Pediatrics

Positive immunogenicity results and lack of adverse events with receipt of the 13-valent pneumococcal conjugate vaccine by 200 children and adolescents in India supports extension of the indication to that population, reported Sharad Agarkhedkar, MD, of the Padmashree Dr. D. Y. Patil Medical College in Pune, India, and associates.

In India, the PCV13 vaccine is indicated for children aged 6 months to 5 years and for adults older than 50 years. The study assessed the safety and immunogenicity of the vaccine in children aged 6-17 years to consider expanding the indication to that age group, the investigators said.

DesignPics/Thinkstock

Positive immunogenicity results and lack of adverse events with receipt of the 13-valent pneumococcal conjugate vaccine by 200 children and adolescents in India supports extension of the indication to that population, reported Sharad Agarkhedkar, MD, of the Padmashree Dr. D. Y. Patil Medical College in Pune, India, and associates.

In India, the PCV13 vaccine is indicated for children aged 6 months to 5 years and for adults older than 50 years. The study assessed the safety and immunogenicity of the vaccine in children aged 6-17 years to consider expanding the indication to that age group, the investigators said.

DesignPics/Thinkstock

Positive immunogenicity results and lack of adverse events with receipt of the 13-valent pneumococcal conjugate vaccine by 200 children and adolescents in India supports extension of the indication to that population, reported Sharad Agarkhedkar, MD, of the Padmashree Dr. D. Y. Patil Medical College in Pune, India, and associates.

In India, the PCV13 vaccine is indicated for children aged 6 months to 5 years and for adults older than 50 years. The study assessed the safety and immunogenicity of the vaccine in children aged 6-17 years to consider expanding the indication to that age group, the investigators said.

DesignPics/Thinkstock

The miniaturization of continuous-flow ventricular assist devices has launched the era of continuous-flow VAD support in pediatric patients, and the trend may accelerate with the introduction of a continuous-flow device designed specifically for small children. In an expert opinion in the Journal of Thoracic and Cardiovascular Surgery, Iki Adachi, MD, of Baylor College of Medicine in Houston, said the emerging science of continuous-flow VADs in children promises to solve problems like device size mismatch, hospital-only VADs, and chronic therapy (J Thorac Cardiovasc Surg. 2017 Oct;154:1358-61). “With ongoing device miniaturization, enthusiasm has been growing among pediatric physicians for the use of continuous-flow VADs in children,” Dr. Adachi said. He noted the introduction of a continuous-flow device for small children, the Infant Jarvik 2015, “may further accelerate the trend.”

Dr. Adachi cited PediMACS reports that stated that more than half of the long-term devices now registered are continuous-flow devices, and that continuous-flow VADs comprised 62% of all durable VAD implants in the third quarter of 2016. “With the encouraging results recorded to date, the use of continuous-flow devices in the pediatric population is rapidly increasing,” he said.

Miniaturization has addressed the problem of size mismatch when using continuous-flow VAD devices in children, he said, noting that use of the Infant Jarvik device may be expanded even further to children as small at 8 kg or less. The PumpKIN trial(Pumps for Kids, Infants, and Neonates), which is evaluating the Infant Jarvik 2015 vs. the Berlin Heart EXCOR, could provide answers on the feasibility of continuous-flow VADs in small children.

“Based on experience with the chronic animal model, I believe that the Infant Jarvik device will properly fit the patients included in the trial,” he said.

Continuous-flow VAD in children also holds potential for managing these patients outside the hospital setting. “Outpatient management of children with continuous-flow VADs has been shown to be feasible,” he said, adding that the PediMACS registry has reported that only 45% of patients have been managed this way. “Nonetheless, with maturation of the pediatric field, outpatient management will become routine rather than the exception,” he said.

Greater use of continuous-flow VADs also may create opportunities to improve the status and suitability for transplantation of children with severe heart failure, he said. He gave as an example his group’s practice at Houston’s Texas Children’s Hospital, which is to deactivate patients on the transplant wait list for 3 months once they start continuous-flow VAD support. “A postoperative ‘grace period’ affords protected opportunities for both physical and psychological recovery,” he said. This timeout of sorts also affords the care team time to assess the myocardium for possible functional recovery.

In patients who are not good candidates for transplantation, durable continuous-flow VADs may provide chronic therapy, and in time, these patients may become suitable transplant candidates, said Dr. Adachi. “Bypassing such an unfavorable period for transplantation with prolonged VAD support may be a reasonable approach,” he said.

Patients with failing single-ventricle circulation also may benefit from VAD support, although the challenges facing this population are more profound than in other groups, Dr. Adachi said. VAD support for single-ventricle disease is sparse, but these patients require careful evaluation of the nature of their condition. “If systolic dysfunction is the predominant cause of circulatory failure, then VAD support for the failing systemic ventricle will likely improve hemodynamics,” said Dr. Adachi. VAD support also could help the patient move through the various stages of palliation.

“Again, the emphasis is not just on simply keeping the patient alive until a donor organ becomes available; rather, attention is refocused on overall health beyond survival, which may eventually affect transplantation candidacy and even post transplantation outcome,” Dr. Adachi concluded.

Dr. Adachi serves as a consultant and proctor for Berlin Heart and HeartWare, and as a consultant for the New England Research Institute related to the PumpKIN trial.
 

The miniaturization of continuous-flow ventricular assist devices has launched the era of continuous-flow VAD support in pediatric patients, and the trend may accelerate with the introduction of a continuous-flow device designed specifically for small children. In an expert opinion in the Journal of Thoracic and Cardiovascular Surgery, Iki Adachi, MD, of Baylor College of Medicine in Houston, said the emerging science of continuous-flow VADs in children promises to solve problems like device size mismatch, hospital-only VADs, and chronic therapy (J Thorac Cardiovasc Surg. 2017 Oct;154:1358-61). “With ongoing device miniaturization, enthusiasm has been growing among pediatric physicians for the use of continuous-flow VADs in children,” Dr. Adachi said. He noted the introduction of a continuous-flow device for small children, the Infant Jarvik 2015, “may further accelerate the trend.”

Dr. Adachi cited PediMACS reports that stated that more than half of the long-term devices now registered are continuous-flow devices, and that continuous-flow VADs comprised 62% of all durable VAD implants in the third quarter of 2016. “With the encouraging results recorded to date, the use of continuous-flow devices in the pediatric population is rapidly increasing,” he said.

Miniaturization has addressed the problem of size mismatch when using continuous-flow VAD devices in children, he said, noting that use of the Infant Jarvik device may be expanded even further to children as small at 8 kg or less. The PumpKIN trial(Pumps for Kids, Infants, and Neonates), which is evaluating the Infant Jarvik 2015 vs. the Berlin Heart EXCOR, could provide answers on the feasibility of continuous-flow VADs in small children.

“Based on experience with the chronic animal model, I believe that the Infant Jarvik device will properly fit the patients included in the trial,” he said.

Continuous-flow VAD in children also holds potential for managing these patients outside the hospital setting. “Outpatient management of children with continuous-flow VADs has been shown to be feasible,” he said, adding that the PediMACS registry has reported that only 45% of patients have been managed this way. “Nonetheless, with maturation of the pediatric field, outpatient management will become routine rather than the exception,” he said.

Greater use of continuous-flow VADs also may create opportunities to improve the status and suitability for transplantation of children with severe heart failure, he said. He gave as an example his group’s practice at Houston’s Texas Children’s Hospital, which is to deactivate patients on the transplant wait list for 3 months once they start continuous-flow VAD support. “A postoperative ‘grace period’ affords protected opportunities for both physical and psychological recovery,” he said. This timeout of sorts also affords the care team time to assess the myocardium for possible functional recovery.

In patients who are not good candidates for transplantation, durable continuous-flow VADs may provide chronic therapy, and in time, these patients may become suitable transplant candidates, said Dr. Adachi. “Bypassing such an unfavorable period for transplantation with prolonged VAD support may be a reasonable approach,” he said.

Patients with failing single-ventricle circulation also may benefit from VAD support, although the challenges facing this population are more profound than in other groups, Dr. Adachi said. VAD support for single-ventricle disease is sparse, but these patients require careful evaluation of the nature of their condition. “If systolic dysfunction is the predominant cause of circulatory failure, then VAD support for the failing systemic ventricle will likely improve hemodynamics,” said Dr. Adachi. VAD support also could help the patient move through the various stages of palliation.

“Again, the emphasis is not just on simply keeping the patient alive until a donor organ becomes available; rather, attention is refocused on overall health beyond survival, which may eventually affect transplantation candidacy and even post transplantation outcome,” Dr. Adachi concluded.

Dr. Adachi serves as a consultant and proctor for Berlin Heart and HeartWare, and as a consultant for the New England Research Institute related to the PumpKIN trial.
 

The miniaturization of continuous-flow ventricular assist devices has launched the era of continuous-flow VAD support in pediatric patients, and the trend may accelerate with the introduction of a continuous-flow device designed specifically for small children. In an expert opinion in the Journal of Thoracic and Cardiovascular Surgery, Iki Adachi, MD, of Baylor College of Medicine in Houston, said the emerging science of continuous-flow VADs in children promises to solve problems like device size mismatch, hospital-only VADs, and chronic therapy (J Thorac Cardiovasc Surg. 2017 Oct;154:1358-61). “With ongoing device miniaturization, enthusiasm has been growing among pediatric physicians for the use of continuous-flow VADs in children,” Dr. Adachi said. He noted the introduction of a continuous-flow device for small children, the Infant Jarvik 2015, “may further accelerate the trend.”

Dr. Adachi cited PediMACS reports that stated that more than half of the long-term devices now registered are continuous-flow devices, and that continuous-flow VADs comprised 62% of all durable VAD implants in the third quarter of 2016. “With the encouraging results recorded to date, the use of continuous-flow devices in the pediatric population is rapidly increasing,” he said.

Miniaturization has addressed the problem of size mismatch when using continuous-flow VAD devices in children, he said, noting that use of the Infant Jarvik device may be expanded even further to children as small at 8 kg or less. The PumpKIN trial(Pumps for Kids, Infants, and Neonates), which is evaluating the Infant Jarvik 2015 vs. the Berlin Heart EXCOR, could provide answers on the feasibility of continuous-flow VADs in small children.

“Based on experience with the chronic animal model, I believe that the Infant Jarvik device will properly fit the patients included in the trial,” he said.

Continuous-flow VAD in children also holds potential for managing these patients outside the hospital setting. “Outpatient management of children with continuous-flow VADs has been shown to be feasible,” he said, adding that the PediMACS registry has reported that only 45% of patients have been managed this way. “Nonetheless, with maturation of the pediatric field, outpatient management will become routine rather than the exception,” he said.

Greater use of continuous-flow VADs also may create opportunities to improve the status and suitability for transplantation of children with severe heart failure, he said. He gave as an example his group’s practice at Houston’s Texas Children’s Hospital, which is to deactivate patients on the transplant wait list for 3 months once they start continuous-flow VAD support. “A postoperative ‘grace period’ affords protected opportunities for both physical and psychological recovery,” he said. This timeout of sorts also affords the care team time to assess the myocardium for possible functional recovery.

In patients who are not good candidates for transplantation, durable continuous-flow VADs may provide chronic therapy, and in time, these patients may become suitable transplant candidates, said Dr. Adachi. “Bypassing such an unfavorable period for transplantation with prolonged VAD support may be a reasonable approach,” he said.

Patients with failing single-ventricle circulation also may benefit from VAD support, although the challenges facing this population are more profound than in other groups, Dr. Adachi said. VAD support for single-ventricle disease is sparse, but these patients require careful evaluation of the nature of their condition. “If systolic dysfunction is the predominant cause of circulatory failure, then VAD support for the failing systemic ventricle will likely improve hemodynamics,” said Dr. Adachi. VAD support also could help the patient move through the various stages of palliation.

“Again, the emphasis is not just on simply keeping the patient alive until a donor organ becomes available; rather, attention is refocused on overall health beyond survival, which may eventually affect transplantation candidacy and even post transplantation outcome,” Dr. Adachi concluded.

Dr. Adachi serves as a consultant and proctor for Berlin Heart and HeartWare, and as a consultant for the New England Research Institute related to the PumpKIN trial.
 

Whether children in Minnesota were up to date on vaccinations from 2 months of age to 36 months depended on if their parents were born in the United States or outside the United States, and, more particularly, on the country of origin of their mother, reported Maureen Leeds and Miriam Halstead Muscoplat of the Minnesota Department of Health, St. Paul.

In a study of 97,885 Minnesota children born during 2011-2012, fewer than half were up to date with their vaccinations by age 18 months and only 70% were up to date by age 36 months.

luiscar/Thinkstock

cnellist@frontlinemedcom.com
 

Whether children in Minnesota were up to date on vaccinations from 2 months of age to 36 months depended on if their parents were born in the United States or outside the United States, and, more particularly, on the country of origin of their mother, reported Maureen Leeds and Miriam Halstead Muscoplat of the Minnesota Department of Health, St. Paul.

In a study of 97,885 Minnesota children born during 2011-2012, fewer than half were up to date with their vaccinations by age 18 months and only 70% were up to date by age 36 months.

luiscar/Thinkstock

cnellist@frontlinemedcom.com
 

Whether children in Minnesota were up to date on vaccinations from 2 months of age to 36 months depended on if their parents were born in the United States or outside the United States, and, more particularly, on the country of origin of their mother, reported Maureen Leeds and Miriam Halstead Muscoplat of the Minnesota Department of Health, St. Paul.

In a study of 97,885 Minnesota children born during 2011-2012, fewer than half were up to date with their vaccinations by age 18 months and only 70% were up to date by age 36 months.

luiscar/Thinkstock

cnellist@frontlinemedcom.com
 

Urinary tract infection (UTI) is one of the most common bacterial infections in young febrile infants, but doctors know that collecting a urine sample to diagnose or exclude UTI can be very challenging in practice.

Recently, researchers in Australia conducted a randomized controlled trial in a pediatric hospital emergency department to test a method that could stimulate voiding within 5 minutes. It’s called the Quick-Wee method, and the technique involves the clinician rubbing the suprapubic area of the child in a circular pattern with gauze soaked in cold saline held with disposable plastic forceps. In the trial, this was done until the sample was obtained or until 5 minutes passed.

Petro Feketa/iStockphoto

Reference

Kaufman J, Fitzpatrick P, Tosif S, et al. Faster clean catch urine collection (Quick-Wee method) from infants: randomised controlled trial. BMJ 2017;357:j1341. doi: 10.1136/bmj.j1341. Accessed June 12, 2017.

Urinary tract infection (UTI) is one of the most common bacterial infections in young febrile infants, but doctors know that collecting a urine sample to diagnose or exclude UTI can be very challenging in practice.

Recently, researchers in Australia conducted a randomized controlled trial in a pediatric hospital emergency department to test a method that could stimulate voiding within 5 minutes. It’s called the Quick-Wee method, and the technique involves the clinician rubbing the suprapubic area of the child in a circular pattern with gauze soaked in cold saline held with disposable plastic forceps. In the trial, this was done until the sample was obtained or until 5 minutes passed.

Petro Feketa/iStockphoto

Reference

Kaufman J, Fitzpatrick P, Tosif S, et al. Faster clean catch urine collection (Quick-Wee method) from infants: randomised controlled trial. BMJ 2017;357:j1341. doi: 10.1136/bmj.j1341. Accessed June 12, 2017.

Urinary tract infection (UTI) is one of the most common bacterial infections in young febrile infants, but doctors know that collecting a urine sample to diagnose or exclude UTI can be very challenging in practice.

Recently, researchers in Australia conducted a randomized controlled trial in a pediatric hospital emergency department to test a method that could stimulate voiding within 5 minutes. It’s called the Quick-Wee method, and the technique involves the clinician rubbing the suprapubic area of the child in a circular pattern with gauze soaked in cold saline held with disposable plastic forceps. In the trial, this was done until the sample was obtained or until 5 minutes passed.

Petro Feketa/iStockphoto

Reference

Kaufman J, Fitzpatrick P, Tosif S, et al. Faster clean catch urine collection (Quick-Wee method) from infants: randomised controlled trial. BMJ 2017;357:j1341. doi: 10.1136/bmj.j1341. Accessed June 12, 2017.

Varicella-zoster virus (VZV) is a neurotropic human herpesvirus that causes varicella (chicken pox) and herpes zoster (shingles). During infection, the virus invades the dorsal root ganglia and establishes permanent latency. It can later reactivate and travel through sensory nerves to the skin where localized viral replication causes herpes zoster (HZ), which manifests with pain in a unilateral dermatomal distribution followed closely by an eruption of grouped macules and papules that evolve into vesicles on an erythematous base.¹ These lesions form pustules and crusts over 7 to 10 days and heal completely within 4 weeks. Although postherpetic neuralgia is rare in children, the pain associated with HZ can last months or years.^1,2

Universal childhood vaccination against VZV has existed in the United States since 1995, with a 2-dose vaccine regimen recommended by the CDC since 2007. Consequently, primary varicella infection in children is uncommon, and the majority of cases now occur in the vaccinated population.³ However, breakthrough varicella infection and postvaccination HZ are rare due to the long-lasting immunity and low virulence of the attenuated vaccine strain. We recount the case of a 6-year-old vaccinated girl with a unique presentation of HZ with no known primary varicella infection.

Case Report

A healthy 6-year-old girl presented with a stabbing burning pain in the left thigh extending down the calf of 4 days’ duration. The intense pain made walking difficult and responded minimally to ibuprofen and naproxen. Poor appetite, nausea, colicky abdominal pain, and fever (temperature, 38°C) accompanied the pain. Three days after the pain began she developed a pruritic rash on the same leg. Notably, she reported falling on a rosebush and sustaining a thorn prick in the left thigh 3 days prior to the onset of pain. Before presenting to our dermatology clinic, she was seen by a pediatrician, an emergency department physician, and an infectious disease specialist. The initial workup included a complete blood cell count, C-reactive protein test, erythrocyte sedimentation rate test, and hip and femur radiograph, which were all unremarkable. She was referred to dermatology with a differential diagnosis of sporotrichosis, contact dermatitis, reactive arthritis, viral myalgia, and Legg-Calvé-Perthes disease.

Physical examination revealed a well-appearing child with pink eczematous patches and plaques extending from the left side of the lower back to the mid shin in an L5 distribution (Figure). The left thigh was tender to palpation, and nontender left inguinal lymphadenopathy was present. A single isolated 2-mm vesicle was found on the anterior aspect of the left lower leg. Direct fluorescent antibody testing of vesicle fluid was positive for VZV antigen, confirming the diagnosis of HZ.

Comment

Herpes zoster is rare in young healthy children, and its incidence has decreased since the introduction of universal varicella vaccination.⁴ Reported incidence rates in vaccinated children vary from approximately 15 to 93 per 100,000 person-years,^5,6 and the reported relative risk is 0.08 to 0.36 in vaccinated compared to unvaccinated children.^6,7 No correlations with gender, race, or ethnicity and postvaccination HZ have been observed.^5,8 Reported intervals between vaccination and HZ presentation are as short as 3 months and as long as 11 years.⁹ Although HZ is uncommon in immunocompetent children, the diagnosis of HZ itself is not an indication for formal workup for an underlying immunodeficiency or malignancy.¹⁰

Both wild-type and vaccine-strain VZV establish latent infection and can cause HZ in vaccinated children. Direct fluorescent antibody testing or polymerase chain reaction of HZ lesions can be used to identify VZV. Genotyping can distinguish the wild-type versus the vaccine strain but is not required for clinical management.³ In previously vaccinated children with HZ, approximately half present with wild-type and half with vaccine-strain VZV. In approximately half of wild-type cases, prior clinical varicella infection also occurred.⁸

Regardless of virus strain, vaccinated children typically present with the characteristic painful, vesicular, dermatomal HZ rash.^8,9 This presentation can be milder with less pain and fewer vesicles than with unvaccinated cases.⁶ When vaccine-strain HZ occurs, the rash often presents at or near the site of initial vaccination, which typically is the arm or thigh.^3,4,6,9 The vaccine strain has lower virulence than the wild-type virus. Eight cases of vaccine-strain zoster severe enough to cause neurological complications such as meningitis or encephalitis have been reported in children, with 6 cases reported in healthy children.^9,11-17 Antiviral drugs hasten the healing of the HZ rash and shorten the duration of associated pain.¹

Although pediatric HZ is uncommon, all physicians should be aware of possible atypical presentations in healthy vaccinated children to appropriately and quickly manage treatment.

Varicella-zoster virus (VZV) is a neurotropic human herpesvirus that causes varicella (chicken pox) and herpes zoster (shingles). During infection, the virus invades the dorsal root ganglia and establishes permanent latency. It can later reactivate and travel through sensory nerves to the skin where localized viral replication causes herpes zoster (HZ), which manifests with pain in a unilateral dermatomal distribution followed closely by an eruption of grouped macules and papules that evolve into vesicles on an erythematous base.¹ These lesions form pustules and crusts over 7 to 10 days and heal completely within 4 weeks. Although postherpetic neuralgia is rare in children, the pain associated with HZ can last months or years.^1,2

Universal childhood vaccination against VZV has existed in the United States since 1995, with a 2-dose vaccine regimen recommended by the CDC since 2007. Consequently, primary varicella infection in children is uncommon, and the majority of cases now occur in the vaccinated population.³ However, breakthrough varicella infection and postvaccination HZ are rare due to the long-lasting immunity and low virulence of the attenuated vaccine strain. We recount the case of a 6-year-old vaccinated girl with a unique presentation of HZ with no known primary varicella infection.

Case Report

A healthy 6-year-old girl presented with a stabbing burning pain in the left thigh extending down the calf of 4 days’ duration. The intense pain made walking difficult and responded minimally to ibuprofen and naproxen. Poor appetite, nausea, colicky abdominal pain, and fever (temperature, 38°C) accompanied the pain. Three days after the pain began she developed a pruritic rash on the same leg. Notably, she reported falling on a rosebush and sustaining a thorn prick in the left thigh 3 days prior to the onset of pain. Before presenting to our dermatology clinic, she was seen by a pediatrician, an emergency department physician, and an infectious disease specialist. The initial workup included a complete blood cell count, C-reactive protein test, erythrocyte sedimentation rate test, and hip and femur radiograph, which were all unremarkable. She was referred to dermatology with a differential diagnosis of sporotrichosis, contact dermatitis, reactive arthritis, viral myalgia, and Legg-Calvé-Perthes disease.

Physical examination revealed a well-appearing child with pink eczematous patches and plaques extending from the left side of the lower back to the mid shin in an L5 distribution (Figure). The left thigh was tender to palpation, and nontender left inguinal lymphadenopathy was present. A single isolated 2-mm vesicle was found on the anterior aspect of the left lower leg. Direct fluorescent antibody testing of vesicle fluid was positive for VZV antigen, confirming the diagnosis of HZ.

Comment

Herpes zoster is rare in young healthy children, and its incidence has decreased since the introduction of universal varicella vaccination.⁴ Reported incidence rates in vaccinated children vary from approximately 15 to 93 per 100,000 person-years,^5,6 and the reported relative risk is 0.08 to 0.36 in vaccinated compared to unvaccinated children.^6,7 No correlations with gender, race, or ethnicity and postvaccination HZ have been observed.^5,8 Reported intervals between vaccination and HZ presentation are as short as 3 months and as long as 11 years.⁹ Although HZ is uncommon in immunocompetent children, the diagnosis of HZ itself is not an indication for formal workup for an underlying immunodeficiency or malignancy.¹⁰

Both wild-type and vaccine-strain VZV establish latent infection and can cause HZ in vaccinated children. Direct fluorescent antibody testing or polymerase chain reaction of HZ lesions can be used to identify VZV. Genotyping can distinguish the wild-type versus the vaccine strain but is not required for clinical management.³ In previously vaccinated children with HZ, approximately half present with wild-type and half with vaccine-strain VZV. In approximately half of wild-type cases, prior clinical varicella infection also occurred.⁸

Regardless of virus strain, vaccinated children typically present with the characteristic painful, vesicular, dermatomal HZ rash.^8,9 This presentation can be milder with less pain and fewer vesicles than with unvaccinated cases.⁶ When vaccine-strain HZ occurs, the rash often presents at or near the site of initial vaccination, which typically is the arm or thigh.^3,4,6,9 The vaccine strain has lower virulence than the wild-type virus. Eight cases of vaccine-strain zoster severe enough to cause neurological complications such as meningitis or encephalitis have been reported in children, with 6 cases reported in healthy children.^9,11-17 Antiviral drugs hasten the healing of the HZ rash and shorten the duration of associated pain.¹

Although pediatric HZ is uncommon, all physicians should be aware of possible atypical presentations in healthy vaccinated children to appropriately and quickly manage treatment.

Varicella-zoster virus (VZV) is a neurotropic human herpesvirus that causes varicella (chicken pox) and herpes zoster (shingles). During infection, the virus invades the dorsal root ganglia and establishes permanent latency. It can later reactivate and travel through sensory nerves to the skin where localized viral replication causes herpes zoster (HZ), which manifests with pain in a unilateral dermatomal distribution followed closely by an eruption of grouped macules and papules that evolve into vesicles on an erythematous base.¹ These lesions form pustules and crusts over 7 to 10 days and heal completely within 4 weeks. Although postherpetic neuralgia is rare in children, the pain associated with HZ can last months or years.^1,2

Universal childhood vaccination against VZV has existed in the United States since 1995, with a 2-dose vaccine regimen recommended by the CDC since 2007. Consequently, primary varicella infection in children is uncommon, and the majority of cases now occur in the vaccinated population.³ However, breakthrough varicella infection and postvaccination HZ are rare due to the long-lasting immunity and low virulence of the attenuated vaccine strain. We recount the case of a 6-year-old vaccinated girl with a unique presentation of HZ with no known primary varicella infection.

Case Report

A healthy 6-year-old girl presented with a stabbing burning pain in the left thigh extending down the calf of 4 days’ duration. The intense pain made walking difficult and responded minimally to ibuprofen and naproxen. Poor appetite, nausea, colicky abdominal pain, and fever (temperature, 38°C) accompanied the pain. Three days after the pain began she developed a pruritic rash on the same leg. Notably, she reported falling on a rosebush and sustaining a thorn prick in the left thigh 3 days prior to the onset of pain. Before presenting to our dermatology clinic, she was seen by a pediatrician, an emergency department physician, and an infectious disease specialist. The initial workup included a complete blood cell count, C-reactive protein test, erythrocyte sedimentation rate test, and hip and femur radiograph, which were all unremarkable. She was referred to dermatology with a differential diagnosis of sporotrichosis, contact dermatitis, reactive arthritis, viral myalgia, and Legg-Calvé-Perthes disease.

Physical examination revealed a well-appearing child with pink eczematous patches and plaques extending from the left side of the lower back to the mid shin in an L5 distribution (Figure). The left thigh was tender to palpation, and nontender left inguinal lymphadenopathy was present. A single isolated 2-mm vesicle was found on the anterior aspect of the left lower leg. Direct fluorescent antibody testing of vesicle fluid was positive for VZV antigen, confirming the diagnosis of HZ.

Comment

Herpes zoster is rare in young healthy children, and its incidence has decreased since the introduction of universal varicella vaccination.⁴ Reported incidence rates in vaccinated children vary from approximately 15 to 93 per 100,000 person-years,^5,6 and the reported relative risk is 0.08 to 0.36 in vaccinated compared to unvaccinated children.^6,7 No correlations with gender, race, or ethnicity and postvaccination HZ have been observed.^5,8 Reported intervals between vaccination and HZ presentation are as short as 3 months and as long as 11 years.⁹ Although HZ is uncommon in immunocompetent children, the diagnosis of HZ itself is not an indication for formal workup for an underlying immunodeficiency or malignancy.¹⁰

Both wild-type and vaccine-strain VZV establish latent infection and can cause HZ in vaccinated children. Direct fluorescent antibody testing or polymerase chain reaction of HZ lesions can be used to identify VZV. Genotyping can distinguish the wild-type versus the vaccine strain but is not required for clinical management.³ In previously vaccinated children with HZ, approximately half present with wild-type and half with vaccine-strain VZV. In approximately half of wild-type cases, prior clinical varicella infection also occurred.⁸

Regardless of virus strain, vaccinated children typically present with the characteristic painful, vesicular, dermatomal HZ rash.^8,9 This presentation can be milder with less pain and fewer vesicles than with unvaccinated cases.⁶ When vaccine-strain HZ occurs, the rash often presents at or near the site of initial vaccination, which typically is the arm or thigh.^3,4,6,9 The vaccine strain has lower virulence than the wild-type virus. Eight cases of vaccine-strain zoster severe enough to cause neurological complications such as meningitis or encephalitis have been reported in children, with 6 cases reported in healthy children.^9,11-17 Antiviral drugs hasten the healing of the HZ rash and shorten the duration of associated pain.¹

Although pediatric HZ is uncommon, all physicians should be aware of possible atypical presentations in healthy vaccinated children to appropriately and quickly manage treatment.

EVIDENCE SUMMARY

A systematic review featured a single RCT (n=185) comparing the effect of a 12-month vs 24-month interval between dental visits on dental caries in low-risk 3- to 5-year-old children with primary teeth and young adults, ages 16 to 20 years, with permanent teeth.¹ The outcomes of caries (ie, decayed, missing, filled surfaces increment) between the 12- and 24-month visits both in younger children (mean difference [MD]= -0.90; 95% confidence interval [CI], -1.96 to 0.16) and young adults (MD= -0.86; 95% CI, -1.75 to 0.03) did not differ.

Gingivitis: Not an issue when visits were delayed in healthy adults

Another systematic review (3 RCTs; N=836) evaluated the benefits associated with scaling and polishing in the prevention of gingivitis (primary outcome measure).² One RCT (n=207) compared scaling and polishing at 6- and 12-month intervals to no treatment for 24 months in adults with healthy dental histories. There was no difference in the percentage of index teeth with bleeding in the 6-month or 12-month treatment groups compared to the group that received no treatment for 24 months (MD= -2%; 95% CI, -10% to 6% and MD= -1%; 95% CI, -9% to 7%, respectively).

2 visits/year prevents tooth loss in high-risk patients

A retrospective cohort study (N=5117) using 16 years of data evaluated the association between one or 2 preventive dental visits per year and tooth extraction events in adults at low risk and those at high risk for progressive periodontitis.³ Those at high risk had at least one of the following risk factors: smoking, diabetes, or interleukin-1 genotype. Low-risk patients had no difference in tooth loss with one visit compared to 2 visits annually (absolute risk reduction [ARR]=2.6%; 95% CI, 0.5%-5.8%; P=.092); however, high-risk patients had fewer events with 2 annual visits (number needed to treat [NNT]=19; ARR 5.2%; 95% CI, 1.8%-8.4%; P=.002).

Visits before age 3 likely benefit only those at high risk

A systematic review of 4 retrospective cohort studies (N=77,291) analyzed the impact of early preventive dental visits (EPDV) on the frequency of future preventive and non-preventive dental visits and related expenditures using data from insurance claims and a kindergarten state dental registry.⁴ One study (n=11,394) used dental disease status at kindergarten (defined as the count of decayed, missing [molar teeth only], and filled primary teeth) as an outcome measure. Children who received EPDV before age 24 months had a comparable number of caries to those who had EPDV at 24 to 36 months. The authors concluded that EPDV before age 3 years is likely to benefit only children at high risk, and that evidence for a first dental visit by age one year is weak.

RECOMMENDATIONS

The National Institute for Health and Care Excellence recommends preventive dental visit intervals based on individual risk.

The National Institute for Health and Care Excellence recommends preventive dental visit intervals based on individual risk (12 months as the longest interval under age 18 years and 24 months as the longest interval for those 18 years and older at low risk).⁵ The American Dental Association recommends preventive dental visits at intervals determined by individual risk.⁶ The American Academy of Pediatric Dentistry recommends a first exam by age one year and preventive dental visits every 6 months through adolescence or as indicated by individual risk.⁷ The US Preventive Services Task Force states there is insufficient evidence to recommend routine dental screening by primary care physicians in children up to age 5 years.⁸

EVIDENCE SUMMARY

A systematic review featured a single RCT (n=185) comparing the effect of a 12-month vs 24-month interval between dental visits on dental caries in low-risk 3- to 5-year-old children with primary teeth and young adults, ages 16 to 20 years, with permanent teeth.¹ The outcomes of caries (ie, decayed, missing, filled surfaces increment) between the 12- and 24-month visits both in younger children (mean difference [MD]= -0.90; 95% confidence interval [CI], -1.96 to 0.16) and young adults (MD= -0.86; 95% CI, -1.75 to 0.03) did not differ.

Gingivitis: Not an issue when visits were delayed in healthy adults

Another systematic review (3 RCTs; N=836) evaluated the benefits associated with scaling and polishing in the prevention of gingivitis (primary outcome measure).² One RCT (n=207) compared scaling and polishing at 6- and 12-month intervals to no treatment for 24 months in adults with healthy dental histories. There was no difference in the percentage of index teeth with bleeding in the 6-month or 12-month treatment groups compared to the group that received no treatment for 24 months (MD= -2%; 95% CI, -10% to 6% and MD= -1%; 95% CI, -9% to 7%, respectively).

2 visits/year prevents tooth loss in high-risk patients

A retrospective cohort study (N=5117) using 16 years of data evaluated the association between one or 2 preventive dental visits per year and tooth extraction events in adults at low risk and those at high risk for progressive periodontitis.³ Those at high risk had at least one of the following risk factors: smoking, diabetes, or interleukin-1 genotype. Low-risk patients had no difference in tooth loss with one visit compared to 2 visits annually (absolute risk reduction [ARR]=2.6%; 95% CI, 0.5%-5.8%; P=.092); however, high-risk patients had fewer events with 2 annual visits (number needed to treat [NNT]=19; ARR 5.2%; 95% CI, 1.8%-8.4%; P=.002).

Visits before age 3 likely benefit only those at high risk

A systematic review of 4 retrospective cohort studies (N=77,291) analyzed the impact of early preventive dental visits (EPDV) on the frequency of future preventive and non-preventive dental visits and related expenditures using data from insurance claims and a kindergarten state dental registry.⁴ One study (n=11,394) used dental disease status at kindergarten (defined as the count of decayed, missing [molar teeth only], and filled primary teeth) as an outcome measure. Children who received EPDV before age 24 months had a comparable number of caries to those who had EPDV at 24 to 36 months. The authors concluded that EPDV before age 3 years is likely to benefit only children at high risk, and that evidence for a first dental visit by age one year is weak.

RECOMMENDATIONS

The National Institute for Health and Care Excellence recommends preventive dental visit intervals based on individual risk.

The National Institute for Health and Care Excellence recommends preventive dental visit intervals based on individual risk (12 months as the longest interval under age 18 years and 24 months as the longest interval for those 18 years and older at low risk).⁵ The American Dental Association recommends preventive dental visits at intervals determined by individual risk.⁶ The American Academy of Pediatric Dentistry recommends a first exam by age one year and preventive dental visits every 6 months through adolescence or as indicated by individual risk.⁷ The US Preventive Services Task Force states there is insufficient evidence to recommend routine dental screening by primary care physicians in children up to age 5 years.⁸

EVIDENCE SUMMARY

A systematic review featured a single RCT (n=185) comparing the effect of a 12-month vs 24-month interval between dental visits on dental caries in low-risk 3- to 5-year-old children with primary teeth and young adults, ages 16 to 20 years, with permanent teeth.¹ The outcomes of caries (ie, decayed, missing, filled surfaces increment) between the 12- and 24-month visits both in younger children (mean difference [MD]= -0.90; 95% confidence interval [CI], -1.96 to 0.16) and young adults (MD= -0.86; 95% CI, -1.75 to 0.03) did not differ.

Gingivitis: Not an issue when visits were delayed in healthy adults

Another systematic review (3 RCTs; N=836) evaluated the benefits associated with scaling and polishing in the prevention of gingivitis (primary outcome measure).² One RCT (n=207) compared scaling and polishing at 6- and 12-month intervals to no treatment for 24 months in adults with healthy dental histories. There was no difference in the percentage of index teeth with bleeding in the 6-month or 12-month treatment groups compared to the group that received no treatment for 24 months (MD= -2%; 95% CI, -10% to 6% and MD= -1%; 95% CI, -9% to 7%, respectively).

2 visits/year prevents tooth loss in high-risk patients

A retrospective cohort study (N=5117) using 16 years of data evaluated the association between one or 2 preventive dental visits per year and tooth extraction events in adults at low risk and those at high risk for progressive periodontitis.³ Those at high risk had at least one of the following risk factors: smoking, diabetes, or interleukin-1 genotype. Low-risk patients had no difference in tooth loss with one visit compared to 2 visits annually (absolute risk reduction [ARR]=2.6%; 95% CI, 0.5%-5.8%; P=.092); however, high-risk patients had fewer events with 2 annual visits (number needed to treat [NNT]=19; ARR 5.2%; 95% CI, 1.8%-8.4%; P=.002).

Visits before age 3 likely benefit only those at high risk

A systematic review of 4 retrospective cohort studies (N=77,291) analyzed the impact of early preventive dental visits (EPDV) on the frequency of future preventive and non-preventive dental visits and related expenditures using data from insurance claims and a kindergarten state dental registry.⁴ One study (n=11,394) used dental disease status at kindergarten (defined as the count of decayed, missing [molar teeth only], and filled primary teeth) as an outcome measure. Children who received EPDV before age 24 months had a comparable number of caries to those who had EPDV at 24 to 36 months. The authors concluded that EPDV before age 3 years is likely to benefit only children at high risk, and that evidence for a first dental visit by age one year is weak.

RECOMMENDATIONS

The National Institute for Health and Care Excellence recommends preventive dental visit intervals based on individual risk.

The National Institute for Health and Care Excellence recommends preventive dental visit intervals based on individual risk (12 months as the longest interval under age 18 years and 24 months as the longest interval for those 18 years and older at low risk).⁵ The American Dental Association recommends preventive dental visits at intervals determined by individual risk.⁶ The American Academy of Pediatric Dentistry recommends a first exam by age one year and preventive dental visits every 6 months through adolescence or as indicated by individual risk.⁷ The US Preventive Services Task Force states there is insufficient evidence to recommend routine dental screening by primary care physicians in children up to age 5 years.⁸

A 15-month-old black male was brought to the pediatric emergency department by his grandmother because she was concerned about his 2 swollen big toes. The patient’s grandmother said that the swelling began 36 hours prior and that her grandson’s big toes had continued to increase in size. She denied trauma, bites, or unusual exposures and said that although her grandson had been fussier than usual that day, he was eating and drinking normally and had normal urine output.

The patient had a history of developmental delay, but was otherwise healthy. He had no rashes, and there was no recent history of vomiting, diarrhea, difficulty breathing, or fever.

Examination of the patient’s skin revealed diffuse edema and erythema of the bilateral great toes (FIGURE 1A), with large overlying bullae extending from the dorsal surface of the base of the great toes around to the plantar (volar) surface of the foot (FIGURE 1B). The bullae on the plantar surface were approximately 4 cm long, extending from the tip of the toes proximally to the region of the head of the first metatarsal.

The patient’s vital signs were notable for a rectal temperature of 100.2° F and a heart rate of 180 beats per minute.

Initial lab tests included a complete blood count (CBC), blood cultures, and urinalysis with urine culture. The CBC revealed a white blood count of 27,000/mcL (normal: 6000-17,500/mcL). Both wound culture and herpes simplex viral culture were negative. An intranasal surveillance culture for methicillin-resistant Staphylococcus aureus (MRSA) was also negative.

Given the patient’s fever and leukocytosis, a 100-mg dose of intravenous clindamycin was administered.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Blistering distal dactylitis

We made a clinical diagnosis of blistering distal dactylitis (BDD), a condition typically caused by infection with Gram-positive bacteria. BDD is generally described as a localized infection of the volar fat pads of one or more fingers. The infection may also occur more proximally on the hand or involve the thumbs or toes.¹

Who’s at risk? BDD occurs among children ages 2 to 16 years, although it has been reported in infants as young as 6 months and in adults. No cases have occurred among the elderly.^2-7

The most common etiologic agents are group A beta-hemolytic Streptococci. Less commonly reported agents include Staphylococcus aureus, S. epidermidis, group B Streptococci, and MRSA.^1,6,8 The presence of multiple bullae may be predictive of infection with S. aureus.⁹

A clinical diagnosis

While blistering distal dactylitis typically affects the volar fat pads of the fingers, it may also occur more proximally on the hand or involve the thumbs or toes.

Diagnosis is usually made on clinical grounds based on the presence of large, tense, superficial, and typically painful bullae, the base of which may be erythematous. Culture of the blister fluid and the base of an unroofed blister may confirm the presence of a Streptococcus or Staphylococcus species.

Lab tests are typically not required to confirm a diagnosis of BDD. However, wound cultures of blister fluid, rapid antigen testing for group A beta-hemolytic Streptococci, and viral culture or polymerase chain reaction testing for herpes simplex virus may be considered.

Rule these conditions out

Lesions similar to those seen with BDD can be caused by the following infections and irritants:^4,5,8

Herpetic whitlow is caused by a herpes simplex virus infection. It presents as a cluster of painful vesicles or ulcers with an erythematous base on the distal part of a finger or toe.

Bullous impetigo is the result of a staphylococcal infection, which produces an epidermolytic toxin leading to bulla formation. Lesions may occur anywhere on the body but are most common on the face.

Irritant or allergic contact dermatitis results from an external topical exposure and is typically localized to the area of contact. The reaction is an eczematous eruption that may include bullae.

Treatment is typically empiric

Treatment of BDD includes wound care with wet-to-dry saline dressings, incision and drainage of the bulla(e), and a systemic beta-lactamase-resistant antibiotic. Topical antibiotics alone are not recommended.⁷

Our patient was transitioned from intravenous to oral clindamycin, 100 mg every 8 hours, and the bullae were incised and drained. His leukocytosis resolved within 24 hours, and he continued to do well. At follow-up one week later, the patient’s blisters were healing well, and he was playful and eating and drinking normally.

CORRESPONDENCE
C. Randall Clinch, DO, MS, Wake Forest University School of Medicine, 1 Medical Center Blvd, Winston-Salem, NC 27157; crclinch@wakehealth.edu.

A 15-month-old black male was brought to the pediatric emergency department by his grandmother because she was concerned about his 2 swollen big toes. The patient’s grandmother said that the swelling began 36 hours prior and that her grandson’s big toes had continued to increase in size. She denied trauma, bites, or unusual exposures and said that although her grandson had been fussier than usual that day, he was eating and drinking normally and had normal urine output.

The patient had a history of developmental delay, but was otherwise healthy. He had no rashes, and there was no recent history of vomiting, diarrhea, difficulty breathing, or fever.

Examination of the patient’s skin revealed diffuse edema and erythema of the bilateral great toes (FIGURE 1A), with large overlying bullae extending from the dorsal surface of the base of the great toes around to the plantar (volar) surface of the foot (FIGURE 1B). The bullae on the plantar surface were approximately 4 cm long, extending from the tip of the toes proximally to the region of the head of the first metatarsal.

The patient’s vital signs were notable for a rectal temperature of 100.2° F and a heart rate of 180 beats per minute.

Initial lab tests included a complete blood count (CBC), blood cultures, and urinalysis with urine culture. The CBC revealed a white blood count of 27,000/mcL (normal: 6000-17,500/mcL). Both wound culture and herpes simplex viral culture were negative. An intranasal surveillance culture for methicillin-resistant Staphylococcus aureus (MRSA) was also negative.

Given the patient’s fever and leukocytosis, a 100-mg dose of intravenous clindamycin was administered.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Blistering distal dactylitis

We made a clinical diagnosis of blistering distal dactylitis (BDD), a condition typically caused by infection with Gram-positive bacteria. BDD is generally described as a localized infection of the volar fat pads of one or more fingers. The infection may also occur more proximally on the hand or involve the thumbs or toes.¹

Who’s at risk? BDD occurs among children ages 2 to 16 years, although it has been reported in infants as young as 6 months and in adults. No cases have occurred among the elderly.^2-7

The most common etiologic agents are group A beta-hemolytic Streptococci. Less commonly reported agents include Staphylococcus aureus, S. epidermidis, group B Streptococci, and MRSA.^1,6,8 The presence of multiple bullae may be predictive of infection with S. aureus.⁹

A clinical diagnosis

While blistering distal dactylitis typically affects the volar fat pads of the fingers, it may also occur more proximally on the hand or involve the thumbs or toes.

Diagnosis is usually made on clinical grounds based on the presence of large, tense, superficial, and typically painful bullae, the base of which may be erythematous. Culture of the blister fluid and the base of an unroofed blister may confirm the presence of a Streptococcus or Staphylococcus species.

Lab tests are typically not required to confirm a diagnosis of BDD. However, wound cultures of blister fluid, rapid antigen testing for group A beta-hemolytic Streptococci, and viral culture or polymerase chain reaction testing for herpes simplex virus may be considered.

Rule these conditions out

Lesions similar to those seen with BDD can be caused by the following infections and irritants:^4,5,8

Herpetic whitlow is caused by a herpes simplex virus infection. It presents as a cluster of painful vesicles or ulcers with an erythematous base on the distal part of a finger or toe.

Bullous impetigo is the result of a staphylococcal infection, which produces an epidermolytic toxin leading to bulla formation. Lesions may occur anywhere on the body but are most common on the face.

Irritant or allergic contact dermatitis results from an external topical exposure and is typically localized to the area of contact. The reaction is an eczematous eruption that may include bullae.

Treatment is typically empiric

Treatment of BDD includes wound care with wet-to-dry saline dressings, incision and drainage of the bulla(e), and a systemic beta-lactamase-resistant antibiotic. Topical antibiotics alone are not recommended.⁷

Our patient was transitioned from intravenous to oral clindamycin, 100 mg every 8 hours, and the bullae were incised and drained. His leukocytosis resolved within 24 hours, and he continued to do well. At follow-up one week later, the patient’s blisters were healing well, and he was playful and eating and drinking normally.

CORRESPONDENCE
C. Randall Clinch, DO, MS, Wake Forest University School of Medicine, 1 Medical Center Blvd, Winston-Salem, NC 27157; crclinch@wakehealth.edu.

A 15-month-old black male was brought to the pediatric emergency department by his grandmother because she was concerned about his 2 swollen big toes. The patient’s grandmother said that the swelling began 36 hours prior and that her grandson’s big toes had continued to increase in size. She denied trauma, bites, or unusual exposures and said that although her grandson had been fussier than usual that day, he was eating and drinking normally and had normal urine output.

The patient had a history of developmental delay, but was otherwise healthy. He had no rashes, and there was no recent history of vomiting, diarrhea, difficulty breathing, or fever.

Examination of the patient’s skin revealed diffuse edema and erythema of the bilateral great toes (FIGURE 1A), with large overlying bullae extending from the dorsal surface of the base of the great toes around to the plantar (volar) surface of the foot (FIGURE 1B). The bullae on the plantar surface were approximately 4 cm long, extending from the tip of the toes proximally to the region of the head of the first metatarsal.

The patient’s vital signs were notable for a rectal temperature of 100.2° F and a heart rate of 180 beats per minute.

Initial lab tests included a complete blood count (CBC), blood cultures, and urinalysis with urine culture. The CBC revealed a white blood count of 27,000/mcL (normal: 6000-17,500/mcL). Both wound culture and herpes simplex viral culture were negative. An intranasal surveillance culture for methicillin-resistant Staphylococcus aureus (MRSA) was also negative.

Given the patient’s fever and leukocytosis, a 100-mg dose of intravenous clindamycin was administered.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Blistering distal dactylitis

We made a clinical diagnosis of blistering distal dactylitis (BDD), a condition typically caused by infection with Gram-positive bacteria. BDD is generally described as a localized infection of the volar fat pads of one or more fingers. The infection may also occur more proximally on the hand or involve the thumbs or toes.¹

Who’s at risk? BDD occurs among children ages 2 to 16 years, although it has been reported in infants as young as 6 months and in adults. No cases have occurred among the elderly.^2-7

The most common etiologic agents are group A beta-hemolytic Streptococci. Less commonly reported agents include Staphylococcus aureus, S. epidermidis, group B Streptococci, and MRSA.^1,6,8 The presence of multiple bullae may be predictive of infection with S. aureus.⁹

A clinical diagnosis

While blistering distal dactylitis typically affects the volar fat pads of the fingers, it may also occur more proximally on the hand or involve the thumbs or toes.

Diagnosis is usually made on clinical grounds based on the presence of large, tense, superficial, and typically painful bullae, the base of which may be erythematous. Culture of the blister fluid and the base of an unroofed blister may confirm the presence of a Streptococcus or Staphylococcus species.

Lab tests are typically not required to confirm a diagnosis of BDD. However, wound cultures of blister fluid, rapid antigen testing for group A beta-hemolytic Streptococci, and viral culture or polymerase chain reaction testing for herpes simplex virus may be considered.

Rule these conditions out

Lesions similar to those seen with BDD can be caused by the following infections and irritants:^4,5,8

Herpetic whitlow is caused by a herpes simplex virus infection. It presents as a cluster of painful vesicles or ulcers with an erythematous base on the distal part of a finger or toe.

Bullous impetigo is the result of a staphylococcal infection, which produces an epidermolytic toxin leading to bulla formation. Lesions may occur anywhere on the body but are most common on the face.

Irritant or allergic contact dermatitis results from an external topical exposure and is typically localized to the area of contact. The reaction is an eczematous eruption that may include bullae.

Treatment is typically empiric

Treatment of BDD includes wound care with wet-to-dry saline dressings, incision and drainage of the bulla(e), and a systemic beta-lactamase-resistant antibiotic. Topical antibiotics alone are not recommended.⁷

Our patient was transitioned from intravenous to oral clindamycin, 100 mg every 8 hours, and the bullae were incised and drained. His leukocytosis resolved within 24 hours, and he continued to do well. At follow-up one week later, the patient’s blisters were healing well, and he was playful and eating and drinking normally.

CORRESPONDENCE
C. Randall Clinch, DO, MS, Wake Forest University School of Medicine, 1 Medical Center Blvd, Winston-Salem, NC 27157; crclinch@wakehealth.edu.

THE CASE

A 14-year-old Caucasian boy presented to our clinic with a complaint of left anterior hip pain. The patient had been running during a flag football match when he suddenly developed a sharp, stabbing pain in his left hip. He said he felt a “pop” in his left groin while his left foot was planted and he was cutting to the right. The patient said this was followed by worsening pain with ambulation and hip flexion.

The patient had considerable difficulty walking into the exam room. On physical examination, he had significant tenderness to palpation along the anteromedial thigh and groin. The patient’s strength was 1/5 with left hip flexion. There was apparent muscle firing, but no significant leg movement. He had full passive range of motion and there was no soft-tissue swelling, erythema, or other integumentary changes.

THE DIAGNOSIS

Plain radiographs revealed a lesser trochanter avulsion fracture with a 2-cm displacement (FIGURE 1).

DISCUSSION

Pelvic and proximal femur avulsion fractures tend to occur during the second decade of life.^1,2 They’re more frequently seen in boys and adolescent athletes, especially those involved in soccer and gymnastics.^3,4

Anterior superior iliac spine (ASIS), ischial tuberosity (IT), and anterior inferior iliac spine (AIIS) avulsion fractures are more prevalent,⁴ while lesser trochanter avulsion fractures are more rare. In one review of 1126 children with femoral neck and proximal 1/3 femoral shaft fractures, only 3 of them had lesser trochanter avulsion fractures.⁵

Clinical presentation. Presenting symptoms of lesser trochanter avulsion fractures can be vague, but are usually localized to the groin and medial hip region. Patients will demonstrate pain and weakness with hip flexion.^3,6 There may be signs of inflammation, tenderness, and ecchymosis near the site of injury.

On physical exam, a positive Ludloff sign helps localize the injury to the iliopsoas muscle, which inserts at the lesser trochanter and is involved in hip flexion.^3,6,7 The Ludloff test is performed by flexing the patient’s hip while he/she is in a seated position.

BIOMECHANICS OF AVULSION FRACTURES

Perhaps surprisingly, the majority of avulsion injuries in children and adolescents are the result of non-contact athletic movement and indirect trauma.⁴ In children, muscles and tendons are often stronger than their bones,⁷ and physes—structurally weak regions—are particularly predisposed to fractures.^2,4,6

The mechanism of injury in children and adolescents is commonly a sudden, forceful contraction of the iliopsoas muscle.^6,7 While similar movement in adults will produce tendon sprains and muscle strains, children often experience a complete avulsion fracture.⁷ So uncommon are these fractures among adults that an adult patient presenting with one should receive further work-up for underlying pathology such as malignancy.^8,9

While other hip and femur avulsion fractures in children and adolescents involve different muscle groups, the etiologic mechanism—forceful muscle contraction—is usually the same.^2,4,7 IT injuries are often seen with sudden, aggressive lengthening of the hamstring muscles, whereas injuries to the ASIS and AIIS are the result of abrupt eccentric contraction of hip extensor muscles while the knee is flexed.⁴

DIFFERENTIAL DIAGNOSIS

There are several entities that can mimic a lesser trochanter avulsion fracture including Legg-Calve-Perthes disease (LCPD), slipped capital femoral epiphysis (SCFE), snapping hip with the iliofemoral ligament, iliopsoas tendonitis, referred pain from the gastrointestinal region, and a genito-urologic etiology.^1,7,10 The work-up and treatment for these alternative diagnoses are quite different and can lead to unnecessary testing.

Diagnostic studies. Physical exam findings of severe pain and reduced strength are clear indications for obtaining baseline imaging. Baseline radiographs are key to the diagnosis of avulsion fractures. They help differentiate between more benign fractures, such as a nondisplaced avulsion fracture, and more substantial conditions, such as LCPD and SCFE, which require significantly different approaches to treatment and follow-up.^1,7

Anteroposterior, oblique, and axial views of the pelvis all assist in assessing avulsion fractures radiographically.^3,4,7 In the event that an avulsion fracture is not radiographically visible, but is still suspected, additional imaging should be obtained.¹⁰ A computerized tomography (CT) scan is an appropriate follow-up, given its meticulous detail of bony anatomy.^3,10 Alternatively, if physes have yet to ossify or there are concerns about soft tissue injury, magnetic resonance imaging can be useful.^3,7,10

MANAGEMENT

The majority of lesser trochanter avulsion fractures are managed conservatively with rest, nonsteroidal anti-inflammatory drugs (NSAIDs), and physical therapy. Patients are often placed on non-weight bearing activity for up to 6 weeks while the fracture repairs and forms a new union.⁷ Current management strategies have moved away from immobilization with splints and braces.

In rare instances when the fragment is displaced >2 cm, or there is inadequate healing or pain relief after 3 months of supportive care, surgery may be required.¹ With appropriate diagnosis and medical care, the injured athlete should fully recover with no impairment or chronic pain.²

Our patient was placed on non-weight-bearing activity and treated with NSAIDs and acetaminophen. We advanced him to weight-bearing activities 4 weeks after injury. After 8 weeks of conservative management, he returned to competitive play with no further complications (FIGURE 2).

THE TAKEAWAY

Pelvic and proximal femur avulsion fractures occur more often in child and adolescent athletes. As this population becomes increasingly competitive in athletics, the risk of injury increases. Infrequent fractures such as lesser trochanter avulsion fractures may become more common, as well. The majority of avulsion fractures don’t require surgical intervention, but it’s important to obtain baseline radiographs to rule out other injuries or pathologies that may lead to poor prognoses if they are left untreated.

THE CASE

A 14-year-old Caucasian boy presented to our clinic with a complaint of left anterior hip pain. The patient had been running during a flag football match when he suddenly developed a sharp, stabbing pain in his left hip. He said he felt a “pop” in his left groin while his left foot was planted and he was cutting to the right. The patient said this was followed by worsening pain with ambulation and hip flexion.

The patient had considerable difficulty walking into the exam room. On physical examination, he had significant tenderness to palpation along the anteromedial thigh and groin. The patient’s strength was 1/5 with left hip flexion. There was apparent muscle firing, but no significant leg movement. He had full passive range of motion and there was no soft-tissue swelling, erythema, or other integumentary changes.

THE DIAGNOSIS

Plain radiographs revealed a lesser trochanter avulsion fracture with a 2-cm displacement (FIGURE 1).

DISCUSSION

Pelvic and proximal femur avulsion fractures tend to occur during the second decade of life.^1,2 They’re more frequently seen in boys and adolescent athletes, especially those involved in soccer and gymnastics.^3,4

Anterior superior iliac spine (ASIS), ischial tuberosity (IT), and anterior inferior iliac spine (AIIS) avulsion fractures are more prevalent,⁴ while lesser trochanter avulsion fractures are more rare. In one review of 1126 children with femoral neck and proximal 1/3 femoral shaft fractures, only 3 of them had lesser trochanter avulsion fractures.⁵

Clinical presentation. Presenting symptoms of lesser trochanter avulsion fractures can be vague, but are usually localized to the groin and medial hip region. Patients will demonstrate pain and weakness with hip flexion.^3,6 There may be signs of inflammation, tenderness, and ecchymosis near the site of injury.

On physical exam, a positive Ludloff sign helps localize the injury to the iliopsoas muscle, which inserts at the lesser trochanter and is involved in hip flexion.^3,6,7 The Ludloff test is performed by flexing the patient’s hip while he/she is in a seated position.

BIOMECHANICS OF AVULSION FRACTURES

Perhaps surprisingly, the majority of avulsion injuries in children and adolescents are the result of non-contact athletic movement and indirect trauma.⁴ In children, muscles and tendons are often stronger than their bones,⁷ and physes—structurally weak regions—are particularly predisposed to fractures.^2,4,6

The mechanism of injury in children and adolescents is commonly a sudden, forceful contraction of the iliopsoas muscle.^6,7 While similar movement in adults will produce tendon sprains and muscle strains, children often experience a complete avulsion fracture.⁷ So uncommon are these fractures among adults that an adult patient presenting with one should receive further work-up for underlying pathology such as malignancy.^8,9

While other hip and femur avulsion fractures in children and adolescents involve different muscle groups, the etiologic mechanism—forceful muscle contraction—is usually the same.^2,4,7 IT injuries are often seen with sudden, aggressive lengthening of the hamstring muscles, whereas injuries to the ASIS and AIIS are the result of abrupt eccentric contraction of hip extensor muscles while the knee is flexed.⁴

DIFFERENTIAL DIAGNOSIS

There are several entities that can mimic a lesser trochanter avulsion fracture including Legg-Calve-Perthes disease (LCPD), slipped capital femoral epiphysis (SCFE), snapping hip with the iliofemoral ligament, iliopsoas tendonitis, referred pain from the gastrointestinal region, and a genito-urologic etiology.^1,7,10 The work-up and treatment for these alternative diagnoses are quite different and can lead to unnecessary testing.

Diagnostic studies. Physical exam findings of severe pain and reduced strength are clear indications for obtaining baseline imaging. Baseline radiographs are key to the diagnosis of avulsion fractures. They help differentiate between more benign fractures, such as a nondisplaced avulsion fracture, and more substantial conditions, such as LCPD and SCFE, which require significantly different approaches to treatment and follow-up.^1,7

Anteroposterior, oblique, and axial views of the pelvis all assist in assessing avulsion fractures radiographically.^3,4,7 In the event that an avulsion fracture is not radiographically visible, but is still suspected, additional imaging should be obtained.¹⁰ A computerized tomography (CT) scan is an appropriate follow-up, given its meticulous detail of bony anatomy.^3,10 Alternatively, if physes have yet to ossify or there are concerns about soft tissue injury, magnetic resonance imaging can be useful.^3,7,10

MANAGEMENT

The majority of lesser trochanter avulsion fractures are managed conservatively with rest, nonsteroidal anti-inflammatory drugs (NSAIDs), and physical therapy. Patients are often placed on non-weight bearing activity for up to 6 weeks while the fracture repairs and forms a new union.⁷ Current management strategies have moved away from immobilization with splints and braces.

In rare instances when the fragment is displaced >2 cm, or there is inadequate healing or pain relief after 3 months of supportive care, surgery may be required.¹ With appropriate diagnosis and medical care, the injured athlete should fully recover with no impairment or chronic pain.²

Our patient was placed on non-weight-bearing activity and treated with NSAIDs and acetaminophen. We advanced him to weight-bearing activities 4 weeks after injury. After 8 weeks of conservative management, he returned to competitive play with no further complications (FIGURE 2).

THE TAKEAWAY

Pelvic and proximal femur avulsion fractures occur more often in child and adolescent athletes. As this population becomes increasingly competitive in athletics, the risk of injury increases. Infrequent fractures such as lesser trochanter avulsion fractures may become more common, as well. The majority of avulsion fractures don’t require surgical intervention, but it’s important to obtain baseline radiographs to rule out other injuries or pathologies that may lead to poor prognoses if they are left untreated.

THE CASE

A 14-year-old Caucasian boy presented to our clinic with a complaint of left anterior hip pain. The patient had been running during a flag football match when he suddenly developed a sharp, stabbing pain in his left hip. He said he felt a “pop” in his left groin while his left foot was planted and he was cutting to the right. The patient said this was followed by worsening pain with ambulation and hip flexion.

The patient had considerable difficulty walking into the exam room. On physical examination, he had significant tenderness to palpation along the anteromedial thigh and groin. The patient’s strength was 1/5 with left hip flexion. There was apparent muscle firing, but no significant leg movement. He had full passive range of motion and there was no soft-tissue swelling, erythema, or other integumentary changes.

THE DIAGNOSIS

Plain radiographs revealed a lesser trochanter avulsion fracture with a 2-cm displacement (FIGURE 1).

DISCUSSION

Pelvic and proximal femur avulsion fractures tend to occur during the second decade of life.^1,2 They’re more frequently seen in boys and adolescent athletes, especially those involved in soccer and gymnastics.^3,4

Anterior superior iliac spine (ASIS), ischial tuberosity (IT), and anterior inferior iliac spine (AIIS) avulsion fractures are more prevalent,⁴ while lesser trochanter avulsion fractures are more rare. In one review of 1126 children with femoral neck and proximal 1/3 femoral shaft fractures, only 3 of them had lesser trochanter avulsion fractures.⁵

Clinical presentation. Presenting symptoms of lesser trochanter avulsion fractures can be vague, but are usually localized to the groin and medial hip region. Patients will demonstrate pain and weakness with hip flexion.^3,6 There may be signs of inflammation, tenderness, and ecchymosis near the site of injury.

On physical exam, a positive Ludloff sign helps localize the injury to the iliopsoas muscle, which inserts at the lesser trochanter and is involved in hip flexion.^3,6,7 The Ludloff test is performed by flexing the patient’s hip while he/she is in a seated position.

BIOMECHANICS OF AVULSION FRACTURES

Perhaps surprisingly, the majority of avulsion injuries in children and adolescents are the result of non-contact athletic movement and indirect trauma.⁴ In children, muscles and tendons are often stronger than their bones,⁷ and physes—structurally weak regions—are particularly predisposed to fractures.^2,4,6

The mechanism of injury in children and adolescents is commonly a sudden, forceful contraction of the iliopsoas muscle.^6,7 While similar movement in adults will produce tendon sprains and muscle strains, children often experience a complete avulsion fracture.⁷ So uncommon are these fractures among adults that an adult patient presenting with one should receive further work-up for underlying pathology such as malignancy.^8,9

While other hip and femur avulsion fractures in children and adolescents involve different muscle groups, the etiologic mechanism—forceful muscle contraction—is usually the same.^2,4,7 IT injuries are often seen with sudden, aggressive lengthening of the hamstring muscles, whereas injuries to the ASIS and AIIS are the result of abrupt eccentric contraction of hip extensor muscles while the knee is flexed.⁴

DIFFERENTIAL DIAGNOSIS

There are several entities that can mimic a lesser trochanter avulsion fracture including Legg-Calve-Perthes disease (LCPD), slipped capital femoral epiphysis (SCFE), snapping hip with the iliofemoral ligament, iliopsoas tendonitis, referred pain from the gastrointestinal region, and a genito-urologic etiology.^1,7,10 The work-up and treatment for these alternative diagnoses are quite different and can lead to unnecessary testing.

Diagnostic studies. Physical exam findings of severe pain and reduced strength are clear indications for obtaining baseline imaging. Baseline radiographs are key to the diagnosis of avulsion fractures. They help differentiate between more benign fractures, such as a nondisplaced avulsion fracture, and more substantial conditions, such as LCPD and SCFE, which require significantly different approaches to treatment and follow-up.^1,7

Anteroposterior, oblique, and axial views of the pelvis all assist in assessing avulsion fractures radiographically.^3,4,7 In the event that an avulsion fracture is not radiographically visible, but is still suspected, additional imaging should be obtained.¹⁰ A computerized tomography (CT) scan is an appropriate follow-up, given its meticulous detail of bony anatomy.^3,10 Alternatively, if physes have yet to ossify or there are concerns about soft tissue injury, magnetic resonance imaging can be useful.^3,7,10

MANAGEMENT

The majority of lesser trochanter avulsion fractures are managed conservatively with rest, nonsteroidal anti-inflammatory drugs (NSAIDs), and physical therapy. Patients are often placed on non-weight bearing activity for up to 6 weeks while the fracture repairs and forms a new union.⁷ Current management strategies have moved away from immobilization with splints and braces.

In rare instances when the fragment is displaced >2 cm, or there is inadequate healing or pain relief after 3 months of supportive care, surgery may be required.¹ With appropriate diagnosis and medical care, the injured athlete should fully recover with no impairment or chronic pain.²

Our patient was placed on non-weight-bearing activity and treated with NSAIDs and acetaminophen. We advanced him to weight-bearing activities 4 weeks after injury. After 8 weeks of conservative management, he returned to competitive play with no further complications (FIGURE 2).

THE TAKEAWAY

Pelvic and proximal femur avulsion fractures occur more often in child and adolescent athletes. As this population becomes increasingly competitive in athletics, the risk of injury increases. Infrequent fractures such as lesser trochanter avulsion fractures may become more common, as well. The majority of avulsion fractures don’t require surgical intervention, but it’s important to obtain baseline radiographs to rule out other injuries or pathologies that may lead to poor prognoses if they are left untreated.

Nearly half of American children have faced one adverse childhood experience (ACE), according to new analysis of the 2016 National Survey of Children’s Health, and more than 20% have had two ACEs or more. This may include abuse or neglect, witnessing violence, parental substance abuse, mental illness, or incarceration. And from news headlines, we are all too aware of other traumas children face, such as natural disasters and mass violence.

Sesame Workshop 2017

Sesame Workshop 2017

Sesame Workshop 2017

Sesame Street Workshop

Dr. Betancourt is the senior vice president for U.S. social impact at Sesame Workshop, the nonprofit media and educational organization behind Sesame Street, in New York.

Nearly half of American children have faced one adverse childhood experience (ACE), according to new analysis of the 2016 National Survey of Children’s Health, and more than 20% have had two ACEs or more. This may include abuse or neglect, witnessing violence, parental substance abuse, mental illness, or incarceration. And from news headlines, we are all too aware of other traumas children face, such as natural disasters and mass violence.

Sesame Workshop 2017

Sesame Workshop 2017

Sesame Workshop 2017

Sesame Street Workshop

Dr. Betancourt is the senior vice president for U.S. social impact at Sesame Workshop, the nonprofit media and educational organization behind Sesame Street, in New York.

Nearly half of American children have faced one adverse childhood experience (ACE), according to new analysis of the 2016 National Survey of Children’s Health, and more than 20% have had two ACEs or more. This may include abuse or neglect, witnessing violence, parental substance abuse, mental illness, or incarceration. And from news headlines, we are all too aware of other traumas children face, such as natural disasters and mass violence.

Sesame Workshop 2017

Sesame Workshop 2017

Sesame Workshop 2017

Sesame Street Workshop

Dr. Betancourt is the senior vice president for U.S. social impact at Sesame Workshop, the nonprofit media and educational organization behind Sesame Street, in New York.

Vesiculobullous eruptions in neonates can readily generate anxiety from parents/guardians and pediatricians over both infectious and noninfectious causes. The role of the dermatology resident is critical to help diminish fear over common vesicular presentations or to escalate care in rarer situations if a more obscure or ominous diagnosis is clouding the patient’s clinical presentation and well-being. This article summarizes both common and uncommon vesiculobullous neonatal diseases to augment precise and efficient diagnoses in this vulnerable patient population.

Steps for Evaluating a Vesiculopustular Eruption

Receiving a consultation for a newborn with widespread vesicles can be a daunting scenario for a dermatology resident. Fear of missing an ominous diagnosis or aggressively treating a newborn for an erroneous infection when the diagnosis is actually a benign presentation can lead to an anxiety-provoking situation. Additionally, performing a procedure on a newborn can cause personal uneasiness. Dr. Lawrence A. Schachner, an eminent pediatric dermatologist at the University of Miami Miller School of Medicine (Miami, Florida), recently lectured on 5 key steps (Table 1) for the evaluation of a vesiculobullous eruption in the newborn to maximize the accuracy of diagnosis and patient care.¹

First, draw out the fluid from the vesicle to send for bacterial and viral culture as well as Gram stain. Second, snip the roof of the vesicle to perform potassium hydroxide examination for yeast or fungi and frozen pathology when indicated. Third, use the base of the vesicle to obtain cells for a Tzanck smear to identify the predominant cell infiltrate, such as multinucleated giant cells in herpes simplex virus or eosinophils in erythema toxicum neonatorum (ETN). Fourth, a mineral oil preparation can be performed on several lesions, especially if a burrow is observed, to rule out bullous scabies in the appropriate clinical presentation. Lastly, a perilesional or lesional punch biopsy can be performed if the above steps have not yet clinched the diagnosis.² By utilizing these steps, the resident efficiently utilizes 1 lesion to narrow down a formidable differential list of bullous disorders in the newborn.

Specific Diagnoses

A number of common diagnoses can present during the newborn period and can usually be readily diagnosed by clinical manifestations alone; a summary of these eruptions is provided in Table 2. Erythema toxicum neonatorum is the most common pustular eruption in neonates and presents in up to 50% of full-term infants at days 1 to 2 of life. Inflammatory pustules surrounded by characteristic blotchy erythema are displayed on the face, trunk, arms, and legs, usually sparing the palms and soles.³ Erythema toxicum neonatorum typically is a clinical diagnosis; however, it can be confirmed by demonstrating the predominance of eosinophils on Tzanck smear.

Transient neonatal pustular melanosis (TNPM) also presents in full-term infants; usually favors darkly pigmented neonates; and exhibits either pustules with a collarette of scale that lack surrounding erythema or with residual brown macules on the face, genitals, and acral surfaces. Postinflammatory pigmentary alteration on lesion clearance is another clue to diagnosis. Similarly, it is a clinical diagnosis but can be confirmed with a Tzanck smear demonstrating neutrophils as the major cell infiltrate.

In a prospective 1-year multicenter study performed by Reginatto et al,⁴ 2831 neonates born in southern Brazil underwent a skin examination by a dermatologist within 72 hours of birth to characterize the prevalence and demographics of ETN and TNPM. They found a 21.3% (602 cases) prevalence of ETN compared to a 3.4% (97 cases) prevalence of TNPM, but they noted that most patients were white, and thus the diagnosis of TNPM likely is less prevalent in this group, as it favors darkly pigmented individuals. Additional predisposing factors associated with ETN were male gender, an Apgar score of 8 to 10 at 1 minute, non–neonatal intensive care unit (NICU) patients, and lack of gestational risk factors. The TNPM population was much smaller, though the authors were able to conclude that the disease also was correlated with healthy, non-NICU patients. The authors hypothesized that there may be a role of immune system maturity in the pathogenesis of ETN and thus dermatology residents should be aware of the setting of their consultation.⁴ A NICU consultation for ETN should raise suspicion, as ETN and TNPM favor healthy infants who likely are not residing in the NICU; we are reminded of the target populations for these disease processes.

Additional common causes of vesicular eruptions in neonates can likewise be diagnosed chiefly with clinical inspection. Miliaria presents with tiny superficial crystalline vesicles on the neck and back of newborns due to elevated temperature and resultant obstruction of the eccrine sweat ducts. Reassurance can be provided, as spontaneous resolution occurs with cooling and limitation of occlusive clothing and swaddling.²

Infants at a few weeks of life may present with a noncomedonal pustular eruption on the cheeks, forehead, and scalp commonly known as neonatal acne or neonatal cephalic pustulosis. The driving factor is thought to be an abnormal response to Malassezia and can be treated with ketoconazole cream or expectant management.²

Cutaneous candidiasis is the most common infectious cause of vesicles in the neonate and can present in 2 fashions. Neonatal candidiasis is common, presenting a week after birth and manifesting as oral thrush and red plaques with satellite pustules in the diaper area. Congenital candidiasis is due to infection in utero, presents prior to 1 week of life, exhibits diffuse erythroderma, and requires timely parenteral antifungals.⁵ Newborns and preterm infants are at higher risk for systemic disease, while full-term infants may experience a mild course of skin-limited lesions.

It is imperative to rule out other infectious etiologies in ill-appearing neonates with vesicles such as herpes simplex virus, bacterial infections, syphilis, and vertically transmitted TORCH (toxoplasmosis, other infections rubella, cytomegalovirus infection, and herpes simplex) diagnoses.⁶ Herpes simplex virus classically presents with grouped vesicles on an erythematous base; however, such characteristic lesions may be subtle in the newborn. The site of skin involvement usually is the area that first comes into contact with maternal lesions, such as the face for a newborn delivered in a cephalic presentation.² It is critical to be cognizant of this diagnosis, as a delay in antiviral therapy can result in neurologic consequences due to disseminated disease. The other TORCH diagnoses may present with blueberry muffin lesions, which are blue to violaceous papules on the trunk, arms, and legs due to extramedullary hematopoiesis. Each disease process may lead to its own characteristic sequelae and should be further investigated based on the maternal history.

If the clinical picture of vesiculobullous disease in the newborn is not as clear, less common causes must be considered. Infantile acropustulosis presents with recurring crops of pustules on the hands and feet at several months of age. The most common differential diagnosis is scabies; therefore, a mineral oil preparation should be performed to rule out this common mimicker. Potent topical corticosteroids are first-line therapy, and episodes generally resolve with time.

Another mimicker of pustules in neonates includes deficiency of IL-1ra, a rare entity described in 2009.⁷ Deficiency of IL-1ra is an autoinflammatory syndrome of skin and bone due to unopposed action of IL-1 with life-threatening inflammation; infants present with pustules, lytic bone lesions, elevated erythrocyte sedimentation rate and C-reactive protein, and failure to thrive.⁸ The characteristic mutation was discovered when the infants dramatically responded to therapy with anakinra, an IL-1ra.

Eosinophilic pustular folliculitis is an additional pustular dermatosis that manifests with lesions predominately in the head and neck area, and unlike the adult population, it usually is self-resolving and not associated with other comorbidities in newborns.²

Incontinentia pigmenti is an X-linked dominant syndrome due to a genetic mutation in NEMO, nuclear factor κβ essential modulator, which protects against apoptosis.³ Incontinentia pigmenti presents in newborn girls shortly after birth with vesicles in a blaschkoid distribution before evolving through 4 unique stages of vesicular lesions, verrucous lesions, hyperpigmentation, and ultimately resolves with residual hypopigmentation in the affected area.

Lastly, neonatal Behçet disease can present with vesicles in the mouth and genital region due to transfer of maternal antibodies. It is self-limiting in nature and would be readily diagnosed with a known maternal history, though judicious screening for infections may be needed in specific settings.²

Conclusion

In summary, a vast array of benign and worrisome dermatoses present in the neonatal period. A thorough history and physical examination, including the temporality of the lesions, the health status of the newborn, and the maternal history, can help delineate the diagnosis. The 5-step method presented can further elucidate the underlying mechanism and reduce an overwhelming differential diagnosis list by reviewing each finding yielded from each step. Dermatology residents should feel comfortable addressing this unique patient population to ameliorate unclear cutaneous diagnoses for pediatricians.

Acknowledgment

A special thank you to Lawrence A. Schachner, MD (Miami, Florida), for his help providing resources and guidance for this topic.

Vesiculobullous eruptions in neonates can readily generate anxiety from parents/guardians and pediatricians over both infectious and noninfectious causes. The role of the dermatology resident is critical to help diminish fear over common vesicular presentations or to escalate care in rarer situations if a more obscure or ominous diagnosis is clouding the patient’s clinical presentation and well-being. This article summarizes both common and uncommon vesiculobullous neonatal diseases to augment precise and efficient diagnoses in this vulnerable patient population.

Steps for Evaluating a Vesiculopustular Eruption

Receiving a consultation for a newborn with widespread vesicles can be a daunting scenario for a dermatology resident. Fear of missing an ominous diagnosis or aggressively treating a newborn for an erroneous infection when the diagnosis is actually a benign presentation can lead to an anxiety-provoking situation. Additionally, performing a procedure on a newborn can cause personal uneasiness. Dr. Lawrence A. Schachner, an eminent pediatric dermatologist at the University of Miami Miller School of Medicine (Miami, Florida), recently lectured on 5 key steps (Table 1) for the evaluation of a vesiculobullous eruption in the newborn to maximize the accuracy of diagnosis and patient care.¹

First, draw out the fluid from the vesicle to send for bacterial and viral culture as well as Gram stain. Second, snip the roof of the vesicle to perform potassium hydroxide examination for yeast or fungi and frozen pathology when indicated. Third, use the base of the vesicle to obtain cells for a Tzanck smear to identify the predominant cell infiltrate, such as multinucleated giant cells in herpes simplex virus or eosinophils in erythema toxicum neonatorum (ETN). Fourth, a mineral oil preparation can be performed on several lesions, especially if a burrow is observed, to rule out bullous scabies in the appropriate clinical presentation. Lastly, a perilesional or lesional punch biopsy can be performed if the above steps have not yet clinched the diagnosis.² By utilizing these steps, the resident efficiently utilizes 1 lesion to narrow down a formidable differential list of bullous disorders in the newborn.

Specific Diagnoses

A number of common diagnoses can present during the newborn period and can usually be readily diagnosed by clinical manifestations alone; a summary of these eruptions is provided in Table 2. Erythema toxicum neonatorum is the most common pustular eruption in neonates and presents in up to 50% of full-term infants at days 1 to 2 of life. Inflammatory pustules surrounded by characteristic blotchy erythema are displayed on the face, trunk, arms, and legs, usually sparing the palms and soles.³ Erythema toxicum neonatorum typically is a clinical diagnosis; however, it can be confirmed by demonstrating the predominance of eosinophils on Tzanck smear.

Transient neonatal pustular melanosis (TNPM) also presents in full-term infants; usually favors darkly pigmented neonates; and exhibits either pustules with a collarette of scale that lack surrounding erythema or with residual brown macules on the face, genitals, and acral surfaces. Postinflammatory pigmentary alteration on lesion clearance is another clue to diagnosis. Similarly, it is a clinical diagnosis but can be confirmed with a Tzanck smear demonstrating neutrophils as the major cell infiltrate.

In a prospective 1-year multicenter study performed by Reginatto et al,⁴ 2831 neonates born in southern Brazil underwent a skin examination by a dermatologist within 72 hours of birth to characterize the prevalence and demographics of ETN and TNPM. They found a 21.3% (602 cases) prevalence of ETN compared to a 3.4% (97 cases) prevalence of TNPM, but they noted that most patients were white, and thus the diagnosis of TNPM likely is less prevalent in this group, as it favors darkly pigmented individuals. Additional predisposing factors associated with ETN were male gender, an Apgar score of 8 to 10 at 1 minute, non–neonatal intensive care unit (NICU) patients, and lack of gestational risk factors. The TNPM population was much smaller, though the authors were able to conclude that the disease also was correlated with healthy, non-NICU patients. The authors hypothesized that there may be a role of immune system maturity in the pathogenesis of ETN and thus dermatology residents should be aware of the setting of their consultation.⁴ A NICU consultation for ETN should raise suspicion, as ETN and TNPM favor healthy infants who likely are not residing in the NICU; we are reminded of the target populations for these disease processes.

Additional common causes of vesicular eruptions in neonates can likewise be diagnosed chiefly with clinical inspection. Miliaria presents with tiny superficial crystalline vesicles on the neck and back of newborns due to elevated temperature and resultant obstruction of the eccrine sweat ducts. Reassurance can be provided, as spontaneous resolution occurs with cooling and limitation of occlusive clothing and swaddling.²

Infants at a few weeks of life may present with a noncomedonal pustular eruption on the cheeks, forehead, and scalp commonly known as neonatal acne or neonatal cephalic pustulosis. The driving factor is thought to be an abnormal response to Malassezia and can be treated with ketoconazole cream or expectant management.²

Cutaneous candidiasis is the most common infectious cause of vesicles in the neonate and can present in 2 fashions. Neonatal candidiasis is common, presenting a week after birth and manifesting as oral thrush and red plaques with satellite pustules in the diaper area. Congenital candidiasis is due to infection in utero, presents prior to 1 week of life, exhibits diffuse erythroderma, and requires timely parenteral antifungals.⁵ Newborns and preterm infants are at higher risk for systemic disease, while full-term infants may experience a mild course of skin-limited lesions.

It is imperative to rule out other infectious etiologies in ill-appearing neonates with vesicles such as herpes simplex virus, bacterial infections, syphilis, and vertically transmitted TORCH (toxoplasmosis, other infections rubella, cytomegalovirus infection, and herpes simplex) diagnoses.⁶ Herpes simplex virus classically presents with grouped vesicles on an erythematous base; however, such characteristic lesions may be subtle in the newborn. The site of skin involvement usually is the area that first comes into contact with maternal lesions, such as the face for a newborn delivered in a cephalic presentation.² It is critical to be cognizant of this diagnosis, as a delay in antiviral therapy can result in neurologic consequences due to disseminated disease. The other TORCH diagnoses may present with blueberry muffin lesions, which are blue to violaceous papules on the trunk, arms, and legs due to extramedullary hematopoiesis. Each disease process may lead to its own characteristic sequelae and should be further investigated based on the maternal history.

If the clinical picture of vesiculobullous disease in the newborn is not as clear, less common causes must be considered. Infantile acropustulosis presents with recurring crops of pustules on the hands and feet at several months of age. The most common differential diagnosis is scabies; therefore, a mineral oil preparation should be performed to rule out this common mimicker. Potent topical corticosteroids are first-line therapy, and episodes generally resolve with time.

Another mimicker of pustules in neonates includes deficiency of IL-1ra, a rare entity described in 2009.⁷ Deficiency of IL-1ra is an autoinflammatory syndrome of skin and bone due to unopposed action of IL-1 with life-threatening inflammation; infants present with pustules, lytic bone lesions, elevated erythrocyte sedimentation rate and C-reactive protein, and failure to thrive.⁸ The characteristic mutation was discovered when the infants dramatically responded to therapy with anakinra, an IL-1ra.

Eosinophilic pustular folliculitis is an additional pustular dermatosis that manifests with lesions predominately in the head and neck area, and unlike the adult population, it usually is self-resolving and not associated with other comorbidities in newborns.²

Incontinentia pigmenti is an X-linked dominant syndrome due to a genetic mutation in NEMO, nuclear factor κβ essential modulator, which protects against apoptosis.³ Incontinentia pigmenti presents in newborn girls shortly after birth with vesicles in a blaschkoid distribution before evolving through 4 unique stages of vesicular lesions, verrucous lesions, hyperpigmentation, and ultimately resolves with residual hypopigmentation in the affected area.

Lastly, neonatal Behçet disease can present with vesicles in the mouth and genital region due to transfer of maternal antibodies. It is self-limiting in nature and would be readily diagnosed with a known maternal history, though judicious screening for infections may be needed in specific settings.²

Conclusion

In summary, a vast array of benign and worrisome dermatoses present in the neonatal period. A thorough history and physical examination, including the temporality of the lesions, the health status of the newborn, and the maternal history, can help delineate the diagnosis. The 5-step method presented can further elucidate the underlying mechanism and reduce an overwhelming differential diagnosis list by reviewing each finding yielded from each step. Dermatology residents should feel comfortable addressing this unique patient population to ameliorate unclear cutaneous diagnoses for pediatricians.

Acknowledgment

A special thank you to Lawrence A. Schachner, MD (Miami, Florida), for his help providing resources and guidance for this topic.

Vesiculobullous eruptions in neonates can readily generate anxiety from parents/guardians and pediatricians over both infectious and noninfectious causes. The role of the dermatology resident is critical to help diminish fear over common vesicular presentations or to escalate care in rarer situations if a more obscure or ominous diagnosis is clouding the patient’s clinical presentation and well-being. This article summarizes both common and uncommon vesiculobullous neonatal diseases to augment precise and efficient diagnoses in this vulnerable patient population.

Steps for Evaluating a Vesiculopustular Eruption

Receiving a consultation for a newborn with widespread vesicles can be a daunting scenario for a dermatology resident. Fear of missing an ominous diagnosis or aggressively treating a newborn for an erroneous infection when the diagnosis is actually a benign presentation can lead to an anxiety-provoking situation. Additionally, performing a procedure on a newborn can cause personal uneasiness. Dr. Lawrence A. Schachner, an eminent pediatric dermatologist at the University of Miami Miller School of Medicine (Miami, Florida), recently lectured on 5 key steps (Table 1) for the evaluation of a vesiculobullous eruption in the newborn to maximize the accuracy of diagnosis and patient care.¹

First, draw out the fluid from the vesicle to send for bacterial and viral culture as well as Gram stain. Second, snip the roof of the vesicle to perform potassium hydroxide examination for yeast or fungi and frozen pathology when indicated. Third, use the base of the vesicle to obtain cells for a Tzanck smear to identify the predominant cell infiltrate, such as multinucleated giant cells in herpes simplex virus or eosinophils in erythema toxicum neonatorum (ETN). Fourth, a mineral oil preparation can be performed on several lesions, especially if a burrow is observed, to rule out bullous scabies in the appropriate clinical presentation. Lastly, a perilesional or lesional punch biopsy can be performed if the above steps have not yet clinched the diagnosis.² By utilizing these steps, the resident efficiently utilizes 1 lesion to narrow down a formidable differential list of bullous disorders in the newborn.

Specific Diagnoses

A number of common diagnoses can present during the newborn period and can usually be readily diagnosed by clinical manifestations alone; a summary of these eruptions is provided in Table 2. Erythema toxicum neonatorum is the most common pustular eruption in neonates and presents in up to 50% of full-term infants at days 1 to 2 of life. Inflammatory pustules surrounded by characteristic blotchy erythema are displayed on the face, trunk, arms, and legs, usually sparing the palms and soles.³ Erythema toxicum neonatorum typically is a clinical diagnosis; however, it can be confirmed by demonstrating the predominance of eosinophils on Tzanck smear.

Transient neonatal pustular melanosis (TNPM) also presents in full-term infants; usually favors darkly pigmented neonates; and exhibits either pustules with a collarette of scale that lack surrounding erythema or with residual brown macules on the face, genitals, and acral surfaces. Postinflammatory pigmentary alteration on lesion clearance is another clue to diagnosis. Similarly, it is a clinical diagnosis but can be confirmed with a Tzanck smear demonstrating neutrophils as the major cell infiltrate.

In a prospective 1-year multicenter study performed by Reginatto et al,⁴ 2831 neonates born in southern Brazil underwent a skin examination by a dermatologist within 72 hours of birth to characterize the prevalence and demographics of ETN and TNPM. They found a 21.3% (602 cases) prevalence of ETN compared to a 3.4% (97 cases) prevalence of TNPM, but they noted that most patients were white, and thus the diagnosis of TNPM likely is less prevalent in this group, as it favors darkly pigmented individuals. Additional predisposing factors associated with ETN were male gender, an Apgar score of 8 to 10 at 1 minute, non–neonatal intensive care unit (NICU) patients, and lack of gestational risk factors. The TNPM population was much smaller, though the authors were able to conclude that the disease also was correlated with healthy, non-NICU patients. The authors hypothesized that there may be a role of immune system maturity in the pathogenesis of ETN and thus dermatology residents should be aware of the setting of their consultation.⁴ A NICU consultation for ETN should raise suspicion, as ETN and TNPM favor healthy infants who likely are not residing in the NICU; we are reminded of the target populations for these disease processes.

Additional common causes of vesicular eruptions in neonates can likewise be diagnosed chiefly with clinical inspection. Miliaria presents with tiny superficial crystalline vesicles on the neck and back of newborns due to elevated temperature and resultant obstruction of the eccrine sweat ducts. Reassurance can be provided, as spontaneous resolution occurs with cooling and limitation of occlusive clothing and swaddling.²

Infants at a few weeks of life may present with a noncomedonal pustular eruption on the cheeks, forehead, and scalp commonly known as neonatal acne or neonatal cephalic pustulosis. The driving factor is thought to be an abnormal response to Malassezia and can be treated with ketoconazole cream or expectant management.²

Cutaneous candidiasis is the most common infectious cause of vesicles in the neonate and can present in 2 fashions. Neonatal candidiasis is common, presenting a week after birth and manifesting as oral thrush and red plaques with satellite pustules in the diaper area. Congenital candidiasis is due to infection in utero, presents prior to 1 week of life, exhibits diffuse erythroderma, and requires timely parenteral antifungals.⁵ Newborns and preterm infants are at higher risk for systemic disease, while full-term infants may experience a mild course of skin-limited lesions.

It is imperative to rule out other infectious etiologies in ill-appearing neonates with vesicles such as herpes simplex virus, bacterial infections, syphilis, and vertically transmitted TORCH (toxoplasmosis, other infections rubella, cytomegalovirus infection, and herpes simplex) diagnoses.⁶ Herpes simplex virus classically presents with grouped vesicles on an erythematous base; however, such characteristic lesions may be subtle in the newborn. The site of skin involvement usually is the area that first comes into contact with maternal lesions, such as the face for a newborn delivered in a cephalic presentation.² It is critical to be cognizant of this diagnosis, as a delay in antiviral therapy can result in neurologic consequences due to disseminated disease. The other TORCH diagnoses may present with blueberry muffin lesions, which are blue to violaceous papules on the trunk, arms, and legs due to extramedullary hematopoiesis. Each disease process may lead to its own characteristic sequelae and should be further investigated based on the maternal history.

If the clinical picture of vesiculobullous disease in the newborn is not as clear, less common causes must be considered. Infantile acropustulosis presents with recurring crops of pustules on the hands and feet at several months of age. The most common differential diagnosis is scabies; therefore, a mineral oil preparation should be performed to rule out this common mimicker. Potent topical corticosteroids are first-line therapy, and episodes generally resolve with time.

Another mimicker of pustules in neonates includes deficiency of IL-1ra, a rare entity described in 2009.⁷ Deficiency of IL-1ra is an autoinflammatory syndrome of skin and bone due to unopposed action of IL-1 with life-threatening inflammation; infants present with pustules, lytic bone lesions, elevated erythrocyte sedimentation rate and C-reactive protein, and failure to thrive.⁸ The characteristic mutation was discovered when the infants dramatically responded to therapy with anakinra, an IL-1ra.

Eosinophilic pustular folliculitis is an additional pustular dermatosis that manifests with lesions predominately in the head and neck area, and unlike the adult population, it usually is self-resolving and not associated with other comorbidities in newborns.²

Incontinentia pigmenti is an X-linked dominant syndrome due to a genetic mutation in NEMO, nuclear factor κβ essential modulator, which protects against apoptosis.³ Incontinentia pigmenti presents in newborn girls shortly after birth with vesicles in a blaschkoid distribution before evolving through 4 unique stages of vesicular lesions, verrucous lesions, hyperpigmentation, and ultimately resolves with residual hypopigmentation in the affected area.

Lastly, neonatal Behçet disease can present with vesicles in the mouth and genital region due to transfer of maternal antibodies. It is self-limiting in nature and would be readily diagnosed with a known maternal history, though judicious screening for infections may be needed in specific settings.²

Conclusion

In summary, a vast array of benign and worrisome dermatoses present in the neonatal period. A thorough history and physical examination, including the temporality of the lesions, the health status of the newborn, and the maternal history, can help delineate the diagnosis. The 5-step method presented can further elucidate the underlying mechanism and reduce an overwhelming differential diagnosis list by reviewing each finding yielded from each step. Dermatology residents should feel comfortable addressing this unique patient population to ameliorate unclear cutaneous diagnoses for pediatricians.

Acknowledgment

A special thank you to Lawrence A. Schachner, MD (Miami, Florida), for his help providing resources and guidance for this topic.