We are in the healing profession. We practice a trade. We are doctors, therapists, counselors. We work with children, adults, and couples. We document the physical form of our patient after examination, setting the stage for interventions that heal and alleviate suffering. With those who we do not touch physically, we hold out our psychological arms to embrace them in a therapeutic relationship.

We are privileged to appreciate their deeper selves through voice, unsaid words, and body language. A trust evolves (or might not); deeper exploration where our intuition and technical skill discover what troubles the soul. Healing begins as a delicate dance: As trust is earned, our patients risk vulnerability by revealing their weakest selves.

As healers, we often find ourselves adrift with our own insecurities, our own histories that make us human; our styles may differ but training and the tenets and guidelines set by our professional societies keep us in safe waters. These guidelines are informed by the science of health care research and vetted through centuries of observation and experience of process. “Do no harm” is perhaps one of the major rules of engaging with patients. The scaffolding that our code of ethics provides healing professions trumps external pressures to deviate. If you violate these codes, the consequences are borne by the patient and the potential loss of your license.

Some of you may have read about Kevin Euceda, an adolescent who reportedly was waiting for his immigration interview and ordered to undergo mandatory therapy as part of the immigration protocol. Kevin revealed to his therapist the history of violence he experienced as a child growing up in Honduras. His subsequent initiation into a gang was the only option he had to escape a violent death. Those of us who work with youth from gang cultures know fully that allegiance to a gang is a means to find an identity and brotherhood with the payment by a lifestyle of violence. A therapist faced with this information does not judge but helps the person deal with PTSD, nightmares, and guilt that become part of an identity just as the memories of mines blowing up in the face of combat affect veterans.

But the therapist, who reportedly holds a master’s in rehabilitation counseling and was “a year away from passing her licensing exam,” according to an article published in the Washington Post, followed policy of the Office of Refugee Resettlement. The therapist betrayed Kevin by reporting the information he shared with her confidentially to Immigration and Customs Enforcement. The reason the therapist gave for the breach was that she was compelled do so because Kevin reported participating in gang activity in Honduras. Subsequently, Kevin was sent to a high-security detention center – and is now facing deportation.
 

Betraying a patient, profession

Therapy begins as a contract between patient and therapist. The contract stipulates that all that transpires in the process of therapy (usually a 50-minute block of time, usually weekly) is information held by the therapist and patient – and is not to be shared with anyone, including parents, guardians, legal entities, and health care agencies. This allows the gradual sharing of events, emotions, behaviors, and reactions akin to peeling an onion. Memories, reactions, and feelings assist the therapist as they start their quest of discovery of the conflict and how to resolve it. Trust is the central tenet of this journey. The patient thinks: “You will hear me; you will see me you will understand me and help me understand myself.” The doctor responds: “Even I don’t yet know fully what ails you; we will discover that together. … I will not fail your trust.”

So how does this interface with external pressures? The constitution of a free country provides some inviolable protections that prevent derailment of the codes of ethics based on science. The fine line between what are considered sacrosanct ethics of a field – be it health care, climatology, or architecture – and what could be sacrificed in the name of prevailing forces (political or otherwise) has to be under constant scrutiny by the members of the guild. In health care, when patients cannot trust the science, its implementation, or is let down by the clinician, they are unlikely to benefit from treatment. A foundation of distrust paves the way for future therapeutic relationships that are stained with distrust and noncompliance.

The ethics guidelines of the American Academy of Psychiatry and the Law specify that psychiatrists in forensic roles “should be clear about limitations on confidentiality in the treatment relationship and ensure that these limitations are communicated to the patient.” Again, the therapist in this case is not a psychiatrist, but I would argue that the same rules would apply.

It is reassuring to know that several key groups, including the American Psychiatric Association, American Academy of Child and Adolescent Psychiatry, and the American Psychological Association, have all condemned the therapist’s actions. Psychiatrists and other mental health professionals must do no harm. We must not stand idly by and allow the kind of professional breach that happened to Kevin continue. Patients who confide in mental health professionals with the promise of confidentiality must be able to do so without fear. Only with confidentiality can the therapeutic relationship thrive.

Dr. Sood is professor of psychiatry and pediatrics, and senior professor of child mental health policy, at Virginia Commonwealth University, Richmond.

We are in the healing profession. We practice a trade. We are doctors, therapists, counselors. We work with children, adults, and couples. We document the physical form of our patient after examination, setting the stage for interventions that heal and alleviate suffering. With those who we do not touch physically, we hold out our psychological arms to embrace them in a therapeutic relationship.

We are privileged to appreciate their deeper selves through voice, unsaid words, and body language. A trust evolves (or might not); deeper exploration where our intuition and technical skill discover what troubles the soul. Healing begins as a delicate dance: As trust is earned, our patients risk vulnerability by revealing their weakest selves.

As healers, we often find ourselves adrift with our own insecurities, our own histories that make us human; our styles may differ but training and the tenets and guidelines set by our professional societies keep us in safe waters. These guidelines are informed by the science of health care research and vetted through centuries of observation and experience of process. “Do no harm” is perhaps one of the major rules of engaging with patients. The scaffolding that our code of ethics provides healing professions trumps external pressures to deviate. If you violate these codes, the consequences are borne by the patient and the potential loss of your license.

Some of you may have read about Kevin Euceda, an adolescent who reportedly was waiting for his immigration interview and ordered to undergo mandatory therapy as part of the immigration protocol. Kevin revealed to his therapist the history of violence he experienced as a child growing up in Honduras. His subsequent initiation into a gang was the only option he had to escape a violent death. Those of us who work with youth from gang cultures know fully that allegiance to a gang is a means to find an identity and brotherhood with the payment by a lifestyle of violence. A therapist faced with this information does not judge but helps the person deal with PTSD, nightmares, and guilt that become part of an identity just as the memories of mines blowing up in the face of combat affect veterans.

But the therapist, who reportedly holds a master’s in rehabilitation counseling and was “a year away from passing her licensing exam,” according to an article published in the Washington Post, followed policy of the Office of Refugee Resettlement. The therapist betrayed Kevin by reporting the information he shared with her confidentially to Immigration and Customs Enforcement. The reason the therapist gave for the breach was that she was compelled do so because Kevin reported participating in gang activity in Honduras. Subsequently, Kevin was sent to a high-security detention center – and is now facing deportation.
 

Betraying a patient, profession

Therapy begins as a contract between patient and therapist. The contract stipulates that all that transpires in the process of therapy (usually a 50-minute block of time, usually weekly) is information held by the therapist and patient – and is not to be shared with anyone, including parents, guardians, legal entities, and health care agencies. This allows the gradual sharing of events, emotions, behaviors, and reactions akin to peeling an onion. Memories, reactions, and feelings assist the therapist as they start their quest of discovery of the conflict and how to resolve it. Trust is the central tenet of this journey. The patient thinks: “You will hear me; you will see me you will understand me and help me understand myself.” The doctor responds: “Even I don’t yet know fully what ails you; we will discover that together. … I will not fail your trust.”

So how does this interface with external pressures? The constitution of a free country provides some inviolable protections that prevent derailment of the codes of ethics based on science. The fine line between what are considered sacrosanct ethics of a field – be it health care, climatology, or architecture – and what could be sacrificed in the name of prevailing forces (political or otherwise) has to be under constant scrutiny by the members of the guild. In health care, when patients cannot trust the science, its implementation, or is let down by the clinician, they are unlikely to benefit from treatment. A foundation of distrust paves the way for future therapeutic relationships that are stained with distrust and noncompliance.

The ethics guidelines of the American Academy of Psychiatry and the Law specify that psychiatrists in forensic roles “should be clear about limitations on confidentiality in the treatment relationship and ensure that these limitations are communicated to the patient.” Again, the therapist in this case is not a psychiatrist, but I would argue that the same rules would apply.

It is reassuring to know that several key groups, including the American Psychiatric Association, American Academy of Child and Adolescent Psychiatry, and the American Psychological Association, have all condemned the therapist’s actions. Psychiatrists and other mental health professionals must do no harm. We must not stand idly by and allow the kind of professional breach that happened to Kevin continue. Patients who confide in mental health professionals with the promise of confidentiality must be able to do so without fear. Only with confidentiality can the therapeutic relationship thrive.

Dr. Sood is professor of psychiatry and pediatrics, and senior professor of child mental health policy, at Virginia Commonwealth University, Richmond.

We are in the healing profession. We practice a trade. We are doctors, therapists, counselors. We work with children, adults, and couples. We document the physical form of our patient after examination, setting the stage for interventions that heal and alleviate suffering. With those who we do not touch physically, we hold out our psychological arms to embrace them in a therapeutic relationship.

We are privileged to appreciate their deeper selves through voice, unsaid words, and body language. A trust evolves (or might not); deeper exploration where our intuition and technical skill discover what troubles the soul. Healing begins as a delicate dance: As trust is earned, our patients risk vulnerability by revealing their weakest selves.

As healers, we often find ourselves adrift with our own insecurities, our own histories that make us human; our styles may differ but training and the tenets and guidelines set by our professional societies keep us in safe waters. These guidelines are informed by the science of health care research and vetted through centuries of observation and experience of process. “Do no harm” is perhaps one of the major rules of engaging with patients. The scaffolding that our code of ethics provides healing professions trumps external pressures to deviate. If you violate these codes, the consequences are borne by the patient and the potential loss of your license.

Some of you may have read about Kevin Euceda, an adolescent who reportedly was waiting for his immigration interview and ordered to undergo mandatory therapy as part of the immigration protocol. Kevin revealed to his therapist the history of violence he experienced as a child growing up in Honduras. His subsequent initiation into a gang was the only option he had to escape a violent death. Those of us who work with youth from gang cultures know fully that allegiance to a gang is a means to find an identity and brotherhood with the payment by a lifestyle of violence. A therapist faced with this information does not judge but helps the person deal with PTSD, nightmares, and guilt that become part of an identity just as the memories of mines blowing up in the face of combat affect veterans.

But the therapist, who reportedly holds a master’s in rehabilitation counseling and was “a year away from passing her licensing exam,” according to an article published in the Washington Post, followed policy of the Office of Refugee Resettlement. The therapist betrayed Kevin by reporting the information he shared with her confidentially to Immigration and Customs Enforcement. The reason the therapist gave for the breach was that she was compelled do so because Kevin reported participating in gang activity in Honduras. Subsequently, Kevin was sent to a high-security detention center – and is now facing deportation.
 

Betraying a patient, profession

Therapy begins as a contract between patient and therapist. The contract stipulates that all that transpires in the process of therapy (usually a 50-minute block of time, usually weekly) is information held by the therapist and patient – and is not to be shared with anyone, including parents, guardians, legal entities, and health care agencies. This allows the gradual sharing of events, emotions, behaviors, and reactions akin to peeling an onion. Memories, reactions, and feelings assist the therapist as they start their quest of discovery of the conflict and how to resolve it. Trust is the central tenet of this journey. The patient thinks: “You will hear me; you will see me you will understand me and help me understand myself.” The doctor responds: “Even I don’t yet know fully what ails you; we will discover that together. … I will not fail your trust.”

So how does this interface with external pressures? The constitution of a free country provides some inviolable protections that prevent derailment of the codes of ethics based on science. The fine line between what are considered sacrosanct ethics of a field – be it health care, climatology, or architecture – and what could be sacrificed in the name of prevailing forces (political or otherwise) has to be under constant scrutiny by the members of the guild. In health care, when patients cannot trust the science, its implementation, or is let down by the clinician, they are unlikely to benefit from treatment. A foundation of distrust paves the way for future therapeutic relationships that are stained with distrust and noncompliance.

The ethics guidelines of the American Academy of Psychiatry and the Law specify that psychiatrists in forensic roles “should be clear about limitations on confidentiality in the treatment relationship and ensure that these limitations are communicated to the patient.” Again, the therapist in this case is not a psychiatrist, but I would argue that the same rules would apply.

It is reassuring to know that several key groups, including the American Psychiatric Association, American Academy of Child and Adolescent Psychiatry, and the American Psychological Association, have all condemned the therapist’s actions. Psychiatrists and other mental health professionals must do no harm. We must not stand idly by and allow the kind of professional breach that happened to Kevin continue. Patients who confide in mental health professionals with the promise of confidentiality must be able to do so without fear. Only with confidentiality can the therapeutic relationship thrive.

Dr. Sood is professor of psychiatry and pediatrics, and senior professor of child mental health policy, at Virginia Commonwealth University, Richmond.

Many pediatric skin conditions can be safely monitored with minimal intervention, but certain skin conditions are emergent and require immediate attention and proper assessment of the neonate, infant, or child. The skin may provide the first presentation of a potentially fatal disease with serious sequelae. Cutaneous findings may indicate the need for further evaluation. Therefore, it is important to differentiate skin conditions with benign etiologies from those that require immediate diagnosis and treatment, as early intervention of some of these conditions can be lifesaving. Herein, we discuss pertinent pediatric dermatology emergencies that dermatologists should keep in mind so that these diagnoses are never missed.

Staphylococcal Scalded Skin Syndrome

Presentation
Staphylococcal scalded skin syndrome (SSSS), or Ritter disease, is a potentially fatal pediatric emergency, especially in newborns.¹ The mortality rate for SSSS in the United States is 3.6% to 11% in children.² It typically presents with a prodrome of tenderness, fever, and confluent erythematous patches on the folds of the skin such as the groin, axillae, nose, and ears, with eventual spread to the legs and trunk.^1,2 Within 24 to 48 hours of symptom onset, blistering and fluid accumulation will appear diffusely. Bullae are flaccid, and tangential and gentle pressure on involved unblistered skin may lead to shearing of the epithelium, which is a positive Nikolsky sign.^1,2

Causes
Staphylococcal scalded skin syndrome is caused by exfoliative toxins A and B, toxigenic strains of Staphylococcus aureus. Exfoliative toxins A and B are serine proteases that target and cleave desmoglein 1, which binds keratinocytes in the stratum granulosum.^1,3 Exfoliative toxins disrupt the adhesion of keratinocytes, resulting in bullae formation and subsequently diffuse sheetlike desquamation.^1,4,5 Although up to 30% of the human population are asymptomatically and permanently colonized with nasal S aureus,⁶ the exfoliative toxins are produced by only 5% of species.¹

In neonates, the immune and renal systems are underdeveloped; therefore, patients are susceptible to SSSS due to lack of neutralizing antibodies and decreased renal toxin excretion.⁴ Potential complications of SSSS are deeper soft-tissue infection, septicemia (blood-borne infection), and fluid and electrolyte imbalance.^1,4

Diagnosis and Treatment
The condition is diagnosed clinically based on the findings of tender erythroderma, bullae, and desquamation with a scalded appearance, especially in friction zones; periorificial crusting; positive Nikolsky sign; and lack of mucosal involvement (Figure 1).¹ Histopathology can aid in complicated clinical scenarios as well as culture from affected areas, including the upper respiratory tract, diaper region, and umbilicus.^1,4 Hospitalization is required for SSSS for intravenous antibiotics, fluids, and electrolyte repletion.

Impetigo

Presentation
Impetigo is the most common bacterial skin infection in children caused by S aureus or Streptococcus pyogenes.^7-9 It begins as erythematous papules transitioning to thin-walled vesicles that rapidly rupture and result in honey-crusted papules.^7,9,10 Individuals of any age can be affected by nonbullous impetigo, but it is the most common skin infection in children aged 2 to 5 years.⁷

Bullous impetigo primarily is seen in children, especially infants, and rarely can occur in teenagers or adults.⁷ It most commonly is caused by the exfoliative toxins of S aureus. Bullous impetigo presents as small vesicles that may converge into larger flaccid bullae or pustules.^7-10 Once the bullae rupture, an erythematous base with a collarette of scale remains without the formation of a honey-colored crust.⁸ Bullous impetigo usually affects moist intertriginous areas such as the axillae, neck, and diaper area^8,10 (Figure 3). Complications may result in cellulitis, septicemia, osteomyelitis, poststreptococcal glomerulonephritis associated with S pyogenes, and S aureus–induced SSSS.^7-9

Eczema Herpeticum

Presentation
Eczema herpeticum (EH), also known as Kaposi varicelliform eruption, is a disseminated herpes simplex virus infection of impaired skin, most commonly in patients with atopic dermatitis (AD).¹¹ Eczema herpeticum presents as a widespread eruption of erythematous monomorphic vesicles that progress to punched-out erosions with hemorrhagic crusting (Figure 4). Patients may have associated fever or lymphadenopathy.^12,13

Causes
The number of children hospitalized annually for EH in the United States is approximately 4 to 7 cases per million children. Less than 3% of pediatric AD patients are affected, with a particularly increased risk in patients with severe and earlier-onset AD.^12-15 Patients with AD have skin barrier defects, and decreased IFN-γ expression and cathelicidins predispose patients with AD to developing EH.^12,16,17

Diagnosis
Viral polymerase chain reaction for herpes simplex virus types 1 and 2 is the standard for confirmatory diagnosis. Herpes simplex virus cultures from cutaneous scrapings, direct fluorescent antibody testing, or Tzanck test revealing multinucleated giant cells also may help establish the diagnosis.^11,12,17

Management
Individuals with severe AD and other dermatologic conditions with cutaneous barrier compromise are at risk for developing EH, which is a medical emergency requiring hospitalization and prompt treatment with antiviral therapy such as acyclovir, often intravenously, as death can result if left untreated.^11,17 Topical or systemic antibiotic therapy should be initiated if there is suspicion for secondary bacterial superinfection. Patients should be evaluated for multiorgan involvement such as keratoconjunctivitis, meningitis, encephalitis, and systemic viremia due to increased mortality, especially in infants.^12,15,16

Langerhans Cell Histiocytosis

Presentation
Langerhans cell histiocytosis (LCH) has a variable clinical presentation and can involve a single or multiple organ systems, including the bones and skin. Cutaneous LCH can present as violaceous papules, nodules, or ulcerations and crusted erosions (Figure 5). The lymph nodes, liver, spleen, oral mucosa, and respiratory and central nervous systems also may be involved.

Langerhans cell histiocytosis affects individuals of any age group but more often is seen in pediatric patients. The incidence of LCH is approximately 4.6 cases per million children.¹⁸ The pathogenesis is secondary to pathologic Langerhans cells, characterized as a clonal myeloid malignancy and dysregulation of the immune system.^18,19

Diagnosis
A thorough physical examination is essential in patients with suspected LCH. Additionally, diagnosis of LCH is heavily based on histopathology of tissue from the involved organ system(s) with features of positive S-100 protein, CD1a, and CD207, and identification of Birbeck granules.²⁰ Imaging and laboratory studies also are indicated and can include a skeletal survey (to assess osteolytic and organ involvement), a complete hematologic panel, coagulation studies, and liver function tests.^18,21

Management
Management of LCH varies based on the organ system(s) involved along with the extent of the disease. Dermatology referral may be indicated in patients presenting with nonresolving cutaneous lesions as well as in severe cases. Single-organ and multisystem disease may require one treatment modality or a combination of chemotherapy, surgery, radiation, and/or immunotherapy.²¹

Infantile Hemangioma

Presentation
Infantile hemangioma (IH) is the most common benign tumor of infancy and usually is apparent a few weeks after birth. Lesions appear as bright red papules, nodules, or plaques. Deep or subcutaneous lesions present as raised, flesh-colored nodules with a blue hue and bruiselike appearance with or without a central patch of telangiectasia^22-24 (Figure 6). Although all IHs eventually resolve, residual skin changes such as scarring, atrophy, and fibrosis can persist.²⁴

The incidence of IH has been reported to occur in up to 4% to 5% of infants in the United States.^23,25 Infantile hemangiomas also have been found to be more common among white, preterm, and multiple-gestation infants.²⁵ The proposed pathogenesis of IHs includes angiogenic and vasogenic factors that cause rapid proliferation of blood vessels, likely driven by tissue hypoxia.^23,26,27

Diagnosis
Infantile hemangioma is diagnosed clinically; however, immunohistochemical staining showing positivity for glucose transporter 1 also is helpful.^26,27 Imaging modalities such as ultrasonography and magnetic resonance imaging also can be utilized to visualize the extent of lesions if necessary.²⁵

Management
Around 15% to 25% of IHs are considered complicated and require intervention.^25,27 Infantile hemangiomas can interfere with function depending on location or have potentially fatal complications. Based on the location and extent of involvement, these findings can include ulceration; hemorrhage; impairment of feeding, hearing, and/or vision; facial deformities; airway obstruction; hypothyroidism; and congestive heart failure.^25,28 Early treatment with topical or oral beta-blockers is imperative for potentially life-threatening IHs, which can be seen due to large size or dangerous location.^28,29 Because the rapid proliferative phase of IHs is thought to begin around 6 weeks of life, treatment should be initiated as early as possible. Initiation of beta-blocker therapy in the first few months of life can prevent functional impairment, ulceration, and permanent cosmetic changes. Additionally, surgery or pulsed dye laser treatment have been found to be effective for skin changes found after involution of IH.^25,29

Differential Diagnosis
The differential diagnosis for IH includes vascular malformations, which are present at birth and do not undergo rapid proliferation; sarcoma; and kaposiform hemangioendothelioma, which causes the Kasabach-Merritt phenomenon secondary to platelet trapping. Careful attention to the history of the skin lesion provides good support for diagnosis of IH in most cases.

IgA Vasculitis

Presentation
IgA vasculitis, or Henoch-Schönlein purpura, classically presents as a tetrad of palpable purpura, acute-onset arthritis or arthralgia, abdominal pain, and renal disease with proteinuria or hematuria.³⁰ Skin involvement is seen in almost all cases and is essential for diagnosis of IgA vasculitis. The initial dermatosis may be pruritic and present as an erythematous macular or urticarial wheal that evolves into petechiae, along with palpable purpura that is most frequently located on the legs or buttocks (Figure 7).^30-34

IgA vasculitis is an immune-mediated small vessel vasculitis with deposition of IgA in the small vessels. The underlying cause remains unknown, though infection, dietary allergens, drugs, vaccinations, and chemical triggers have been recognized in literature.^32,35,36 IgA vasculitis is largely a pediatric diagnosis, with 90% of affected individuals younger than 10 years worldwide.³⁷ In the pediatric population, the incidence has been reported to be 3 to 26.7 cases per 100,000 children.³²

Diagnosis
Diagnosis is based on the clinical presentation and histopathology.³⁰ On direct immunofluorescence, IgA deposition is seen in the vessel walls.³⁵ Laboratory testing is not diagnostic, but urinalysis is mandatory to identify involvement of renal vasculature. Imaging studies may be used in patients with abdominal symptoms, as an ultrasound can be used to visualize bowel structure and abnormalities such as intussusception.³³

Management
The majority of cases of IgA vasculitis recover spontaneously, with patients requiring hospital admission based on severity of symptoms.³⁰ The primary approach to management involves providing supportive care including hydration, adequate rest, and symptomatic pain relief of the joints and abdomen with oral analgesics. Systemic corticosteroids or steroid-sparing agents such as dapsone or colchicine can be used to treat cutaneous manifestations in addition to severe pain symptoms.^30,31 Patients with IgA vasculitis must be monitored for proteinuria or hematuria to assess the extent of renal involvement. Although much more common in adults, long-term renal impairment can result from childhood cases of IgA vasculitis.³⁴ 

Final Thoughts

Pediatric dermatology emergencies can be difficult to detect and accurately diagnose. Many of these diseases are potential emergencies that that may result in delayed treatment and considerable morbidity and mortality if missed. Clinicians should be aware that timely recognition and diagnosis, along with possible referral to pediatric dermatology, are essential to avoid complications.

Many pediatric skin conditions can be safely monitored with minimal intervention, but certain skin conditions are emergent and require immediate attention and proper assessment of the neonate, infant, or child. The skin may provide the first presentation of a potentially fatal disease with serious sequelae. Cutaneous findings may indicate the need for further evaluation. Therefore, it is important to differentiate skin conditions with benign etiologies from those that require immediate diagnosis and treatment, as early intervention of some of these conditions can be lifesaving. Herein, we discuss pertinent pediatric dermatology emergencies that dermatologists should keep in mind so that these diagnoses are never missed.

Staphylococcal Scalded Skin Syndrome

Presentation
Staphylococcal scalded skin syndrome (SSSS), or Ritter disease, is a potentially fatal pediatric emergency, especially in newborns.¹ The mortality rate for SSSS in the United States is 3.6% to 11% in children.² It typically presents with a prodrome of tenderness, fever, and confluent erythematous patches on the folds of the skin such as the groin, axillae, nose, and ears, with eventual spread to the legs and trunk.^1,2 Within 24 to 48 hours of symptom onset, blistering and fluid accumulation will appear diffusely. Bullae are flaccid, and tangential and gentle pressure on involved unblistered skin may lead to shearing of the epithelium, which is a positive Nikolsky sign.^1,2

Causes
Staphylococcal scalded skin syndrome is caused by exfoliative toxins A and B, toxigenic strains of Staphylococcus aureus. Exfoliative toxins A and B are serine proteases that target and cleave desmoglein 1, which binds keratinocytes in the stratum granulosum.^1,3 Exfoliative toxins disrupt the adhesion of keratinocytes, resulting in bullae formation and subsequently diffuse sheetlike desquamation.^1,4,5 Although up to 30% of the human population are asymptomatically and permanently colonized with nasal S aureus,⁶ the exfoliative toxins are produced by only 5% of species.¹

In neonates, the immune and renal systems are underdeveloped; therefore, patients are susceptible to SSSS due to lack of neutralizing antibodies and decreased renal toxin excretion.⁴ Potential complications of SSSS are deeper soft-tissue infection, septicemia (blood-borne infection), and fluid and electrolyte imbalance.^1,4

Diagnosis and Treatment
The condition is diagnosed clinically based on the findings of tender erythroderma, bullae, and desquamation with a scalded appearance, especially in friction zones; periorificial crusting; positive Nikolsky sign; and lack of mucosal involvement (Figure 1).¹ Histopathology can aid in complicated clinical scenarios as well as culture from affected areas, including the upper respiratory tract, diaper region, and umbilicus.^1,4 Hospitalization is required for SSSS for intravenous antibiotics, fluids, and electrolyte repletion.

Impetigo

Presentation
Impetigo is the most common bacterial skin infection in children caused by S aureus or Streptococcus pyogenes.^7-9 It begins as erythematous papules transitioning to thin-walled vesicles that rapidly rupture and result in honey-crusted papules.^7,9,10 Individuals of any age can be affected by nonbullous impetigo, but it is the most common skin infection in children aged 2 to 5 years.⁷

Bullous impetigo primarily is seen in children, especially infants, and rarely can occur in teenagers or adults.⁷ It most commonly is caused by the exfoliative toxins of S aureus. Bullous impetigo presents as small vesicles that may converge into larger flaccid bullae or pustules.^7-10 Once the bullae rupture, an erythematous base with a collarette of scale remains without the formation of a honey-colored crust.⁸ Bullous impetigo usually affects moist intertriginous areas such as the axillae, neck, and diaper area^8,10 (Figure 3). Complications may result in cellulitis, septicemia, osteomyelitis, poststreptococcal glomerulonephritis associated with S pyogenes, and S aureus–induced SSSS.^7-9

Eczema Herpeticum

Presentation
Eczema herpeticum (EH), also known as Kaposi varicelliform eruption, is a disseminated herpes simplex virus infection of impaired skin, most commonly in patients with atopic dermatitis (AD).¹¹ Eczema herpeticum presents as a widespread eruption of erythematous monomorphic vesicles that progress to punched-out erosions with hemorrhagic crusting (Figure 4). Patients may have associated fever or lymphadenopathy.^12,13

Causes
The number of children hospitalized annually for EH in the United States is approximately 4 to 7 cases per million children. Less than 3% of pediatric AD patients are affected, with a particularly increased risk in patients with severe and earlier-onset AD.^12-15 Patients with AD have skin barrier defects, and decreased IFN-γ expression and cathelicidins predispose patients with AD to developing EH.^12,16,17

Diagnosis
Viral polymerase chain reaction for herpes simplex virus types 1 and 2 is the standard for confirmatory diagnosis. Herpes simplex virus cultures from cutaneous scrapings, direct fluorescent antibody testing, or Tzanck test revealing multinucleated giant cells also may help establish the diagnosis.^11,12,17

Management
Individuals with severe AD and other dermatologic conditions with cutaneous barrier compromise are at risk for developing EH, which is a medical emergency requiring hospitalization and prompt treatment with antiviral therapy such as acyclovir, often intravenously, as death can result if left untreated.^11,17 Topical or systemic antibiotic therapy should be initiated if there is suspicion for secondary bacterial superinfection. Patients should be evaluated for multiorgan involvement such as keratoconjunctivitis, meningitis, encephalitis, and systemic viremia due to increased mortality, especially in infants.^12,15,16

Langerhans Cell Histiocytosis

Presentation
Langerhans cell histiocytosis (LCH) has a variable clinical presentation and can involve a single or multiple organ systems, including the bones and skin. Cutaneous LCH can present as violaceous papules, nodules, or ulcerations and crusted erosions (Figure 5). The lymph nodes, liver, spleen, oral mucosa, and respiratory and central nervous systems also may be involved.

Langerhans cell histiocytosis affects individuals of any age group but more often is seen in pediatric patients. The incidence of LCH is approximately 4.6 cases per million children.¹⁸ The pathogenesis is secondary to pathologic Langerhans cells, characterized as a clonal myeloid malignancy and dysregulation of the immune system.^18,19

Diagnosis
A thorough physical examination is essential in patients with suspected LCH. Additionally, diagnosis of LCH is heavily based on histopathology of tissue from the involved organ system(s) with features of positive S-100 protein, CD1a, and CD207, and identification of Birbeck granules.²⁰ Imaging and laboratory studies also are indicated and can include a skeletal survey (to assess osteolytic and organ involvement), a complete hematologic panel, coagulation studies, and liver function tests.^18,21

Management
Management of LCH varies based on the organ system(s) involved along with the extent of the disease. Dermatology referral may be indicated in patients presenting with nonresolving cutaneous lesions as well as in severe cases. Single-organ and multisystem disease may require one treatment modality or a combination of chemotherapy, surgery, radiation, and/or immunotherapy.²¹

Infantile Hemangioma

Presentation
Infantile hemangioma (IH) is the most common benign tumor of infancy and usually is apparent a few weeks after birth. Lesions appear as bright red papules, nodules, or plaques. Deep or subcutaneous lesions present as raised, flesh-colored nodules with a blue hue and bruiselike appearance with or without a central patch of telangiectasia^22-24 (Figure 6). Although all IHs eventually resolve, residual skin changes such as scarring, atrophy, and fibrosis can persist.²⁴

The incidence of IH has been reported to occur in up to 4% to 5% of infants in the United States.^23,25 Infantile hemangiomas also have been found to be more common among white, preterm, and multiple-gestation infants.²⁵ The proposed pathogenesis of IHs includes angiogenic and vasogenic factors that cause rapid proliferation of blood vessels, likely driven by tissue hypoxia.^23,26,27

Diagnosis
Infantile hemangioma is diagnosed clinically; however, immunohistochemical staining showing positivity for glucose transporter 1 also is helpful.^26,27 Imaging modalities such as ultrasonography and magnetic resonance imaging also can be utilized to visualize the extent of lesions if necessary.²⁵

Management
Around 15% to 25% of IHs are considered complicated and require intervention.^25,27 Infantile hemangiomas can interfere with function depending on location or have potentially fatal complications. Based on the location and extent of involvement, these findings can include ulceration; hemorrhage; impairment of feeding, hearing, and/or vision; facial deformities; airway obstruction; hypothyroidism; and congestive heart failure.^25,28 Early treatment with topical or oral beta-blockers is imperative for potentially life-threatening IHs, which can be seen due to large size or dangerous location.^28,29 Because the rapid proliferative phase of IHs is thought to begin around 6 weeks of life, treatment should be initiated as early as possible. Initiation of beta-blocker therapy in the first few months of life can prevent functional impairment, ulceration, and permanent cosmetic changes. Additionally, surgery or pulsed dye laser treatment have been found to be effective for skin changes found after involution of IH.^25,29

Differential Diagnosis
The differential diagnosis for IH includes vascular malformations, which are present at birth and do not undergo rapid proliferation; sarcoma; and kaposiform hemangioendothelioma, which causes the Kasabach-Merritt phenomenon secondary to platelet trapping. Careful attention to the history of the skin lesion provides good support for diagnosis of IH in most cases.

IgA Vasculitis

Presentation
IgA vasculitis, or Henoch-Schönlein purpura, classically presents as a tetrad of palpable purpura, acute-onset arthritis or arthralgia, abdominal pain, and renal disease with proteinuria or hematuria.³⁰ Skin involvement is seen in almost all cases and is essential for diagnosis of IgA vasculitis. The initial dermatosis may be pruritic and present as an erythematous macular or urticarial wheal that evolves into petechiae, along with palpable purpura that is most frequently located on the legs or buttocks (Figure 7).^30-34

IgA vasculitis is an immune-mediated small vessel vasculitis with deposition of IgA in the small vessels. The underlying cause remains unknown, though infection, dietary allergens, drugs, vaccinations, and chemical triggers have been recognized in literature.^32,35,36 IgA vasculitis is largely a pediatric diagnosis, with 90% of affected individuals younger than 10 years worldwide.³⁷ In the pediatric population, the incidence has been reported to be 3 to 26.7 cases per 100,000 children.³²

Diagnosis
Diagnosis is based on the clinical presentation and histopathology.³⁰ On direct immunofluorescence, IgA deposition is seen in the vessel walls.³⁵ Laboratory testing is not diagnostic, but urinalysis is mandatory to identify involvement of renal vasculature. Imaging studies may be used in patients with abdominal symptoms, as an ultrasound can be used to visualize bowel structure and abnormalities such as intussusception.³³

Management
The majority of cases of IgA vasculitis recover spontaneously, with patients requiring hospital admission based on severity of symptoms.³⁰ The primary approach to management involves providing supportive care including hydration, adequate rest, and symptomatic pain relief of the joints and abdomen with oral analgesics. Systemic corticosteroids or steroid-sparing agents such as dapsone or colchicine can be used to treat cutaneous manifestations in addition to severe pain symptoms.^30,31 Patients with IgA vasculitis must be monitored for proteinuria or hematuria to assess the extent of renal involvement. Although much more common in adults, long-term renal impairment can result from childhood cases of IgA vasculitis.³⁴ 

Final Thoughts

Pediatric dermatology emergencies can be difficult to detect and accurately diagnose. Many of these diseases are potential emergencies that that may result in delayed treatment and considerable morbidity and mortality if missed. Clinicians should be aware that timely recognition and diagnosis, along with possible referral to pediatric dermatology, are essential to avoid complications.

Many pediatric skin conditions can be safely monitored with minimal intervention, but certain skin conditions are emergent and require immediate attention and proper assessment of the neonate, infant, or child. The skin may provide the first presentation of a potentially fatal disease with serious sequelae. Cutaneous findings may indicate the need for further evaluation. Therefore, it is important to differentiate skin conditions with benign etiologies from those that require immediate diagnosis and treatment, as early intervention of some of these conditions can be lifesaving. Herein, we discuss pertinent pediatric dermatology emergencies that dermatologists should keep in mind so that these diagnoses are never missed.

Staphylococcal Scalded Skin Syndrome

Presentation
Staphylococcal scalded skin syndrome (SSSS), or Ritter disease, is a potentially fatal pediatric emergency, especially in newborns.¹ The mortality rate for SSSS in the United States is 3.6% to 11% in children.² It typically presents with a prodrome of tenderness, fever, and confluent erythematous patches on the folds of the skin such as the groin, axillae, nose, and ears, with eventual spread to the legs and trunk.^1,2 Within 24 to 48 hours of symptom onset, blistering and fluid accumulation will appear diffusely. Bullae are flaccid, and tangential and gentle pressure on involved unblistered skin may lead to shearing of the epithelium, which is a positive Nikolsky sign.^1,2

Causes
Staphylococcal scalded skin syndrome is caused by exfoliative toxins A and B, toxigenic strains of Staphylococcus aureus. Exfoliative toxins A and B are serine proteases that target and cleave desmoglein 1, which binds keratinocytes in the stratum granulosum.^1,3 Exfoliative toxins disrupt the adhesion of keratinocytes, resulting in bullae formation and subsequently diffuse sheetlike desquamation.^1,4,5 Although up to 30% of the human population are asymptomatically and permanently colonized with nasal S aureus,⁶ the exfoliative toxins are produced by only 5% of species.¹

In neonates, the immune and renal systems are underdeveloped; therefore, patients are susceptible to SSSS due to lack of neutralizing antibodies and decreased renal toxin excretion.⁴ Potential complications of SSSS are deeper soft-tissue infection, septicemia (blood-borne infection), and fluid and electrolyte imbalance.^1,4

Diagnosis and Treatment
The condition is diagnosed clinically based on the findings of tender erythroderma, bullae, and desquamation with a scalded appearance, especially in friction zones; periorificial crusting; positive Nikolsky sign; and lack of mucosal involvement (Figure 1).¹ Histopathology can aid in complicated clinical scenarios as well as culture from affected areas, including the upper respiratory tract, diaper region, and umbilicus.^1,4 Hospitalization is required for SSSS for intravenous antibiotics, fluids, and electrolyte repletion.

Impetigo

Presentation
Impetigo is the most common bacterial skin infection in children caused by S aureus or Streptococcus pyogenes.^7-9 It begins as erythematous papules transitioning to thin-walled vesicles that rapidly rupture and result in honey-crusted papules.^7,9,10 Individuals of any age can be affected by nonbullous impetigo, but it is the most common skin infection in children aged 2 to 5 years.⁷

Bullous impetigo primarily is seen in children, especially infants, and rarely can occur in teenagers or adults.⁷ It most commonly is caused by the exfoliative toxins of S aureus. Bullous impetigo presents as small vesicles that may converge into larger flaccid bullae or pustules.^7-10 Once the bullae rupture, an erythematous base with a collarette of scale remains without the formation of a honey-colored crust.⁸ Bullous impetigo usually affects moist intertriginous areas such as the axillae, neck, and diaper area^8,10 (Figure 3). Complications may result in cellulitis, septicemia, osteomyelitis, poststreptococcal glomerulonephritis associated with S pyogenes, and S aureus–induced SSSS.^7-9

Eczema Herpeticum

Presentation
Eczema herpeticum (EH), also known as Kaposi varicelliform eruption, is a disseminated herpes simplex virus infection of impaired skin, most commonly in patients with atopic dermatitis (AD).¹¹ Eczema herpeticum presents as a widespread eruption of erythematous monomorphic vesicles that progress to punched-out erosions with hemorrhagic crusting (Figure 4). Patients may have associated fever or lymphadenopathy.^12,13

Causes
The number of children hospitalized annually for EH in the United States is approximately 4 to 7 cases per million children. Less than 3% of pediatric AD patients are affected, with a particularly increased risk in patients with severe and earlier-onset AD.^12-15 Patients with AD have skin barrier defects, and decreased IFN-γ expression and cathelicidins predispose patients with AD to developing EH.^12,16,17

Diagnosis
Viral polymerase chain reaction for herpes simplex virus types 1 and 2 is the standard for confirmatory diagnosis. Herpes simplex virus cultures from cutaneous scrapings, direct fluorescent antibody testing, or Tzanck test revealing multinucleated giant cells also may help establish the diagnosis.^11,12,17

Management
Individuals with severe AD and other dermatologic conditions with cutaneous barrier compromise are at risk for developing EH, which is a medical emergency requiring hospitalization and prompt treatment with antiviral therapy such as acyclovir, often intravenously, as death can result if left untreated.^11,17 Topical or systemic antibiotic therapy should be initiated if there is suspicion for secondary bacterial superinfection. Patients should be evaluated for multiorgan involvement such as keratoconjunctivitis, meningitis, encephalitis, and systemic viremia due to increased mortality, especially in infants.^12,15,16

Langerhans Cell Histiocytosis

Presentation
Langerhans cell histiocytosis (LCH) has a variable clinical presentation and can involve a single or multiple organ systems, including the bones and skin. Cutaneous LCH can present as violaceous papules, nodules, or ulcerations and crusted erosions (Figure 5). The lymph nodes, liver, spleen, oral mucosa, and respiratory and central nervous systems also may be involved.

Langerhans cell histiocytosis affects individuals of any age group but more often is seen in pediatric patients. The incidence of LCH is approximately 4.6 cases per million children.¹⁸ The pathogenesis is secondary to pathologic Langerhans cells, characterized as a clonal myeloid malignancy and dysregulation of the immune system.^18,19

Diagnosis
A thorough physical examination is essential in patients with suspected LCH. Additionally, diagnosis of LCH is heavily based on histopathology of tissue from the involved organ system(s) with features of positive S-100 protein, CD1a, and CD207, and identification of Birbeck granules.²⁰ Imaging and laboratory studies also are indicated and can include a skeletal survey (to assess osteolytic and organ involvement), a complete hematologic panel, coagulation studies, and liver function tests.^18,21

Management
Management of LCH varies based on the organ system(s) involved along with the extent of the disease. Dermatology referral may be indicated in patients presenting with nonresolving cutaneous lesions as well as in severe cases. Single-organ and multisystem disease may require one treatment modality or a combination of chemotherapy, surgery, radiation, and/or immunotherapy.²¹

Infantile Hemangioma

Presentation
Infantile hemangioma (IH) is the most common benign tumor of infancy and usually is apparent a few weeks after birth. Lesions appear as bright red papules, nodules, or plaques. Deep or subcutaneous lesions present as raised, flesh-colored nodules with a blue hue and bruiselike appearance with or without a central patch of telangiectasia^22-24 (Figure 6). Although all IHs eventually resolve, residual skin changes such as scarring, atrophy, and fibrosis can persist.²⁴

The incidence of IH has been reported to occur in up to 4% to 5% of infants in the United States.^23,25 Infantile hemangiomas also have been found to be more common among white, preterm, and multiple-gestation infants.²⁵ The proposed pathogenesis of IHs includes angiogenic and vasogenic factors that cause rapid proliferation of blood vessels, likely driven by tissue hypoxia.^23,26,27

Diagnosis
Infantile hemangioma is diagnosed clinically; however, immunohistochemical staining showing positivity for glucose transporter 1 also is helpful.^26,27 Imaging modalities such as ultrasonography and magnetic resonance imaging also can be utilized to visualize the extent of lesions if necessary.²⁵

Management
Around 15% to 25% of IHs are considered complicated and require intervention.^25,27 Infantile hemangiomas can interfere with function depending on location or have potentially fatal complications. Based on the location and extent of involvement, these findings can include ulceration; hemorrhage; impairment of feeding, hearing, and/or vision; facial deformities; airway obstruction; hypothyroidism; and congestive heart failure.^25,28 Early treatment with topical or oral beta-blockers is imperative for potentially life-threatening IHs, which can be seen due to large size or dangerous location.^28,29 Because the rapid proliferative phase of IHs is thought to begin around 6 weeks of life, treatment should be initiated as early as possible. Initiation of beta-blocker therapy in the first few months of life can prevent functional impairment, ulceration, and permanent cosmetic changes. Additionally, surgery or pulsed dye laser treatment have been found to be effective for skin changes found after involution of IH.^25,29

Differential Diagnosis
The differential diagnosis for IH includes vascular malformations, which are present at birth and do not undergo rapid proliferation; sarcoma; and kaposiform hemangioendothelioma, which causes the Kasabach-Merritt phenomenon secondary to platelet trapping. Careful attention to the history of the skin lesion provides good support for diagnosis of IH in most cases.

IgA Vasculitis

Presentation
IgA vasculitis, or Henoch-Schönlein purpura, classically presents as a tetrad of palpable purpura, acute-onset arthritis or arthralgia, abdominal pain, and renal disease with proteinuria or hematuria.³⁰ Skin involvement is seen in almost all cases and is essential for diagnosis of IgA vasculitis. The initial dermatosis may be pruritic and present as an erythematous macular or urticarial wheal that evolves into petechiae, along with palpable purpura that is most frequently located on the legs or buttocks (Figure 7).^30-34

IgA vasculitis is an immune-mediated small vessel vasculitis with deposition of IgA in the small vessels. The underlying cause remains unknown, though infection, dietary allergens, drugs, vaccinations, and chemical triggers have been recognized in literature.^32,35,36 IgA vasculitis is largely a pediatric diagnosis, with 90% of affected individuals younger than 10 years worldwide.³⁷ In the pediatric population, the incidence has been reported to be 3 to 26.7 cases per 100,000 children.³²

Diagnosis
Diagnosis is based on the clinical presentation and histopathology.³⁰ On direct immunofluorescence, IgA deposition is seen in the vessel walls.³⁵ Laboratory testing is not diagnostic, but urinalysis is mandatory to identify involvement of renal vasculature. Imaging studies may be used in patients with abdominal symptoms, as an ultrasound can be used to visualize bowel structure and abnormalities such as intussusception.³³

Management
The majority of cases of IgA vasculitis recover spontaneously, with patients requiring hospital admission based on severity of symptoms.³⁰ The primary approach to management involves providing supportive care including hydration, adequate rest, and symptomatic pain relief of the joints and abdomen with oral analgesics. Systemic corticosteroids or steroid-sparing agents such as dapsone or colchicine can be used to treat cutaneous manifestations in addition to severe pain symptoms.^30,31 Patients with IgA vasculitis must be monitored for proteinuria or hematuria to assess the extent of renal involvement. Although much more common in adults, long-term renal impairment can result from childhood cases of IgA vasculitis.³⁴ 

Final Thoughts

Pediatric dermatology emergencies can be difficult to detect and accurately diagnose. Many of these diseases are potential emergencies that that may result in delayed treatment and considerable morbidity and mortality if missed. Clinicians should be aware that timely recognition and diagnosis, along with possible referral to pediatric dermatology, are essential to avoid complications.

Epidemiology and Transmission

Pediculus humanus corporis, commonly known as the human body louse, is one in a family of 3 ectoparasites of the same suborder that also encompasses pubic lice (Phthirus pubis) and head lice (Pediculus humanus capitis). Adults are approximately 2 mm in size, with the same life cycle as head lice (Figure 1). They require blood meals roughly 5 times per day and cannot survive longer than 2 days without feeding.¹ Although similar in structure to head lice, body lice differ behaviorally in that they do not reside on their human host’s body; instead, they infest the host’s clothing, localizing to seams (Figure 2), and migrate to the host for blood meals. In fact, based on this behavior, genetic analysis of early human body lice has been used to postulate when clothing was first used by humans as well as to determine early human migration patterns.^2,3

Although clinicians in developed countries may be less familiar with body lice compared to their counterparts, body lice nevertheless remain a global health concern in impoverished, densely populated areas, as well as in homeless populations due to poor hygiene. Transmission frequently occurs via physical contact with an affected individual and his/her personal items (eg, linens) via fomites.^4,5 Body louse infestation is more prevalent in homeless individuals who sleep outside vs in shelters; a history of pubic lice and lack of regular bathing have been reported as additional risk factors.⁶ Outbreaks have been noted in the wake of natural disasters, in the setting of political upheavals, and in refugee camps, as well as in individuals seeking political asylum.⁷ Unlike head and pubic lice, body lice can serve as vectors for infectious diseases including Rickettsia prowazekii (epidemic typhus), Borrelia recurrentis (louse-borne relapsing fever), Bartonella quintana (trench fever), and Yersinia pestis (plague).^5,8,9 Several Acinetobacter species were isolated from nearly one-third of collected body louse specimens in a French study.¹⁰ Additionally, serology for B quintana was found to be positive in up to 30% of cases in one United States urban homeless population.⁴

Clinical Manifestations

Patients often present with generalized pruritus, usually considerably more severe than with P humanus capitis, with lesions concentrated on the trunk.¹¹ In addition to often impetiginized, self-inflicted excoriations, feeding sites may present as erythematous macules (Figure 3), papules, or papular urticaria with a central hemorrhagic punctum. Extensive infestation also can manifest as the colloquial vagabond disease, characterized by postinflammatory hyperpigmentation and thickening of the involved skin. Remarkably, patients also may present with considerable iron-deficiency anemia secondary to high parasite load and large volume blood feeding. Multiple case reports have demonstrated associated morbidity.^12-14 The differential diagnosis for pediculosis may include scabies, lichen simplex chronicus, and eczematous dermatitis, though the clinician should prudently consider whether both scabies and pediculosis may be present, as coexistence is possible.^4,15

Diagnosis

Diagnosis can be reached by visualizing adult lice, nymphs, or viable nits on the body or more commonly within inner clothing seams; nits also fluoresce under Wood light.¹⁵ Although dermoscopy has proven useful for increased sensitivity and differentiation between viable and hatched nits, the insects also can be viewed with the unaided eye.¹⁶

Treatment: New Concerns and Strategies

The mainstay of treatment for body lice has long consisted of thorough washing and drying of all clothing and linens in a hot dryer. Treatment can be augmented with the addition of pharmacotherapy, plus antibiotics as warranted for louse-borne disease. Pharmacologic intervention often is used in cases of mass infestation and is similar to head lice.

Options for head lice include topical permethrin, malathion, lindane, spinosad, benzyl alcohol, and ivermectin. Pyrethroids, derived from the chrysanthemum, generally are considered safe for human use with a side-effect profile limited to irritation and allergy¹⁷; however, neurotoxicity and leukemia are clinical concerns, with an association more recently shown between large-volume use of pyrethroids and acute lymphoblastic leukemia.^18,19 Use of lindane is not recommended due to a greater potential for central nervous system neurotoxicity, manifested by seizures, with repeated large surface application. Malathion is problematic due to the risk for mucosal irritation, flammability of some formulations, and theoretical organophosphate poisoning, as its mechanism of action involves inhibition of acetylcholinesterase.¹⁵ However, in the context of head lice treatment, a randomized controlled trial reported no incidence of acetylcholinesterase inhibition.²⁰ Spinosad, manufactured from the soil bacterium Saccharopolyspora spinosa, functions similarly by interfering with the nicotinic acetylcholine receptor and also carries a risk for skin irritation.²¹ Among all the treatment options, we prefer benzyl alcohol, particularly in the context of resistance, as it is effective via a physical mechanism of action and lacks notable neurotoxic effects to the host. Use of benzyl alcohol is approved for patients as young as 6 months; it functions by asphyxiating the lice via paralysis of the respiratory spiracle with occlusion by inert ingredients. Itching, episodic numbness, and scalp or mucosal irritation are possible complications of treatment.²²

Treatment resistance of body lice has increased in recent years, warranting exploration of additional management strategies. Moreover, developing resistance to lindane and malathion has been reported.²³ Resistance to pyrethroids has been attributed to mutations in a voltage-gated sodium channel, one of which was universally present in the sampling of a single population.²⁴ A randomized controlled trial showed that off-label oral ivermectin 400 μg/kg was superior to malathion lotion 0.5% in difficult-to-treat cases of head lice²⁵; utility of oral ivermectin also has been reported in body lice.²⁶ In vitro studies also have shown promise for pursuing synergistic treatment of body lice with both ivermectin and antibiotics.²⁷

A novel primary prophylaxis approach for at-risk homeless individuals recently utilized permethrin-impregnated underwear. Although the intervention provided short-term infestation improvement, longer-term use did not show improvement from placebo and also increased prevalence of permethrin-resistant haplotypes.²

Epidemiology and Transmission

Pediculus humanus corporis, commonly known as the human body louse, is one in a family of 3 ectoparasites of the same suborder that also encompasses pubic lice (Phthirus pubis) and head lice (Pediculus humanus capitis). Adults are approximately 2 mm in size, with the same life cycle as head lice (Figure 1). They require blood meals roughly 5 times per day and cannot survive longer than 2 days without feeding.¹ Although similar in structure to head lice, body lice differ behaviorally in that they do not reside on their human host’s body; instead, they infest the host’s clothing, localizing to seams (Figure 2), and migrate to the host for blood meals. In fact, based on this behavior, genetic analysis of early human body lice has been used to postulate when clothing was first used by humans as well as to determine early human migration patterns.^2,3

Although clinicians in developed countries may be less familiar with body lice compared to their counterparts, body lice nevertheless remain a global health concern in impoverished, densely populated areas, as well as in homeless populations due to poor hygiene. Transmission frequently occurs via physical contact with an affected individual and his/her personal items (eg, linens) via fomites.^4,5 Body louse infestation is more prevalent in homeless individuals who sleep outside vs in shelters; a history of pubic lice and lack of regular bathing have been reported as additional risk factors.⁶ Outbreaks have been noted in the wake of natural disasters, in the setting of political upheavals, and in refugee camps, as well as in individuals seeking political asylum.⁷ Unlike head and pubic lice, body lice can serve as vectors for infectious diseases including Rickettsia prowazekii (epidemic typhus), Borrelia recurrentis (louse-borne relapsing fever), Bartonella quintana (trench fever), and Yersinia pestis (plague).^5,8,9 Several Acinetobacter species were isolated from nearly one-third of collected body louse specimens in a French study.¹⁰ Additionally, serology for B quintana was found to be positive in up to 30% of cases in one United States urban homeless population.⁴

Clinical Manifestations

Patients often present with generalized pruritus, usually considerably more severe than with P humanus capitis, with lesions concentrated on the trunk.¹¹ In addition to often impetiginized, self-inflicted excoriations, feeding sites may present as erythematous macules (Figure 3), papules, or papular urticaria with a central hemorrhagic punctum. Extensive infestation also can manifest as the colloquial vagabond disease, characterized by postinflammatory hyperpigmentation and thickening of the involved skin. Remarkably, patients also may present with considerable iron-deficiency anemia secondary to high parasite load and large volume blood feeding. Multiple case reports have demonstrated associated morbidity.^12-14 The differential diagnosis for pediculosis may include scabies, lichen simplex chronicus, and eczematous dermatitis, though the clinician should prudently consider whether both scabies and pediculosis may be present, as coexistence is possible.^4,15

Diagnosis

Diagnosis can be reached by visualizing adult lice, nymphs, or viable nits on the body or more commonly within inner clothing seams; nits also fluoresce under Wood light.¹⁵ Although dermoscopy has proven useful for increased sensitivity and differentiation between viable and hatched nits, the insects also can be viewed with the unaided eye.¹⁶

Treatment: New Concerns and Strategies

The mainstay of treatment for body lice has long consisted of thorough washing and drying of all clothing and linens in a hot dryer. Treatment can be augmented with the addition of pharmacotherapy, plus antibiotics as warranted for louse-borne disease. Pharmacologic intervention often is used in cases of mass infestation and is similar to head lice.

Options for head lice include topical permethrin, malathion, lindane, spinosad, benzyl alcohol, and ivermectin. Pyrethroids, derived from the chrysanthemum, generally are considered safe for human use with a side-effect profile limited to irritation and allergy¹⁷; however, neurotoxicity and leukemia are clinical concerns, with an association more recently shown between large-volume use of pyrethroids and acute lymphoblastic leukemia.^18,19 Use of lindane is not recommended due to a greater potential for central nervous system neurotoxicity, manifested by seizures, with repeated large surface application. Malathion is problematic due to the risk for mucosal irritation, flammability of some formulations, and theoretical organophosphate poisoning, as its mechanism of action involves inhibition of acetylcholinesterase.¹⁵ However, in the context of head lice treatment, a randomized controlled trial reported no incidence of acetylcholinesterase inhibition.²⁰ Spinosad, manufactured from the soil bacterium Saccharopolyspora spinosa, functions similarly by interfering with the nicotinic acetylcholine receptor and also carries a risk for skin irritation.²¹ Among all the treatment options, we prefer benzyl alcohol, particularly in the context of resistance, as it is effective via a physical mechanism of action and lacks notable neurotoxic effects to the host. Use of benzyl alcohol is approved for patients as young as 6 months; it functions by asphyxiating the lice via paralysis of the respiratory spiracle with occlusion by inert ingredients. Itching, episodic numbness, and scalp or mucosal irritation are possible complications of treatment.²²

Treatment resistance of body lice has increased in recent years, warranting exploration of additional management strategies. Moreover, developing resistance to lindane and malathion has been reported.²³ Resistance to pyrethroids has been attributed to mutations in a voltage-gated sodium channel, one of which was universally present in the sampling of a single population.²⁴ A randomized controlled trial showed that off-label oral ivermectin 400 μg/kg was superior to malathion lotion 0.5% in difficult-to-treat cases of head lice²⁵; utility of oral ivermectin also has been reported in body lice.²⁶ In vitro studies also have shown promise for pursuing synergistic treatment of body lice with both ivermectin and antibiotics.²⁷

A novel primary prophylaxis approach for at-risk homeless individuals recently utilized permethrin-impregnated underwear. Although the intervention provided short-term infestation improvement, longer-term use did not show improvement from placebo and also increased prevalence of permethrin-resistant haplotypes.²

Epidemiology and Transmission

Pediculus humanus corporis, commonly known as the human body louse, is one in a family of 3 ectoparasites of the same suborder that also encompasses pubic lice (Phthirus pubis) and head lice (Pediculus humanus capitis). Adults are approximately 2 mm in size, with the same life cycle as head lice (Figure 1). They require blood meals roughly 5 times per day and cannot survive longer than 2 days without feeding.¹ Although similar in structure to head lice, body lice differ behaviorally in that they do not reside on their human host’s body; instead, they infest the host’s clothing, localizing to seams (Figure 2), and migrate to the host for blood meals. In fact, based on this behavior, genetic analysis of early human body lice has been used to postulate when clothing was first used by humans as well as to determine early human migration patterns.^2,3

Although clinicians in developed countries may be less familiar with body lice compared to their counterparts, body lice nevertheless remain a global health concern in impoverished, densely populated areas, as well as in homeless populations due to poor hygiene. Transmission frequently occurs via physical contact with an affected individual and his/her personal items (eg, linens) via fomites.^4,5 Body louse infestation is more prevalent in homeless individuals who sleep outside vs in shelters; a history of pubic lice and lack of regular bathing have been reported as additional risk factors.⁶ Outbreaks have been noted in the wake of natural disasters, in the setting of political upheavals, and in refugee camps, as well as in individuals seeking political asylum.⁷ Unlike head and pubic lice, body lice can serve as vectors for infectious diseases including Rickettsia prowazekii (epidemic typhus), Borrelia recurrentis (louse-borne relapsing fever), Bartonella quintana (trench fever), and Yersinia pestis (plague).^5,8,9 Several Acinetobacter species were isolated from nearly one-third of collected body louse specimens in a French study.¹⁰ Additionally, serology for B quintana was found to be positive in up to 30% of cases in one United States urban homeless population.⁴

Clinical Manifestations

Patients often present with generalized pruritus, usually considerably more severe than with P humanus capitis, with lesions concentrated on the trunk.¹¹ In addition to often impetiginized, self-inflicted excoriations, feeding sites may present as erythematous macules (Figure 3), papules, or papular urticaria with a central hemorrhagic punctum. Extensive infestation also can manifest as the colloquial vagabond disease, characterized by postinflammatory hyperpigmentation and thickening of the involved skin. Remarkably, patients also may present with considerable iron-deficiency anemia secondary to high parasite load and large volume blood feeding. Multiple case reports have demonstrated associated morbidity.^12-14 The differential diagnosis for pediculosis may include scabies, lichen simplex chronicus, and eczematous dermatitis, though the clinician should prudently consider whether both scabies and pediculosis may be present, as coexistence is possible.^4,15

Diagnosis

Diagnosis can be reached by visualizing adult lice, nymphs, or viable nits on the body or more commonly within inner clothing seams; nits also fluoresce under Wood light.¹⁵ Although dermoscopy has proven useful for increased sensitivity and differentiation between viable and hatched nits, the insects also can be viewed with the unaided eye.¹⁶

Treatment: New Concerns and Strategies

The mainstay of treatment for body lice has long consisted of thorough washing and drying of all clothing and linens in a hot dryer. Treatment can be augmented with the addition of pharmacotherapy, plus antibiotics as warranted for louse-borne disease. Pharmacologic intervention often is used in cases of mass infestation and is similar to head lice.

Options for head lice include topical permethrin, malathion, lindane, spinosad, benzyl alcohol, and ivermectin. Pyrethroids, derived from the chrysanthemum, generally are considered safe for human use with a side-effect profile limited to irritation and allergy¹⁷; however, neurotoxicity and leukemia are clinical concerns, with an association more recently shown between large-volume use of pyrethroids and acute lymphoblastic leukemia.^18,19 Use of lindane is not recommended due to a greater potential for central nervous system neurotoxicity, manifested by seizures, with repeated large surface application. Malathion is problematic due to the risk for mucosal irritation, flammability of some formulations, and theoretical organophosphate poisoning, as its mechanism of action involves inhibition of acetylcholinesterase.¹⁵ However, in the context of head lice treatment, a randomized controlled trial reported no incidence of acetylcholinesterase inhibition.²⁰ Spinosad, manufactured from the soil bacterium Saccharopolyspora spinosa, functions similarly by interfering with the nicotinic acetylcholine receptor and also carries a risk for skin irritation.²¹ Among all the treatment options, we prefer benzyl alcohol, particularly in the context of resistance, as it is effective via a physical mechanism of action and lacks notable neurotoxic effects to the host. Use of benzyl alcohol is approved for patients as young as 6 months; it functions by asphyxiating the lice via paralysis of the respiratory spiracle with occlusion by inert ingredients. Itching, episodic numbness, and scalp or mucosal irritation are possible complications of treatment.²²

Treatment resistance of body lice has increased in recent years, warranting exploration of additional management strategies. Moreover, developing resistance to lindane and malathion has been reported.²³ Resistance to pyrethroids has been attributed to mutations in a voltage-gated sodium channel, one of which was universally present in the sampling of a single population.²⁴ A randomized controlled trial showed that off-label oral ivermectin 400 μg/kg was superior to malathion lotion 0.5% in difficult-to-treat cases of head lice²⁵; utility of oral ivermectin also has been reported in body lice.²⁶ In vitro studies also have shown promise for pursuing synergistic treatment of body lice with both ivermectin and antibiotics.²⁷

A novel primary prophylaxis approach for at-risk homeless individuals recently utilized permethrin-impregnated underwear. Although the intervention provided short-term infestation improvement, longer-term use did not show improvement from placebo and also increased prevalence of permethrin-resistant haplotypes.²

The use of skin emollients early in infancy and early introduction of certain foods failed to prevent atopic dermatitis (AD) in infants, including those at high risk, in two new clinical trials.

The BEEP (Barrier Enhancement for Eczema Prevention) study compared the rates of AD among infants identified as at risk of AD because of family history who had daily applications of emollients (Diprobase cream or Doublebase gel) for the first year of life, compared with a standard skin care group. PreventADALL (Preventing Atopic Dermatitis and Allergies in Children) is a randomized, primary-prevention study conducted in Norway and Sweden that randomized infants into one of four groups: controls whose parents followed regular skin care advice and nutrition guidelines; those who received skin emollients (the addition of emulsified oil to their bath and application of facial cream on at least 4 days a week from age 2 weeks to 8 months); those who received early complementary feeding of peanut, cow’s milk, wheat, and egg introduced between aged 12 and 16 weeks; and a group that combined both the emollient and diet interventions.

Neither of the studies, published in the Lancet, found statistically significant differences in AD rates between the intervention and control groups.

The results put a damper on hopes raised by previous studies that included two small pilot studies, which found that daily use of leave-on emollients in infants considered at high risk of AD prevented the development of AD (J Allergy Clin Immunol 2014 Oct;134:824-30.e6; J Allergy Clin Immunol Oct 2014;134:818-23).

“It was maybe a little bit overly hopeful to think that we could just moisturize and prevent such a complex disorder,” Robert Sidbury, MD, chief of dermatology at Seattle Children’s Hospital, said in an interview. He emphasized that the studies only addressed emollients as a preventative, and that “there’s no question that emollients are still critical for the therapy of eczema.”

Bruce Brod, MD, clinical professor of dermatology at the University of Pennsylvania, Philadelphia, suggested that homogeneous patient populations or insufficient numbers might explain the negative findings. PreventADALL drew patients from Norway and Sweden, while BEEP recruited from the United Kingdom. “They’re important studies, but I think they still lend themselves to further studies with different patient populations and larger groups of patients,” Dr. Brod said in an interview.

BEEP was headed by Joanne Chalmers, PhD, and Hywel Williams, DSc, of the Centre of Evidence-Based Dermatology at the University of Nottingham (England). Håvard Ove Skjerven, PhD, and Karin C Lødrup Carlsen, PhD, of Oslo University Hospital led the PreventADALL study.

The BEEP study randomized 1,394 newborns at 16 sites in the United Kingdom to daily emollient treatment with standard skin care, or standard skin care alone. At one year, compliance was 74% in the intervention group. At age 2, 23% of the intervention group had AD, compared with 25% of controls (hazard ratio, 0.95; P =.61). Skin infections were also higher in the treatment arm (mean, 0.23 per year vs. 0.15 per year; adjusted incidence ratio, 1.55; 95% confidence interval, 1.15-2.09).

“Our study does not support the use of emollients for preventing eczema in high-risk infants, a finding supported by PreventADALL, another large trial using a skin barrier enhancing intervention,” they concluded. Their data “relate only to prevention of eczema and do not directly challenge the practice of using emollients as first-line treatment for eczema.”

In the PreventADALL study, 2,397 newborn infants born between 2015 and 2017 were randomized to one of the four groups. Use of facial cream and emollients during bathing began at 2 weeks, and early complementary feeding of peanut, cow’s milk, wheat, and egg at 3-4 months. The frequency of AD at aged 12 months in the control group was 8%, compared with 11% in the skin-intervention group, 9% in the food-intervention group, and 5% in the combined-intervention group.

These differences were not statistically significant, and “the primary hypothesis that either skin intervention or food intervention reduced atopic dermatitis were not confirmed,” the authors wrote. Parental atopy did not influence the effects of the interventions. Their results were in line with the BEEP results, and the authors “cannot recommend these interventions as primary prevention strategies.”

The researchers will continue to follow children until age 3 years to evaluate the food allergy rates, if the combined-treatment group experiences a long-term benefit. Adherence to the protocol was poor, with 44% compliance with the facial cream application and 27% compliance with bathing emollients; 32% fully adhered to the diet protocols.

The studies were funded by the National Institute for Health Research Health Technology Assessment (BEEP); and a range of public and private funders (PreventADALL). One author of the PreventADALL study disclosed receiving honoraria for presentations from several pharmaceutical companies, and one author received honoraria for presentations from Thermo Fisher Scientific; the rest had no disclosures. Dr. Sidbury has been an investigator for Regeneron. Dr. Brod had no relevant financial disclosures.

SOURCES: Chalmers JR et al. Lancet. 2020 Feb 19. doi: 10.1016/S0140-6736(19)32984-8; Skjerven HO et al. Lancet. 2020 Feb 19. doi: 10.1016/S0140-6736(19)32983-6.
 

The use of skin emollients early in infancy and early introduction of certain foods failed to prevent atopic dermatitis (AD) in infants, including those at high risk, in two new clinical trials.

The BEEP (Barrier Enhancement for Eczema Prevention) study compared the rates of AD among infants identified as at risk of AD because of family history who had daily applications of emollients (Diprobase cream or Doublebase gel) for the first year of life, compared with a standard skin care group. PreventADALL (Preventing Atopic Dermatitis and Allergies in Children) is a randomized, primary-prevention study conducted in Norway and Sweden that randomized infants into one of four groups: controls whose parents followed regular skin care advice and nutrition guidelines; those who received skin emollients (the addition of emulsified oil to their bath and application of facial cream on at least 4 days a week from age 2 weeks to 8 months); those who received early complementary feeding of peanut, cow’s milk, wheat, and egg introduced between aged 12 and 16 weeks; and a group that combined both the emollient and diet interventions.

Neither of the studies, published in the Lancet, found statistically significant differences in AD rates between the intervention and control groups.

The results put a damper on hopes raised by previous studies that included two small pilot studies, which found that daily use of leave-on emollients in infants considered at high risk of AD prevented the development of AD (J Allergy Clin Immunol 2014 Oct;134:824-30.e6; J Allergy Clin Immunol Oct 2014;134:818-23).

“It was maybe a little bit overly hopeful to think that we could just moisturize and prevent such a complex disorder,” Robert Sidbury, MD, chief of dermatology at Seattle Children’s Hospital, said in an interview. He emphasized that the studies only addressed emollients as a preventative, and that “there’s no question that emollients are still critical for the therapy of eczema.”

Bruce Brod, MD, clinical professor of dermatology at the University of Pennsylvania, Philadelphia, suggested that homogeneous patient populations or insufficient numbers might explain the negative findings. PreventADALL drew patients from Norway and Sweden, while BEEP recruited from the United Kingdom. “They’re important studies, but I think they still lend themselves to further studies with different patient populations and larger groups of patients,” Dr. Brod said in an interview.

BEEP was headed by Joanne Chalmers, PhD, and Hywel Williams, DSc, of the Centre of Evidence-Based Dermatology at the University of Nottingham (England). Håvard Ove Skjerven, PhD, and Karin C Lødrup Carlsen, PhD, of Oslo University Hospital led the PreventADALL study.

The BEEP study randomized 1,394 newborns at 16 sites in the United Kingdom to daily emollient treatment with standard skin care, or standard skin care alone. At one year, compliance was 74% in the intervention group. At age 2, 23% of the intervention group had AD, compared with 25% of controls (hazard ratio, 0.95; P =.61). Skin infections were also higher in the treatment arm (mean, 0.23 per year vs. 0.15 per year; adjusted incidence ratio, 1.55; 95% confidence interval, 1.15-2.09).

“Our study does not support the use of emollients for preventing eczema in high-risk infants, a finding supported by PreventADALL, another large trial using a skin barrier enhancing intervention,” they concluded. Their data “relate only to prevention of eczema and do not directly challenge the practice of using emollients as first-line treatment for eczema.”

In the PreventADALL study, 2,397 newborn infants born between 2015 and 2017 were randomized to one of the four groups. Use of facial cream and emollients during bathing began at 2 weeks, and early complementary feeding of peanut, cow’s milk, wheat, and egg at 3-4 months. The frequency of AD at aged 12 months in the control group was 8%, compared with 11% in the skin-intervention group, 9% in the food-intervention group, and 5% in the combined-intervention group.

These differences were not statistically significant, and “the primary hypothesis that either skin intervention or food intervention reduced atopic dermatitis were not confirmed,” the authors wrote. Parental atopy did not influence the effects of the interventions. Their results were in line with the BEEP results, and the authors “cannot recommend these interventions as primary prevention strategies.”

The researchers will continue to follow children until age 3 years to evaluate the food allergy rates, if the combined-treatment group experiences a long-term benefit. Adherence to the protocol was poor, with 44% compliance with the facial cream application and 27% compliance with bathing emollients; 32% fully adhered to the diet protocols.

The studies were funded by the National Institute for Health Research Health Technology Assessment (BEEP); and a range of public and private funders (PreventADALL). One author of the PreventADALL study disclosed receiving honoraria for presentations from several pharmaceutical companies, and one author received honoraria for presentations from Thermo Fisher Scientific; the rest had no disclosures. Dr. Sidbury has been an investigator for Regeneron. Dr. Brod had no relevant financial disclosures.

SOURCES: Chalmers JR et al. Lancet. 2020 Feb 19. doi: 10.1016/S0140-6736(19)32984-8; Skjerven HO et al. Lancet. 2020 Feb 19. doi: 10.1016/S0140-6736(19)32983-6.
 

The use of skin emollients early in infancy and early introduction of certain foods failed to prevent atopic dermatitis (AD) in infants, including those at high risk, in two new clinical trials.

The BEEP (Barrier Enhancement for Eczema Prevention) study compared the rates of AD among infants identified as at risk of AD because of family history who had daily applications of emollients (Diprobase cream or Doublebase gel) for the first year of life, compared with a standard skin care group. PreventADALL (Preventing Atopic Dermatitis and Allergies in Children) is a randomized, primary-prevention study conducted in Norway and Sweden that randomized infants into one of four groups: controls whose parents followed regular skin care advice and nutrition guidelines; those who received skin emollients (the addition of emulsified oil to their bath and application of facial cream on at least 4 days a week from age 2 weeks to 8 months); those who received early complementary feeding of peanut, cow’s milk, wheat, and egg introduced between aged 12 and 16 weeks; and a group that combined both the emollient and diet interventions.

Neither of the studies, published in the Lancet, found statistically significant differences in AD rates between the intervention and control groups.

The results put a damper on hopes raised by previous studies that included two small pilot studies, which found that daily use of leave-on emollients in infants considered at high risk of AD prevented the development of AD (J Allergy Clin Immunol 2014 Oct;134:824-30.e6; J Allergy Clin Immunol Oct 2014;134:818-23).

“It was maybe a little bit overly hopeful to think that we could just moisturize and prevent such a complex disorder,” Robert Sidbury, MD, chief of dermatology at Seattle Children’s Hospital, said in an interview. He emphasized that the studies only addressed emollients as a preventative, and that “there’s no question that emollients are still critical for the therapy of eczema.”

Bruce Brod, MD, clinical professor of dermatology at the University of Pennsylvania, Philadelphia, suggested that homogeneous patient populations or insufficient numbers might explain the negative findings. PreventADALL drew patients from Norway and Sweden, while BEEP recruited from the United Kingdom. “They’re important studies, but I think they still lend themselves to further studies with different patient populations and larger groups of patients,” Dr. Brod said in an interview.

BEEP was headed by Joanne Chalmers, PhD, and Hywel Williams, DSc, of the Centre of Evidence-Based Dermatology at the University of Nottingham (England). Håvard Ove Skjerven, PhD, and Karin C Lødrup Carlsen, PhD, of Oslo University Hospital led the PreventADALL study.

The BEEP study randomized 1,394 newborns at 16 sites in the United Kingdom to daily emollient treatment with standard skin care, or standard skin care alone. At one year, compliance was 74% in the intervention group. At age 2, 23% of the intervention group had AD, compared with 25% of controls (hazard ratio, 0.95; P =.61). Skin infections were also higher in the treatment arm (mean, 0.23 per year vs. 0.15 per year; adjusted incidence ratio, 1.55; 95% confidence interval, 1.15-2.09).

“Our study does not support the use of emollients for preventing eczema in high-risk infants, a finding supported by PreventADALL, another large trial using a skin barrier enhancing intervention,” they concluded. Their data “relate only to prevention of eczema and do not directly challenge the practice of using emollients as first-line treatment for eczema.”

In the PreventADALL study, 2,397 newborn infants born between 2015 and 2017 were randomized to one of the four groups. Use of facial cream and emollients during bathing began at 2 weeks, and early complementary feeding of peanut, cow’s milk, wheat, and egg at 3-4 months. The frequency of AD at aged 12 months in the control group was 8%, compared with 11% in the skin-intervention group, 9% in the food-intervention group, and 5% in the combined-intervention group.

These differences were not statistically significant, and “the primary hypothesis that either skin intervention or food intervention reduced atopic dermatitis were not confirmed,” the authors wrote. Parental atopy did not influence the effects of the interventions. Their results were in line with the BEEP results, and the authors “cannot recommend these interventions as primary prevention strategies.”

The researchers will continue to follow children until age 3 years to evaluate the food allergy rates, if the combined-treatment group experiences a long-term benefit. Adherence to the protocol was poor, with 44% compliance with the facial cream application and 27% compliance with bathing emollients; 32% fully adhered to the diet protocols.

The studies were funded by the National Institute for Health Research Health Technology Assessment (BEEP); and a range of public and private funders (PreventADALL). One author of the PreventADALL study disclosed receiving honoraria for presentations from several pharmaceutical companies, and one author received honoraria for presentations from Thermo Fisher Scientific; the rest had no disclosures. Dr. Sidbury has been an investigator for Regeneron. Dr. Brod had no relevant financial disclosures.

SOURCES: Chalmers JR et al. Lancet. 2020 Feb 19. doi: 10.1016/S0140-6736(19)32984-8; Skjerven HO et al. Lancet. 2020 Feb 19. doi: 10.1016/S0140-6736(19)32983-6.
 

The treatment failure with the terbinafine made onychomycosis unlikely, and the appearance of the finger did not suggest that this was a wart. So, the physician opted for a 4-mm punch biopsy of the lateral nail fold, which confirmed that this was a well-differentiated squamous cell carcinoma (SCC) of the fingertip.

Periungual SCC is twice as common in men as women. Lesions tend to appear as hyperkeratotic plaques or nodules, pushing the nail plate away from the nail bed. With onychomycosis, one would expect the nail to be more thickened and discolored. A wart would not be as keratotic as this lesion was, and there would be thrombosed capillaries on closer inspection.

SCC is the second most common skin cancer in humans. It is most common on sun-exposed areas but may present in sites not exposed to the sun. It has been hypothesized that high risk human papillomavirus (HPV) types—particularly HPV 16—may contribute to diseases of the fingertips and nail unit in older adults. (There was no known history of HPV in this patient.)

A surgical approach often is curative. Achieving appropriate margins occasionally requires partial amputation. Mohs micrographic surgery (MMS) offers the highest cure rate and spares as much uninvolved tissue as possible. Radiation therapy is another tissue-sparing technique. It requires 15 to 30 sessions over 3 to 6 weeks and has a lower cure rate than MMS.

In this case, the patient underwent MMS. Follow-up skin surveillance exams revealed other small nonmelanoma skin cancers at other sites. The patient also developed a dystrophic nail spicule near the surgical site that was re-excised and deemed benign.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

The treatment failure with the terbinafine made onychomycosis unlikely, and the appearance of the finger did not suggest that this was a wart. So, the physician opted for a 4-mm punch biopsy of the lateral nail fold, which confirmed that this was a well-differentiated squamous cell carcinoma (SCC) of the fingertip.

Periungual SCC is twice as common in men as women. Lesions tend to appear as hyperkeratotic plaques or nodules, pushing the nail plate away from the nail bed. With onychomycosis, one would expect the nail to be more thickened and discolored. A wart would not be as keratotic as this lesion was, and there would be thrombosed capillaries on closer inspection.

SCC is the second most common skin cancer in humans. It is most common on sun-exposed areas but may present in sites not exposed to the sun. It has been hypothesized that high risk human papillomavirus (HPV) types—particularly HPV 16—may contribute to diseases of the fingertips and nail unit in older adults. (There was no known history of HPV in this patient.)

A surgical approach often is curative. Achieving appropriate margins occasionally requires partial amputation. Mohs micrographic surgery (MMS) offers the highest cure rate and spares as much uninvolved tissue as possible. Radiation therapy is another tissue-sparing technique. It requires 15 to 30 sessions over 3 to 6 weeks and has a lower cure rate than MMS.

In this case, the patient underwent MMS. Follow-up skin surveillance exams revealed other small nonmelanoma skin cancers at other sites. The patient also developed a dystrophic nail spicule near the surgical site that was re-excised and deemed benign.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

The treatment failure with the terbinafine made onychomycosis unlikely, and the appearance of the finger did not suggest that this was a wart. So, the physician opted for a 4-mm punch biopsy of the lateral nail fold, which confirmed that this was a well-differentiated squamous cell carcinoma (SCC) of the fingertip.

Periungual SCC is twice as common in men as women. Lesions tend to appear as hyperkeratotic plaques or nodules, pushing the nail plate away from the nail bed. With onychomycosis, one would expect the nail to be more thickened and discolored. A wart would not be as keratotic as this lesion was, and there would be thrombosed capillaries on closer inspection.

SCC is the second most common skin cancer in humans. It is most common on sun-exposed areas but may present in sites not exposed to the sun. It has been hypothesized that high risk human papillomavirus (HPV) types—particularly HPV 16—may contribute to diseases of the fingertips and nail unit in older adults. (There was no known history of HPV in this patient.)

A surgical approach often is curative. Achieving appropriate margins occasionally requires partial amputation. Mohs micrographic surgery (MMS) offers the highest cure rate and spares as much uninvolved tissue as possible. Radiation therapy is another tissue-sparing technique. It requires 15 to 30 sessions over 3 to 6 weeks and has a lower cure rate than MMS.

In this case, the patient underwent MMS. Follow-up skin surveillance exams revealed other small nonmelanoma skin cancers at other sites. The patient also developed a dystrophic nail spicule near the surgical site that was re-excised and deemed benign.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

Health care systems need to take urgent action to address social isolation and loneliness among U.S. seniors, experts say.

A new report from the National Academies of Sciences, Engineering, and Medicine (NAS) points out that social isolation in this population is a major public health concern that contributes to heart disease, depression, and premature death.

The report authors note that the health care system remains an underused partner in preventing, identifying, and intervening in social isolation and loneliness among adults over age 50.

For seniors who are homebound, have no family, or do not belong to community or faith groups, a medical appointment or home health visit may be one of the few social interactions they have, the report notes.

Health care providers and systems may be “first responders” in recognizing lonely or socially isolated patients, committee chair Dan Blazer, MD, from Duke University School of Medicine, Durham, N.C., said during a press briefing.
 

As deadly as obesity, smoking

Committee member Julianne Holt-Lunstad, PhD, from Brigham Young University, Provo, Utah, noted that social isolation and loneliness are “distinctly different.”

Social isolation is defined as an objective lack of (or limited) social connections, while loneliness is a subjective perception of social isolation or the subjective feeling of being lonely.

Not all older adults are isolated or lonely, but they are more likely to face predisposing factors such as living alone and the loss of loved ones, she explained.

The issue may be compounded for LGBT, minority, and immigrant older adults, who may already face barriers to care, stigma, and discrimination. Social isolation and loneliness may also directly stem from chronic illness, hearing or vision loss, or mobility issues. In these cases, health care providers might be able to help prevent or reduce social isolation and loneliness by directly addressing the underlying health-related causes.

Some evidence suggests that the magnitude of the effect of social isolation on premature mortality may be comparable to or greater than smoking, obesity, and physical inactivity, Holt-Lunstad told the briefing. The report offers a vision for how the health care system can identify people at risk of social isolation and loneliness, intervene, and engage other community partners.

It recommends that providers use validated tools to periodically assess patients who may be at risk for social isolation and loneliness and connect them to community resources for help.

The report also calls for greater education and training among health providers. Schools of health professions and training programs for direct care workers (eg, home health aides, nurse aides, and personal care aides) should incorporate social isolation and loneliness in their curricula, the report says.

It also offers recommendations for leveraging digital health and health technology, improving community partnerships, increasing funding for research, and creation of a national resource center under the Department of Health and Human Services.

Blazer said there remains “much to be learned” about what approaches to mitigating social isolation and loneliness work best in which populations.

The report, from the Committee on the Health and Medical Dimensions of Social Isolation and Loneliness in Older Adults, was sponsored by the AARP Foundation.

This article first appeared on Medscape.com.

Health care systems need to take urgent action to address social isolation and loneliness among U.S. seniors, experts say.

A new report from the National Academies of Sciences, Engineering, and Medicine (NAS) points out that social isolation in this population is a major public health concern that contributes to heart disease, depression, and premature death.

The report authors note that the health care system remains an underused partner in preventing, identifying, and intervening in social isolation and loneliness among adults over age 50.

For seniors who are homebound, have no family, or do not belong to community or faith groups, a medical appointment or home health visit may be one of the few social interactions they have, the report notes.

Health care providers and systems may be “first responders” in recognizing lonely or socially isolated patients, committee chair Dan Blazer, MD, from Duke University School of Medicine, Durham, N.C., said during a press briefing.
 

As deadly as obesity, smoking

Committee member Julianne Holt-Lunstad, PhD, from Brigham Young University, Provo, Utah, noted that social isolation and loneliness are “distinctly different.”

Social isolation is defined as an objective lack of (or limited) social connections, while loneliness is a subjective perception of social isolation or the subjective feeling of being lonely.

Not all older adults are isolated or lonely, but they are more likely to face predisposing factors such as living alone and the loss of loved ones, she explained.

The issue may be compounded for LGBT, minority, and immigrant older adults, who may already face barriers to care, stigma, and discrimination. Social isolation and loneliness may also directly stem from chronic illness, hearing or vision loss, or mobility issues. In these cases, health care providers might be able to help prevent or reduce social isolation and loneliness by directly addressing the underlying health-related causes.

Some evidence suggests that the magnitude of the effect of social isolation on premature mortality may be comparable to or greater than smoking, obesity, and physical inactivity, Holt-Lunstad told the briefing. The report offers a vision for how the health care system can identify people at risk of social isolation and loneliness, intervene, and engage other community partners.

It recommends that providers use validated tools to periodically assess patients who may be at risk for social isolation and loneliness and connect them to community resources for help.

The report also calls for greater education and training among health providers. Schools of health professions and training programs for direct care workers (eg, home health aides, nurse aides, and personal care aides) should incorporate social isolation and loneliness in their curricula, the report says.

It also offers recommendations for leveraging digital health and health technology, improving community partnerships, increasing funding for research, and creation of a national resource center under the Department of Health and Human Services.

Blazer said there remains “much to be learned” about what approaches to mitigating social isolation and loneliness work best in which populations.

The report, from the Committee on the Health and Medical Dimensions of Social Isolation and Loneliness in Older Adults, was sponsored by the AARP Foundation.

This article first appeared on Medscape.com.

Health care systems need to take urgent action to address social isolation and loneliness among U.S. seniors, experts say.

A new report from the National Academies of Sciences, Engineering, and Medicine (NAS) points out that social isolation in this population is a major public health concern that contributes to heart disease, depression, and premature death.

The report authors note that the health care system remains an underused partner in preventing, identifying, and intervening in social isolation and loneliness among adults over age 50.

For seniors who are homebound, have no family, or do not belong to community or faith groups, a medical appointment or home health visit may be one of the few social interactions they have, the report notes.

Health care providers and systems may be “first responders” in recognizing lonely or socially isolated patients, committee chair Dan Blazer, MD, from Duke University School of Medicine, Durham, N.C., said during a press briefing.
 

As deadly as obesity, smoking

Committee member Julianne Holt-Lunstad, PhD, from Brigham Young University, Provo, Utah, noted that social isolation and loneliness are “distinctly different.”

Social isolation is defined as an objective lack of (or limited) social connections, while loneliness is a subjective perception of social isolation or the subjective feeling of being lonely.

Not all older adults are isolated or lonely, but they are more likely to face predisposing factors such as living alone and the loss of loved ones, she explained.

The issue may be compounded for LGBT, minority, and immigrant older adults, who may already face barriers to care, stigma, and discrimination. Social isolation and loneliness may also directly stem from chronic illness, hearing or vision loss, or mobility issues. In these cases, health care providers might be able to help prevent or reduce social isolation and loneliness by directly addressing the underlying health-related causes.

Some evidence suggests that the magnitude of the effect of social isolation on premature mortality may be comparable to or greater than smoking, obesity, and physical inactivity, Holt-Lunstad told the briefing. The report offers a vision for how the health care system can identify people at risk of social isolation and loneliness, intervene, and engage other community partners.

It recommends that providers use validated tools to periodically assess patients who may be at risk for social isolation and loneliness and connect them to community resources for help.

The report also calls for greater education and training among health providers. Schools of health professions and training programs for direct care workers (eg, home health aides, nurse aides, and personal care aides) should incorporate social isolation and loneliness in their curricula, the report says.

It also offers recommendations for leveraging digital health and health technology, improving community partnerships, increasing funding for research, and creation of a national resource center under the Department of Health and Human Services.

Blazer said there remains “much to be learned” about what approaches to mitigating social isolation and loneliness work best in which populations.

The report, from the Committee on the Health and Medical Dimensions of Social Isolation and Loneliness in Older Adults, was sponsored by the AARP Foundation.

This article first appeared on Medscape.com.

Combining magnetic resonance imaging (MRI)–targeted biopsy and systematic biopsy improved detection of prostate cancer among men with MRI-visible lesions in a single-center study.

Compared with either method alone, a combination of the two biopsy methods resulted in 9.9% more prostate cancer diagnoses, explained study author Michael Ahdoot, MD, of the National Institutes of Health and colleagues. Their report was published in the New England Journal of Medicine.

“With the addition of MRI-targeted biopsy to systematic biopsy, we may have entered an era of increased diagnostic certainty in prostate cancer,” the researchers wrote.

Their single-center, comparative diagnostic study included 2,103 patients with MRI-visible prostate lesions who underwent both systematic and MRI-targeted biopsy. In cases of multiple biopsies, only the results of the initial biopsies were included.

Each individual specimen was assigned a Gleason score by a genitourinary pathologist and was subsequently categorized into a grade group on a scale of 1-5, with higher scores reflecting greater cancer risk. Grade group 1 was defined as clinically insignificant disease. Grade group 2 was defined as favorable intermediate-risk disease. Grade group 3 or higher was defined as unfavorable intermediate-risk disease or worse.

The primary endpoints were cancer detection rates for each biopsy method, based on grade group. “Among the men who underwent subsequent radical prostatectomy, upgrading and downgrading of grade group from biopsy to whole-mount histopathological analysis of surgical specimens [was also assessed],” the researchers explained.

Among patients who underwent combined biopsy, prostate cancer was identified in 62.4% of patients, and 19.2% underwent radical prostatectomy.

For grade groups 3-5, rates of cancer detection were significantly higher with MRI-targeted biopsy than with systematic biopsy (P less than .01 for all). For grade group 1, detection rates were significantly lower with MRI-targeted biopsy (P less than .01).

“Although many of [the] benefits resulted from MRI-targeted biopsy alone, omission of systematic biopsy would have led to missing the diagnosis of 8.8% of clinically significant cancers,” the researchers reported.

In addition, among patients who underwent radical prostatectomy, the rates of upgrading (grade group 3 or higher) on histopathological analysis were lower for combined biopsy (3.5%) than for MRI-targeted biopsy (8.7%) and systematic biopsy (16.8%).

The researchers acknowledged that a key limitation of this study was the single-center design. As a result, the findings may not be generalizable to other institutions.

However, the researchers concluded that “these findings suggest that combined biopsy provides improved diagnostic accuracy over either systematic or MRI-targeted biopsy alone and better predicts the results of final histopathological analysis.”

The study was funded by the National Institutes of Health, Philips, and the Dr. Mildred Scheel Foundation for Cancer Research. The authors disclosed financial affiliations with Philips, Biocompatibles UK, Boston Scientific, Celsion, and other companies.

SOURCE: Ahdoot M et al. N Engl J Med. 2020 Mar 4. doi: 10.1056/NEJMoa1910038.

Combining magnetic resonance imaging (MRI)–targeted biopsy and systematic biopsy improved detection of prostate cancer among men with MRI-visible lesions in a single-center study.

Compared with either method alone, a combination of the two biopsy methods resulted in 9.9% more prostate cancer diagnoses, explained study author Michael Ahdoot, MD, of the National Institutes of Health and colleagues. Their report was published in the New England Journal of Medicine.

“With the addition of MRI-targeted biopsy to systematic biopsy, we may have entered an era of increased diagnostic certainty in prostate cancer,” the researchers wrote.

Their single-center, comparative diagnostic study included 2,103 patients with MRI-visible prostate lesions who underwent both systematic and MRI-targeted biopsy. In cases of multiple biopsies, only the results of the initial biopsies were included.

Each individual specimen was assigned a Gleason score by a genitourinary pathologist and was subsequently categorized into a grade group on a scale of 1-5, with higher scores reflecting greater cancer risk. Grade group 1 was defined as clinically insignificant disease. Grade group 2 was defined as favorable intermediate-risk disease. Grade group 3 or higher was defined as unfavorable intermediate-risk disease or worse.

The primary endpoints were cancer detection rates for each biopsy method, based on grade group. “Among the men who underwent subsequent radical prostatectomy, upgrading and downgrading of grade group from biopsy to whole-mount histopathological analysis of surgical specimens [was also assessed],” the researchers explained.

Among patients who underwent combined biopsy, prostate cancer was identified in 62.4% of patients, and 19.2% underwent radical prostatectomy.

For grade groups 3-5, rates of cancer detection were significantly higher with MRI-targeted biopsy than with systematic biopsy (P less than .01 for all). For grade group 1, detection rates were significantly lower with MRI-targeted biopsy (P less than .01).

“Although many of [the] benefits resulted from MRI-targeted biopsy alone, omission of systematic biopsy would have led to missing the diagnosis of 8.8% of clinically significant cancers,” the researchers reported.

In addition, among patients who underwent radical prostatectomy, the rates of upgrading (grade group 3 or higher) on histopathological analysis were lower for combined biopsy (3.5%) than for MRI-targeted biopsy (8.7%) and systematic biopsy (16.8%).

The researchers acknowledged that a key limitation of this study was the single-center design. As a result, the findings may not be generalizable to other institutions.

However, the researchers concluded that “these findings suggest that combined biopsy provides improved diagnostic accuracy over either systematic or MRI-targeted biopsy alone and better predicts the results of final histopathological analysis.”

The study was funded by the National Institutes of Health, Philips, and the Dr. Mildred Scheel Foundation for Cancer Research. The authors disclosed financial affiliations with Philips, Biocompatibles UK, Boston Scientific, Celsion, and other companies.

SOURCE: Ahdoot M et al. N Engl J Med. 2020 Mar 4. doi: 10.1056/NEJMoa1910038.

Combining magnetic resonance imaging (MRI)–targeted biopsy and systematic biopsy improved detection of prostate cancer among men with MRI-visible lesions in a single-center study.

Compared with either method alone, a combination of the two biopsy methods resulted in 9.9% more prostate cancer diagnoses, explained study author Michael Ahdoot, MD, of the National Institutes of Health and colleagues. Their report was published in the New England Journal of Medicine.

“With the addition of MRI-targeted biopsy to systematic biopsy, we may have entered an era of increased diagnostic certainty in prostate cancer,” the researchers wrote.

Their single-center, comparative diagnostic study included 2,103 patients with MRI-visible prostate lesions who underwent both systematic and MRI-targeted biopsy. In cases of multiple biopsies, only the results of the initial biopsies were included.

Each individual specimen was assigned a Gleason score by a genitourinary pathologist and was subsequently categorized into a grade group on a scale of 1-5, with higher scores reflecting greater cancer risk. Grade group 1 was defined as clinically insignificant disease. Grade group 2 was defined as favorable intermediate-risk disease. Grade group 3 or higher was defined as unfavorable intermediate-risk disease or worse.

The primary endpoints were cancer detection rates for each biopsy method, based on grade group. “Among the men who underwent subsequent radical prostatectomy, upgrading and downgrading of grade group from biopsy to whole-mount histopathological analysis of surgical specimens [was also assessed],” the researchers explained.

Among patients who underwent combined biopsy, prostate cancer was identified in 62.4% of patients, and 19.2% underwent radical prostatectomy.

For grade groups 3-5, rates of cancer detection were significantly higher with MRI-targeted biopsy than with systematic biopsy (P less than .01 for all). For grade group 1, detection rates were significantly lower with MRI-targeted biopsy (P less than .01).

“Although many of [the] benefits resulted from MRI-targeted biopsy alone, omission of systematic biopsy would have led to missing the diagnosis of 8.8% of clinically significant cancers,” the researchers reported.

In addition, among patients who underwent radical prostatectomy, the rates of upgrading (grade group 3 or higher) on histopathological analysis were lower for combined biopsy (3.5%) than for MRI-targeted biopsy (8.7%) and systematic biopsy (16.8%).

The researchers acknowledged that a key limitation of this study was the single-center design. As a result, the findings may not be generalizable to other institutions.

However, the researchers concluded that “these findings suggest that combined biopsy provides improved diagnostic accuracy over either systematic or MRI-targeted biopsy alone and better predicts the results of final histopathological analysis.”

The study was funded by the National Institutes of Health, Philips, and the Dr. Mildred Scheel Foundation for Cancer Research. The authors disclosed financial affiliations with Philips, Biocompatibles UK, Boston Scientific, Celsion, and other companies.

SOURCE: Ahdoot M et al. N Engl J Med. 2020 Mar 4. doi: 10.1056/NEJMoa1910038.

When physicians gaze into their crystal balls to predict what’s coming in 2020, they see continued efforts to defund the Affordable Care Act – meaning the ACA will still be around to be defunded – but they don’t see a lot of support for universal health care, according to health care market research company InCrowd.

Expectations for universal health care came in at 18% of the 100 generalists and 101 specialists who responded to InCrowd’s fifth annual health care predictions survey, which left 82% who thought that “election outcomes will result in universal healthcare support” was somewhat or very unlikely in 2020.

One respondent, a specialist from California, commented that “the global data on universal healthcare for all shows that it results in overall improved population health. Unfortunately, we are so polarized in the US against universal healthcare driven by bias from health insurance companies and decision makers that are quick to ignore scientific data.”

This was the first time InCrowd asked physicians about universal health care, but ACA-related predictions have been included before, and all three scenarios presented were deemed to be increasingly likely, compared with 2019.

Respondents thought that federal government defunding was more likely to occur in 2020 (80%) than in 2019 (73%), but increased majorities also said that preexisting conditions coverage would continue (78% in 2020 vs. 70% in 2019) and that the ACA would remain in place (74% in 2020 vs. 60% in 2019), InCrowd reported after the survey, which was conducted from Dec. 30, 2019, to Jan. 2, 2020.

A respondent who thought the ACA will be eliminated said, “I have as many uninsured today as before the ACA. They are just different. Mainly younger patients who spend less in a year on healthcare than one month’s premium.” Another suggested that eliminateing it “will limit access to care and overload [emergency departments]. More people will die.”

Cost was addressed in a separate survey question that asked how physicians could help to reduce health care spending in 2020.

The leading answer, given by 37% of respondents, was for physicians to “inform themselves of costs and adapt cost-saving prescription practices.” Next came “limit use of expensive tests and scans” with 21%, followed by “prescribe generics when possible” at 20%, which was a substantial drop from the 38% it garnered in 2019, InCrowd noted.

“Participation in [shared savings] programs and risk-based incentive programs and pay-for-performance programs” would provide “better stewardship of resources,” a primary care physician from Michigan wrote.

When the survey turned to pharmaceutical industry predictions for 2020, cost was the major issue.

“What’s interesting about this year’s data is that we’re seeing less emphasis on the importance of bringing innovative, new therapies to market faster … versus expanding affordability, which was nearly a unanimous top priority for respondents,” Daniel S. Fitzgerald, InCrowd’s CEO and president, said in a separate statement.

rfranki@mdedge.com

When physicians gaze into their crystal balls to predict what’s coming in 2020, they see continued efforts to defund the Affordable Care Act – meaning the ACA will still be around to be defunded – but they don’t see a lot of support for universal health care, according to health care market research company InCrowd.

Expectations for universal health care came in at 18% of the 100 generalists and 101 specialists who responded to InCrowd’s fifth annual health care predictions survey, which left 82% who thought that “election outcomes will result in universal healthcare support” was somewhat or very unlikely in 2020.

One respondent, a specialist from California, commented that “the global data on universal healthcare for all shows that it results in overall improved population health. Unfortunately, we are so polarized in the US against universal healthcare driven by bias from health insurance companies and decision makers that are quick to ignore scientific data.”

This was the first time InCrowd asked physicians about universal health care, but ACA-related predictions have been included before, and all three scenarios presented were deemed to be increasingly likely, compared with 2019.

Respondents thought that federal government defunding was more likely to occur in 2020 (80%) than in 2019 (73%), but increased majorities also said that preexisting conditions coverage would continue (78% in 2020 vs. 70% in 2019) and that the ACA would remain in place (74% in 2020 vs. 60% in 2019), InCrowd reported after the survey, which was conducted from Dec. 30, 2019, to Jan. 2, 2020.

A respondent who thought the ACA will be eliminated said, “I have as many uninsured today as before the ACA. They are just different. Mainly younger patients who spend less in a year on healthcare than one month’s premium.” Another suggested that eliminateing it “will limit access to care and overload [emergency departments]. More people will die.”

Cost was addressed in a separate survey question that asked how physicians could help to reduce health care spending in 2020.

The leading answer, given by 37% of respondents, was for physicians to “inform themselves of costs and adapt cost-saving prescription practices.” Next came “limit use of expensive tests and scans” with 21%, followed by “prescribe generics when possible” at 20%, which was a substantial drop from the 38% it garnered in 2019, InCrowd noted.

“Participation in [shared savings] programs and risk-based incentive programs and pay-for-performance programs” would provide “better stewardship of resources,” a primary care physician from Michigan wrote.

When the survey turned to pharmaceutical industry predictions for 2020, cost was the major issue.

“What’s interesting about this year’s data is that we’re seeing less emphasis on the importance of bringing innovative, new therapies to market faster … versus expanding affordability, which was nearly a unanimous top priority for respondents,” Daniel S. Fitzgerald, InCrowd’s CEO and president, said in a separate statement.

rfranki@mdedge.com

When physicians gaze into their crystal balls to predict what’s coming in 2020, they see continued efforts to defund the Affordable Care Act – meaning the ACA will still be around to be defunded – but they don’t see a lot of support for universal health care, according to health care market research company InCrowd.

Expectations for universal health care came in at 18% of the 100 generalists and 101 specialists who responded to InCrowd’s fifth annual health care predictions survey, which left 82% who thought that “election outcomes will result in universal healthcare support” was somewhat or very unlikely in 2020.

One respondent, a specialist from California, commented that “the global data on universal healthcare for all shows that it results in overall improved population health. Unfortunately, we are so polarized in the US against universal healthcare driven by bias from health insurance companies and decision makers that are quick to ignore scientific data.”

This was the first time InCrowd asked physicians about universal health care, but ACA-related predictions have been included before, and all three scenarios presented were deemed to be increasingly likely, compared with 2019.

Respondents thought that federal government defunding was more likely to occur in 2020 (80%) than in 2019 (73%), but increased majorities also said that preexisting conditions coverage would continue (78% in 2020 vs. 70% in 2019) and that the ACA would remain in place (74% in 2020 vs. 60% in 2019), InCrowd reported after the survey, which was conducted from Dec. 30, 2019, to Jan. 2, 2020.

A respondent who thought the ACA will be eliminated said, “I have as many uninsured today as before the ACA. They are just different. Mainly younger patients who spend less in a year on healthcare than one month’s premium.” Another suggested that eliminateing it “will limit access to care and overload [emergency departments]. More people will die.”

Cost was addressed in a separate survey question that asked how physicians could help to reduce health care spending in 2020.

The leading answer, given by 37% of respondents, was for physicians to “inform themselves of costs and adapt cost-saving prescription practices.” Next came “limit use of expensive tests and scans” with 21%, followed by “prescribe generics when possible” at 20%, which was a substantial drop from the 38% it garnered in 2019, InCrowd noted.

“Participation in [shared savings] programs and risk-based incentive programs and pay-for-performance programs” would provide “better stewardship of resources,” a primary care physician from Michigan wrote.

When the survey turned to pharmaceutical industry predictions for 2020, cost was the major issue.

“What’s interesting about this year’s data is that we’re seeing less emphasis on the importance of bringing innovative, new therapies to market faster … versus expanding affordability, which was nearly a unanimous top priority for respondents,” Daniel S. Fitzgerald, InCrowd’s CEO and president, said in a separate statement.

rfranki@mdedge.com

MAUI, HAWAII – Alvin F. Wells, MD, PhD, believes he’s seen the future of rheumatology. So he’s taken a deep dive into telerheumatology, going all in.

Bruce Jancin/MDedge News

“Whether you’re in academic, private, or hospital-based practice, in 2020 if you are not thinking about telerheumatology, you and your practice will not be able to compete with growing patient demands, expectations, and need for clinical monitoring. If you do not have a digital/virtual strategy, you do not have a health care strategy,” he asserted at the 2020 Rheumatology Winter Clinical Symposium.

“Begin now,” the rheumatologist advised.

In pursuit of his own telerheumatology strategy, he holds licenses to practice medicine in five states and has licensure pending in five others.

“My goal is to cover 20% of the U.S., so if the local guys can’t see the patients, I can see them virtually,” he explained. “The days of waiting 4-6 months to be seen by a rheumatologist are gone.”

Rheumatologists are already in short supply in most of the country, and a major shortage looms ahead as older practitioners retire. Telerheumatology can help fill that unmet need. But the specialty is behind the curve. In a survey that rated the medical specialties most engaged in telemedicine, the top three spots were held by radiology, psychiatry, and internal medicine. Rheumatology didn’t even crack the top 10, noted Dr. Wells, director of the Rheumatology and Immunotherapy Center in Franklin, Wisc., and a part-time faculty member at Duke University, the Medical College of Wisconsin, and the Karolinska Institute.

Yet telemedicine is primed for rheumatologic takeoff. Notably, the 2019 update of the American College of Rheumatology recommendations on rheumatoid arthritis disease activity measures incorporates the RAPID3 (Routine Assessment of Patient Index Data) as an endorsed three-question clinical assessment that doesn’t involve a physical exam or laboratory work. The ACR update is recognition that, while every rheumatology patient needs an initial physical exam along with follow-up physical exams at various rates, many patients with well-controlled disease don’t need a physical exam at every physician encounter, he said.

Telerheumatology saves time for both patient and physician. The patient saves travel time, doesn’t miss work, avoids having to arrange for child care in order to make a face-to-face clinic visit, and can schedule more frequent virtual follow-up visits. For the practitioner, telerheumatology means additional consults and – here’s the big one – “You never run behind,” according to Dr. Wells. “For a 15-minute appointment, the patient gets a 5-minute warning, then a 2-minute warning, and at 15 minutes the link is cut. If the fibromyalgia patients want 30 minutes, they pay for 30 minutes.”

He sees the strictly enforced, impersonally delivered electronic time limits as key to running an efficient practice.

“The patients with osteoarthritis who hate the nodules, the fibromyalgia patients because they’re hurting all over, the patients with back pain – you’ve really got to limit those patients because otherwise you’ll be running 30-40 minutes behind for a scheduled 15-minute visit,” he explained.

One rheumatologist’s telemedicine practice

Dr. Wells currently utilizes the Epic electronic health record integrated with a Zoom videoconferencing platform for real-time virtual patient encounters. But he noted that other virtual platforms are available, including Health Tap, American Well, MySpecialistMD, MDLIVE, and TelaDoc. The American Telemedicine Association is a valuable resource for state-by-state medicolegal, reimbursement, and how-to-do-it questions.

At present, he reserves two daily time slots for telerheumatology: one at 8:30-9:00 a.m., the other at 4:30-5:00 p.m. These can be filled with four 15-minute live consults or two 30-minute consults. His goal is to eventually make telerheumatology 20% of his patient load of about 100 patients per week.

His typical 15-minute virtual visit proceeds as follows: It begins with a 3-minute subjective patient assessment, followed by a 5-minute objective assessment which includes the RAPID3, a brief Health Assessment Questionnaire (HAQ) addressing the patient’s pain and overall satisfaction, a virtual joint inspection, the use of high-quality teleultrasound and other technology when warranted, and capture of relevant still photos. This is followed by 5 minutes to relay the treatment plan, and finally a 2-minute recap and summary.

“No niceties. We cut right to the chase,” he noted.

He documents the patient encounter as he goes, dictating his notes throughout the visit.

“When I walk out of the room, I’m done. It’s on to the next patient,” Dr. Wells said.

The reimbursement picture is improving, although major hurdles remain. At present, 48 states and the District of Columbia reimburse for live video telemedicine through Medicaid. And in January 2020, Aetna announced it covers reimbursement for telemedicine in all of its fully insured health plans via the Teladoc platform. Dr. Wells’ patients pay for their telerheumatology out of pocket if their insurance doesn’t cover it.
 

Telemedicine caveats

Dr. Wells shared his telerheumatology experience as the first half of a point/counterpoint session on telemedicine’s future in the specialty. His debate opponent, Orrin M. Troum, MD, announced at the outset that he is quite interested in getting into telerheumatology; however, while looking into it he has come across issues that for now give him pause and that other rheumatologists need to be aware of.

Bruce Jancin/MDedge News

“Just imagine who might come knocking on your door,” he said.

Among the most common offenses, according to the OIG, were claims for services outside the limited range currently covered; lack of the requisite HIPAA-compliant two-way audio and visual communication technology with fully encrypted data transmission; services billed by institutional providers not defined by Medicare as telemedicine-eligible; and claims for services received by patients who weren’t located in an officially designated Health Professional Shortage Area or in a rural county as determined by the U.S. Census Bureau.

Telemedicine is no panacea for out-of-control health care costs. A RAND study of participants in the California Public Employees’ Retirement System (CalPERS) concluded that only 12% of beneficiaries who used direct-to-consumer telemedicine did so to replace provider visits. The other 88% added on telemedicine as an additional service. So while telemedicine increased patient access to health care, it also increased the overall cost, observed Dr. Troum, a rheumatologist at the University of Southern California, Los Angeles, and in private practice in Santa Monica, Calif.

Talk to your attorney and malpractice insurer before embarking on telerheumatology. Physicians could potentially lose their medical malpractice insurance if they use telemedicine to treat patients located in states where they aren’t licensed to practice, even if through inadvertent error.

Telemedicine isn’t appropriate for all patients. Nearly a decade ago, rheumatologists at Dartmouth-Hitchcock Medical Center launched a telerheumatology service in order to bring specialty care to the largely rural populations of New Hampshire and Vermont. In a review of the experience that included interviews with both patients and providers, investigators concluded that telerheumatology successfully increased access to specialty care in underserved locations and got good satisfaction scores from both providers and beneficiaries. However, fully 19% of patients were found to be inappropriate for their telerheumatology visit, mainly because their disease was too complex or the underlying diagnosis was unclear.

“Almost one-fifth of their patients were inappropriate for telerheumatology. The question is, how are you supposed to know that ahead of time?” Dr. Troum asked.

Patient satisfaction. Dr. Troum’s reading of the literature on patient satisfaction with telerheumatology, coupled with his own extensive experience in clinical practice, makes him think that many of his younger patients with less disease activity might welcome a telerheumatology option, even with strict time boundaries. But his older patients with more disease activity are a different story.

“Typically my middle-aged and older patients won’t accept that without a lot of convincing,” he commented.

Dr. Wells and Dr. Troum had no relevant disclosures regarding their presentations.

bjancin@mdedge.com

MAUI, HAWAII – Alvin F. Wells, MD, PhD, believes he’s seen the future of rheumatology. So he’s taken a deep dive into telerheumatology, going all in.

Bruce Jancin/MDedge News

“Whether you’re in academic, private, or hospital-based practice, in 2020 if you are not thinking about telerheumatology, you and your practice will not be able to compete with growing patient demands, expectations, and need for clinical monitoring. If you do not have a digital/virtual strategy, you do not have a health care strategy,” he asserted at the 2020 Rheumatology Winter Clinical Symposium.

“Begin now,” the rheumatologist advised.

In pursuit of his own telerheumatology strategy, he holds licenses to practice medicine in five states and has licensure pending in five others.

“My goal is to cover 20% of the U.S., so if the local guys can’t see the patients, I can see them virtually,” he explained. “The days of waiting 4-6 months to be seen by a rheumatologist are gone.”

Rheumatologists are already in short supply in most of the country, and a major shortage looms ahead as older practitioners retire. Telerheumatology can help fill that unmet need. But the specialty is behind the curve. In a survey that rated the medical specialties most engaged in telemedicine, the top three spots were held by radiology, psychiatry, and internal medicine. Rheumatology didn’t even crack the top 10, noted Dr. Wells, director of the Rheumatology and Immunotherapy Center in Franklin, Wisc., and a part-time faculty member at Duke University, the Medical College of Wisconsin, and the Karolinska Institute.

Yet telemedicine is primed for rheumatologic takeoff. Notably, the 2019 update of the American College of Rheumatology recommendations on rheumatoid arthritis disease activity measures incorporates the RAPID3 (Routine Assessment of Patient Index Data) as an endorsed three-question clinical assessment that doesn’t involve a physical exam or laboratory work. The ACR update is recognition that, while every rheumatology patient needs an initial physical exam along with follow-up physical exams at various rates, many patients with well-controlled disease don’t need a physical exam at every physician encounter, he said.

Telerheumatology saves time for both patient and physician. The patient saves travel time, doesn’t miss work, avoids having to arrange for child care in order to make a face-to-face clinic visit, and can schedule more frequent virtual follow-up visits. For the practitioner, telerheumatology means additional consults and – here’s the big one – “You never run behind,” according to Dr. Wells. “For a 15-minute appointment, the patient gets a 5-minute warning, then a 2-minute warning, and at 15 minutes the link is cut. If the fibromyalgia patients want 30 minutes, they pay for 30 minutes.”

He sees the strictly enforced, impersonally delivered electronic time limits as key to running an efficient practice.

“The patients with osteoarthritis who hate the nodules, the fibromyalgia patients because they’re hurting all over, the patients with back pain – you’ve really got to limit those patients because otherwise you’ll be running 30-40 minutes behind for a scheduled 15-minute visit,” he explained.

One rheumatologist’s telemedicine practice

Dr. Wells currently utilizes the Epic electronic health record integrated with a Zoom videoconferencing platform for real-time virtual patient encounters. But he noted that other virtual platforms are available, including Health Tap, American Well, MySpecialistMD, MDLIVE, and TelaDoc. The American Telemedicine Association is a valuable resource for state-by-state medicolegal, reimbursement, and how-to-do-it questions.

At present, he reserves two daily time slots for telerheumatology: one at 8:30-9:00 a.m., the other at 4:30-5:00 p.m. These can be filled with four 15-minute live consults or two 30-minute consults. His goal is to eventually make telerheumatology 20% of his patient load of about 100 patients per week.

His typical 15-minute virtual visit proceeds as follows: It begins with a 3-minute subjective patient assessment, followed by a 5-minute objective assessment which includes the RAPID3, a brief Health Assessment Questionnaire (HAQ) addressing the patient’s pain and overall satisfaction, a virtual joint inspection, the use of high-quality teleultrasound and other technology when warranted, and capture of relevant still photos. This is followed by 5 minutes to relay the treatment plan, and finally a 2-minute recap and summary.

“No niceties. We cut right to the chase,” he noted.

He documents the patient encounter as he goes, dictating his notes throughout the visit.

“When I walk out of the room, I’m done. It’s on to the next patient,” Dr. Wells said.

The reimbursement picture is improving, although major hurdles remain. At present, 48 states and the District of Columbia reimburse for live video telemedicine through Medicaid. And in January 2020, Aetna announced it covers reimbursement for telemedicine in all of its fully insured health plans via the Teladoc platform. Dr. Wells’ patients pay for their telerheumatology out of pocket if their insurance doesn’t cover it.
 

Telemedicine caveats

Dr. Wells shared his telerheumatology experience as the first half of a point/counterpoint session on telemedicine’s future in the specialty. His debate opponent, Orrin M. Troum, MD, announced at the outset that he is quite interested in getting into telerheumatology; however, while looking into it he has come across issues that for now give him pause and that other rheumatologists need to be aware of.

Bruce Jancin/MDedge News

“Just imagine who might come knocking on your door,” he said.

Among the most common offenses, according to the OIG, were claims for services outside the limited range currently covered; lack of the requisite HIPAA-compliant two-way audio and visual communication technology with fully encrypted data transmission; services billed by institutional providers not defined by Medicare as telemedicine-eligible; and claims for services received by patients who weren’t located in an officially designated Health Professional Shortage Area or in a rural county as determined by the U.S. Census Bureau.

Telemedicine is no panacea for out-of-control health care costs. A RAND study of participants in the California Public Employees’ Retirement System (CalPERS) concluded that only 12% of beneficiaries who used direct-to-consumer telemedicine did so to replace provider visits. The other 88% added on telemedicine as an additional service. So while telemedicine increased patient access to health care, it also increased the overall cost, observed Dr. Troum, a rheumatologist at the University of Southern California, Los Angeles, and in private practice in Santa Monica, Calif.

Talk to your attorney and malpractice insurer before embarking on telerheumatology. Physicians could potentially lose their medical malpractice insurance if they use telemedicine to treat patients located in states where they aren’t licensed to practice, even if through inadvertent error.

Telemedicine isn’t appropriate for all patients. Nearly a decade ago, rheumatologists at Dartmouth-Hitchcock Medical Center launched a telerheumatology service in order to bring specialty care to the largely rural populations of New Hampshire and Vermont. In a review of the experience that included interviews with both patients and providers, investigators concluded that telerheumatology successfully increased access to specialty care in underserved locations and got good satisfaction scores from both providers and beneficiaries. However, fully 19% of patients were found to be inappropriate for their telerheumatology visit, mainly because their disease was too complex or the underlying diagnosis was unclear.

“Almost one-fifth of their patients were inappropriate for telerheumatology. The question is, how are you supposed to know that ahead of time?” Dr. Troum asked.

Patient satisfaction. Dr. Troum’s reading of the literature on patient satisfaction with telerheumatology, coupled with his own extensive experience in clinical practice, makes him think that many of his younger patients with less disease activity might welcome a telerheumatology option, even with strict time boundaries. But his older patients with more disease activity are a different story.

“Typically my middle-aged and older patients won’t accept that without a lot of convincing,” he commented.

Dr. Wells and Dr. Troum had no relevant disclosures regarding their presentations.

bjancin@mdedge.com

MAUI, HAWAII – Alvin F. Wells, MD, PhD, believes he’s seen the future of rheumatology. So he’s taken a deep dive into telerheumatology, going all in.

Bruce Jancin/MDedge News

“Whether you’re in academic, private, or hospital-based practice, in 2020 if you are not thinking about telerheumatology, you and your practice will not be able to compete with growing patient demands, expectations, and need for clinical monitoring. If you do not have a digital/virtual strategy, you do not have a health care strategy,” he asserted at the 2020 Rheumatology Winter Clinical Symposium.

“Begin now,” the rheumatologist advised.

In pursuit of his own telerheumatology strategy, he holds licenses to practice medicine in five states and has licensure pending in five others.

“My goal is to cover 20% of the U.S., so if the local guys can’t see the patients, I can see them virtually,” he explained. “The days of waiting 4-6 months to be seen by a rheumatologist are gone.”

Rheumatologists are already in short supply in most of the country, and a major shortage looms ahead as older practitioners retire. Telerheumatology can help fill that unmet need. But the specialty is behind the curve. In a survey that rated the medical specialties most engaged in telemedicine, the top three spots were held by radiology, psychiatry, and internal medicine. Rheumatology didn’t even crack the top 10, noted Dr. Wells, director of the Rheumatology and Immunotherapy Center in Franklin, Wisc., and a part-time faculty member at Duke University, the Medical College of Wisconsin, and the Karolinska Institute.

Yet telemedicine is primed for rheumatologic takeoff. Notably, the 2019 update of the American College of Rheumatology recommendations on rheumatoid arthritis disease activity measures incorporates the RAPID3 (Routine Assessment of Patient Index Data) as an endorsed three-question clinical assessment that doesn’t involve a physical exam or laboratory work. The ACR update is recognition that, while every rheumatology patient needs an initial physical exam along with follow-up physical exams at various rates, many patients with well-controlled disease don’t need a physical exam at every physician encounter, he said.

Telerheumatology saves time for both patient and physician. The patient saves travel time, doesn’t miss work, avoids having to arrange for child care in order to make a face-to-face clinic visit, and can schedule more frequent virtual follow-up visits. For the practitioner, telerheumatology means additional consults and – here’s the big one – “You never run behind,” according to Dr. Wells. “For a 15-minute appointment, the patient gets a 5-minute warning, then a 2-minute warning, and at 15 minutes the link is cut. If the fibromyalgia patients want 30 minutes, they pay for 30 minutes.”

He sees the strictly enforced, impersonally delivered electronic time limits as key to running an efficient practice.

“The patients with osteoarthritis who hate the nodules, the fibromyalgia patients because they’re hurting all over, the patients with back pain – you’ve really got to limit those patients because otherwise you’ll be running 30-40 minutes behind for a scheduled 15-minute visit,” he explained.

One rheumatologist’s telemedicine practice

Dr. Wells currently utilizes the Epic electronic health record integrated with a Zoom videoconferencing platform for real-time virtual patient encounters. But he noted that other virtual platforms are available, including Health Tap, American Well, MySpecialistMD, MDLIVE, and TelaDoc. The American Telemedicine Association is a valuable resource for state-by-state medicolegal, reimbursement, and how-to-do-it questions.

At present, he reserves two daily time slots for telerheumatology: one at 8:30-9:00 a.m., the other at 4:30-5:00 p.m. These can be filled with four 15-minute live consults or two 30-minute consults. His goal is to eventually make telerheumatology 20% of his patient load of about 100 patients per week.

His typical 15-minute virtual visit proceeds as follows: It begins with a 3-minute subjective patient assessment, followed by a 5-minute objective assessment which includes the RAPID3, a brief Health Assessment Questionnaire (HAQ) addressing the patient’s pain and overall satisfaction, a virtual joint inspection, the use of high-quality teleultrasound and other technology when warranted, and capture of relevant still photos. This is followed by 5 minutes to relay the treatment plan, and finally a 2-minute recap and summary.

“No niceties. We cut right to the chase,” he noted.

He documents the patient encounter as he goes, dictating his notes throughout the visit.

“When I walk out of the room, I’m done. It’s on to the next patient,” Dr. Wells said.

The reimbursement picture is improving, although major hurdles remain. At present, 48 states and the District of Columbia reimburse for live video telemedicine through Medicaid. And in January 2020, Aetna announced it covers reimbursement for telemedicine in all of its fully insured health plans via the Teladoc platform. Dr. Wells’ patients pay for their telerheumatology out of pocket if their insurance doesn’t cover it.
 

Telemedicine caveats

Dr. Wells shared his telerheumatology experience as the first half of a point/counterpoint session on telemedicine’s future in the specialty. His debate opponent, Orrin M. Troum, MD, announced at the outset that he is quite interested in getting into telerheumatology; however, while looking into it he has come across issues that for now give him pause and that other rheumatologists need to be aware of.

Bruce Jancin/MDedge News

“Just imagine who might come knocking on your door,” he said.

Among the most common offenses, according to the OIG, were claims for services outside the limited range currently covered; lack of the requisite HIPAA-compliant two-way audio and visual communication technology with fully encrypted data transmission; services billed by institutional providers not defined by Medicare as telemedicine-eligible; and claims for services received by patients who weren’t located in an officially designated Health Professional Shortage Area or in a rural county as determined by the U.S. Census Bureau.

Telemedicine is no panacea for out-of-control health care costs. A RAND study of participants in the California Public Employees’ Retirement System (CalPERS) concluded that only 12% of beneficiaries who used direct-to-consumer telemedicine did so to replace provider visits. The other 88% added on telemedicine as an additional service. So while telemedicine increased patient access to health care, it also increased the overall cost, observed Dr. Troum, a rheumatologist at the University of Southern California, Los Angeles, and in private practice in Santa Monica, Calif.

Talk to your attorney and malpractice insurer before embarking on telerheumatology. Physicians could potentially lose their medical malpractice insurance if they use telemedicine to treat patients located in states where they aren’t licensed to practice, even if through inadvertent error.

Telemedicine isn’t appropriate for all patients. Nearly a decade ago, rheumatologists at Dartmouth-Hitchcock Medical Center launched a telerheumatology service in order to bring specialty care to the largely rural populations of New Hampshire and Vermont. In a review of the experience that included interviews with both patients and providers, investigators concluded that telerheumatology successfully increased access to specialty care in underserved locations and got good satisfaction scores from both providers and beneficiaries. However, fully 19% of patients were found to be inappropriate for their telerheumatology visit, mainly because their disease was too complex or the underlying diagnosis was unclear.

“Almost one-fifth of their patients were inappropriate for telerheumatology. The question is, how are you supposed to know that ahead of time?” Dr. Troum asked.

Patient satisfaction. Dr. Troum’s reading of the literature on patient satisfaction with telerheumatology, coupled with his own extensive experience in clinical practice, makes him think that many of his younger patients with less disease activity might welcome a telerheumatology option, even with strict time boundaries. But his older patients with more disease activity are a different story.

“Typically my middle-aged and older patients won’t accept that without a lot of convincing,” he commented.

Dr. Wells and Dr. Troum had no relevant disclosures regarding their presentations.

bjancin@mdedge.com

LOS ANGELES – When a patient with atrial fibrillation (AFib) has a cardioembolic stroke, the best blood thinner to start may be a direct-acting oral anticoagulant (DOAC), possibly beginning 7-10 days after the index stroke, according to an analysis of 90-day, observational outcomes data from nearly 1,300 patients.

Mitchel L. Zoler/MDedge News

The analysis also suggested that the use of “bridging” anticoagulant treatment by injection before a patient with atrial fibrillation (AFib) starts a daily oral anticoagulant regimen following a cardioembolic stroke is not a good idea. Patients who received bridging anticoagulation had a nearly threefold higher rate of symptomatic intracranial hemorrhage than did patients who did not, and their bridging treatment failed to protect them from recurrent ischemic events, Shadi Yaghi, MD, said at the International Stroke Conference, sponsored by the American Heart Association. The bridging regimens delivered either heparin or low-molecular-weight heparin.

Based on the findings, “it seems reasonable to avoid bridging unless absolutely necessary, to initiate a DOAC unless it’s contraindicated, and to start the DOAC on day 7-10 following the stroke in most patients,” said Dr. Yaghi, a vascular neurologist and director of stroke research at NYU Langone Health in New York.

“It’s been hard to develop a broad guideline on when to start oral anticoagulation” after a cardioembolic stroke in AFib patients. The best time “depends on a lot of variables and how the patient responded to acute treatment,” commented Alexis Simpkins, MD, a vascular and stroke neurologist at the University of Florida in Gainesville. “You want to start treatment before the patient has another stroke, but not so soon that the treatment causes symptomatic hemorrhagic transformation.”

Dr. Yaghi’s suggestion, based on his findings, to start treatment for most patients with a DOAC 7-10 days after their index stroke “shows consistency” with the prevailing guideline recommendation from the AHA/American Stroke Association to start oral anticoagulation in this patient population 4-14 days after the index stroke (Stroke. 2018 March;49[3]:e46-e99), she noted.

A recent article reviewed the uncertainty about the best time to start oral anticoagulation in AFib patients after a cardioembolic stroke and the subtle differences that distinguish various international medical groups that, like the ASA, have made recommendations (Lancet Neurol. 2019 Jan 1;18[1]:117-26). According to this review, a major limitation of these various recommendations has been the lack of actual evidence collected from AFib patients who began receiving a DOAC shortly after a cardioembolic stroke, although the article added that several studies in progress are collecting these data.

The study reported by Dr. Yaghi pooled data collected from 2,084 recent AFib patients with a cardioembolic stroke treated at any of eight comprehensive U.S. stroke centers. They excluded patients who died from causes unrelated to the primary endpoint, those who did not receive an anticoagulant or had incomplete data, and patients lost to follow-up, leaving 1,289 evaluable patients. During their 90-day follow-up, 10% of the patients had an ischemic event, a symptomatic intracranial hemorrhage, or an extracranial hemorrhage.

The study’s primary analysis showed no statistically significant difference in the incidence of recurrent ischemic events, symptomatic intracranial hemorrhage, or both based on when oral anticoagulant treatment began: 0-3 days, 4-14 days, or more than 14 days after the index stroke.

The investigators then subdivided patients into the subgroup that started treatment with a DOAC and the subgroup that started treatment with warfarin and also further subdivided the 4-14 day time window for starting treatment. Results of this analysis showed that patients who received a DOAC and began this treatment 7-10 days after their stroke had a 50% cut in their 90-day events compared with other patients, a difference that fell just short of statistical significance at P = .07. All the other combinations of oral anticoagulant and time of treatment initiation analyzed showed neutral effects that never came near statistical significance.

Secondary data analyses also showed that both patients with a history of a stroke prior to their index stroke and patients with ipsilateral atherosclerosis came close to having a statistically significant increased rate of a subsequent ischemic event during 90-day follow-up. Furthermore, women, patients with a history of hyperlipidemia, and patients who developed hemorrhagic transformation of their index stroke all had significantly increased rates of developing a symptomatic intracranial hemorrhage during 90-day follow-up. When the endpoint was limited to recurrent ischemic events only, patients who received a DOAC were 50% less likely to have an event than were patients treated with warfarin, a statistically significant difference.

Although starting a DOAC 7-10 days after the index stroke seems reasonable based on this analysis, the question needs a prospective, randomized study to create an appropriate evidence base, Dr. Yaghi said.

Dr. Yaghi disclosed a financial relationship with Medtronic. Dr. Simpkins had no disclosures.

mzoler@mdedge.com

SOURCE: Yaghi S et al. Stroke. 2020 Feb;51(suppl 1):A119.

LOS ANGELES – When a patient with atrial fibrillation (AFib) has a cardioembolic stroke, the best blood thinner to start may be a direct-acting oral anticoagulant (DOAC), possibly beginning 7-10 days after the index stroke, according to an analysis of 90-day, observational outcomes data from nearly 1,300 patients.

Mitchel L. Zoler/MDedge News

The analysis also suggested that the use of “bridging” anticoagulant treatment by injection before a patient with atrial fibrillation (AFib) starts a daily oral anticoagulant regimen following a cardioembolic stroke is not a good idea. Patients who received bridging anticoagulation had a nearly threefold higher rate of symptomatic intracranial hemorrhage than did patients who did not, and their bridging treatment failed to protect them from recurrent ischemic events, Shadi Yaghi, MD, said at the International Stroke Conference, sponsored by the American Heart Association. The bridging regimens delivered either heparin or low-molecular-weight heparin.

Based on the findings, “it seems reasonable to avoid bridging unless absolutely necessary, to initiate a DOAC unless it’s contraindicated, and to start the DOAC on day 7-10 following the stroke in most patients,” said Dr. Yaghi, a vascular neurologist and director of stroke research at NYU Langone Health in New York.

“It’s been hard to develop a broad guideline on when to start oral anticoagulation” after a cardioembolic stroke in AFib patients. The best time “depends on a lot of variables and how the patient responded to acute treatment,” commented Alexis Simpkins, MD, a vascular and stroke neurologist at the University of Florida in Gainesville. “You want to start treatment before the patient has another stroke, but not so soon that the treatment causes symptomatic hemorrhagic transformation.”

Dr. Yaghi’s suggestion, based on his findings, to start treatment for most patients with a DOAC 7-10 days after their index stroke “shows consistency” with the prevailing guideline recommendation from the AHA/American Stroke Association to start oral anticoagulation in this patient population 4-14 days after the index stroke (Stroke. 2018 March;49[3]:e46-e99), she noted.

A recent article reviewed the uncertainty about the best time to start oral anticoagulation in AFib patients after a cardioembolic stroke and the subtle differences that distinguish various international medical groups that, like the ASA, have made recommendations (Lancet Neurol. 2019 Jan 1;18[1]:117-26). According to this review, a major limitation of these various recommendations has been the lack of actual evidence collected from AFib patients who began receiving a DOAC shortly after a cardioembolic stroke, although the article added that several studies in progress are collecting these data.

The study reported by Dr. Yaghi pooled data collected from 2,084 recent AFib patients with a cardioembolic stroke treated at any of eight comprehensive U.S. stroke centers. They excluded patients who died from causes unrelated to the primary endpoint, those who did not receive an anticoagulant or had incomplete data, and patients lost to follow-up, leaving 1,289 evaluable patients. During their 90-day follow-up, 10% of the patients had an ischemic event, a symptomatic intracranial hemorrhage, or an extracranial hemorrhage.

The study’s primary analysis showed no statistically significant difference in the incidence of recurrent ischemic events, symptomatic intracranial hemorrhage, or both based on when oral anticoagulant treatment began: 0-3 days, 4-14 days, or more than 14 days after the index stroke.

The investigators then subdivided patients into the subgroup that started treatment with a DOAC and the subgroup that started treatment with warfarin and also further subdivided the 4-14 day time window for starting treatment. Results of this analysis showed that patients who received a DOAC and began this treatment 7-10 days after their stroke had a 50% cut in their 90-day events compared with other patients, a difference that fell just short of statistical significance at P = .07. All the other combinations of oral anticoagulant and time of treatment initiation analyzed showed neutral effects that never came near statistical significance.

Secondary data analyses also showed that both patients with a history of a stroke prior to their index stroke and patients with ipsilateral atherosclerosis came close to having a statistically significant increased rate of a subsequent ischemic event during 90-day follow-up. Furthermore, women, patients with a history of hyperlipidemia, and patients who developed hemorrhagic transformation of their index stroke all had significantly increased rates of developing a symptomatic intracranial hemorrhage during 90-day follow-up. When the endpoint was limited to recurrent ischemic events only, patients who received a DOAC were 50% less likely to have an event than were patients treated with warfarin, a statistically significant difference.

Although starting a DOAC 7-10 days after the index stroke seems reasonable based on this analysis, the question needs a prospective, randomized study to create an appropriate evidence base, Dr. Yaghi said.

Dr. Yaghi disclosed a financial relationship with Medtronic. Dr. Simpkins had no disclosures.

mzoler@mdedge.com

SOURCE: Yaghi S et al. Stroke. 2020 Feb;51(suppl 1):A119.

LOS ANGELES – When a patient with atrial fibrillation (AFib) has a cardioembolic stroke, the best blood thinner to start may be a direct-acting oral anticoagulant (DOAC), possibly beginning 7-10 days after the index stroke, according to an analysis of 90-day, observational outcomes data from nearly 1,300 patients.

Mitchel L. Zoler/MDedge News

The analysis also suggested that the use of “bridging” anticoagulant treatment by injection before a patient with atrial fibrillation (AFib) starts a daily oral anticoagulant regimen following a cardioembolic stroke is not a good idea. Patients who received bridging anticoagulation had a nearly threefold higher rate of symptomatic intracranial hemorrhage than did patients who did not, and their bridging treatment failed to protect them from recurrent ischemic events, Shadi Yaghi, MD, said at the International Stroke Conference, sponsored by the American Heart Association. The bridging regimens delivered either heparin or low-molecular-weight heparin.

Based on the findings, “it seems reasonable to avoid bridging unless absolutely necessary, to initiate a DOAC unless it’s contraindicated, and to start the DOAC on day 7-10 following the stroke in most patients,” said Dr. Yaghi, a vascular neurologist and director of stroke research at NYU Langone Health in New York.

“It’s been hard to develop a broad guideline on when to start oral anticoagulation” after a cardioembolic stroke in AFib patients. The best time “depends on a lot of variables and how the patient responded to acute treatment,” commented Alexis Simpkins, MD, a vascular and stroke neurologist at the University of Florida in Gainesville. “You want to start treatment before the patient has another stroke, but not so soon that the treatment causes symptomatic hemorrhagic transformation.”

Dr. Yaghi’s suggestion, based on his findings, to start treatment for most patients with a DOAC 7-10 days after their index stroke “shows consistency” with the prevailing guideline recommendation from the AHA/American Stroke Association to start oral anticoagulation in this patient population 4-14 days after the index stroke (Stroke. 2018 March;49[3]:e46-e99), she noted.

A recent article reviewed the uncertainty about the best time to start oral anticoagulation in AFib patients after a cardioembolic stroke and the subtle differences that distinguish various international medical groups that, like the ASA, have made recommendations (Lancet Neurol. 2019 Jan 1;18[1]:117-26). According to this review, a major limitation of these various recommendations has been the lack of actual evidence collected from AFib patients who began receiving a DOAC shortly after a cardioembolic stroke, although the article added that several studies in progress are collecting these data.

The study reported by Dr. Yaghi pooled data collected from 2,084 recent AFib patients with a cardioembolic stroke treated at any of eight comprehensive U.S. stroke centers. They excluded patients who died from causes unrelated to the primary endpoint, those who did not receive an anticoagulant or had incomplete data, and patients lost to follow-up, leaving 1,289 evaluable patients. During their 90-day follow-up, 10% of the patients had an ischemic event, a symptomatic intracranial hemorrhage, or an extracranial hemorrhage.

The study’s primary analysis showed no statistically significant difference in the incidence of recurrent ischemic events, symptomatic intracranial hemorrhage, or both based on when oral anticoagulant treatment began: 0-3 days, 4-14 days, or more than 14 days after the index stroke.

The investigators then subdivided patients into the subgroup that started treatment with a DOAC and the subgroup that started treatment with warfarin and also further subdivided the 4-14 day time window for starting treatment. Results of this analysis showed that patients who received a DOAC and began this treatment 7-10 days after their stroke had a 50% cut in their 90-day events compared with other patients, a difference that fell just short of statistical significance at P = .07. All the other combinations of oral anticoagulant and time of treatment initiation analyzed showed neutral effects that never came near statistical significance.

Secondary data analyses also showed that both patients with a history of a stroke prior to their index stroke and patients with ipsilateral atherosclerosis came close to having a statistically significant increased rate of a subsequent ischemic event during 90-day follow-up. Furthermore, women, patients with a history of hyperlipidemia, and patients who developed hemorrhagic transformation of their index stroke all had significantly increased rates of developing a symptomatic intracranial hemorrhage during 90-day follow-up. When the endpoint was limited to recurrent ischemic events only, patients who received a DOAC were 50% less likely to have an event than were patients treated with warfarin, a statistically significant difference.

Although starting a DOAC 7-10 days after the index stroke seems reasonable based on this analysis, the question needs a prospective, randomized study to create an appropriate evidence base, Dr. Yaghi said.

Dr. Yaghi disclosed a financial relationship with Medtronic. Dr. Simpkins had no disclosures.

mzoler@mdedge.com

SOURCE: Yaghi S et al. Stroke. 2020 Feb;51(suppl 1):A119.