bacterial endocarditis. J Am Acad Dermatol. 1996;35:984-985. doi:10.1016/S0190-9622(96)90125-5
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From Virginia Commonwealth University Health System, Richmond. Ms. Tisdale is from the School of Medicine, Dr. Massoud is from the Department of Dermatology, and Dr. Mochel is from the Departments of Dermatology and Pathology.

The authors report no conflict of interest.

Correspondence: Mark C. Mochel, MD, Department of Pathology, Virginia Commonwealth University Health System, 1200 E Marshall St, Gateway 6, Richmond, VA 23298 ([email protected]).

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From Virginia Commonwealth University Health System, Richmond. Ms. Tisdale is from the School of Medicine, Dr. Massoud is from the Department of Dermatology, and Dr. Mochel is from the Departments of Dermatology and Pathology.

The authors report no conflict of interest.

Correspondence: Mark C. Mochel, MD, Department of Pathology, Virginia Commonwealth University Health System, 1200 E Marshall St, Gateway 6, Richmond, VA 23298 ([email protected]).

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From Virginia Commonwealth University Health System, Richmond. Ms. Tisdale is from the School of Medicine, Dr. Massoud is from the Department of Dermatology, and Dr. Mochel is from the Departments of Dermatology and Pathology.

The authors report no conflict of interest.

Correspondence: Mark C. Mochel, MD, Department of Pathology, Virginia Commonwealth University Health System, 1200 E Marshall St, Gateway 6, Richmond, VA 23298 ([email protected]).

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To the Editor:

A 44-year-old woman presented with a low-grade fever (temperature, 38.0 °C) and painful acral lesions of 1 week’s duration. She had a history of hepatitis C viral infection and intravenous (IV) drug use, as well as polymicrobial infective endocarditis that involved the tricuspid and aortic valves; pathogenic organisms were identified via blood culture as Enterococcus faecalis, Serratia species, Streptococcus viridans, and Candida albicans. The patient had received a mechanical aortic valve and bioprosthetic tricuspid valve replacement 5 months prior with warfarin therapy and had completed a postsurgical 6-week course of high-dose micafungin. She reported that she had developed painful, violaceous, thin papules on the plantar surface of the left foot 2 weeks prior to presentation. Her symptoms improved with a short systemic steroid taper; however, within a week she developed new tender, erythematous, thin papules on the plantar surface of the right foot and the palmar surface of the left hand with associated lower extremity swelling. She denied other symptoms, including fever, chills, neurologic symptoms, shortness of breath, chest pain, nausea, vomiting, hematuria, and hematochezia. Due to worsening cutaneous findings, the patient presented to the emergency department, prompting hospital admission for empiric antibacterial therapy with vancomycin and piperacillin-tazobactam for suspected infectious endocarditis. Dermatology was consulted after 1 day of antibacterial therapy without improvement to determine the etiology of the patient’s skin findings.

Physical examination revealed the patient was afebrile with partially blanching violaceous to purpuric, tender, edematous papules on the left fourth and fifth finger pads, as well as scattered, painful, purpuric patches with stellate borders on the right plantar foot (Figure 1). Laboratory test results revealed mild anemia (hemoglobin, 11.9 g/dL [reference range, 12.0–15.0 g/dL], mild neutrophilia (neutrophils, 8.4×109/L [reference range, 1.9–7.9×109/L], elevated acute-phase reactants (erythrocyte sedimentation rate, 71 mm/h [reference range, 0–20 mm/h]; C-reactive protein, 5.7 mg/dL [reference range, 0.0–0.5 mg/dL]), and positive hepatitis C virus antibody with an undetectable viral load. At the time of dermatologic evaluation, admission blood cultures and transthoracic echocardiogram were negative. Additionally, a transesophageal echocardiogram, limited by artifact from the mechanical aortic valve, was equivocal for valvular pathology. Subsequent ophthalmologic evaluation was negative for lesions associated with endocarditis, such as retinal hemorrhages.

A, Left fourth and fifth distal volar fingers with tender, edematous, purpuric papules. B, Right plantar foot with a purpuric stellate patch; similar lesions were present on the left plantar foot (not pictured).
FIGURE 1. A, Left fourth and fifth distal volar fingers with tender, edematous, purpuric papules. B, Right plantar foot with a purpuric stellate patch; similar lesions were present on the left plantar foot (not pictured).

Punch biopsies of the left fourth finger pad were submitted for histopathologic analysis and tissue cultures. Histopathology demonstrated deep dermal perivascular neutrophilic inflammation with multiple intravascular thrombi, perivascular fibrin, and karyorrhectic debris (Figure 2). Periodic acid–Schiff and Grocott-Gomori methenamine-silver stains revealed fungal spores with rare pseudohyphae within the thrombosed vascular spaces and the perivascular dermis, consistent with fungal septic emboli (Figure 3).

A, A punch biopsy of the left fourth finger pad revealed multiple intravascular microthrombi with edema and a dense perivascular neutrophilic infiltrate (H&E, original magnification ×40). B, Higher power showed a thrombus with surrounding fibrin...
FIGURE 2. A, A punch biopsy of the left fourth finger pad revealed multiple intravascular microthrombi with edema and a dense perivascular neutrophilic infiltrate (H&E, original magnification ×40). B, Higher power showed a thrombus with surrounding fibrin deposition and a dense perivascular neutrophilic infiltrate (H&E, original magnification ×100).

Empiric systemic antifungal coverage composed of IV liposomal amphotericin B and oral flucytosine was initiated, and the patient’s tender acral papules rapidly improved. Within 48 hours of biopsy, skin tissue culture confirmed the presence of C albicans. Four days after the preliminary dermatopathology report, confirmatory blood cultures resulted with pansensitive C albicans. Final tissue and blood cultures were negative for bacteria including mycobacteria. In addition to a 6-week course of IV amphotericin B and flucytosine, repeat surgical intervention was considered, and lifelong suppressive antifungal oral therapy was recommended. Unfortunately, the patient did not present for follow-up. Three months later, she presented to the emergency department with peritonitis; in the operating room, she was found to have ischemia of the entirety of the small and large intestines and died shortly thereafter.

 A, Periodic acid–Schiff stain highlighted fungal spores and pseudohyphae within the thrombosed vascular spaces (original magnification ×100). B, Grocott-Gomori methenamine-silver stain demonstrated fungal spores in the thrombosed vascular space
FIGURE 3. A, Periodic acid–Schiff stain highlighted fungal spores and pseudohyphae within the thrombosed vascular spaces (original magnification ×100). B, Grocott-Gomori methenamine-silver stain demonstrated fungal spores in the thrombosed vascular space (original magnification ×100).

Fungal endocarditis is rare, tending to develop in patient populations with particular risk factors such as immune compromise, structural heart defects or prosthetic valves, and IV drug use. Candida infective endocarditis (CIE) represents less than 2% of infective endocarditis cases and carries a high mortality rate (30%–80%).1-3 Diagnosis may be challenging, as the clinical presentation varies widely. Although some patients may present with classic features of infective endocarditis, including fever, cardiac murmurs, and positive blood cultures, many cases of infective endocarditis present with nonspecific symptoms, raising a broad clinical differential diagnosis. Delay in diagnosis, which is seen in 82% of patients with fungal endocarditis, may be attributed to the slow progression of symptoms, inconclusive cardiac imaging, or negative blood cultures seen in almost one-third of cases.2,3 The feared complication of systemic embolization via infective endocarditis may occur in up to one-half of cases, with the highest rates associated with staphylococcal or fungal pathogens.2 The risk for embolization in fungal endocarditis is independent of the size of the cardiac valve vegetations; accordingly, sequelae of embolic complications may arise despite negative cardiac imaging.4 Embolic complications, which typically are seen within the first 2 to 4 weeks of treatment, may serve as the presenting feature of endocarditis and may even occur after completion of antimicrobial therapy.

Detection of cutaneous manifestations of infective endocarditis, including Janeway lesions, Osler nodes, and splinter hemorrhages, may allow for earlier diagnosis. Despite eponymous recognition, Janeway lesions and Osler nodes are relatively uncommon manifestations of infective endocarditis and may be found in only 5% to 15% of cases.5 Biopsies of suspected Janeway lesions and Osler nodes may allow for recognition of relevant vascular pathology, identification of the causative pathogen, and strong support for the diagnosis of infective endocarditis.4-7

The initial photomicrograph of corresponding Janeway lesion histopathology was published by Kerr in 1955 and revealed dermal microabscesses posited to be secondary to bacterial emboli.8,9 Additional cases through the years have reported overlapping histopathologic features of Janeway lesions and Osler nodes, with the latter often defined by the presence of vasculitis.4 Although there appears to be ongoing debate and overlap between the 2 integumentary findings, a general consensus on differentiation takes into account both the clinical signs and symptoms as well as the histopathologic findings.10,11

 

 

Osler nodes present as tender, violaceous, subcutaneous nodules on the acral surfaces, usually on the pads of the fingers and toes.5 The pathogenesis involves the deposition of immune complexes as a sequela of vascular occlusion by microthrombi classically seen in the late phase of subacute endocarditis. Janeway lesions present as nontender erythematous macules on the acral surfaces and are thought to represent microthrombi with dermal microabscesses, more common in acute endocarditis. Our patient demonstrated features of both Osler nodes and Janeway lesions. Despite the presence of fungal thrombi—a pathophysiology closer to that of Janeway lesions—the clinical presentation of painful acral nodules affecting finger pads and histologic features of vasculitis may be better characterized as Osler nodes. Regardless of pathogenesis, these cutaneous findings serve as a minor clinical criterion in the Duke criteria for the diagnosis of infective endocarditis when present.12

Candida infective endocarditis should be suspected in a patient with a history of valvular disease or prior infective endocarditis with fungemia, unexplained neurologic signs, or manifestations of peripheral embolization despite negative blood cultures.3 Particularly in the setting of negative cardiac imaging, recognition of CIE requires heightened diagnostic acumen and clinicopathologic correlation. Although culture and pathologic examination of valvular vegetations represents the gold standard for diagnosis of CIE, aspiration and culture of easily accessible septic emboli may provide rapid identification of the etiologic pathogen. In 1976, Alpert et al13 identified C albicans from an aspirated Osler node. Postmortem examination revealed extensive involvement of the homograft valve and aortic root with C albicans.13 Many other examples exist in the literature demonstrating matching pathogenic isolates from microbiologic cultures of skin and blood.4,9,14,15 Thadepalli and Francis7 investigated 26 cases of endocarditis in heroin users in which the admitting diagnosis was endocarditis in only 4 cases. The etiologic pathogen was aspirated from secondary sites of localized infections secondary to emboli, including cutaneous lesions in 10 of the cases. Gram stain and culture revealed the causative organism leading to the ultimate diagnosis and management in 17 of 26 patients with endocarditis.7

The incidence of fungal endocarditis is increasing, with a reported 67% of cases caused by nosocomial infection.1 Given the rising incidence of fungal endocarditis and its accompanying diagnostic difficulties, including frequently negative blood cultures and cardiac imaging, clinicians must perform careful skin examinations, employ judicious use of skin biopsy, and carefully correlate clinical and pathologic findings to improve recognition of this disease and guide patient care.

To the Editor:

A 44-year-old woman presented with a low-grade fever (temperature, 38.0 °C) and painful acral lesions of 1 week’s duration. She had a history of hepatitis C viral infection and intravenous (IV) drug use, as well as polymicrobial infective endocarditis that involved the tricuspid and aortic valves; pathogenic organisms were identified via blood culture as Enterococcus faecalis, Serratia species, Streptococcus viridans, and Candida albicans. The patient had received a mechanical aortic valve and bioprosthetic tricuspid valve replacement 5 months prior with warfarin therapy and had completed a postsurgical 6-week course of high-dose micafungin. She reported that she had developed painful, violaceous, thin papules on the plantar surface of the left foot 2 weeks prior to presentation. Her symptoms improved with a short systemic steroid taper; however, within a week she developed new tender, erythematous, thin papules on the plantar surface of the right foot and the palmar surface of the left hand with associated lower extremity swelling. She denied other symptoms, including fever, chills, neurologic symptoms, shortness of breath, chest pain, nausea, vomiting, hematuria, and hematochezia. Due to worsening cutaneous findings, the patient presented to the emergency department, prompting hospital admission for empiric antibacterial therapy with vancomycin and piperacillin-tazobactam for suspected infectious endocarditis. Dermatology was consulted after 1 day of antibacterial therapy without improvement to determine the etiology of the patient’s skin findings.

Physical examination revealed the patient was afebrile with partially blanching violaceous to purpuric, tender, edematous papules on the left fourth and fifth finger pads, as well as scattered, painful, purpuric patches with stellate borders on the right plantar foot (Figure 1). Laboratory test results revealed mild anemia (hemoglobin, 11.9 g/dL [reference range, 12.0–15.0 g/dL], mild neutrophilia (neutrophils, 8.4×109/L [reference range, 1.9–7.9×109/L], elevated acute-phase reactants (erythrocyte sedimentation rate, 71 mm/h [reference range, 0–20 mm/h]; C-reactive protein, 5.7 mg/dL [reference range, 0.0–0.5 mg/dL]), and positive hepatitis C virus antibody with an undetectable viral load. At the time of dermatologic evaluation, admission blood cultures and transthoracic echocardiogram were negative. Additionally, a transesophageal echocardiogram, limited by artifact from the mechanical aortic valve, was equivocal for valvular pathology. Subsequent ophthalmologic evaluation was negative for lesions associated with endocarditis, such as retinal hemorrhages.

A, Left fourth and fifth distal volar fingers with tender, edematous, purpuric papules. B, Right plantar foot with a purpuric stellate patch; similar lesions were present on the left plantar foot (not pictured).
FIGURE 1. A, Left fourth and fifth distal volar fingers with tender, edematous, purpuric papules. B, Right plantar foot with a purpuric stellate patch; similar lesions were present on the left plantar foot (not pictured).

Punch biopsies of the left fourth finger pad were submitted for histopathologic analysis and tissue cultures. Histopathology demonstrated deep dermal perivascular neutrophilic inflammation with multiple intravascular thrombi, perivascular fibrin, and karyorrhectic debris (Figure 2). Periodic acid–Schiff and Grocott-Gomori methenamine-silver stains revealed fungal spores with rare pseudohyphae within the thrombosed vascular spaces and the perivascular dermis, consistent with fungal septic emboli (Figure 3).

A, A punch biopsy of the left fourth finger pad revealed multiple intravascular microthrombi with edema and a dense perivascular neutrophilic infiltrate (H&E, original magnification ×40). B, Higher power showed a thrombus with surrounding fibrin...
FIGURE 2. A, A punch biopsy of the left fourth finger pad revealed multiple intravascular microthrombi with edema and a dense perivascular neutrophilic infiltrate (H&E, original magnification ×40). B, Higher power showed a thrombus with surrounding fibrin deposition and a dense perivascular neutrophilic infiltrate (H&E, original magnification ×100).

Empiric systemic antifungal coverage composed of IV liposomal amphotericin B and oral flucytosine was initiated, and the patient’s tender acral papules rapidly improved. Within 48 hours of biopsy, skin tissue culture confirmed the presence of C albicans. Four days after the preliminary dermatopathology report, confirmatory blood cultures resulted with pansensitive C albicans. Final tissue and blood cultures were negative for bacteria including mycobacteria. In addition to a 6-week course of IV amphotericin B and flucytosine, repeat surgical intervention was considered, and lifelong suppressive antifungal oral therapy was recommended. Unfortunately, the patient did not present for follow-up. Three months later, she presented to the emergency department with peritonitis; in the operating room, she was found to have ischemia of the entirety of the small and large intestines and died shortly thereafter.

 A, Periodic acid–Schiff stain highlighted fungal spores and pseudohyphae within the thrombosed vascular spaces (original magnification ×100). B, Grocott-Gomori methenamine-silver stain demonstrated fungal spores in the thrombosed vascular space
FIGURE 3. A, Periodic acid–Schiff stain highlighted fungal spores and pseudohyphae within the thrombosed vascular spaces (original magnification ×100). B, Grocott-Gomori methenamine-silver stain demonstrated fungal spores in the thrombosed vascular space (original magnification ×100).

Fungal endocarditis is rare, tending to develop in patient populations with particular risk factors such as immune compromise, structural heart defects or prosthetic valves, and IV drug use. Candida infective endocarditis (CIE) represents less than 2% of infective endocarditis cases and carries a high mortality rate (30%–80%).1-3 Diagnosis may be challenging, as the clinical presentation varies widely. Although some patients may present with classic features of infective endocarditis, including fever, cardiac murmurs, and positive blood cultures, many cases of infective endocarditis present with nonspecific symptoms, raising a broad clinical differential diagnosis. Delay in diagnosis, which is seen in 82% of patients with fungal endocarditis, may be attributed to the slow progression of symptoms, inconclusive cardiac imaging, or negative blood cultures seen in almost one-third of cases.2,3 The feared complication of systemic embolization via infective endocarditis may occur in up to one-half of cases, with the highest rates associated with staphylococcal or fungal pathogens.2 The risk for embolization in fungal endocarditis is independent of the size of the cardiac valve vegetations; accordingly, sequelae of embolic complications may arise despite negative cardiac imaging.4 Embolic complications, which typically are seen within the first 2 to 4 weeks of treatment, may serve as the presenting feature of endocarditis and may even occur after completion of antimicrobial therapy.

Detection of cutaneous manifestations of infective endocarditis, including Janeway lesions, Osler nodes, and splinter hemorrhages, may allow for earlier diagnosis. Despite eponymous recognition, Janeway lesions and Osler nodes are relatively uncommon manifestations of infective endocarditis and may be found in only 5% to 15% of cases.5 Biopsies of suspected Janeway lesions and Osler nodes may allow for recognition of relevant vascular pathology, identification of the causative pathogen, and strong support for the diagnosis of infective endocarditis.4-7

The initial photomicrograph of corresponding Janeway lesion histopathology was published by Kerr in 1955 and revealed dermal microabscesses posited to be secondary to bacterial emboli.8,9 Additional cases through the years have reported overlapping histopathologic features of Janeway lesions and Osler nodes, with the latter often defined by the presence of vasculitis.4 Although there appears to be ongoing debate and overlap between the 2 integumentary findings, a general consensus on differentiation takes into account both the clinical signs and symptoms as well as the histopathologic findings.10,11

 

 

Osler nodes present as tender, violaceous, subcutaneous nodules on the acral surfaces, usually on the pads of the fingers and toes.5 The pathogenesis involves the deposition of immune complexes as a sequela of vascular occlusion by microthrombi classically seen in the late phase of subacute endocarditis. Janeway lesions present as nontender erythematous macules on the acral surfaces and are thought to represent microthrombi with dermal microabscesses, more common in acute endocarditis. Our patient demonstrated features of both Osler nodes and Janeway lesions. Despite the presence of fungal thrombi—a pathophysiology closer to that of Janeway lesions—the clinical presentation of painful acral nodules affecting finger pads and histologic features of vasculitis may be better characterized as Osler nodes. Regardless of pathogenesis, these cutaneous findings serve as a minor clinical criterion in the Duke criteria for the diagnosis of infective endocarditis when present.12

Candida infective endocarditis should be suspected in a patient with a history of valvular disease or prior infective endocarditis with fungemia, unexplained neurologic signs, or manifestations of peripheral embolization despite negative blood cultures.3 Particularly in the setting of negative cardiac imaging, recognition of CIE requires heightened diagnostic acumen and clinicopathologic correlation. Although culture and pathologic examination of valvular vegetations represents the gold standard for diagnosis of CIE, aspiration and culture of easily accessible septic emboli may provide rapid identification of the etiologic pathogen. In 1976, Alpert et al13 identified C albicans from an aspirated Osler node. Postmortem examination revealed extensive involvement of the homograft valve and aortic root with C albicans.13 Many other examples exist in the literature demonstrating matching pathogenic isolates from microbiologic cultures of skin and blood.4,9,14,15 Thadepalli and Francis7 investigated 26 cases of endocarditis in heroin users in which the admitting diagnosis was endocarditis in only 4 cases. The etiologic pathogen was aspirated from secondary sites of localized infections secondary to emboli, including cutaneous lesions in 10 of the cases. Gram stain and culture revealed the causative organism leading to the ultimate diagnosis and management in 17 of 26 patients with endocarditis.7

The incidence of fungal endocarditis is increasing, with a reported 67% of cases caused by nosocomial infection.1 Given the rising incidence of fungal endocarditis and its accompanying diagnostic difficulties, including frequently negative blood cultures and cardiac imaging, clinicians must perform careful skin examinations, employ judicious use of skin biopsy, and carefully correlate clinical and pathologic findings to improve recognition of this disease and guide patient care.

References
  1. Arnold CJ, Johnson M, Bayer AS, et al. Infective endocarditis: an observational cohort study with a focus on therapy. Antimicrob Agents Chemother. 2015;59:2365. doi:10.1128/AAC.04867-14
  2. Chaudhary SC, Sawlani KK, Arora R, et al. Native aortic valve fungal endocarditis. BMJ Case Rep. 2013;2013:bcr2012007144. doi:10.1136/bcr-2012-007144
  3. Ellis ME, Al-Abdely H, Sandridge A, et al. Fungal endocarditis: evidence in the world literature, 1965–1995. Clin Infect Dis. 2001;32:50-62. doi:10.1086/317550
  4. Gil MP, Velasco M, Botella R, et al. Janeway lesions: differential diagnosis with Osler’s nodes. Int J Dermatol. 1993;32:673-674. doi:10.1111/j.1365-4362.1993.tb04025.x
  5. Gomes RT, Tiberto LR, Bello VNM, et al. Dermatologic manifestations of infective endocarditis. An Bras Dermatol. 2016;91:92-94.
  6. Yee JM. Osler’s nodes and the recognition of infective endocarditis: a lesion of diagnostic importance. South Med J. 1987;80:753-757.
  7. Thadepalli H, Francis C. Diagnostic clues in metastatic lesions of endocarditia in addicts. West J Med. 1978;128:1-5.
  8. Kerr A Jr. Subacute Bacterial Endocarditis. Charles C. Thomas; 1955.
  9. Kerr A Jr, Tan JS. Biopsies of the Janeway lesion of infective endocarditis. J Cutan Pathol. 1979;6:124-129. doi:10.1111/j.1600-0560.1979.tb01113.x
  10. Marrie TJ. Osler’s nodes and Janeway lesions. Am J Med. 2008;121:105-106. doi:10.1016/j.amjmed.2007.07.035
  11. Gunson TH, Oliver GF. Osler’s nodes and Janeway lesions. Australas J Dermatol. 2007;48:251-255. doi:10.1111/j.1440-0960.2007.00397.x
  12. Durack DT, Lukes AS, Bright DK, et al. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Am J Med. 1994;96:200-209.
  13. Alpert JS, Krous HF, Dalen JE, et al. Pathogenesis of Osler’s nodes. Ann Intern Med. 1976;85:471-473. doi:10.7326/0003-4819-85-4-471
  14. Cardullo AC, Silvers DN, Grossman ME. Janeway lesions and Osler’s nodes: a review of histopathologic findings. J Am Acad Dermatol. 1990;22:1088-1090. doi:10.1016/0190-9622(90)70157-D
  15. Vinson RP, Chung A, Elston DM, et al. Septic microemboli in a Janeway lesion of bacterial endocarditis. J Am Acad Dermatol. 1996;35:984-985. doi:10.1016/S0190-9622(96)90125-5
References
  1. Arnold CJ, Johnson M, Bayer AS, et al. Infective endocarditis: an observational cohort study with a focus on therapy. Antimicrob Agents Chemother. 2015;59:2365. doi:10.1128/AAC.04867-14
  2. Chaudhary SC, Sawlani KK, Arora R, et al. Native aortic valve fungal endocarditis. BMJ Case Rep. 2013;2013:bcr2012007144. doi:10.1136/bcr-2012-007144
  3. Ellis ME, Al-Abdely H, Sandridge A, et al. Fungal endocarditis: evidence in the world literature, 1965–1995. Clin Infect Dis. 2001;32:50-62. doi:10.1086/317550
  4. Gil MP, Velasco M, Botella R, et al. Janeway lesions: differential diagnosis with Osler’s nodes. Int J Dermatol. 1993;32:673-674. doi:10.1111/j.1365-4362.1993.tb04025.x
  5. Gomes RT, Tiberto LR, Bello VNM, et al. Dermatologic manifestations of infective endocarditis. An Bras Dermatol. 2016;91:92-94.
  6. Yee JM. Osler’s nodes and the recognition of infective endocarditis: a lesion of diagnostic importance. South Med J. 1987;80:753-757.
  7. Thadepalli H, Francis C. Diagnostic clues in metastatic lesions of endocarditia in addicts. West J Med. 1978;128:1-5.
  8. Kerr A Jr. Subacute Bacterial Endocarditis. Charles C. Thomas; 1955.
  9. Kerr A Jr, Tan JS. Biopsies of the Janeway lesion of infective endocarditis. J Cutan Pathol. 1979;6:124-129. doi:10.1111/j.1600-0560.1979.tb01113.x
  10. Marrie TJ. Osler’s nodes and Janeway lesions. Am J Med. 2008;121:105-106. doi:10.1016/j.amjmed.2007.07.035
  11. Gunson TH, Oliver GF. Osler’s nodes and Janeway lesions. Australas J Dermatol. 2007;48:251-255. doi:10.1111/j.1440-0960.2007.00397.x
  12. Durack DT, Lukes AS, Bright DK, et al. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Am J Med. 1994;96:200-209.
  13. Alpert JS, Krous HF, Dalen JE, et al. Pathogenesis of Osler’s nodes. Ann Intern Med. 1976;85:471-473. doi:10.7326/0003-4819-85-4-471
  14. Cardullo AC, Silvers DN, Grossman ME. Janeway lesions and Osler’s nodes: a review of histopathologic findings. J Am Acad Dermatol. 1990;22:1088-1090. doi:10.1016/0190-9622(90)70157-D
  15. Vinson RP, Chung A, Elston DM, et al. Septic microemboli in a Janeway lesion of bacterial endocarditis. J Am Acad Dermatol. 1996;35:984-985. doi:10.1016/S0190-9622(96)90125-5
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PRACTICE POINTS

  • Fungal infective endocarditis is rare, and diagnostic tests such as blood cultures and echocardiography may not detect the disease.
  • The mortality rate of fungal endocarditis is high, with improved clinical outcomes if diagnosed and treated early.
  • Clinicopathologic correlation between integumentary examination and skin biopsy findings may provide timely diagnosis, thereby guiding appropriate therapy.
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Citing workplace violence, one-fourth of critical care workers are ready to quit

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A surgeon in Tulsa shot by a disgruntled patient. A doctor in India beaten by a group of bereaved family members. A general practitioner in the United Kingdom threatened with stabbing. The reality is grim: Health care workers across the globe experience violence while at work. A new study identifies this trend and finds that 25% of health care workers polled were willing to quit because of such violence.

“That was pretty appalling,” Rahul Kashyap, MD, MBA, MBBS, recalls. Dr. Kashyap is one of the leaders of the Violence Study of Healthcare Workers and Systems (ViSHWaS), which polled an international sample of physicians, nurses, and hospital staff. This study has worrying implications, Dr. Kashyap says. In a time when hospital staff are reporting burnout in record numbers, further deterrents may be the last thing our health care system needs. But Dr. Kashyap hopes that bringing awareness to these trends may allow physicians, policymakers, and the public to mobilize and intervene before it’s too late.

Previous studies have revealed similar trends. The rate of workplace violence directed at U.S. health care workers is five times that of workers in any other industry, according to the Bureau of Labor Statistics. The same study found that attacks had increased 63% from 2011 to 2018. Other polls that focus on the pandemic show that nearly half of U.S. nurses believe that violence increased since the world shut down. Well before the pandemic, however, a study from the Indian Medical Association found that 75% of doctors experienced workplace violence.

With this history in mind, perhaps it’s not surprising that the idea for the study came from the authors’ personal experiences. They had seen coworkers go through attacks, or they had endured attacks themselves, Dr. Kashyap says. But they couldn’t find any global data to back up these experiences. So Dr. Kashyap and his colleagues formed a web of volunteers dedicated to creating a cross-sectional study.

They got in touch with researchers from countries across Asia, the Middle East, South America, North America, and Africa. The initial group agreed to reach out to their contacts, casting a wide net. Researchers used WhatsApp, LinkedIn, and text messages to distribute the survey. Health care workers in each country completed the brief questionnaire, recalling their prepandemic world and evaluating their current one.

Within 2 months, they had reached health care workers in more than 100 countries. They concluded the study when they received about 5,000 results, according to Dr. Kashyap, and then began the process of stratifying the data. For this report, they focused on critical care, emergency medicine, and anesthesiology, which resulted in 598 responses from 69 countries. Of these, India and the United States had the highest number of participants.

In all, 73% of participants reported facing physical or verbal violence while in the hospital; 48% said they felt less motivated to work because of that violence; 39% of respondents believed that the amount of violence they experienced was the same as before the COVID-19 pandemic; and 36% of respondents believed that violence had increased. Even though they were trained on guidelines from the Occupational Safety and Health Administration, 20% of participants felt unprepared to face violence.

Although the study didn’t analyze the reasons workers felt this way, Dr. Kashyap speculates that it could be related to the medical distrust that grew during the pandemic or the stress patients and health care professionals experienced during its peak.

Regardless, the researchers say their study is a starting point. Now that the trend has been highlighted, it may be acted on.

Moving forward, Dr. Kashyap believes that controlling for different variables could determine whether factors like gender or shift time put a worker at higher risk for violence. He hopes it’s possible to interrupt these patterns and reestablish trust in the hospital environment. “It’s aspirational, but you’re hoping that through studies like ViSHWaS, which means trust in Hindi ... [we could restore] the trust and confidence among health care providers for the patients and family members.”

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

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A surgeon in Tulsa shot by a disgruntled patient. A doctor in India beaten by a group of bereaved family members. A general practitioner in the United Kingdom threatened with stabbing. The reality is grim: Health care workers across the globe experience violence while at work. A new study identifies this trend and finds that 25% of health care workers polled were willing to quit because of such violence.

“That was pretty appalling,” Rahul Kashyap, MD, MBA, MBBS, recalls. Dr. Kashyap is one of the leaders of the Violence Study of Healthcare Workers and Systems (ViSHWaS), which polled an international sample of physicians, nurses, and hospital staff. This study has worrying implications, Dr. Kashyap says. In a time when hospital staff are reporting burnout in record numbers, further deterrents may be the last thing our health care system needs. But Dr. Kashyap hopes that bringing awareness to these trends may allow physicians, policymakers, and the public to mobilize and intervene before it’s too late.

Previous studies have revealed similar trends. The rate of workplace violence directed at U.S. health care workers is five times that of workers in any other industry, according to the Bureau of Labor Statistics. The same study found that attacks had increased 63% from 2011 to 2018. Other polls that focus on the pandemic show that nearly half of U.S. nurses believe that violence increased since the world shut down. Well before the pandemic, however, a study from the Indian Medical Association found that 75% of doctors experienced workplace violence.

With this history in mind, perhaps it’s not surprising that the idea for the study came from the authors’ personal experiences. They had seen coworkers go through attacks, or they had endured attacks themselves, Dr. Kashyap says. But they couldn’t find any global data to back up these experiences. So Dr. Kashyap and his colleagues formed a web of volunteers dedicated to creating a cross-sectional study.

They got in touch with researchers from countries across Asia, the Middle East, South America, North America, and Africa. The initial group agreed to reach out to their contacts, casting a wide net. Researchers used WhatsApp, LinkedIn, and text messages to distribute the survey. Health care workers in each country completed the brief questionnaire, recalling their prepandemic world and evaluating their current one.

Within 2 months, they had reached health care workers in more than 100 countries. They concluded the study when they received about 5,000 results, according to Dr. Kashyap, and then began the process of stratifying the data. For this report, they focused on critical care, emergency medicine, and anesthesiology, which resulted in 598 responses from 69 countries. Of these, India and the United States had the highest number of participants.

In all, 73% of participants reported facing physical or verbal violence while in the hospital; 48% said they felt less motivated to work because of that violence; 39% of respondents believed that the amount of violence they experienced was the same as before the COVID-19 pandemic; and 36% of respondents believed that violence had increased. Even though they were trained on guidelines from the Occupational Safety and Health Administration, 20% of participants felt unprepared to face violence.

Although the study didn’t analyze the reasons workers felt this way, Dr. Kashyap speculates that it could be related to the medical distrust that grew during the pandemic or the stress patients and health care professionals experienced during its peak.

Regardless, the researchers say their study is a starting point. Now that the trend has been highlighted, it may be acted on.

Moving forward, Dr. Kashyap believes that controlling for different variables could determine whether factors like gender or shift time put a worker at higher risk for violence. He hopes it’s possible to interrupt these patterns and reestablish trust in the hospital environment. “It’s aspirational, but you’re hoping that through studies like ViSHWaS, which means trust in Hindi ... [we could restore] the trust and confidence among health care providers for the patients and family members.”

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

A surgeon in Tulsa shot by a disgruntled patient. A doctor in India beaten by a group of bereaved family members. A general practitioner in the United Kingdom threatened with stabbing. The reality is grim: Health care workers across the globe experience violence while at work. A new study identifies this trend and finds that 25% of health care workers polled were willing to quit because of such violence.

“That was pretty appalling,” Rahul Kashyap, MD, MBA, MBBS, recalls. Dr. Kashyap is one of the leaders of the Violence Study of Healthcare Workers and Systems (ViSHWaS), which polled an international sample of physicians, nurses, and hospital staff. This study has worrying implications, Dr. Kashyap says. In a time when hospital staff are reporting burnout in record numbers, further deterrents may be the last thing our health care system needs. But Dr. Kashyap hopes that bringing awareness to these trends may allow physicians, policymakers, and the public to mobilize and intervene before it’s too late.

Previous studies have revealed similar trends. The rate of workplace violence directed at U.S. health care workers is five times that of workers in any other industry, according to the Bureau of Labor Statistics. The same study found that attacks had increased 63% from 2011 to 2018. Other polls that focus on the pandemic show that nearly half of U.S. nurses believe that violence increased since the world shut down. Well before the pandemic, however, a study from the Indian Medical Association found that 75% of doctors experienced workplace violence.

With this history in mind, perhaps it’s not surprising that the idea for the study came from the authors’ personal experiences. They had seen coworkers go through attacks, or they had endured attacks themselves, Dr. Kashyap says. But they couldn’t find any global data to back up these experiences. So Dr. Kashyap and his colleagues formed a web of volunteers dedicated to creating a cross-sectional study.

They got in touch with researchers from countries across Asia, the Middle East, South America, North America, and Africa. The initial group agreed to reach out to their contacts, casting a wide net. Researchers used WhatsApp, LinkedIn, and text messages to distribute the survey. Health care workers in each country completed the brief questionnaire, recalling their prepandemic world and evaluating their current one.

Within 2 months, they had reached health care workers in more than 100 countries. They concluded the study when they received about 5,000 results, according to Dr. Kashyap, and then began the process of stratifying the data. For this report, they focused on critical care, emergency medicine, and anesthesiology, which resulted in 598 responses from 69 countries. Of these, India and the United States had the highest number of participants.

In all, 73% of participants reported facing physical or verbal violence while in the hospital; 48% said they felt less motivated to work because of that violence; 39% of respondents believed that the amount of violence they experienced was the same as before the COVID-19 pandemic; and 36% of respondents believed that violence had increased. Even though they were trained on guidelines from the Occupational Safety and Health Administration, 20% of participants felt unprepared to face violence.

Although the study didn’t analyze the reasons workers felt this way, Dr. Kashyap speculates that it could be related to the medical distrust that grew during the pandemic or the stress patients and health care professionals experienced during its peak.

Regardless, the researchers say their study is a starting point. Now that the trend has been highlighted, it may be acted on.

Moving forward, Dr. Kashyap believes that controlling for different variables could determine whether factors like gender or shift time put a worker at higher risk for violence. He hopes it’s possible to interrupt these patterns and reestablish trust in the hospital environment. “It’s aspirational, but you’re hoping that through studies like ViSHWaS, which means trust in Hindi ... [we could restore] the trust and confidence among health care providers for the patients and family members.”

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

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Feds charge 25 nursing school execs, staff in fake diploma scheme

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At least one state licensing agency is revoking nursing licenses allegedly obtained in a multistate fake diploma scheme.

The U.S. Department of Justice recently announced charges against 25 owners, operators, and employees of three Florida nursing schools in a fraud scheme in which they sold as many as 7,600 fake nursing degrees.

The purchasers in the diploma scheme paid $10,000 to $15,000 for degrees and transcripts and some 2,800 of the buyers passed the national nursing licensing exam to become registered nurses (RNs) and licensed practice nurses/vocational nurses (LPN/VNs) around the country, according to The New York Times.

Many of the degree recipients went on to work at hospitals, nursing homes, and Veterans Affairs medical centers, according to the U.S. Attorney’s Office for the Southern District of Florida.

Several national nursing organizations cooperated with the investigation, and the Delaware Division of Professional Regulation already annulled 26 licenses, according to the Delaware Nurses Association. Fake licenses were issued in five states, according to federal reports.

“We are deeply unsettled by this egregious act,” DNA President Stephanie McClellan, MSN, RN, CMSRN, said in the group’s press statement. “We want all Delaware nurses to be aware of this active issue and to speak up if there is a concern regarding capacity to practice safely by a colleague/peer,” she said.

The Oregon State Board of Nursing is also investigating at least a dozen nurses who may have paid for their degrees, according to a Portland CBS affiliate.

The National Council of State Boards of Nursing said in a statement that it had helped authorities identify and monitor the individuals who allegedly provided the false degrees.
 

Nursing community reacts

News of the fraud scheme spread through the nursing community, including social media. “The recent report on falsified nursing school degrees is both heartbreaking and serves as an eye-opener,” tweeted Usha Menon, PhD, RN, FAAN, dean and health professor of the University of South Florida Health College of Nursing. “There was enough of a need that prompted these bad actors to develop a scheme that could’ve endangered dozens of lives.”

Jennifer Mensik Kennedy, PhD, MBA, RN, the new president of the American Nurses Association, also weighed in. “The accusation that personnel at once-accredited nursing schools allegedly participated in this scheme is simply deplorable. These unlawful and unethical acts disparage the reputation of actual nurses everywhere who have rightfully earned [their titles] through their education, hard work, dedication, and time.”

The false degrees and transcripts were issued by three once-accredited and now-shuttered nursing schools in South Florida: Palm Beach School of Nursing, Sacred Heart International Institute, and Sienna College.

The alleged co-conspirators reportedly made $114 million from the scheme, which dates back to 2016, according to several news reports. Each defendant faces up to 20 years in prison.

Most LPN programs charge $10,000 to $15,000 to complete a program, Robert Rosseter, a spokesperson for the American Association of Colleges of Nursing (AACN), told this news organization.

None were AACN members, and none were accredited by the Commission on Collegiate Nursing Education, which is AACN’s autonomous accrediting agency, Mr. Rosseter said. AACN membership is voluntary and is open to schools offering baccalaureate or higher degrees, he explained.

“What is disturbing about this investigation is that there are over 7,600 people around the country with fraudulent nursing credentials who are potentially in critical health care roles treating patients,” Chad Yarbrough, acting special agent in charge for the FBI in Miami, said in the federal justice department release.
 

 

 

‘Operation Nightingale’ based on tip

The federal action, dubbed “Operation Nightingale” after the nursing pioneer Florence Nightingale, began in 2019. It was based on a tip related to a case in Maryland, according to Nurse.org.

That case ensnared Palm Beach School of Nursing owner Johanah Napoleon, who reportedly was selling fake degrees for $6,000 to $18,000 each to two individuals in Maryland and Virginia. Ms. Napoleon was charged in 2021 and eventually pled guilty. The Florida Board of Nursing shut down the Palm Beach school in 2017 owing to its students’ low passing rate on the national licensing exam.

Two participants in the bigger scheme who had also worked with Ms. Napoleon – Geralda Adrien and Woosvelt Predestin – were indicted in 2021. Ms. Adrien owned private education companies for people who at aspired to be nurses, and Mr. Predestin was an employee. They were sentenced to 27 months in prison last year and helped the federal officials build the larger case.

The 25 individuals who were charged Jan. 25 operated in Delaware, New York, New Jersey, Texas, and Florida.
 

Schemes lured immigrants

In the scheme involving Siena College, some of the individuals acted as recruiters to direct nurses who were looking for employment to the school, where they allegedly would then pay for an RN or LPN/VN degree. The recipients of the false documents then used them to obtain jobs, including at a hospital in Georgia and a Veterans Affairs medical center in Maryland, according to one indictment. The president of Siena and her co-conspirators sold more than 2,000 fake diplomas, according to charging documents.

At the Palm Beach College of Nursing, individuals at various nursing prep and education programs allegedly helped others obtain fake degrees and transcripts, which were then used to pass RN and LPN/VN licensing exams in states that included Massachusetts, New Jersey, New York, and Ohio, according to the indictment.

Some individuals then secured employment with a nursing home in Ohio, a home health agency for pediatric patients in Massachusetts, and skilled nursing facilities in New York and New Jersey.

Prosecutors allege that the president of Sacred Heart International Institute and two other co-conspirators sold 588 fake diplomas.

The FBI said that some of the aspiring nurses who were talked into buying the degrees were LPNs who wanted to become RNs and that most of those lured into the scheme were from South Florida’s Haitian American immigrant community, Nurse.org reported.

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

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At least one state licensing agency is revoking nursing licenses allegedly obtained in a multistate fake diploma scheme.

The U.S. Department of Justice recently announced charges against 25 owners, operators, and employees of three Florida nursing schools in a fraud scheme in which they sold as many as 7,600 fake nursing degrees.

The purchasers in the diploma scheme paid $10,000 to $15,000 for degrees and transcripts and some 2,800 of the buyers passed the national nursing licensing exam to become registered nurses (RNs) and licensed practice nurses/vocational nurses (LPN/VNs) around the country, according to The New York Times.

Many of the degree recipients went on to work at hospitals, nursing homes, and Veterans Affairs medical centers, according to the U.S. Attorney’s Office for the Southern District of Florida.

Several national nursing organizations cooperated with the investigation, and the Delaware Division of Professional Regulation already annulled 26 licenses, according to the Delaware Nurses Association. Fake licenses were issued in five states, according to federal reports.

“We are deeply unsettled by this egregious act,” DNA President Stephanie McClellan, MSN, RN, CMSRN, said in the group’s press statement. “We want all Delaware nurses to be aware of this active issue and to speak up if there is a concern regarding capacity to practice safely by a colleague/peer,” she said.

The Oregon State Board of Nursing is also investigating at least a dozen nurses who may have paid for their degrees, according to a Portland CBS affiliate.

The National Council of State Boards of Nursing said in a statement that it had helped authorities identify and monitor the individuals who allegedly provided the false degrees.
 

Nursing community reacts

News of the fraud scheme spread through the nursing community, including social media. “The recent report on falsified nursing school degrees is both heartbreaking and serves as an eye-opener,” tweeted Usha Menon, PhD, RN, FAAN, dean and health professor of the University of South Florida Health College of Nursing. “There was enough of a need that prompted these bad actors to develop a scheme that could’ve endangered dozens of lives.”

Jennifer Mensik Kennedy, PhD, MBA, RN, the new president of the American Nurses Association, also weighed in. “The accusation that personnel at once-accredited nursing schools allegedly participated in this scheme is simply deplorable. These unlawful and unethical acts disparage the reputation of actual nurses everywhere who have rightfully earned [their titles] through their education, hard work, dedication, and time.”

The false degrees and transcripts were issued by three once-accredited and now-shuttered nursing schools in South Florida: Palm Beach School of Nursing, Sacred Heart International Institute, and Sienna College.

The alleged co-conspirators reportedly made $114 million from the scheme, which dates back to 2016, according to several news reports. Each defendant faces up to 20 years in prison.

Most LPN programs charge $10,000 to $15,000 to complete a program, Robert Rosseter, a spokesperson for the American Association of Colleges of Nursing (AACN), told this news organization.

None were AACN members, and none were accredited by the Commission on Collegiate Nursing Education, which is AACN’s autonomous accrediting agency, Mr. Rosseter said. AACN membership is voluntary and is open to schools offering baccalaureate or higher degrees, he explained.

“What is disturbing about this investigation is that there are over 7,600 people around the country with fraudulent nursing credentials who are potentially in critical health care roles treating patients,” Chad Yarbrough, acting special agent in charge for the FBI in Miami, said in the federal justice department release.
 

 

 

‘Operation Nightingale’ based on tip

The federal action, dubbed “Operation Nightingale” after the nursing pioneer Florence Nightingale, began in 2019. It was based on a tip related to a case in Maryland, according to Nurse.org.

That case ensnared Palm Beach School of Nursing owner Johanah Napoleon, who reportedly was selling fake degrees for $6,000 to $18,000 each to two individuals in Maryland and Virginia. Ms. Napoleon was charged in 2021 and eventually pled guilty. The Florida Board of Nursing shut down the Palm Beach school in 2017 owing to its students’ low passing rate on the national licensing exam.

Two participants in the bigger scheme who had also worked with Ms. Napoleon – Geralda Adrien and Woosvelt Predestin – were indicted in 2021. Ms. Adrien owned private education companies for people who at aspired to be nurses, and Mr. Predestin was an employee. They were sentenced to 27 months in prison last year and helped the federal officials build the larger case.

The 25 individuals who were charged Jan. 25 operated in Delaware, New York, New Jersey, Texas, and Florida.
 

Schemes lured immigrants

In the scheme involving Siena College, some of the individuals acted as recruiters to direct nurses who were looking for employment to the school, where they allegedly would then pay for an RN or LPN/VN degree. The recipients of the false documents then used them to obtain jobs, including at a hospital in Georgia and a Veterans Affairs medical center in Maryland, according to one indictment. The president of Siena and her co-conspirators sold more than 2,000 fake diplomas, according to charging documents.

At the Palm Beach College of Nursing, individuals at various nursing prep and education programs allegedly helped others obtain fake degrees and transcripts, which were then used to pass RN and LPN/VN licensing exams in states that included Massachusetts, New Jersey, New York, and Ohio, according to the indictment.

Some individuals then secured employment with a nursing home in Ohio, a home health agency for pediatric patients in Massachusetts, and skilled nursing facilities in New York and New Jersey.

Prosecutors allege that the president of Sacred Heart International Institute and two other co-conspirators sold 588 fake diplomas.

The FBI said that some of the aspiring nurses who were talked into buying the degrees were LPNs who wanted to become RNs and that most of those lured into the scheme were from South Florida’s Haitian American immigrant community, Nurse.org reported.

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

At least one state licensing agency is revoking nursing licenses allegedly obtained in a multistate fake diploma scheme.

The U.S. Department of Justice recently announced charges against 25 owners, operators, and employees of three Florida nursing schools in a fraud scheme in which they sold as many as 7,600 fake nursing degrees.

The purchasers in the diploma scheme paid $10,000 to $15,000 for degrees and transcripts and some 2,800 of the buyers passed the national nursing licensing exam to become registered nurses (RNs) and licensed practice nurses/vocational nurses (LPN/VNs) around the country, according to The New York Times.

Many of the degree recipients went on to work at hospitals, nursing homes, and Veterans Affairs medical centers, according to the U.S. Attorney’s Office for the Southern District of Florida.

Several national nursing organizations cooperated with the investigation, and the Delaware Division of Professional Regulation already annulled 26 licenses, according to the Delaware Nurses Association. Fake licenses were issued in five states, according to federal reports.

“We are deeply unsettled by this egregious act,” DNA President Stephanie McClellan, MSN, RN, CMSRN, said in the group’s press statement. “We want all Delaware nurses to be aware of this active issue and to speak up if there is a concern regarding capacity to practice safely by a colleague/peer,” she said.

The Oregon State Board of Nursing is also investigating at least a dozen nurses who may have paid for their degrees, according to a Portland CBS affiliate.

The National Council of State Boards of Nursing said in a statement that it had helped authorities identify and monitor the individuals who allegedly provided the false degrees.
 

Nursing community reacts

News of the fraud scheme spread through the nursing community, including social media. “The recent report on falsified nursing school degrees is both heartbreaking and serves as an eye-opener,” tweeted Usha Menon, PhD, RN, FAAN, dean and health professor of the University of South Florida Health College of Nursing. “There was enough of a need that prompted these bad actors to develop a scheme that could’ve endangered dozens of lives.”

Jennifer Mensik Kennedy, PhD, MBA, RN, the new president of the American Nurses Association, also weighed in. “The accusation that personnel at once-accredited nursing schools allegedly participated in this scheme is simply deplorable. These unlawful and unethical acts disparage the reputation of actual nurses everywhere who have rightfully earned [their titles] through their education, hard work, dedication, and time.”

The false degrees and transcripts were issued by three once-accredited and now-shuttered nursing schools in South Florida: Palm Beach School of Nursing, Sacred Heart International Institute, and Sienna College.

The alleged co-conspirators reportedly made $114 million from the scheme, which dates back to 2016, according to several news reports. Each defendant faces up to 20 years in prison.

Most LPN programs charge $10,000 to $15,000 to complete a program, Robert Rosseter, a spokesperson for the American Association of Colleges of Nursing (AACN), told this news organization.

None were AACN members, and none were accredited by the Commission on Collegiate Nursing Education, which is AACN’s autonomous accrediting agency, Mr. Rosseter said. AACN membership is voluntary and is open to schools offering baccalaureate or higher degrees, he explained.

“What is disturbing about this investigation is that there are over 7,600 people around the country with fraudulent nursing credentials who are potentially in critical health care roles treating patients,” Chad Yarbrough, acting special agent in charge for the FBI in Miami, said in the federal justice department release.
 

 

 

‘Operation Nightingale’ based on tip

The federal action, dubbed “Operation Nightingale” after the nursing pioneer Florence Nightingale, began in 2019. It was based on a tip related to a case in Maryland, according to Nurse.org.

That case ensnared Palm Beach School of Nursing owner Johanah Napoleon, who reportedly was selling fake degrees for $6,000 to $18,000 each to two individuals in Maryland and Virginia. Ms. Napoleon was charged in 2021 and eventually pled guilty. The Florida Board of Nursing shut down the Palm Beach school in 2017 owing to its students’ low passing rate on the national licensing exam.

Two participants in the bigger scheme who had also worked with Ms. Napoleon – Geralda Adrien and Woosvelt Predestin – were indicted in 2021. Ms. Adrien owned private education companies for people who at aspired to be nurses, and Mr. Predestin was an employee. They were sentenced to 27 months in prison last year and helped the federal officials build the larger case.

The 25 individuals who were charged Jan. 25 operated in Delaware, New York, New Jersey, Texas, and Florida.
 

Schemes lured immigrants

In the scheme involving Siena College, some of the individuals acted as recruiters to direct nurses who were looking for employment to the school, where they allegedly would then pay for an RN or LPN/VN degree. The recipients of the false documents then used them to obtain jobs, including at a hospital in Georgia and a Veterans Affairs medical center in Maryland, according to one indictment. The president of Siena and her co-conspirators sold more than 2,000 fake diplomas, according to charging documents.

At the Palm Beach College of Nursing, individuals at various nursing prep and education programs allegedly helped others obtain fake degrees and transcripts, which were then used to pass RN and LPN/VN licensing exams in states that included Massachusetts, New Jersey, New York, and Ohio, according to the indictment.

Some individuals then secured employment with a nursing home in Ohio, a home health agency for pediatric patients in Massachusetts, and skilled nursing facilities in New York and New Jersey.

Prosecutors allege that the president of Sacred Heart International Institute and two other co-conspirators sold 588 fake diplomas.

The FBI said that some of the aspiring nurses who were talked into buying the degrees were LPNs who wanted to become RNs and that most of those lured into the scheme were from South Florida’s Haitian American immigrant community, Nurse.org reported.

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

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Biden to end COVID emergencies in May

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The two national emergency declarations dealing with the COVID-19 pandemic will end May 11, President Joe Biden said on Jan. 30.

Doing so will have many effects, including the end of free vaccines and health services to fight the pandemic. The public health emergency has been renewed every 90 days since it was declared by the Trump administration in January 2020.

The declaration allowed major changes throughout the health care system to deal with the pandemic, including the free distribution of vaccines, testing, and treatments. In addition, telehealth services were expanded, and Medicaid and the Children’s Health Insurance Program were extended to millions more Americans.

Biden said the COVID-19 national emergency is set to expire March 1 while the declared public health emergency would currently expire on April 11. The president said both will be extended to end May 11.

There were nearly 300,000 newly reported COVID-19 cases in the United States for the week ending Jan. 25, according to CDC data, as well as more than 3,750 deaths.

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

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The two national emergency declarations dealing with the COVID-19 pandemic will end May 11, President Joe Biden said on Jan. 30.

Doing so will have many effects, including the end of free vaccines and health services to fight the pandemic. The public health emergency has been renewed every 90 days since it was declared by the Trump administration in January 2020.

The declaration allowed major changes throughout the health care system to deal with the pandemic, including the free distribution of vaccines, testing, and treatments. In addition, telehealth services were expanded, and Medicaid and the Children’s Health Insurance Program were extended to millions more Americans.

Biden said the COVID-19 national emergency is set to expire March 1 while the declared public health emergency would currently expire on April 11. The president said both will be extended to end May 11.

There were nearly 300,000 newly reported COVID-19 cases in the United States for the week ending Jan. 25, according to CDC data, as well as more than 3,750 deaths.

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

The two national emergency declarations dealing with the COVID-19 pandemic will end May 11, President Joe Biden said on Jan. 30.

Doing so will have many effects, including the end of free vaccines and health services to fight the pandemic. The public health emergency has been renewed every 90 days since it was declared by the Trump administration in January 2020.

The declaration allowed major changes throughout the health care system to deal with the pandemic, including the free distribution of vaccines, testing, and treatments. In addition, telehealth services were expanded, and Medicaid and the Children’s Health Insurance Program were extended to millions more Americans.

Biden said the COVID-19 national emergency is set to expire March 1 while the declared public health emergency would currently expire on April 11. The president said both will be extended to end May 11.

There were nearly 300,000 newly reported COVID-19 cases in the United States for the week ending Jan. 25, according to CDC data, as well as more than 3,750 deaths.

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

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