ROME – Early administration of high-dose N-acetylcysteine and low-dose glyceryl trinitrate in ST-segment elevation acute myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI) achieved a 30% reduction in myocardial infarct size, compared with placebo in a randomized, double-blind, multicenter clinical trial, Sivabaskari Pasupathy reported at the annual congress of the European Society of Cardiology.

The adjunctive regimen also resulted in a doubling of myocardial salvage, the secondary endpoint in the NACIAM (N-acetylcysteine in acute myocardial infarction) trial, said Ms. Pasupathy of the University of Adelaide, Australia.

Bruce Jancin/Frontline Medical News

NACIAM, which she stressed was a pilot study, included 75 randomized STEMI patients with follow-up cardiac MRIs obtained at about 5 days post-PCI, most of whom had another MRI at about 8 months.

All participants received IV glycerol trinitrate at a rate of 25 mcg/min for 48 hours starting in the emergency department. Patients in the active treatment arm received IV N-acetylcysteine (NAC) at 20 mg/min for the first hour and 10 mg/min for the next 47 hours. Controls got placebo at 40 mL/hour for the first hour and 20 mL/hour thereafter.

Cardiac MRI at 5 days showed a myocardial infarct size of 16.5% in the control group and 11% with active treatment. This absolute 5.5% reduction in infarct size in NAC recipients was achieved despite no difference between the two groups in myocardial area at risk by MRI, which was roughly 24%. Nor did the groups differ in rates of anterior MI or microvascular obstruction. The myocardial salvage rate was 60% in the NAC group and just 27% in controls.

Creatine kinase levels, measured hourly during the first 24 hours of hospitalization, were consistently lower in the NAC group, although the difference didn’t reach statistical significance.

In-hospital rates of hypotension, bleeding, or renal dysfunction were similar in the two study arms. However, at 2 years of follow-up the composite rate of death or cardiac rehospitalization was 27% in the control group, compared with 6% in patients who got NAC.

A key to the demonstrable success of the adjunctive NAC/nitrate treatment strategy was that it began early, in the emergency department, when patients initially presented with STEMI. The mean total ischemia time for study participants was 2.4 hours, and the shorter the duration of ischemia, the larger the reduction seen in infarct size, according to Ms. Pasupathy.

The rationale for this therapy is that NAC is thought to reduce oxidative stress by scavenging reactive oxygen species and inhibiting their release, thereby minimizing reperfusion injury. The Australian investigators also believe that NAC potentiates the effects of glycerol trinitrate in improving tissue reperfusion through enhanced vasodilation, inhibition of platelet aggregation, and dampening of inflammation. A reduction in reperfusion injury accompanied by increased tissue reperfusion could result in reduced infarct size, she explained.

Bruce Jancin/Frontline Medical News

John F. Beltrame, MD, lead investigator in the NACIAM study, noted that infarct size and myocardial salvage are surrogate endpoints. The investigators plan to conduct a larger trial with hard clinical outcomes.

“The key thing we need to do before we start using this in widespread fashion and changing practice guidelines is to look at clinical endpoints,” said Dr. Beltrame, professor of medicine at the University of Adelaide.

Nonetheless, he added, this therapy is given routinely in the setting of primary PCI for STEMI where he practices. That has been the case for 20 years because he and colleagues in his department did some of the early studies suggesting NAC was beneficial.

“Hospitals have different practices, and this is one of our particular practices,” the cardiologist said.

It all sounded pretty good to Jorge A. Belardi, MD, who co-chaired a press conference devoted to the NACIAM trial and other hotline presentations.

“It’s a very benign combination of medicines to use. So why not use it? We already use it to prevent contrast nephropathy. And there are no contraindications, to my knowledge,” said Dr. Belardi, director of the department of cardiology at the Buenos Aires Cardiovascular Institute.

Michel Ovize, MD, of the University of Lyon (France), the formal discussant designated for NACIAM, took a more flinty eyed view, noting that the study was small and previous studies of NAC during the past 2 decades have yielded conflicting results.

Ms. Pasupathy responded that a likely explanation for the disparate results is the fact that other investigators didn’t start NAC at the soonest possible time in the ED.

The NACIAM trial was funded by the Australian National Heart Foundation. Ms. Pasupathy and Dr. Beltrame reported having no financial conflicts of interest.

[email protected]

ROME – Early administration of high-dose N-acetylcysteine and low-dose glyceryl trinitrate in ST-segment elevation acute myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI) achieved a 30% reduction in myocardial infarct size, compared with placebo in a randomized, double-blind, multicenter clinical trial, Sivabaskari Pasupathy reported at the annual congress of the European Society of Cardiology.

The adjunctive regimen also resulted in a doubling of myocardial salvage, the secondary endpoint in the NACIAM (N-acetylcysteine in acute myocardial infarction) trial, said Ms. Pasupathy of the University of Adelaide, Australia.

Bruce Jancin/Frontline Medical News

NACIAM, which she stressed was a pilot study, included 75 randomized STEMI patients with follow-up cardiac MRIs obtained at about 5 days post-PCI, most of whom had another MRI at about 8 months.

All participants received IV glycerol trinitrate at a rate of 25 mcg/min for 48 hours starting in the emergency department. Patients in the active treatment arm received IV N-acetylcysteine (NAC) at 20 mg/min for the first hour and 10 mg/min for the next 47 hours. Controls got placebo at 40 mL/hour for the first hour and 20 mL/hour thereafter.

Cardiac MRI at 5 days showed a myocardial infarct size of 16.5% in the control group and 11% with active treatment. This absolute 5.5% reduction in infarct size in NAC recipients was achieved despite no difference between the two groups in myocardial area at risk by MRI, which was roughly 24%. Nor did the groups differ in rates of anterior MI or microvascular obstruction. The myocardial salvage rate was 60% in the NAC group and just 27% in controls.

Creatine kinase levels, measured hourly during the first 24 hours of hospitalization, were consistently lower in the NAC group, although the difference didn’t reach statistical significance.

In-hospital rates of hypotension, bleeding, or renal dysfunction were similar in the two study arms. However, at 2 years of follow-up the composite rate of death or cardiac rehospitalization was 27% in the control group, compared with 6% in patients who got NAC.

A key to the demonstrable success of the adjunctive NAC/nitrate treatment strategy was that it began early, in the emergency department, when patients initially presented with STEMI. The mean total ischemia time for study participants was 2.4 hours, and the shorter the duration of ischemia, the larger the reduction seen in infarct size, according to Ms. Pasupathy.

The rationale for this therapy is that NAC is thought to reduce oxidative stress by scavenging reactive oxygen species and inhibiting their release, thereby minimizing reperfusion injury. The Australian investigators also believe that NAC potentiates the effects of glycerol trinitrate in improving tissue reperfusion through enhanced vasodilation, inhibition of platelet aggregation, and dampening of inflammation. A reduction in reperfusion injury accompanied by increased tissue reperfusion could result in reduced infarct size, she explained.

Bruce Jancin/Frontline Medical News

John F. Beltrame, MD, lead investigator in the NACIAM study, noted that infarct size and myocardial salvage are surrogate endpoints. The investigators plan to conduct a larger trial with hard clinical outcomes.

“The key thing we need to do before we start using this in widespread fashion and changing practice guidelines is to look at clinical endpoints,” said Dr. Beltrame, professor of medicine at the University of Adelaide.

Nonetheless, he added, this therapy is given routinely in the setting of primary PCI for STEMI where he practices. That has been the case for 20 years because he and colleagues in his department did some of the early studies suggesting NAC was beneficial.

“Hospitals have different practices, and this is one of our particular practices,” the cardiologist said.

It all sounded pretty good to Jorge A. Belardi, MD, who co-chaired a press conference devoted to the NACIAM trial and other hotline presentations.

“It’s a very benign combination of medicines to use. So why not use it? We already use it to prevent contrast nephropathy. And there are no contraindications, to my knowledge,” said Dr. Belardi, director of the department of cardiology at the Buenos Aires Cardiovascular Institute.

Michel Ovize, MD, of the University of Lyon (France), the formal discussant designated for NACIAM, took a more flinty eyed view, noting that the study was small and previous studies of NAC during the past 2 decades have yielded conflicting results.

Ms. Pasupathy responded that a likely explanation for the disparate results is the fact that other investigators didn’t start NAC at the soonest possible time in the ED.

The NACIAM trial was funded by the Australian National Heart Foundation. Ms. Pasupathy and Dr. Beltrame reported having no financial conflicts of interest.

[email protected]

ROME – Early administration of high-dose N-acetylcysteine and low-dose glyceryl trinitrate in ST-segment elevation acute myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI) achieved a 30% reduction in myocardial infarct size, compared with placebo in a randomized, double-blind, multicenter clinical trial, Sivabaskari Pasupathy reported at the annual congress of the European Society of Cardiology.

The adjunctive regimen also resulted in a doubling of myocardial salvage, the secondary endpoint in the NACIAM (N-acetylcysteine in acute myocardial infarction) trial, said Ms. Pasupathy of the University of Adelaide, Australia.

Bruce Jancin/Frontline Medical News

NACIAM, which she stressed was a pilot study, included 75 randomized STEMI patients with follow-up cardiac MRIs obtained at about 5 days post-PCI, most of whom had another MRI at about 8 months.

All participants received IV glycerol trinitrate at a rate of 25 mcg/min for 48 hours starting in the emergency department. Patients in the active treatment arm received IV N-acetylcysteine (NAC) at 20 mg/min for the first hour and 10 mg/min for the next 47 hours. Controls got placebo at 40 mL/hour for the first hour and 20 mL/hour thereafter.

Cardiac MRI at 5 days showed a myocardial infarct size of 16.5% in the control group and 11% with active treatment. This absolute 5.5% reduction in infarct size in NAC recipients was achieved despite no difference between the two groups in myocardial area at risk by MRI, which was roughly 24%. Nor did the groups differ in rates of anterior MI or microvascular obstruction. The myocardial salvage rate was 60% in the NAC group and just 27% in controls.

Creatine kinase levels, measured hourly during the first 24 hours of hospitalization, were consistently lower in the NAC group, although the difference didn’t reach statistical significance.

In-hospital rates of hypotension, bleeding, or renal dysfunction were similar in the two study arms. However, at 2 years of follow-up the composite rate of death or cardiac rehospitalization was 27% in the control group, compared with 6% in patients who got NAC.

A key to the demonstrable success of the adjunctive NAC/nitrate treatment strategy was that it began early, in the emergency department, when patients initially presented with STEMI. The mean total ischemia time for study participants was 2.4 hours, and the shorter the duration of ischemia, the larger the reduction seen in infarct size, according to Ms. Pasupathy.

The rationale for this therapy is that NAC is thought to reduce oxidative stress by scavenging reactive oxygen species and inhibiting their release, thereby minimizing reperfusion injury. The Australian investigators also believe that NAC potentiates the effects of glycerol trinitrate in improving tissue reperfusion through enhanced vasodilation, inhibition of platelet aggregation, and dampening of inflammation. A reduction in reperfusion injury accompanied by increased tissue reperfusion could result in reduced infarct size, she explained.

Bruce Jancin/Frontline Medical News

John F. Beltrame, MD, lead investigator in the NACIAM study, noted that infarct size and myocardial salvage are surrogate endpoints. The investigators plan to conduct a larger trial with hard clinical outcomes.

“The key thing we need to do before we start using this in widespread fashion and changing practice guidelines is to look at clinical endpoints,” said Dr. Beltrame, professor of medicine at the University of Adelaide.

Nonetheless, he added, this therapy is given routinely in the setting of primary PCI for STEMI where he practices. That has been the case for 20 years because he and colleagues in his department did some of the early studies suggesting NAC was beneficial.

“Hospitals have different practices, and this is one of our particular practices,” the cardiologist said.

It all sounded pretty good to Jorge A. Belardi, MD, who co-chaired a press conference devoted to the NACIAM trial and other hotline presentations.

“It’s a very benign combination of medicines to use. So why not use it? We already use it to prevent contrast nephropathy. And there are no contraindications, to my knowledge,” said Dr. Belardi, director of the department of cardiology at the Buenos Aires Cardiovascular Institute.

Michel Ovize, MD, of the University of Lyon (France), the formal discussant designated for NACIAM, took a more flinty eyed view, noting that the study was small and previous studies of NAC during the past 2 decades have yielded conflicting results.

Ms. Pasupathy responded that a likely explanation for the disparate results is the fact that other investigators didn’t start NAC at the soonest possible time in the ED.

The NACIAM trial was funded by the Australian National Heart Foundation. Ms. Pasupathy and Dr. Beltrame reported having no financial conflicts of interest.

[email protected]

Dr. Tunc's literature review and retrospective review of headache clinic data provide food for thought with regard to chronic daily headache (CDH) in younger children. The rate of CDH in the papers reviewed ranged from 8% to 30%. I think this range represents the differences in nature between the pediatric headache clinics included in the sample. In some areas, the local primary care providers refer all children with headache to headache clinics. In other areas, the primary care providers hold on to "easy" headache patients and refer only the "tough cases." For that reason, it is hard to generalize from Dr. Tunc's finding. Suffice it to say that tertiary pediatric headache clinics do see some younger children with CDH. The Cleveland Clinic experience showed a prevalence of 58%, so that clinic sees the harder cases.

Dr. Tunc did not find MRI to be useful in children with CDH. I just want to caution readers to order MRIs when patients have systemic signs (eg, growth failure or secondary amenorrhea), neurologic signs (eg, ataxia, slurred speech, one-sided weakness, or facial asymmetry), abrupt onset of headache (think of ruptured aneurysm), or a new change in headache pattern. We must be careful with conclusions drawn from retrospective studies because we can't control for any factors. Although no MRIs were positive, we don't know about patients who came to the neurosurgeon through other pathways besides the headache clinic.

Dr. Tunc mentioned that younger patients had a longer duration of illness before seeking tertiary care, and she speculated as to why. Further clarification is needed to develop a plausible explanation. How was the time measured? Was it measured from the first headache until the tertiary care visit, or from onset of CDH until the tertiary care visit? If the former is true, then I might reach a different conclusion. Perhaps it takes longer for younger children to chronify than older children. If, on the other hand, time was measured from the onset of CDH until presentation, then the authors' explanations may indeed be sound.

In summary, this is a great study that shows that small children presenting to a tertiary care center do get CDH at a higher rate than we thought. It would be terrific to poll other pediatric headache programs to compare and contrast with the findings of this study.

—Jack Gladstein, MD
Professor of Pediatrics and Neurology
Director of the Pediatric Headache Clinic
University of Maryland School of Medicine
Baltimore

Dr. Tunc's literature review and retrospective review of headache clinic data provide food for thought with regard to chronic daily headache (CDH) in younger children. The rate of CDH in the papers reviewed ranged from 8% to 30%. I think this range represents the differences in nature between the pediatric headache clinics included in the sample. In some areas, the local primary care providers refer all children with headache to headache clinics. In other areas, the primary care providers hold on to "easy" headache patients and refer only the "tough cases." For that reason, it is hard to generalize from Dr. Tunc's finding. Suffice it to say that tertiary pediatric headache clinics do see some younger children with CDH. The Cleveland Clinic experience showed a prevalence of 58%, so that clinic sees the harder cases.

Dr. Tunc did not find MRI to be useful in children with CDH. I just want to caution readers to order MRIs when patients have systemic signs (eg, growth failure or secondary amenorrhea), neurologic signs (eg, ataxia, slurred speech, one-sided weakness, or facial asymmetry), abrupt onset of headache (think of ruptured aneurysm), or a new change in headache pattern. We must be careful with conclusions drawn from retrospective studies because we can't control for any factors. Although no MRIs were positive, we don't know about patients who came to the neurosurgeon through other pathways besides the headache clinic.

Dr. Tunc mentioned that younger patients had a longer duration of illness before seeking tertiary care, and she speculated as to why. Further clarification is needed to develop a plausible explanation. How was the time measured? Was it measured from the first headache until the tertiary care visit, or from onset of CDH until the tertiary care visit? If the former is true, then I might reach a different conclusion. Perhaps it takes longer for younger children to chronify than older children. If, on the other hand, time was measured from the onset of CDH until presentation, then the authors' explanations may indeed be sound.

In summary, this is a great study that shows that small children presenting to a tertiary care center do get CDH at a higher rate than we thought. It would be terrific to poll other pediatric headache programs to compare and contrast with the findings of this study.

—Jack Gladstein, MD
Professor of Pediatrics and Neurology
Director of the Pediatric Headache Clinic
University of Maryland School of Medicine
Baltimore

Dr. Tunc's literature review and retrospective review of headache clinic data provide food for thought with regard to chronic daily headache (CDH) in younger children. The rate of CDH in the papers reviewed ranged from 8% to 30%. I think this range represents the differences in nature between the pediatric headache clinics included in the sample. In some areas, the local primary care providers refer all children with headache to headache clinics. In other areas, the primary care providers hold on to "easy" headache patients and refer only the "tough cases." For that reason, it is hard to generalize from Dr. Tunc's finding. Suffice it to say that tertiary pediatric headache clinics do see some younger children with CDH. The Cleveland Clinic experience showed a prevalence of 58%, so that clinic sees the harder cases.

Dr. Tunc did not find MRI to be useful in children with CDH. I just want to caution readers to order MRIs when patients have systemic signs (eg, growth failure or secondary amenorrhea), neurologic signs (eg, ataxia, slurred speech, one-sided weakness, or facial asymmetry), abrupt onset of headache (think of ruptured aneurysm), or a new change in headache pattern. We must be careful with conclusions drawn from retrospective studies because we can't control for any factors. Although no MRIs were positive, we don't know about patients who came to the neurosurgeon through other pathways besides the headache clinic.

Dr. Tunc mentioned that younger patients had a longer duration of illness before seeking tertiary care, and she speculated as to why. Further clarification is needed to develop a plausible explanation. How was the time measured? Was it measured from the first headache until the tertiary care visit, or from onset of CDH until the tertiary care visit? If the former is true, then I might reach a different conclusion. Perhaps it takes longer for younger children to chronify than older children. If, on the other hand, time was measured from the onset of CDH until presentation, then the authors' explanations may indeed be sound.

In summary, this is a great study that shows that small children presenting to a tertiary care center do get CDH at a higher rate than we thought. It would be terrific to poll other pediatric headache programs to compare and contrast with the findings of this study.

—Jack Gladstein, MD
Professor of Pediatrics and Neurology
Director of the Pediatric Headache Clinic
University of Maryland School of Medicine
Baltimore

A 19-year-old man presented to our clinic with erythematous, pruritic, lightly-scaled, and annular patches on his dorsal wrists. The rash had first appeared 3 weeks earlier on the patient’s left wrist, which is where he’d been wearing a chrome-colored watch for a couple of years. After the rash appeared on his left wrist, the patient began wearing the watch on his right wrist. Soon after the switch, the rash appeared on his right wrist. The patient was otherwise healthy and denied any previous rashes, had no body piercings or allergies of any kind, and was not on any medications.

On physical exam, we noted 2 erythematous, scaly, annular, and slightly raised plaques on the distal dorsal aspects of both forearms/wrists with a few erythematous papular lesions (FIGURE). There was also scaling on the soles of the patient’s feet and white, moist scaling in the web space between his 4th and 5th toes bilaterally.

COURTESY OF STEPHEN E. HELMS, MD, FAAD

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

Diagnosis: Tinea corporis (ringworm)

The patient and physician initially considered the possibility of allergic contact dermatitis due to nickel because of the history of redness, scaling, and itching underneath the watch when it was worn on the left wrist, and then when it was worn on the right wrist. Nickel dermatitis is common and it is easy to attribute the cause of a condition like this to the most obvious diagnosis without considering a more complete differential diagnosis.¹

However, there were clues that prompted us to suspect tinea corporis (ringworm). The red, scaly rash spread centrifugally over several weeks, and fomites, such as a watch, can spread infectious diseases. Also, our patient had a few erythematous papular lesions, and the presence of papules in addition to scaling rings is typical of fungal infections involving hair follicles (Majocchi’s granuloma).

A positive potassium hydroxide (KOH) preparation confirmed the diagnosis and eliminated the need for nickel patch testing.²

Warmth and moisture could explain tinea on the wrists

Dermatophytes are fungi that can cause infections in the skin, hair, and nails. They are classified by where they are found—anthropophilic (humans), geophilic (soil), or zoophilic (animals). Anthropophilic and zoophilic dermatophytes from the genera Trichophyton, Microsporum, and Epidermophyton are primarily responsible for human fungal infections.³ It is estimated that superficial fungal infections affect up to a quarter of the world’s population.³

The wrists are not a common place for tinea corporis, but the condition can occur anywhere on the body.

Tinea corporis mainly occurs in prepubertal children, presenting as a red, annular, scaly, pruritic patch with central clearing and an active border.⁴ Tinea corporis includes all superficial dermatophyte infections of the glabrous skin and is particularly common in areas of excessive heat and moisture.⁵ Patients can pick up tinea corporis via fomites at the gym, through soil in the garden, or by touching a pet’s fur or a child’s scalp when either has the fungal infection.

The wrists are not a common place for tinea corporis, but the condition can occur anywhere on the body. This patient may well have contracted tinea from his own interdigital tinea pedis. Warmth and moisture under the watch could also explain the predilection for fungus to grow on the wrists.

Distinguish between contact dermatitis and tinea corporis

The differential diagnosis for tinea corporis includes allergic contact dermatitis, granuloma annulare, annular elastolytic granuloma, and erythema chronicum migrans.

Allergic contact dermatitis is caused by an allergy to a substance, such as the metal nickel. A preliminary diagnosis of contact dermatitis could easily be made in error if one were to assume that a patient was having a type IV hypersensitivity response to nickel from a watch.⁶

Granuloma annulare produces slowly expanding annular plaques that are not itchy and do not scale. This commonly occurs over the joints and is of unknown etiology.⁷

Annular elastolytic granuloma is a variant of granuloma annulare that occurs on skin that has been exposed to the sun. It presents with a red, ring-like pattern and is associated with little scaling or pruritus.⁸

Erythema chronicum migrans produces annular lesions at the site of a tick bite and is the primary sign of Lyme disease. The tick must be in place for 24 hours for infection to occur.⁹ (Our patient did not notice a tick attached at either site.)

In this case, a KOH preparation of skin scrapings identified septate hyphae, which supported our diagnosis of tinea corporis.² A history of red, scaly, itchy, and expanding round/oval patches or plaques and evidence of “athlete’s foot” can also help one to make the diagnosis.

Antifungal agents will clear the rash

Proper treatment of tinea corporis consists of antifungal creams containing ketoconazole, econazole, or naftifine on non-hair-bearing areas. The creams should be applied twice daily and rarely cause adverse effects. Bandages are not usually necessary, but may be used if contact with others is anticipated. For the scalp and other hair-bearing areas, systemic treatment with terbinafine 250 mg daily for one month in an adult is necessary. Oral agents will usually clear the rash within 4 to 6 weeks.^10,11

Because our patient had bilateral involvement and some papule formation indicating Majocchi’s granuloma, we prescribed oral terbinafine 250 mg daily for 2 weeks in addition to econazole cream. The patient was to apply the cream for a total of 4 weeks to ensure the rash did not recur.

CORRESPONDENCE
Stephen E. Helms, MD, Department of Dermatology, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216; [email protected].

A 19-year-old man presented to our clinic with erythematous, pruritic, lightly-scaled, and annular patches on his dorsal wrists. The rash had first appeared 3 weeks earlier on the patient’s left wrist, which is where he’d been wearing a chrome-colored watch for a couple of years. After the rash appeared on his left wrist, the patient began wearing the watch on his right wrist. Soon after the switch, the rash appeared on his right wrist. The patient was otherwise healthy and denied any previous rashes, had no body piercings or allergies of any kind, and was not on any medications.

On physical exam, we noted 2 erythematous, scaly, annular, and slightly raised plaques on the distal dorsal aspects of both forearms/wrists with a few erythematous papular lesions (FIGURE). There was also scaling on the soles of the patient’s feet and white, moist scaling in the web space between his 4th and 5th toes bilaterally.

COURTESY OF STEPHEN E. HELMS, MD, FAAD

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

Diagnosis: Tinea corporis (ringworm)

The patient and physician initially considered the possibility of allergic contact dermatitis due to nickel because of the history of redness, scaling, and itching underneath the watch when it was worn on the left wrist, and then when it was worn on the right wrist. Nickel dermatitis is common and it is easy to attribute the cause of a condition like this to the most obvious diagnosis without considering a more complete differential diagnosis.¹

However, there were clues that prompted us to suspect tinea corporis (ringworm). The red, scaly rash spread centrifugally over several weeks, and fomites, such as a watch, can spread infectious diseases. Also, our patient had a few erythematous papular lesions, and the presence of papules in addition to scaling rings is typical of fungal infections involving hair follicles (Majocchi’s granuloma).

A positive potassium hydroxide (KOH) preparation confirmed the diagnosis and eliminated the need for nickel patch testing.²

Warmth and moisture could explain tinea on the wrists

Dermatophytes are fungi that can cause infections in the skin, hair, and nails. They are classified by where they are found—anthropophilic (humans), geophilic (soil), or zoophilic (animals). Anthropophilic and zoophilic dermatophytes from the genera Trichophyton, Microsporum, and Epidermophyton are primarily responsible for human fungal infections.³ It is estimated that superficial fungal infections affect up to a quarter of the world’s population.³

The wrists are not a common place for tinea corporis, but the condition can occur anywhere on the body.

Tinea corporis mainly occurs in prepubertal children, presenting as a red, annular, scaly, pruritic patch with central clearing and an active border.⁴ Tinea corporis includes all superficial dermatophyte infections of the glabrous skin and is particularly common in areas of excessive heat and moisture.⁵ Patients can pick up tinea corporis via fomites at the gym, through soil in the garden, or by touching a pet’s fur or a child’s scalp when either has the fungal infection.

The wrists are not a common place for tinea corporis, but the condition can occur anywhere on the body. This patient may well have contracted tinea from his own interdigital tinea pedis. Warmth and moisture under the watch could also explain the predilection for fungus to grow on the wrists.

Distinguish between contact dermatitis and tinea corporis

The differential diagnosis for tinea corporis includes allergic contact dermatitis, granuloma annulare, annular elastolytic granuloma, and erythema chronicum migrans.

Allergic contact dermatitis is caused by an allergy to a substance, such as the metal nickel. A preliminary diagnosis of contact dermatitis could easily be made in error if one were to assume that a patient was having a type IV hypersensitivity response to nickel from a watch.⁶

Granuloma annulare produces slowly expanding annular plaques that are not itchy and do not scale. This commonly occurs over the joints and is of unknown etiology.⁷

Annular elastolytic granuloma is a variant of granuloma annulare that occurs on skin that has been exposed to the sun. It presents with a red, ring-like pattern and is associated with little scaling or pruritus.⁸

Erythema chronicum migrans produces annular lesions at the site of a tick bite and is the primary sign of Lyme disease. The tick must be in place for 24 hours for infection to occur.⁹ (Our patient did not notice a tick attached at either site.)

In this case, a KOH preparation of skin scrapings identified septate hyphae, which supported our diagnosis of tinea corporis.² A history of red, scaly, itchy, and expanding round/oval patches or plaques and evidence of “athlete’s foot” can also help one to make the diagnosis.

Antifungal agents will clear the rash

Proper treatment of tinea corporis consists of antifungal creams containing ketoconazole, econazole, or naftifine on non-hair-bearing areas. The creams should be applied twice daily and rarely cause adverse effects. Bandages are not usually necessary, but may be used if contact with others is anticipated. For the scalp and other hair-bearing areas, systemic treatment with terbinafine 250 mg daily for one month in an adult is necessary. Oral agents will usually clear the rash within 4 to 6 weeks.^10,11

Because our patient had bilateral involvement and some papule formation indicating Majocchi’s granuloma, we prescribed oral terbinafine 250 mg daily for 2 weeks in addition to econazole cream. The patient was to apply the cream for a total of 4 weeks to ensure the rash did not recur.

CORRESPONDENCE
Stephen E. Helms, MD, Department of Dermatology, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216; [email protected].

A 19-year-old man presented to our clinic with erythematous, pruritic, lightly-scaled, and annular patches on his dorsal wrists. The rash had first appeared 3 weeks earlier on the patient’s left wrist, which is where he’d been wearing a chrome-colored watch for a couple of years. After the rash appeared on his left wrist, the patient began wearing the watch on his right wrist. Soon after the switch, the rash appeared on his right wrist. The patient was otherwise healthy and denied any previous rashes, had no body piercings or allergies of any kind, and was not on any medications.

On physical exam, we noted 2 erythematous, scaly, annular, and slightly raised plaques on the distal dorsal aspects of both forearms/wrists with a few erythematous papular lesions (FIGURE). There was also scaling on the soles of the patient’s feet and white, moist scaling in the web space between his 4th and 5th toes bilaterally.

COURTESY OF STEPHEN E. HELMS, MD, FAAD

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

Diagnosis: Tinea corporis (ringworm)

The patient and physician initially considered the possibility of allergic contact dermatitis due to nickel because of the history of redness, scaling, and itching underneath the watch when it was worn on the left wrist, and then when it was worn on the right wrist. Nickel dermatitis is common and it is easy to attribute the cause of a condition like this to the most obvious diagnosis without considering a more complete differential diagnosis.¹

However, there were clues that prompted us to suspect tinea corporis (ringworm). The red, scaly rash spread centrifugally over several weeks, and fomites, such as a watch, can spread infectious diseases. Also, our patient had a few erythematous papular lesions, and the presence of papules in addition to scaling rings is typical of fungal infections involving hair follicles (Majocchi’s granuloma).

A positive potassium hydroxide (KOH) preparation confirmed the diagnosis and eliminated the need for nickel patch testing.²

Warmth and moisture could explain tinea on the wrists

Dermatophytes are fungi that can cause infections in the skin, hair, and nails. They are classified by where they are found—anthropophilic (humans), geophilic (soil), or zoophilic (animals). Anthropophilic and zoophilic dermatophytes from the genera Trichophyton, Microsporum, and Epidermophyton are primarily responsible for human fungal infections.³ It is estimated that superficial fungal infections affect up to a quarter of the world’s population.³

The wrists are not a common place for tinea corporis, but the condition can occur anywhere on the body.

Tinea corporis mainly occurs in prepubertal children, presenting as a red, annular, scaly, pruritic patch with central clearing and an active border.⁴ Tinea corporis includes all superficial dermatophyte infections of the glabrous skin and is particularly common in areas of excessive heat and moisture.⁵ Patients can pick up tinea corporis via fomites at the gym, through soil in the garden, or by touching a pet’s fur or a child’s scalp when either has the fungal infection.

The wrists are not a common place for tinea corporis, but the condition can occur anywhere on the body. This patient may well have contracted tinea from his own interdigital tinea pedis. Warmth and moisture under the watch could also explain the predilection for fungus to grow on the wrists.

Distinguish between contact dermatitis and tinea corporis

The differential diagnosis for tinea corporis includes allergic contact dermatitis, granuloma annulare, annular elastolytic granuloma, and erythema chronicum migrans.

Allergic contact dermatitis is caused by an allergy to a substance, such as the metal nickel. A preliminary diagnosis of contact dermatitis could easily be made in error if one were to assume that a patient was having a type IV hypersensitivity response to nickel from a watch.⁶

Granuloma annulare produces slowly expanding annular plaques that are not itchy and do not scale. This commonly occurs over the joints and is of unknown etiology.⁷

Annular elastolytic granuloma is a variant of granuloma annulare that occurs on skin that has been exposed to the sun. It presents with a red, ring-like pattern and is associated with little scaling or pruritus.⁸

Erythema chronicum migrans produces annular lesions at the site of a tick bite and is the primary sign of Lyme disease. The tick must be in place for 24 hours for infection to occur.⁹ (Our patient did not notice a tick attached at either site.)

In this case, a KOH preparation of skin scrapings identified septate hyphae, which supported our diagnosis of tinea corporis.² A history of red, scaly, itchy, and expanding round/oval patches or plaques and evidence of “athlete’s foot” can also help one to make the diagnosis.

Antifungal agents will clear the rash

Proper treatment of tinea corporis consists of antifungal creams containing ketoconazole, econazole, or naftifine on non-hair-bearing areas. The creams should be applied twice daily and rarely cause adverse effects. Bandages are not usually necessary, but may be used if contact with others is anticipated. For the scalp and other hair-bearing areas, systemic treatment with terbinafine 250 mg daily for one month in an adult is necessary. Oral agents will usually clear the rash within 4 to 6 weeks.^10,11

Because our patient had bilateral involvement and some papule formation indicating Majocchi’s granuloma, we prescribed oral terbinafine 250 mg daily for 2 weeks in addition to econazole cream. The patient was to apply the cream for a total of 4 weeks to ensure the rash did not recur.

CORRESPONDENCE
Stephen E. Helms, MD, Department of Dermatology, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216; [email protected].

SAN DIEGO—Chronic daily headache is common in younger children and manifests with similar characteristics as it does among older children, according to research presented at the 58th Annual Scientific Meeting of the American Headache Society. Because younger children often present for evaluation later in the disease process, compared with older children, earlier diagnosis would decrease morbidity significantly. Greater effort is needed to decrease medication overuse and school absenteeism, which contribute to headache chronification, said Emine Tunc, MD, research scholar at the Cleveland Clinic Foundation.

To increase the awareness of chronic headache among children between ages 3 and 11, Dr. Tunc and colleagues performed a literature review. The group identified 29 articles that examined the prevalence and characteristics of chronic daily headache in children. Six of them included information specific to younger children.

Dr. Tunc and her colleague A. David Rothner, MD, a child neurologist at the Cleveland Clinic, also reviewed the charts of patients who presented to the Cleveland Clinic's headache clinic for evaluation between May 2014 and May 2015. They defined chronic daily headache as more than 15 days of headache per month for at least two months and excluded patients with secondary headache disorders.

Pediatric Incidence of Chronic Daily Headache

The mean frequency of chronic daily headache in children and adolescents reported in the literature ranged from 8% to 30%, with a weighted mean of 23%. Between 28% and 56% of patients in the literature were younger than 12. Dr. Tunc and colleagues identified 327 patients with primary headache in their chart review. Of those patients, 57% had chronic daily headache. Approximately 28% of patients with chronic daily headache were younger than 12. The most common type of chronic daily headache was chronic migraine (a combination of migraine and tension-type headaches).

In the literature review and in the chart review, the male-to-female ratio was 1:2 among older patients (ie, between ages 11 and 18), which is similar to the ratio among adults, and 1:1 among younger patients (ie, ages 3 to 11). "This follows the concept that males develop headaches earlier than females, and later on, females [predominate]," said Dr. Tunc.

Younger Children Present Later in the Disease Process

The most interesting finding, she added, was that younger patients had greater duration of illness before initial evaluation, compared with older patients. One possible explanation for this finding is that children younger than 11 may not be articulate enough to state that they are having a headache, or parents may misinterpret signs and symptoms of headaches (eg, cessation of play and retreat to a dark, quiet room). In addition, parents may doubt that their young children are having headaches and may ignore them.

The chart review also showed that 61% of younger children and 52% of older children had medication overuse. "This difference between younger and older children is not statistically significant, but we were not expecting to see this at all," said Dr. Tunc. "One possible explanation, which we come across most commonly, is that parents are eager to stop the pain of little ones, but they are less concerned in older children. But the information that they are lacking is that pain killers themselves can initiate headaches."

About 38% of younger patients and 59% of older patients underwent brain MRI. All MRI results were within normal limits. "This proves to us that if there is no neurologic symptom and the physical exam is not concerning for underlying neurologic diseases such as tumor or increased CSF, MRI is not going to help us to diagnose these patients," said Dr. Tunc. "A comprehensive history and a really good physical exam will help us to diagnose these patients without an MRI."

Finally, the investigators observed that 30% of younger patients and 41% of older patients had excessive school absences, which they defined as missing more than 10 full days of school in the previous three months. "This school absenteeism is not only a result of the headaches, but also contributes to the chronicity of the headaches and makes those headaches harder to treat," said Dr. Tunc.

"As a next step, we should find ways to share this information with the pediatricians," she continued. Pediatricians are the first physicians to see children with headache and should be able to provide early diagnosis, treatment, or at least refer patients to a headache specialist or child neurologist, Dr. Tunc concluded.

—Erik Greb

SAN DIEGO—Chronic daily headache is common in younger children and manifests with similar characteristics as it does among older children, according to research presented at the 58th Annual Scientific Meeting of the American Headache Society. Because younger children often present for evaluation later in the disease process, compared with older children, earlier diagnosis would decrease morbidity significantly. Greater effort is needed to decrease medication overuse and school absenteeism, which contribute to headache chronification, said Emine Tunc, MD, research scholar at the Cleveland Clinic Foundation.

To increase the awareness of chronic headache among children between ages 3 and 11, Dr. Tunc and colleagues performed a literature review. The group identified 29 articles that examined the prevalence and characteristics of chronic daily headache in children. Six of them included information specific to younger children.

Dr. Tunc and her colleague A. David Rothner, MD, a child neurologist at the Cleveland Clinic, also reviewed the charts of patients who presented to the Cleveland Clinic's headache clinic for evaluation between May 2014 and May 2015. They defined chronic daily headache as more than 15 days of headache per month for at least two months and excluded patients with secondary headache disorders.

Pediatric Incidence of Chronic Daily Headache

The mean frequency of chronic daily headache in children and adolescents reported in the literature ranged from 8% to 30%, with a weighted mean of 23%. Between 28% and 56% of patients in the literature were younger than 12. Dr. Tunc and colleagues identified 327 patients with primary headache in their chart review. Of those patients, 57% had chronic daily headache. Approximately 28% of patients with chronic daily headache were younger than 12. The most common type of chronic daily headache was chronic migraine (a combination of migraine and tension-type headaches).

In the literature review and in the chart review, the male-to-female ratio was 1:2 among older patients (ie, between ages 11 and 18), which is similar to the ratio among adults, and 1:1 among younger patients (ie, ages 3 to 11). "This follows the concept that males develop headaches earlier than females, and later on, females [predominate]," said Dr. Tunc.

Younger Children Present Later in the Disease Process

The most interesting finding, she added, was that younger patients had greater duration of illness before initial evaluation, compared with older patients. One possible explanation for this finding is that children younger than 11 may not be articulate enough to state that they are having a headache, or parents may misinterpret signs and symptoms of headaches (eg, cessation of play and retreat to a dark, quiet room). In addition, parents may doubt that their young children are having headaches and may ignore them.

The chart review also showed that 61% of younger children and 52% of older children had medication overuse. "This difference between younger and older children is not statistically significant, but we were not expecting to see this at all," said Dr. Tunc. "One possible explanation, which we come across most commonly, is that parents are eager to stop the pain of little ones, but they are less concerned in older children. But the information that they are lacking is that pain killers themselves can initiate headaches."

About 38% of younger patients and 59% of older patients underwent brain MRI. All MRI results were within normal limits. "This proves to us that if there is no neurologic symptom and the physical exam is not concerning for underlying neurologic diseases such as tumor or increased CSF, MRI is not going to help us to diagnose these patients," said Dr. Tunc. "A comprehensive history and a really good physical exam will help us to diagnose these patients without an MRI."

Finally, the investigators observed that 30% of younger patients and 41% of older patients had excessive school absences, which they defined as missing more than 10 full days of school in the previous three months. "This school absenteeism is not only a result of the headaches, but also contributes to the chronicity of the headaches and makes those headaches harder to treat," said Dr. Tunc.

"As a next step, we should find ways to share this information with the pediatricians," she continued. Pediatricians are the first physicians to see children with headache and should be able to provide early diagnosis, treatment, or at least refer patients to a headache specialist or child neurologist, Dr. Tunc concluded.

—Erik Greb

SAN DIEGO—Chronic daily headache is common in younger children and manifests with similar characteristics as it does among older children, according to research presented at the 58th Annual Scientific Meeting of the American Headache Society. Because younger children often present for evaluation later in the disease process, compared with older children, earlier diagnosis would decrease morbidity significantly. Greater effort is needed to decrease medication overuse and school absenteeism, which contribute to headache chronification, said Emine Tunc, MD, research scholar at the Cleveland Clinic Foundation.

To increase the awareness of chronic headache among children between ages 3 and 11, Dr. Tunc and colleagues performed a literature review. The group identified 29 articles that examined the prevalence and characteristics of chronic daily headache in children. Six of them included information specific to younger children.

Dr. Tunc and her colleague A. David Rothner, MD, a child neurologist at the Cleveland Clinic, also reviewed the charts of patients who presented to the Cleveland Clinic's headache clinic for evaluation between May 2014 and May 2015. They defined chronic daily headache as more than 15 days of headache per month for at least two months and excluded patients with secondary headache disorders.

Pediatric Incidence of Chronic Daily Headache

The mean frequency of chronic daily headache in children and adolescents reported in the literature ranged from 8% to 30%, with a weighted mean of 23%. Between 28% and 56% of patients in the literature were younger than 12. Dr. Tunc and colleagues identified 327 patients with primary headache in their chart review. Of those patients, 57% had chronic daily headache. Approximately 28% of patients with chronic daily headache were younger than 12. The most common type of chronic daily headache was chronic migraine (a combination of migraine and tension-type headaches).

In the literature review and in the chart review, the male-to-female ratio was 1:2 among older patients (ie, between ages 11 and 18), which is similar to the ratio among adults, and 1:1 among younger patients (ie, ages 3 to 11). "This follows the concept that males develop headaches earlier than females, and later on, females [predominate]," said Dr. Tunc.

Younger Children Present Later in the Disease Process

The most interesting finding, she added, was that younger patients had greater duration of illness before initial evaluation, compared with older patients. One possible explanation for this finding is that children younger than 11 may not be articulate enough to state that they are having a headache, or parents may misinterpret signs and symptoms of headaches (eg, cessation of play and retreat to a dark, quiet room). In addition, parents may doubt that their young children are having headaches and may ignore them.

The chart review also showed that 61% of younger children and 52% of older children had medication overuse. "This difference between younger and older children is not statistically significant, but we were not expecting to see this at all," said Dr. Tunc. "One possible explanation, which we come across most commonly, is that parents are eager to stop the pain of little ones, but they are less concerned in older children. But the information that they are lacking is that pain killers themselves can initiate headaches."

About 38% of younger patients and 59% of older patients underwent brain MRI. All MRI results were within normal limits. "This proves to us that if there is no neurologic symptom and the physical exam is not concerning for underlying neurologic diseases such as tumor or increased CSF, MRI is not going to help us to diagnose these patients," said Dr. Tunc. "A comprehensive history and a really good physical exam will help us to diagnose these patients without an MRI."

Finally, the investigators observed that 30% of younger patients and 41% of older patients had excessive school absences, which they defined as missing more than 10 full days of school in the previous three months. "This school absenteeism is not only a result of the headaches, but also contributes to the chronicity of the headaches and makes those headaches harder to treat," said Dr. Tunc.

"As a next step, we should find ways to share this information with the pediatricians," she continued. Pediatricians are the first physicians to see children with headache and should be able to provide early diagnosis, treatment, or at least refer patients to a headache specialist or child neurologist, Dr. Tunc concluded.

—Erik Greb

Primary care physicians can play an important role in managing thyroid disease in children and teens by proactive screening and evaluation, based on data from a literature review of 83 articles published between Jan. 1, 2010, and Dec. 31, 2015. The review was published online Aug. 29 in JAMA Pediatrics.

“Early diagnosis and treatment of thyroid hormone deficiency is crucial to ensure normal development and cognition,” wrote Dr. Patrick Hanley of the Children’s Hospital of Philadelphia and his colleagues.

Thyroid dysgenesis accounts for 80%-85% of cases of primary congenital hypothyroidism, and many newborns with the condition are asymptomatic at birth because of protection by maternal thyroid hormones. Early signs of thyroid problems include a hoarse cry, prolonged jaundice, lethargy, poor feeding, and constipation, the researchers said (JAMA Pediatr. 2016. doi:10.1001/jamapediatrics.2016.0486).

“Once the diagnosis has been made, additional testing can be considered to determine the etiology of the hypothyroidism so that the family can receive anticipatory guidance in regard to the potential need for lifelong thyroid hormone replacement therapy,” the researchers wrote.

The treatment of choice for congenital hypothyroidism is levothyroxine at a starting dose of 10-15 mcg/kg once daily, they noted.

Read the full study here: http://archpedi.jamanetwork.com/article.aspx?doi=10.1001/jamapediatrics.2016.0486.

Primary care physicians can play an important role in managing thyroid disease in children and teens by proactive screening and evaluation, based on data from a literature review of 83 articles published between Jan. 1, 2010, and Dec. 31, 2015. The review was published online Aug. 29 in JAMA Pediatrics.

“Early diagnosis and treatment of thyroid hormone deficiency is crucial to ensure normal development and cognition,” wrote Dr. Patrick Hanley of the Children’s Hospital of Philadelphia and his colleagues.

Thyroid dysgenesis accounts for 80%-85% of cases of primary congenital hypothyroidism, and many newborns with the condition are asymptomatic at birth because of protection by maternal thyroid hormones. Early signs of thyroid problems include a hoarse cry, prolonged jaundice, lethargy, poor feeding, and constipation, the researchers said (JAMA Pediatr. 2016. doi:10.1001/jamapediatrics.2016.0486).

“Once the diagnosis has been made, additional testing can be considered to determine the etiology of the hypothyroidism so that the family can receive anticipatory guidance in regard to the potential need for lifelong thyroid hormone replacement therapy,” the researchers wrote.

The treatment of choice for congenital hypothyroidism is levothyroxine at a starting dose of 10-15 mcg/kg once daily, they noted.

Read the full study here: http://archpedi.jamanetwork.com/article.aspx?doi=10.1001/jamapediatrics.2016.0486.

Primary care physicians can play an important role in managing thyroid disease in children and teens by proactive screening and evaluation, based on data from a literature review of 83 articles published between Jan. 1, 2010, and Dec. 31, 2015. The review was published online Aug. 29 in JAMA Pediatrics.

“Early diagnosis and treatment of thyroid hormone deficiency is crucial to ensure normal development and cognition,” wrote Dr. Patrick Hanley of the Children’s Hospital of Philadelphia and his colleagues.

Thyroid dysgenesis accounts for 80%-85% of cases of primary congenital hypothyroidism, and many newborns with the condition are asymptomatic at birth because of protection by maternal thyroid hormones. Early signs of thyroid problems include a hoarse cry, prolonged jaundice, lethargy, poor feeding, and constipation, the researchers said (JAMA Pediatr. 2016. doi:10.1001/jamapediatrics.2016.0486).

“Once the diagnosis has been made, additional testing can be considered to determine the etiology of the hypothyroidism so that the family can receive anticipatory guidance in regard to the potential need for lifelong thyroid hormone replacement therapy,” the researchers wrote.

The treatment of choice for congenital hypothyroidism is levothyroxine at a starting dose of 10-15 mcg/kg once daily, they noted.

Read the full study here: http://archpedi.jamanetwork.com/article.aspx?doi=10.1001/jamapediatrics.2016.0486.

A new consensus statement provides recommendations for transitioning adolescents and young adults with neurologic disorders to adult care. Created by the Child Neurology Foundation, the recommendations were published online ahead of print July 27 in Neurology.

"The goal of this research is to help make the transition easier for millions of parents and caregivers of children who are reaching the age where they will be dealing with complex teenage and adult life situations," said study author Lawrence W. Brown, MD, a pediatric neurologist at the Children's Hospital of Philadelphia.

The consensus statement is the work of the Neurology Transition Consensus Panel, an interdisciplinary team including child neurologists, child neurology nurses, adult neurologists, rehabilitation specialists, patients, and family members of neurology patients.

The research team reviewed studies published within the last 10 years focused mainly on transition of care for those with neurologic disorders. Older studies and book chapters that were relevant to transition in general were also included. The consensus statement addresses the great majority of adolescents and young adults whose care shifts from pediatric to adult providers. The paper does not directly address children with brain diseases who are not expected to live to adulthood or those children who are managed by adult neurologists. However, it strongly recommends that adult models of care be introduced even if providers are unchanged.

The consensus statement identifies the following eight best practices for making the transition from pediatric to adult care as smooth as possible:

· Expectation of future transition to the adult care system with the youth and family is discussed before age 13.

· Self-management skills should be assessed at age 12 and reevaluated on a yearly basis.

· Yearly transition planning sessions should also address the youth's medical condition, including current medications and potential side effects; signs and symptoms of concern; genetic counseling and reproductive implications of the condition; issues of puberty and sexuality; driving, alcohol, substance use, and other risks; and emotional or psychological concerns and wellness.

· If appropriate, a discussion with the caregivers regarding the youth's expected legal competency (ie, whether there is a need for legal guardianship and powers of attorney) should begin by age 14. If the youth's expected legal competency is unclear, assessment of that capacity should be made yearly.

· A comprehensive transition plan should be developed by age 14 in collaboration with the youth, caregivers, other health care providers, school personnel, vocational professionals, community services providers, and legal services regarding all aspects of health, financial, and legal care. This is usually the responsibility of the primary care provider.

· The child neurology team is responsible for the neurologic component of the comprehensive transition plan and should update it annually.

· Adult providers are identified in collaboration with the youth and caregivers prior to the anticipated time of transfer. A medical transfer packet is prepared for the adult provider and provided to the youth; it includes the transition plan and medical summary with pertinent history, diagnostic evaluations, previous drug trials, current medications, and protocol for emergency care.

· The child neurology team communicates directly with the new adult provider to ensure smooth completion of the transition process, which is finalized after the first appointment. It is recommended that the child neurologist be available to the youth and the adult provider for continuity and support.

"We believe that following these steps will make a real difference in the lives of our patients as they become independent and self-sufficient adults to the greatest extent possible," said Dr. Brown.

The consensus statement was endorsed by the American Academy of Neurology, the Child Neurology Society, and the American Academy of Pediatrics and was cosponsored by Eisai.

A new consensus statement provides recommendations for transitioning adolescents and young adults with neurologic disorders to adult care. Created by the Child Neurology Foundation, the recommendations were published online ahead of print July 27 in Neurology.

"The goal of this research is to help make the transition easier for millions of parents and caregivers of children who are reaching the age where they will be dealing with complex teenage and adult life situations," said study author Lawrence W. Brown, MD, a pediatric neurologist at the Children's Hospital of Philadelphia.

The consensus statement is the work of the Neurology Transition Consensus Panel, an interdisciplinary team including child neurologists, child neurology nurses, adult neurologists, rehabilitation specialists, patients, and family members of neurology patients.

The research team reviewed studies published within the last 10 years focused mainly on transition of care for those with neurologic disorders. Older studies and book chapters that were relevant to transition in general were also included. The consensus statement addresses the great majority of adolescents and young adults whose care shifts from pediatric to adult providers. The paper does not directly address children with brain diseases who are not expected to live to adulthood or those children who are managed by adult neurologists. However, it strongly recommends that adult models of care be introduced even if providers are unchanged.

The consensus statement identifies the following eight best practices for making the transition from pediatric to adult care as smooth as possible:

· Expectation of future transition to the adult care system with the youth and family is discussed before age 13.

· Self-management skills should be assessed at age 12 and reevaluated on a yearly basis.

· Yearly transition planning sessions should also address the youth's medical condition, including current medications and potential side effects; signs and symptoms of concern; genetic counseling and reproductive implications of the condition; issues of puberty and sexuality; driving, alcohol, substance use, and other risks; and emotional or psychological concerns and wellness.

· If appropriate, a discussion with the caregivers regarding the youth's expected legal competency (ie, whether there is a need for legal guardianship and powers of attorney) should begin by age 14. If the youth's expected legal competency is unclear, assessment of that capacity should be made yearly.

· A comprehensive transition plan should be developed by age 14 in collaboration with the youth, caregivers, other health care providers, school personnel, vocational professionals, community services providers, and legal services regarding all aspects of health, financial, and legal care. This is usually the responsibility of the primary care provider.

· The child neurology team is responsible for the neurologic component of the comprehensive transition plan and should update it annually.

· Adult providers are identified in collaboration with the youth and caregivers prior to the anticipated time of transfer. A medical transfer packet is prepared for the adult provider and provided to the youth; it includes the transition plan and medical summary with pertinent history, diagnostic evaluations, previous drug trials, current medications, and protocol for emergency care.

· The child neurology team communicates directly with the new adult provider to ensure smooth completion of the transition process, which is finalized after the first appointment. It is recommended that the child neurologist be available to the youth and the adult provider for continuity and support.

"We believe that following these steps will make a real difference in the lives of our patients as they become independent and self-sufficient adults to the greatest extent possible," said Dr. Brown.

The consensus statement was endorsed by the American Academy of Neurology, the Child Neurology Society, and the American Academy of Pediatrics and was cosponsored by Eisai.

A new consensus statement provides recommendations for transitioning adolescents and young adults with neurologic disorders to adult care. Created by the Child Neurology Foundation, the recommendations were published online ahead of print July 27 in Neurology.

"The goal of this research is to help make the transition easier for millions of parents and caregivers of children who are reaching the age where they will be dealing with complex teenage and adult life situations," said study author Lawrence W. Brown, MD, a pediatric neurologist at the Children's Hospital of Philadelphia.

The consensus statement is the work of the Neurology Transition Consensus Panel, an interdisciplinary team including child neurologists, child neurology nurses, adult neurologists, rehabilitation specialists, patients, and family members of neurology patients.

The research team reviewed studies published within the last 10 years focused mainly on transition of care for those with neurologic disorders. Older studies and book chapters that were relevant to transition in general were also included. The consensus statement addresses the great majority of adolescents and young adults whose care shifts from pediatric to adult providers. The paper does not directly address children with brain diseases who are not expected to live to adulthood or those children who are managed by adult neurologists. However, it strongly recommends that adult models of care be introduced even if providers are unchanged.

The consensus statement identifies the following eight best practices for making the transition from pediatric to adult care as smooth as possible:

· Expectation of future transition to the adult care system with the youth and family is discussed before age 13.

· Self-management skills should be assessed at age 12 and reevaluated on a yearly basis.

· Yearly transition planning sessions should also address the youth's medical condition, including current medications and potential side effects; signs and symptoms of concern; genetic counseling and reproductive implications of the condition; issues of puberty and sexuality; driving, alcohol, substance use, and other risks; and emotional or psychological concerns and wellness.

· If appropriate, a discussion with the caregivers regarding the youth's expected legal competency (ie, whether there is a need for legal guardianship and powers of attorney) should begin by age 14. If the youth's expected legal competency is unclear, assessment of that capacity should be made yearly.

· A comprehensive transition plan should be developed by age 14 in collaboration with the youth, caregivers, other health care providers, school personnel, vocational professionals, community services providers, and legal services regarding all aspects of health, financial, and legal care. This is usually the responsibility of the primary care provider.

· The child neurology team is responsible for the neurologic component of the comprehensive transition plan and should update it annually.

· Adult providers are identified in collaboration with the youth and caregivers prior to the anticipated time of transfer. A medical transfer packet is prepared for the adult provider and provided to the youth; it includes the transition plan and medical summary with pertinent history, diagnostic evaluations, previous drug trials, current medications, and protocol for emergency care.

· The child neurology team communicates directly with the new adult provider to ensure smooth completion of the transition process, which is finalized after the first appointment. It is recommended that the child neurologist be available to the youth and the adult provider for continuity and support.

"We believe that following these steps will make a real difference in the lives of our patients as they become independent and self-sufficient adults to the greatest extent possible," said Dr. Brown.

The consensus statement was endorsed by the American Academy of Neurology, the Child Neurology Society, and the American Academy of Pediatrics and was cosponsored by Eisai.

This supplement is sponsored by Medtronic.

The retained surgical sponge or gauze after surgical intervention or a birth can have serious consequences for patients and poses a challenging problem for clinicians. This supplement explores the causes and consequences of sponge retention and how the Situate™ Delivery System can help reduce the incidence of gossypiboma, which is responsible for approximately 2000 cases of retained surgical items each year in the US.

Hector Chapa, MD
Clinical Assistant Professor
Texas A&M College of Medicine – College Station
Department of ObGyn, Brazos Valley ObGyn
ObGyn Hospitalist Group
CHI St. Joseph Regional Hospital
Bryan, Texas

Click here to read the Clinical Update

This supplement is sponsored by Medtronic.

The retained surgical sponge or gauze after surgical intervention or a birth can have serious consequences for patients and poses a challenging problem for clinicians. This supplement explores the causes and consequences of sponge retention and how the Situate™ Delivery System can help reduce the incidence of gossypiboma, which is responsible for approximately 2000 cases of retained surgical items each year in the US.

Hector Chapa, MD
Clinical Assistant Professor
Texas A&M College of Medicine – College Station
Department of ObGyn, Brazos Valley ObGyn
ObGyn Hospitalist Group
CHI St. Joseph Regional Hospital
Bryan, Texas

Click here to read the Clinical Update

This supplement is sponsored by Medtronic.

The retained surgical sponge or gauze after surgical intervention or a birth can have serious consequences for patients and poses a challenging problem for clinicians. This supplement explores the causes and consequences of sponge retention and how the Situate™ Delivery System can help reduce the incidence of gossypiboma, which is responsible for approximately 2000 cases of retained surgical items each year in the US.

Hector Chapa, MD
Clinical Assistant Professor
Texas A&M College of Medicine – College Station
Department of ObGyn, Brazos Valley ObGyn
ObGyn Hospitalist Group
CHI St. Joseph Regional Hospital
Bryan, Texas

Click here to read the Clinical Update

The Diagnosis: Livedoid Vasculopathy

Livedoid vasculopathy (LV) is a rare cutaneous disorder that most commonly affects the lower legs. It has an estimated incidence of 1 case per 100,000 per year and predominantly affects women.¹ The disease pathogenesis is not fully understood but is thought to involve thrombosis and occlusion of dermal vessels resulting in tissue hypoxia.² Both inherited and acquired thrombophilic conditions frequently are seen in patients with LV.^3,4 Livedoid vasculopathy also has been described as idiopathic⁵ and is associated with immune complex deposition.⁶ However, the number of cases of idiopathic LV may be overestimated; as technological advancements to detect coagulation abnormalities improve, it is hypothesized that this entity will be identified less often.^2,4

Livedoid vasculopathy has been described in the literature using the term PPURPLE (painful purpuric ulcers with reticular pattern of lower extremities).⁷ The triad of livedo racemosa, recurrent painful ulcerations, and residual healing with atrophie blanche characterizes the clinical manifestations of LV; however, all 3 characteristics do not need to appear simultaneously for a diagnosis to be made. The condition has a chronic course with spontaneous remissions and exacerbations. Episodic ulcerations occur, especially in the summertime, and heal slowly, leaving behind atrophic, porcelain white, stellate-shaped scars called atrophie blanche. Livedo racemosa also may be seen in Sneddon syndrome; however, these patients experience neurologic symptoms secondary to cerebrovascular occlusion. In contrast to livedo racemosa, acquired livedo reticularis represents a physiologic hypoperfusion pattern that occurs in response to cold exposure.⁸ A localized sharp pain, known as angina cutis, typically precedes the clinical symptom of painful ulcerations.⁹ Atrophie blanche once was thought to be specific to LV but has been seen in other diseases such as systemic lupus erythematosus and chronic venous insufficiency.²

The diagnosis of LV is based on identification of characteristic clinical features and skin biopsy. In almost all biopsy specimens, histopathology reveals fibrinoid occlusion of vessels in the superficial and mid dermis.⁴ Other findings may include epidermal necrosis and vessel wall hyalinization and infarction² (Figure). Because LV is commonly misdiagnosed as vasculitis, the absence of hallmark features of vasculitis such as neutrophilic infiltrate of blood vessel walls and fibrinoid necrosis suggest the diagnosis. Extensive laboratory evaluation for inherited and acquired coagulation abnormalities should be performed.

Treatment of LV is difficult, as there is currently no consensus on optimal therapy. The mainstay of therapy is to reduce pain, prevent infection, and reduce ulceration and development of atrophie blanche. Underlying causes should be identified and appropriately treated. Because the primary pathogenesis of LV is considered to be a hypercoagulable state, first-line treatment often includes therapies to enhance blood flow and prevent thrombosis such as smoking cessation, antiplatelet therapy, and pentoxifylline. Vasodilating agents, anti-inflammatory agents, anticoagulation, and fibrinolytic therapy also have been used with varying degrees of success.⁷

The Diagnosis: Livedoid Vasculopathy

Livedoid vasculopathy (LV) is a rare cutaneous disorder that most commonly affects the lower legs. It has an estimated incidence of 1 case per 100,000 per year and predominantly affects women.¹ The disease pathogenesis is not fully understood but is thought to involve thrombosis and occlusion of dermal vessels resulting in tissue hypoxia.² Both inherited and acquired thrombophilic conditions frequently are seen in patients with LV.^3,4 Livedoid vasculopathy also has been described as idiopathic⁵ and is associated with immune complex deposition.⁶ However, the number of cases of idiopathic LV may be overestimated; as technological advancements to detect coagulation abnormalities improve, it is hypothesized that this entity will be identified less often.^2,4

Livedoid vasculopathy has been described in the literature using the term PPURPLE (painful purpuric ulcers with reticular pattern of lower extremities).⁷ The triad of livedo racemosa, recurrent painful ulcerations, and residual healing with atrophie blanche characterizes the clinical manifestations of LV; however, all 3 characteristics do not need to appear simultaneously for a diagnosis to be made. The condition has a chronic course with spontaneous remissions and exacerbations. Episodic ulcerations occur, especially in the summertime, and heal slowly, leaving behind atrophic, porcelain white, stellate-shaped scars called atrophie blanche. Livedo racemosa also may be seen in Sneddon syndrome; however, these patients experience neurologic symptoms secondary to cerebrovascular occlusion. In contrast to livedo racemosa, acquired livedo reticularis represents a physiologic hypoperfusion pattern that occurs in response to cold exposure.⁸ A localized sharp pain, known as angina cutis, typically precedes the clinical symptom of painful ulcerations.⁹ Atrophie blanche once was thought to be specific to LV but has been seen in other diseases such as systemic lupus erythematosus and chronic venous insufficiency.²

The diagnosis of LV is based on identification of characteristic clinical features and skin biopsy. In almost all biopsy specimens, histopathology reveals fibrinoid occlusion of vessels in the superficial and mid dermis.⁴ Other findings may include epidermal necrosis and vessel wall hyalinization and infarction² (Figure). Because LV is commonly misdiagnosed as vasculitis, the absence of hallmark features of vasculitis such as neutrophilic infiltrate of blood vessel walls and fibrinoid necrosis suggest the diagnosis. Extensive laboratory evaluation for inherited and acquired coagulation abnormalities should be performed.

Treatment of LV is difficult, as there is currently no consensus on optimal therapy. The mainstay of therapy is to reduce pain, prevent infection, and reduce ulceration and development of atrophie blanche. Underlying causes should be identified and appropriately treated. Because the primary pathogenesis of LV is considered to be a hypercoagulable state, first-line treatment often includes therapies to enhance blood flow and prevent thrombosis such as smoking cessation, antiplatelet therapy, and pentoxifylline. Vasodilating agents, anti-inflammatory agents, anticoagulation, and fibrinolytic therapy also have been used with varying degrees of success.⁷

The Diagnosis: Livedoid Vasculopathy

Livedoid vasculopathy (LV) is a rare cutaneous disorder that most commonly affects the lower legs. It has an estimated incidence of 1 case per 100,000 per year and predominantly affects women.¹ The disease pathogenesis is not fully understood but is thought to involve thrombosis and occlusion of dermal vessels resulting in tissue hypoxia.² Both inherited and acquired thrombophilic conditions frequently are seen in patients with LV.^3,4 Livedoid vasculopathy also has been described as idiopathic⁵ and is associated with immune complex deposition.⁶ However, the number of cases of idiopathic LV may be overestimated; as technological advancements to detect coagulation abnormalities improve, it is hypothesized that this entity will be identified less often.^2,4

Livedoid vasculopathy has been described in the literature using the term PPURPLE (painful purpuric ulcers with reticular pattern of lower extremities).⁷ The triad of livedo racemosa, recurrent painful ulcerations, and residual healing with atrophie blanche characterizes the clinical manifestations of LV; however, all 3 characteristics do not need to appear simultaneously for a diagnosis to be made. The condition has a chronic course with spontaneous remissions and exacerbations. Episodic ulcerations occur, especially in the summertime, and heal slowly, leaving behind atrophic, porcelain white, stellate-shaped scars called atrophie blanche. Livedo racemosa also may be seen in Sneddon syndrome; however, these patients experience neurologic symptoms secondary to cerebrovascular occlusion. In contrast to livedo racemosa, acquired livedo reticularis represents a physiologic hypoperfusion pattern that occurs in response to cold exposure.⁸ A localized sharp pain, known as angina cutis, typically precedes the clinical symptom of painful ulcerations.⁹ Atrophie blanche once was thought to be specific to LV but has been seen in other diseases such as systemic lupus erythematosus and chronic venous insufficiency.²

The diagnosis of LV is based on identification of characteristic clinical features and skin biopsy. In almost all biopsy specimens, histopathology reveals fibrinoid occlusion of vessels in the superficial and mid dermis.⁴ Other findings may include epidermal necrosis and vessel wall hyalinization and infarction² (Figure). Because LV is commonly misdiagnosed as vasculitis, the absence of hallmark features of vasculitis such as neutrophilic infiltrate of blood vessel walls and fibrinoid necrosis suggest the diagnosis. Extensive laboratory evaluation for inherited and acquired coagulation abnormalities should be performed.

Treatment of LV is difficult, as there is currently no consensus on optimal therapy. The mainstay of therapy is to reduce pain, prevent infection, and reduce ulceration and development of atrophie blanche. Underlying causes should be identified and appropriately treated. Because the primary pathogenesis of LV is considered to be a hypercoagulable state, first-line treatment often includes therapies to enhance blood flow and prevent thrombosis such as smoking cessation, antiplatelet therapy, and pentoxifylline. Vasodilating agents, anti-inflammatory agents, anticoagulation, and fibrinolytic therapy also have been used with varying degrees of success.⁷