Quiz

The Diagnosis: Phrynoderma

Phrynoderma, meaning “toad skin,” was first described by Nicholls¹ in 1933 as a condition due to vitamin A deficiency and characterized by follicular hyperkeratosis. Since then, there has been debate in the literature over the etiology of phrynoderma, as studies have demonstrated different causes for this condition,^2-5 which suggests that it is prudent to check several markers of nutritional status including vitamin A, vitamin B, vitamin E, and essential fatty acid studies.

Phrynoderma is most commonly seen in South and East Asia with relatively rare occurrences in the United States. Although it characteristically occurs in children and adolescents aged 5 to 15 years, almost all of the cases reported in the United States have occurred in adults.^6,7 A clear gender predilection has not been established.⁷

Phrynoderma tends to favor the extensor surfaces. In particular, the elbows, thighs, and buttocks are the most commonly affected locations. The face is typically the last site to become involved. On physical examination of a patient with phrynoderma, there are various-sized, discrete, red-brown to flesh-colored papules with a conical keratotic follicular plug (Figure).³ The eruption is often asymptomatic, but mild pruritus may be reported.⁷ Additional signs of vitamin A deficiency may be present, including night blindness, hyperpigmentation, or xerosis. Patients with phrynoderma also may have evidence of other nutritional deficiencies, such as angular stomatitis, cheilitis, or glossitis. The differential diagnosis for a patient with this type of papular eruption may include pityriasis rubra pilaris, keratosis pilaris, lichen spinulosus, crusted scabies, and follicular lichen planus.⁷ History and clinical presentation can generally help to distinguish these diagnoses.

Generalized follicular, erythematous, and scaly papular eruption on the chest (A) and abdomen (B).

Histopathology typically shows moderate hyperkeratosis with distension of the upper portion of the follicle by large keratotic plugs. Sebaceous glands are greatly reduced in size and may exhibit epithelial atrophy.^8,9

A reduced serum vitamin A level can confirm the diagnosis of phrynoderma. Our patient’s laboratory results revealed a vitamin A value of 26 mg/100 dL (reference range, 38–106 mg/100 dL), consistent with his clinical presentation of phrynoderma. Other markers of nutritional status, including vitamins D, E, and K₁, were all within reference range. Treatment consists of replacing the nutritional deficit. High doses of vitamin A, such as 200,000 to 500,000 IU daily for 3 to 5 days or daily doses of 2000 to 50,000 IU, can lead to resolution of the rash in 1 to 4 months.^8,9 Our patient was started on 10,000 IU of oral vitamin A daily at discharge but unfortunately died a few months later.

Vitamin A has been shown to promote maturation and differentiation of the basal keratinocytes as they move up through the epidermis, which may in part explain why this treatment is effective.¹⁰ It is important to be aware of this condition when seeing a patient with follicular hyperkeratosis because even patients in developed countries with malnutrition due to diet or gastrointestinal disease may develop phrynoderma.

The Diagnosis: Phrynoderma

Phrynoderma, meaning “toad skin,” was first described by Nicholls¹ in 1933 as a condition due to vitamin A deficiency and characterized by follicular hyperkeratosis. Since then, there has been debate in the literature over the etiology of phrynoderma, as studies have demonstrated different causes for this condition,^2-5 which suggests that it is prudent to check several markers of nutritional status including vitamin A, vitamin B, vitamin E, and essential fatty acid studies.

Phrynoderma is most commonly seen in South and East Asia with relatively rare occurrences in the United States. Although it characteristically occurs in children and adolescents aged 5 to 15 years, almost all of the cases reported in the United States have occurred in adults.^6,7 A clear gender predilection has not been established.⁷

Phrynoderma tends to favor the extensor surfaces. In particular, the elbows, thighs, and buttocks are the most commonly affected locations. The face is typically the last site to become involved. On physical examination of a patient with phrynoderma, there are various-sized, discrete, red-brown to flesh-colored papules with a conical keratotic follicular plug (Figure).³ The eruption is often asymptomatic, but mild pruritus may be reported.⁷ Additional signs of vitamin A deficiency may be present, including night blindness, hyperpigmentation, or xerosis. Patients with phrynoderma also may have evidence of other nutritional deficiencies, such as angular stomatitis, cheilitis, or glossitis. The differential diagnosis for a patient with this type of papular eruption may include pityriasis rubra pilaris, keratosis pilaris, lichen spinulosus, crusted scabies, and follicular lichen planus.⁷ History and clinical presentation can generally help to distinguish these diagnoses.

Generalized follicular, erythematous, and scaly papular eruption on the chest (A) and abdomen (B).

Histopathology typically shows moderate hyperkeratosis with distension of the upper portion of the follicle by large keratotic plugs. Sebaceous glands are greatly reduced in size and may exhibit epithelial atrophy.^8,9

A reduced serum vitamin A level can confirm the diagnosis of phrynoderma. Our patient’s laboratory results revealed a vitamin A value of 26 mg/100 dL (reference range, 38–106 mg/100 dL), consistent with his clinical presentation of phrynoderma. Other markers of nutritional status, including vitamins D, E, and K₁, were all within reference range. Treatment consists of replacing the nutritional deficit. High doses of vitamin A, such as 200,000 to 500,000 IU daily for 3 to 5 days or daily doses of 2000 to 50,000 IU, can lead to resolution of the rash in 1 to 4 months.^8,9 Our patient was started on 10,000 IU of oral vitamin A daily at discharge but unfortunately died a few months later.

Vitamin A has been shown to promote maturation and differentiation of the basal keratinocytes as they move up through the epidermis, which may in part explain why this treatment is effective.¹⁰ It is important to be aware of this condition when seeing a patient with follicular hyperkeratosis because even patients in developed countries with malnutrition due to diet or gastrointestinal disease may develop phrynoderma.

The Diagnosis: Phrynoderma

Phrynoderma, meaning “toad skin,” was first described by Nicholls¹ in 1933 as a condition due to vitamin A deficiency and characterized by follicular hyperkeratosis. Since then, there has been debate in the literature over the etiology of phrynoderma, as studies have demonstrated different causes for this condition,^2-5 which suggests that it is prudent to check several markers of nutritional status including vitamin A, vitamin B, vitamin E, and essential fatty acid studies.

Phrynoderma is most commonly seen in South and East Asia with relatively rare occurrences in the United States. Although it characteristically occurs in children and adolescents aged 5 to 15 years, almost all of the cases reported in the United States have occurred in adults.^6,7 A clear gender predilection has not been established.⁷

Phrynoderma tends to favor the extensor surfaces. In particular, the elbows, thighs, and buttocks are the most commonly affected locations. The face is typically the last site to become involved. On physical examination of a patient with phrynoderma, there are various-sized, discrete, red-brown to flesh-colored papules with a conical keratotic follicular plug (Figure).³ The eruption is often asymptomatic, but mild pruritus may be reported.⁷ Additional signs of vitamin A deficiency may be present, including night blindness, hyperpigmentation, or xerosis. Patients with phrynoderma also may have evidence of other nutritional deficiencies, such as angular stomatitis, cheilitis, or glossitis. The differential diagnosis for a patient with this type of papular eruption may include pityriasis rubra pilaris, keratosis pilaris, lichen spinulosus, crusted scabies, and follicular lichen planus.⁷ History and clinical presentation can generally help to distinguish these diagnoses.

Generalized follicular, erythematous, and scaly papular eruption on the chest (A) and abdomen (B).

Histopathology typically shows moderate hyperkeratosis with distension of the upper portion of the follicle by large keratotic plugs. Sebaceous glands are greatly reduced in size and may exhibit epithelial atrophy.^8,9

A reduced serum vitamin A level can confirm the diagnosis of phrynoderma. Our patient’s laboratory results revealed a vitamin A value of 26 mg/100 dL (reference range, 38–106 mg/100 dL), consistent with his clinical presentation of phrynoderma. Other markers of nutritional status, including vitamins D, E, and K₁, were all within reference range. Treatment consists of replacing the nutritional deficit. High doses of vitamin A, such as 200,000 to 500,000 IU daily for 3 to 5 days or daily doses of 2000 to 50,000 IU, can lead to resolution of the rash in 1 to 4 months.^8,9 Our patient was started on 10,000 IU of oral vitamin A daily at discharge but unfortunately died a few months later.

Vitamin A has been shown to promote maturation and differentiation of the basal keratinocytes as they move up through the epidermis, which may in part explain why this treatment is effective.¹⁰ It is important to be aware of this condition when seeing a patient with follicular hyperkeratosis because even patients in developed countries with malnutrition due to diet or gastrointestinal disease may develop phrynoderma.

The Diagnosis: Crusted Scabies

Approximately 1 year prior to presentation the patient completed a course of therapy comprised of repeat doses of ivermectin and permethrin for crusted scabies. He stated that the crusts had recurred shortly after treatment (Figure 1). The initial differential diagnosis included crusted scabies, pityriasis rubra pilaris, and psoriasis. Scraping from the interdigital web space (Figure 2) revealed multiple scabies mites, scabella, and ova (Figure 3). The patient was diagnosed with crusted scabies. Laboratory test results revealed a normal white blood cell count of 7300/μL, with an elevated eosinophil count of 1900/μL (reference range, <500/μL). Human T-lymphotropic virus 1 (HTLV-1) was found to be positive. Serum protein electrophoresis showed a moderate polyclonal increase in gamma globulins. Treatment was promptly initiated with permethrin cream 5% applied to the whole body for a total of 2 treatments that were administered 7 days apart. Ivermectin also was started at 200 μg/kg and was given on days 1, 7, 14, and 29. Salicylic acid cream 25% was applied daily to help hasten resolution of the crusts.

Human T-lymphotropic virus 1 is endemic to Japan, Central and South America, the Middle East, and regions of Africa and the Caribbean.¹ Multiple cases of HTLV-1 associated with crusted scabies have been reported in endemic areas.^2-6 In the present case, we encountered a patient with crusted scabies and HTLV-1 in a nonendemic area.

Cases of HTLV-1 and crusted scabies have been reported in Brazil, Peru, and Central Australia.^3,4,7 A retrospective study in Brazil showed a notable association between HTLV-1 infection and crusted scabies; of 23 patients with crusted scabies, 21 were HTLV-1 positive.³ In another small study from Peru, 23 patients with crusted scabies were tested for HTLV-1 and 16 (70%) were seropositive.⁴ Neither study had a control group for comparison; however, interestingly, the estimated seroprevalence in the general population (based on blood donors) is only 0.04% to 1% and 1.2% to 1.7% in Brazil and Peru, respectively, thus reinforcing the association between HTLV-1 and crusted scabies.¹ Crusted scabies and HTLV-1 seropositivity acting as a predictor for adult T-cell leukemia/lymphoma (ATL) has been reported⁸ but not consistently.³ Our patient had abnormal serum protein electrophoresis findings. Although the results were not diagnostic of ATL, patients with HTLV-1 are at increased risk for ATL and the pres-ence of this virus is important to document when there is a high index of suspicion for ATL, as with crusted scabies.

Our patient resided in the northeastern United States and there was no evidence in support of underlying immunosuppression. This case of crusted scabies is unique because the patient was HTLV-1 positive without other underlying immunocompromise and he resided in a region where HTLV-1 is nonendemic. In light of these findings, the present case serves as a reminder to check for HTLV-1 infection in those patients with severe or crusted scabies and without an identifiable reason for immunosuppression, even if the patient resides in an area that is nonendemic for HTLV-1.

The Diagnosis: Crusted Scabies

Approximately 1 year prior to presentation the patient completed a course of therapy comprised of repeat doses of ivermectin and permethrin for crusted scabies. He stated that the crusts had recurred shortly after treatment (Figure 1). The initial differential diagnosis included crusted scabies, pityriasis rubra pilaris, and psoriasis. Scraping from the interdigital web space (Figure 2) revealed multiple scabies mites, scabella, and ova (Figure 3). The patient was diagnosed with crusted scabies. Laboratory test results revealed a normal white blood cell count of 7300/μL, with an elevated eosinophil count of 1900/μL (reference range, <500/μL). Human T-lymphotropic virus 1 (HTLV-1) was found to be positive. Serum protein electrophoresis showed a moderate polyclonal increase in gamma globulins. Treatment was promptly initiated with permethrin cream 5% applied to the whole body for a total of 2 treatments that were administered 7 days apart. Ivermectin also was started at 200 μg/kg and was given on days 1, 7, 14, and 29. Salicylic acid cream 25% was applied daily to help hasten resolution of the crusts.

Human T-lymphotropic virus 1 is endemic to Japan, Central and South America, the Middle East, and regions of Africa and the Caribbean.¹ Multiple cases of HTLV-1 associated with crusted scabies have been reported in endemic areas.^2-6 In the present case, we encountered a patient with crusted scabies and HTLV-1 in a nonendemic area.

Cases of HTLV-1 and crusted scabies have been reported in Brazil, Peru, and Central Australia.^3,4,7 A retrospective study in Brazil showed a notable association between HTLV-1 infection and crusted scabies; of 23 patients with crusted scabies, 21 were HTLV-1 positive.³ In another small study from Peru, 23 patients with crusted scabies were tested for HTLV-1 and 16 (70%) were seropositive.⁴ Neither study had a control group for comparison; however, interestingly, the estimated seroprevalence in the general population (based on blood donors) is only 0.04% to 1% and 1.2% to 1.7% in Brazil and Peru, respectively, thus reinforcing the association between HTLV-1 and crusted scabies.¹ Crusted scabies and HTLV-1 seropositivity acting as a predictor for adult T-cell leukemia/lymphoma (ATL) has been reported⁸ but not consistently.³ Our patient had abnormal serum protein electrophoresis findings. Although the results were not diagnostic of ATL, patients with HTLV-1 are at increased risk for ATL and the pres-ence of this virus is important to document when there is a high index of suspicion for ATL, as with crusted scabies.

Our patient resided in the northeastern United States and there was no evidence in support of underlying immunosuppression. This case of crusted scabies is unique because the patient was HTLV-1 positive without other underlying immunocompromise and he resided in a region where HTLV-1 is nonendemic. In light of these findings, the present case serves as a reminder to check for HTLV-1 infection in those patients with severe or crusted scabies and without an identifiable reason for immunosuppression, even if the patient resides in an area that is nonendemic for HTLV-1.

The Diagnosis: Crusted Scabies

Approximately 1 year prior to presentation the patient completed a course of therapy comprised of repeat doses of ivermectin and permethrin for crusted scabies. He stated that the crusts had recurred shortly after treatment (Figure 1). The initial differential diagnosis included crusted scabies, pityriasis rubra pilaris, and psoriasis. Scraping from the interdigital web space (Figure 2) revealed multiple scabies mites, scabella, and ova (Figure 3). The patient was diagnosed with crusted scabies. Laboratory test results revealed a normal white blood cell count of 7300/μL, with an elevated eosinophil count of 1900/μL (reference range, <500/μL). Human T-lymphotropic virus 1 (HTLV-1) was found to be positive. Serum protein electrophoresis showed a moderate polyclonal increase in gamma globulins. Treatment was promptly initiated with permethrin cream 5% applied to the whole body for a total of 2 treatments that were administered 7 days apart. Ivermectin also was started at 200 μg/kg and was given on days 1, 7, 14, and 29. Salicylic acid cream 25% was applied daily to help hasten resolution of the crusts.

Human T-lymphotropic virus 1 is endemic to Japan, Central and South America, the Middle East, and regions of Africa and the Caribbean.¹ Multiple cases of HTLV-1 associated with crusted scabies have been reported in endemic areas.^2-6 In the present case, we encountered a patient with crusted scabies and HTLV-1 in a nonendemic area.

Cases of HTLV-1 and crusted scabies have been reported in Brazil, Peru, and Central Australia.^3,4,7 A retrospective study in Brazil showed a notable association between HTLV-1 infection and crusted scabies; of 23 patients with crusted scabies, 21 were HTLV-1 positive.³ In another small study from Peru, 23 patients with crusted scabies were tested for HTLV-1 and 16 (70%) were seropositive.⁴ Neither study had a control group for comparison; however, interestingly, the estimated seroprevalence in the general population (based on blood donors) is only 0.04% to 1% and 1.2% to 1.7% in Brazil and Peru, respectively, thus reinforcing the association between HTLV-1 and crusted scabies.¹ Crusted scabies and HTLV-1 seropositivity acting as a predictor for adult T-cell leukemia/lymphoma (ATL) has been reported⁸ but not consistently.³ Our patient had abnormal serum protein electrophoresis findings. Although the results were not diagnostic of ATL, patients with HTLV-1 are at increased risk for ATL and the pres-ence of this virus is important to document when there is a high index of suspicion for ATL, as with crusted scabies.

Our patient resided in the northeastern United States and there was no evidence in support of underlying immunosuppression. This case of crusted scabies is unique because the patient was HTLV-1 positive without other underlying immunocompromise and he resided in a region where HTLV-1 is nonendemic. In light of these findings, the present case serves as a reminder to check for HTLV-1 infection in those patients with severe or crusted scabies and without an identifiable reason for immunosuppression, even if the patient resides in an area that is nonendemic for HTLV-1.

ANSWER
The correct answer is lichen striatus (choice “d”), a rare, self-limited condition usually seen on the extremities of children. It will be discussed further in the next  section.

The differential for lichen striatus includes psoriasis (choice “a”). However, typical psoriatic lesions would not assume this configuration and would likely manifest with other corroborative areas of involvement.

Eczema (choice “b”) is certainly common in children, but it is unlikely to be relegated to one linear area. The same can be said of pityriasis rosea (choice “c”).

DISCUSSION 
Lichen striatus, also known as Blaschko linear acquired skin inflammation, is an unusual self-limited condition of unknown etiology seen mostly on the extremities of children ages 3 to 10. More common on legs than on arms, it can occasionally appear on the face.

Its linear configuration is instantly diagnostic: The lesion typically follows the Blaschko lines, which represent a segmental clone of cutaneous cells deposited at an embryonic stage of development.

As seen in this case, post­inflammatory hypopigmentation is common. In a minority of cases, the condition can involve the entire length of the extremity—even the digits, where it can lead to dystrophy of the affected nail. It almost always resolves within a few weeks to months, with or without treatment (which is limited to symptom relief).

Several potential causes of lichen striatus have been posited. The most convincing theory is a possible connection with human herpesviruses 6 and 7, which are also triggers for pityriasis rosea. There have been cases in which both conditions are present, ­producing somewhat similar microscopic changes in the skin (and both resolving without ­treatment). Additional items in the differential include lichen planus, lichen nitidus, and warts.

TREATMENT
For most cases of lichen striatus, treatment is supportive: topical steroids for the itching, which is seldom severe. Given the self-limited but prolonged nature of the problem, patient education is the more important component; these days, there are web-based sources to which you can direct your patients for reliable information, including the Mayo Clinic and the American Academy of Dermatology.

ANSWER
The correct answer is lichen striatus (choice “d”), a rare, self-limited condition usually seen on the extremities of children. It will be discussed further in the next  section.

The differential for lichen striatus includes psoriasis (choice “a”). However, typical psoriatic lesions would not assume this configuration and would likely manifest with other corroborative areas of involvement.

Eczema (choice “b”) is certainly common in children, but it is unlikely to be relegated to one linear area. The same can be said of pityriasis rosea (choice “c”).

DISCUSSION 
Lichen striatus, also known as Blaschko linear acquired skin inflammation, is an unusual self-limited condition of unknown etiology seen mostly on the extremities of children ages 3 to 10. More common on legs than on arms, it can occasionally appear on the face.

Its linear configuration is instantly diagnostic: The lesion typically follows the Blaschko lines, which represent a segmental clone of cutaneous cells deposited at an embryonic stage of development.

As seen in this case, post­inflammatory hypopigmentation is common. In a minority of cases, the condition can involve the entire length of the extremity—even the digits, where it can lead to dystrophy of the affected nail. It almost always resolves within a few weeks to months, with or without treatment (which is limited to symptom relief).

Several potential causes of lichen striatus have been posited. The most convincing theory is a possible connection with human herpesviruses 6 and 7, which are also triggers for pityriasis rosea. There have been cases in which both conditions are present, ­producing somewhat similar microscopic changes in the skin (and both resolving without ­treatment). Additional items in the differential include lichen planus, lichen nitidus, and warts.

TREATMENT
For most cases of lichen striatus, treatment is supportive: topical steroids for the itching, which is seldom severe. Given the self-limited but prolonged nature of the problem, patient education is the more important component; these days, there are web-based sources to which you can direct your patients for reliable information, including the Mayo Clinic and the American Academy of Dermatology.

ANSWER
The correct answer is lichen striatus (choice “d”), a rare, self-limited condition usually seen on the extremities of children. It will be discussed further in the next  section.

The differential for lichen striatus includes psoriasis (choice “a”). However, typical psoriatic lesions would not assume this configuration and would likely manifest with other corroborative areas of involvement.

Eczema (choice “b”) is certainly common in children, but it is unlikely to be relegated to one linear area. The same can be said of pityriasis rosea (choice “c”).

DISCUSSION 
Lichen striatus, also known as Blaschko linear acquired skin inflammation, is an unusual self-limited condition of unknown etiology seen mostly on the extremities of children ages 3 to 10. More common on legs than on arms, it can occasionally appear on the face.

Its linear configuration is instantly diagnostic: The lesion typically follows the Blaschko lines, which represent a segmental clone of cutaneous cells deposited at an embryonic stage of development.

As seen in this case, post­inflammatory hypopigmentation is common. In a minority of cases, the condition can involve the entire length of the extremity—even the digits, where it can lead to dystrophy of the affected nail. It almost always resolves within a few weeks to months, with or without treatment (which is limited to symptom relief).

Several potential causes of lichen striatus have been posited. The most convincing theory is a possible connection with human herpesviruses 6 and 7, which are also triggers for pityriasis rosea. There have been cases in which both conditions are present, ­producing somewhat similar microscopic changes in the skin (and both resolving without ­treatment). Additional items in the differential include lichen planus, lichen nitidus, and warts.

TREATMENT
For most cases of lichen striatus, treatment is supportive: topical steroids for the itching, which is seldom severe. Given the self-limited but prolonged nature of the problem, patient education is the more important component; these days, there are web-based sources to which you can direct your patients for reliable information, including the Mayo Clinic and the American Academy of Dermatology.

ANSWER
The correct interpretation of this ECG is atrial fibrillation with a rapid ventricular response and aberrantly conducted QRS complexes. The latter were misinterpreted as ventricular tachycardia. Although they represent a wide complex at a rate of more than 100 beats/min, the rhythm is irregular and the intrinsic (initial) inflection of normally conducted and aberrant beats is the same. (See lead I rhythm strip at bottom.)

What is unusual (and doesn’t make sense) regarding this ECG is the machine’s reading of the PR interval (128 ms) and the QRS duration (88 ms). For one thing, there is no measurable PR interval. And for another, the measured QRS duration accounts for the normally conducted complex and not the aberrantly conducted ones.

The technician was reassured, and the patient underwent successful cardioversion back to normal sinus rhythm. 

ANSWER
The correct interpretation of this ECG is atrial fibrillation with a rapid ventricular response and aberrantly conducted QRS complexes. The latter were misinterpreted as ventricular tachycardia. Although they represent a wide complex at a rate of more than 100 beats/min, the rhythm is irregular and the intrinsic (initial) inflection of normally conducted and aberrant beats is the same. (See lead I rhythm strip at bottom.)

What is unusual (and doesn’t make sense) regarding this ECG is the machine’s reading of the PR interval (128 ms) and the QRS duration (88 ms). For one thing, there is no measurable PR interval. And for another, the measured QRS duration accounts for the normally conducted complex and not the aberrantly conducted ones.

The technician was reassured, and the patient underwent successful cardioversion back to normal sinus rhythm. 

ANSWER
The correct interpretation of this ECG is atrial fibrillation with a rapid ventricular response and aberrantly conducted QRS complexes. The latter were misinterpreted as ventricular tachycardia. Although they represent a wide complex at a rate of more than 100 beats/min, the rhythm is irregular and the intrinsic (initial) inflection of normally conducted and aberrant beats is the same. (See lead I rhythm strip at bottom.)

What is unusual (and doesn’t make sense) regarding this ECG is the machine’s reading of the PR interval (128 ms) and the QRS duration (88 ms). For one thing, there is no measurable PR interval. And for another, the measured QRS duration accounts for the normally conducted complex and not the aberrantly conducted ones.

The technician was reassured, and the patient underwent successful cardioversion back to normal sinus rhythm. 

ANSWER
The radiograph shows complete opacification of the left hemithorax. The differential includes total atelectasis of the lung, mucus plug within the left bronchus, or possible blood or fluid collection. Of note, the patient has a catheter within the left subclavian vein, the distal tip of which appears to be in an unusual location. In this case, it was determined that the displaced catheter tip, resulting in hemothorax, was the etiology. The line was removed, and urgent cardiothoracic consultation was obtained. A left chest tube was promptly placed, with a resultant 2 L of immediate output. The patient improved clinically as well.

ANSWER
The radiograph shows complete opacification of the left hemithorax. The differential includes total atelectasis of the lung, mucus plug within the left bronchus, or possible blood or fluid collection. Of note, the patient has a catheter within the left subclavian vein, the distal tip of which appears to be in an unusual location. In this case, it was determined that the displaced catheter tip, resulting in hemothorax, was the etiology. The line was removed, and urgent cardiothoracic consultation was obtained. A left chest tube was promptly placed, with a resultant 2 L of immediate output. The patient improved clinically as well.

ANSWER
The radiograph shows complete opacification of the left hemithorax. The differential includes total atelectasis of the lung, mucus plug within the left bronchus, or possible blood or fluid collection. Of note, the patient has a catheter within the left subclavian vein, the distal tip of which appears to be in an unusual location. In this case, it was determined that the displaced catheter tip, resulting in hemothorax, was the etiology. The line was removed, and urgent cardiothoracic consultation was obtained. A left chest tube was promptly placed, with a resultant 2 L of immediate output. The patient improved clinically as well.

ANSWER
The radiographs demonstrate a left inferior pubic ramus fracture. The patient was referred to orthopedics for follow-up. She was given a walker and a series of home exercises for hip stretching and strengthening, as well as anti-inflammatories as needed for discomfort. She was scheduled for a four-week follow-up visit and repeat radiographs of the pelvis.

ANSWER
The radiographs demonstrate a left inferior pubic ramus fracture. The patient was referred to orthopedics for follow-up. She was given a walker and a series of home exercises for hip stretching and strengthening, as well as anti-inflammatories as needed for discomfort. She was scheduled for a four-week follow-up visit and repeat radiographs of the pelvis.

ANSWER
The radiographs demonstrate a left inferior pubic ramus fracture. The patient was referred to orthopedics for follow-up. She was given a walker and a series of home exercises for hip stretching and strengthening, as well as anti-inflammatories as needed for discomfort. She was scheduled for a four-week follow-up visit and repeat radiographs of the pelvis.

The Diagnosis: Linear Vesiculobullous Keratosis Follicularis (Darier Disease)

Darier disease (DD), or keratosis follicularis, is typically an autosomal-dominant disorder that is characterized by greasy hyperkeratotic papules that coalesce into warty plaques with a predilection for seborrheic areas. The lesions usually are pruritic; malodorous; and may be exacerbated by sunlight, heat, or sweating. Darier disease may be accompanied by oral mucosal involvement including fine white papules on the palate.¹ The condition also can be accompanied by hand and nail involvement (95% of cases) including palmar pitting, punctate keratoses, hemorrhagic macules, palmoplantar keratoderma, and acrokeratosis verruciformis–like lesions on the dorsal aspects of the hands and feet. Nail changes predominately occur on the fingers, manifesting as longitudinal splitting, subungual hyperkeratosis, or characteristic white and red longitudinal bands with V-shaped nicks at the free margin of the nail. In linear DD, hand and nail involvement is rare and, when present, ipsilateral to the primary lesions.^1,2

The clinical variants of DD are classified by lesion morphology or distribution, or both. Morphological variants include vesiculobullous, cornified, erosive, acral hemorrhagic, and guttate leukodermic macular.^1,2 The clinical features of chronic relapsing vesicular lesions and histologic findings described in this case are consistent with vesiculobullous DD, though genetic testing was not performed.^3,4 As in our case, some patients lack a family history and the disease is thought to be the result of genetic mosaicism or somatic postzygotic mutations that affect a limited number of cells. These mosaic variants are named by their cutaneous distribution (ie, linear, segmental, unilateral, localized) and tend to course along the Blaschko lines, most commonly on the trunk. Studies have shown various types of mutations specific to the ATP2A2 gene in the affected tissue but not in the unaffected skin.⁵ This gene encodes for sarcoplasmic/endoplasmic reticulum ATPase SERCA2, which is responsible for intracellular calcium signaling. These mosaic forms of DD are unlikely to be inherited by offspring, in contrast to patients with mosaic epidermal nevi with epidermolytic hyperkeratosis who have a high likelihood of having children with generalized epidermolytic hyperkeratosis.⁶

Darier disease is a chronic incurable disease. Topical corticosteroid, retinoid, 5-fluorouracil, keratolytics, and laser ablation or excision are used in mild and limited disease with mixed outcomes.⁷ Oral retinoids are effective in severe or systemic cases of DD by inhibiting hyperkeratosis.⁸ Individuals with DD are predisposed to infection, warranting regular surveillance and use of antimicrobials and bleach baths. In addition to prophylaxis for bacterial superinfection, patients also are predisposed to getting disseminated herpes simplex virus in the form of eczema herpeticum.

In our patient, the diagnosis was confirmed by performing a punch biopsy from one of the vesicular lesions. Histopathologic examination revealed suprabasal acantholytic dyskeratosis with superficial perivascular and interstitial inflammation with eosinophils (Figure). Immunohistochemical staining showed no evidence of varicella-zoster virus or herpes simplex virus type 1 or type 2.

Histopathology revealed suprabasal acantholysis forming an intraepidermal cleft with superficial perivascular inflammation (A)(H&E, original magnification ×100) and acantholysis with dyskeratotic keratinocytes floating within the intraepidermal cleft (B)(H&E, original magnification ×200).

Our patient was prescribed tretinoin cream 0.1% daily and was advised to use sun protection and stop valacyclovir. At follow-up she noted decreased frequency of outbreaks after starting the tretinoin cream and the patient has now been free of any outbreaks for 8 months.

The Diagnosis: Linear Vesiculobullous Keratosis Follicularis (Darier Disease)

Darier disease (DD), or keratosis follicularis, is typically an autosomal-dominant disorder that is characterized by greasy hyperkeratotic papules that coalesce into warty plaques with a predilection for seborrheic areas. The lesions usually are pruritic; malodorous; and may be exacerbated by sunlight, heat, or sweating. Darier disease may be accompanied by oral mucosal involvement including fine white papules on the palate.¹ The condition also can be accompanied by hand and nail involvement (95% of cases) including palmar pitting, punctate keratoses, hemorrhagic macules, palmoplantar keratoderma, and acrokeratosis verruciformis–like lesions on the dorsal aspects of the hands and feet. Nail changes predominately occur on the fingers, manifesting as longitudinal splitting, subungual hyperkeratosis, or characteristic white and red longitudinal bands with V-shaped nicks at the free margin of the nail. In linear DD, hand and nail involvement is rare and, when present, ipsilateral to the primary lesions.^1,2

The clinical variants of DD are classified by lesion morphology or distribution, or both. Morphological variants include vesiculobullous, cornified, erosive, acral hemorrhagic, and guttate leukodermic macular.^1,2 The clinical features of chronic relapsing vesicular lesions and histologic findings described in this case are consistent with vesiculobullous DD, though genetic testing was not performed.^3,4 As in our case, some patients lack a family history and the disease is thought to be the result of genetic mosaicism or somatic postzygotic mutations that affect a limited number of cells. These mosaic variants are named by their cutaneous distribution (ie, linear, segmental, unilateral, localized) and tend to course along the Blaschko lines, most commonly on the trunk. Studies have shown various types of mutations specific to the ATP2A2 gene in the affected tissue but not in the unaffected skin.⁵ This gene encodes for sarcoplasmic/endoplasmic reticulum ATPase SERCA2, which is responsible for intracellular calcium signaling. These mosaic forms of DD are unlikely to be inherited by offspring, in contrast to patients with mosaic epidermal nevi with epidermolytic hyperkeratosis who have a high likelihood of having children with generalized epidermolytic hyperkeratosis.⁶

Darier disease is a chronic incurable disease. Topical corticosteroid, retinoid, 5-fluorouracil, keratolytics, and laser ablation or excision are used in mild and limited disease with mixed outcomes.⁷ Oral retinoids are effective in severe or systemic cases of DD by inhibiting hyperkeratosis.⁸ Individuals with DD are predisposed to infection, warranting regular surveillance and use of antimicrobials and bleach baths. In addition to prophylaxis for bacterial superinfection, patients also are predisposed to getting disseminated herpes simplex virus in the form of eczema herpeticum.

In our patient, the diagnosis was confirmed by performing a punch biopsy from one of the vesicular lesions. Histopathologic examination revealed suprabasal acantholytic dyskeratosis with superficial perivascular and interstitial inflammation with eosinophils (Figure). Immunohistochemical staining showed no evidence of varicella-zoster virus or herpes simplex virus type 1 or type 2.

Histopathology revealed suprabasal acantholysis forming an intraepidermal cleft with superficial perivascular inflammation (A)(H&E, original magnification ×100) and acantholysis with dyskeratotic keratinocytes floating within the intraepidermal cleft (B)(H&E, original magnification ×200).

Our patient was prescribed tretinoin cream 0.1% daily and was advised to use sun protection and stop valacyclovir. At follow-up she noted decreased frequency of outbreaks after starting the tretinoin cream and the patient has now been free of any outbreaks for 8 months.

The Diagnosis: Linear Vesiculobullous Keratosis Follicularis (Darier Disease)

Darier disease (DD), or keratosis follicularis, is typically an autosomal-dominant disorder that is characterized by greasy hyperkeratotic papules that coalesce into warty plaques with a predilection for seborrheic areas. The lesions usually are pruritic; malodorous; and may be exacerbated by sunlight, heat, or sweating. Darier disease may be accompanied by oral mucosal involvement including fine white papules on the palate.¹ The condition also can be accompanied by hand and nail involvement (95% of cases) including palmar pitting, punctate keratoses, hemorrhagic macules, palmoplantar keratoderma, and acrokeratosis verruciformis–like lesions on the dorsal aspects of the hands and feet. Nail changes predominately occur on the fingers, manifesting as longitudinal splitting, subungual hyperkeratosis, or characteristic white and red longitudinal bands with V-shaped nicks at the free margin of the nail. In linear DD, hand and nail involvement is rare and, when present, ipsilateral to the primary lesions.^1,2

The clinical variants of DD are classified by lesion morphology or distribution, or both. Morphological variants include vesiculobullous, cornified, erosive, acral hemorrhagic, and guttate leukodermic macular.^1,2 The clinical features of chronic relapsing vesicular lesions and histologic findings described in this case are consistent with vesiculobullous DD, though genetic testing was not performed.^3,4 As in our case, some patients lack a family history and the disease is thought to be the result of genetic mosaicism or somatic postzygotic mutations that affect a limited number of cells. These mosaic variants are named by their cutaneous distribution (ie, linear, segmental, unilateral, localized) and tend to course along the Blaschko lines, most commonly on the trunk. Studies have shown various types of mutations specific to the ATP2A2 gene in the affected tissue but not in the unaffected skin.⁵ This gene encodes for sarcoplasmic/endoplasmic reticulum ATPase SERCA2, which is responsible for intracellular calcium signaling. These mosaic forms of DD are unlikely to be inherited by offspring, in contrast to patients with mosaic epidermal nevi with epidermolytic hyperkeratosis who have a high likelihood of having children with generalized epidermolytic hyperkeratosis.⁶

Darier disease is a chronic incurable disease. Topical corticosteroid, retinoid, 5-fluorouracil, keratolytics, and laser ablation or excision are used in mild and limited disease with mixed outcomes.⁷ Oral retinoids are effective in severe or systemic cases of DD by inhibiting hyperkeratosis.⁸ Individuals with DD are predisposed to infection, warranting regular surveillance and use of antimicrobials and bleach baths. In addition to prophylaxis for bacterial superinfection, patients also are predisposed to getting disseminated herpes simplex virus in the form of eczema herpeticum.

In our patient, the diagnosis was confirmed by performing a punch biopsy from one of the vesicular lesions. Histopathologic examination revealed suprabasal acantholytic dyskeratosis with superficial perivascular and interstitial inflammation with eosinophils (Figure). Immunohistochemical staining showed no evidence of varicella-zoster virus or herpes simplex virus type 1 or type 2.

Histopathology revealed suprabasal acantholysis forming an intraepidermal cleft with superficial perivascular inflammation (A)(H&E, original magnification ×100) and acantholysis with dyskeratotic keratinocytes floating within the intraepidermal cleft (B)(H&E, original magnification ×200).

Our patient was prescribed tretinoin cream 0.1% daily and was advised to use sun protection and stop valacyclovir. At follow-up she noted decreased frequency of outbreaks after starting the tretinoin cream and the patient has now been free of any outbreaks for 8 months.

The Diagnosis: Asymmetric Periflexural Exanthem of Childhood (Unilateral Laterothoracic Exanthem)

Asymmetric periflexural exanthem of childhood (APEC), also known as unilateral laterothoracic exanthem, is a self-limited eruptive dermatosis that occurs most frequently in infants and young children. The term unilateral laterothoracic exanthem was first coined by Bodemer and de Prost¹ in 1992 due to its characteristic distribution. The eruption occurs in children aged 4 months to 10 years, with most cases presenting between 2 and 3 years of age.² Isolated cases also have been reported in adults.³ It affects girls more often than boys (2:1), and the majority of reported cases have occurred in white individuals. The disease is seen throughout Europe and North America, and seasonal variation has been noted with most cases occurring in late winter and early spring.^4,5

Fine erythematous macules coalescing to form morbilliform plaques with a reticulated pattern on the right axilla, flank, and chest (A). Unaffected contralateral left axilla and flank (B).

Clinically, APEC is characterized by its asymmetric localization and unilateral onset. In the majority of patients, the eruption presents as discrete erythematous papules that coalesce to form morbilliform plaques that may have reticular or annular configuration (Figure).⁴ The exanthem begins unilaterally near a flexural area, most commonly the axilla (75% of cases), and spreads centrifugally to the adjacent trunk and proximal extremity. There is no right or left dominance.^4,6 There is eventual involvement of the contralateral side in 70% of cases, but a unilateral predominance is maintained throughout the disease course.⁴ Rarely, the eruption may involve the face, genitals, and palmoplantar surfaces. As in our case, up to three-quarters of affected children report symptoms of an upper respiratory tract or gastrointestinal prodrome, including mild fever, diarrhea, and rhinitis.⁴ Accompanying regional lymphadenopathy has been reported in the majority of cases, and mild to moderate pruritus is not uncommon. The syndrome is self-limited, with spontaneous resolution commonly occurring 3 to 6 weeks after onset. Although no treatment is required, systemic antihistamines and topical steroids have been used to alleviate pruritus in symptomatic patients. Our patient was treated with triamcinolone cream 0.1% twice daily as well as oral diphenhydramine 25 mg every 6 hours as needed for associated pruritus. The eruption spontaneously resolved over the following 4 weeks.

Although the cause of APEC remains unknown, an infectious etiology has been presumed. The seasonal pattern, lack of efficacy of broad-spectrum antibiotics, frequently reported prodromal symptoms, and reports of familial cases suggest a viral etiology.¹ Additionally, the predilection to affect infants and young children as well as lack of recurrence in the same patient suggests that immunity may develop. Although no etiologic agent has been consistently detected, several reports have suggested a possible relationship to parvovirus B19.^7,8 Parainfluenzavirus 2, parainfluenzavirus 3, and adenovirus also have been isolated but may represent incidental viral infection.² An inoculation dermatosis from an arthropod bite also has been suggested, but this claim has not been substantiated.¹

The diagnosis often can be made on clinical features alone, and histopathologic evaluation is not required. Histologic features are nonspecific and include a superficial perivascular infiltrate of lymphocytes, often involving the dermal eccrine ducts without involvement of the secretory coils.^4,6 Mild lichenoid changes as well as spongiosis with exocytosis of lymphocytes into the acrosyringium also may be present.⁴ The clinical differential diagnosis of APEC includes allergic contact dermatitis, a nonspecific drug or viral eruption, atypical pityriasis rosea, miliaria, scabies, tinea corporis, and Gianotti-Crosti syndrome. Asymmetric periflexural exanthem of childhood lacks the peripheral scale present in tinea corporis or pityriasis rosea, but when an annular or reticular configuration predominates, a potassium hydroxide preparation of skin scrapings can exclude the presence of a dermatophyte. Similar to APEC, Gianotti-Crosti syndrome affects young children, is preceded by symptoms of a viral prodrome, and spontaneously resolves over several weeks. This condition is distinguished from APEC by the presence of papulovesicles located symmetrically on the face, buttocks, and extensor surface of the extremities, which largely spare the trunk. 

Asymmetric periflexural exanthem of childhood is a unique morbilliform eruption of infants and young children characterized by a stereotypical distribution and self-limited course. The cause of this syndrome remains unclear, but most authors suggest a viral etiology. Recognition of this entity and an ability to distinguish it from other common pediatric dermatoses is required to provide reassurance to parents and avoid unnecessary diagnostic procedures and treatments.

The Diagnosis: Asymmetric Periflexural Exanthem of Childhood (Unilateral Laterothoracic Exanthem)

Asymmetric periflexural exanthem of childhood (APEC), also known as unilateral laterothoracic exanthem, is a self-limited eruptive dermatosis that occurs most frequently in infants and young children. The term unilateral laterothoracic exanthem was first coined by Bodemer and de Prost¹ in 1992 due to its characteristic distribution. The eruption occurs in children aged 4 months to 10 years, with most cases presenting between 2 and 3 years of age.² Isolated cases also have been reported in adults.³ It affects girls more often than boys (2:1), and the majority of reported cases have occurred in white individuals. The disease is seen throughout Europe and North America, and seasonal variation has been noted with most cases occurring in late winter and early spring.^4,5

Fine erythematous macules coalescing to form morbilliform plaques with a reticulated pattern on the right axilla, flank, and chest (A). Unaffected contralateral left axilla and flank (B).

Clinically, APEC is characterized by its asymmetric localization and unilateral onset. In the majority of patients, the eruption presents as discrete erythematous papules that coalesce to form morbilliform plaques that may have reticular or annular configuration (Figure).⁴ The exanthem begins unilaterally near a flexural area, most commonly the axilla (75% of cases), and spreads centrifugally to the adjacent trunk and proximal extremity. There is no right or left dominance.^4,6 There is eventual involvement of the contralateral side in 70% of cases, but a unilateral predominance is maintained throughout the disease course.⁴ Rarely, the eruption may involve the face, genitals, and palmoplantar surfaces. As in our case, up to three-quarters of affected children report symptoms of an upper respiratory tract or gastrointestinal prodrome, including mild fever, diarrhea, and rhinitis.⁴ Accompanying regional lymphadenopathy has been reported in the majority of cases, and mild to moderate pruritus is not uncommon. The syndrome is self-limited, with spontaneous resolution commonly occurring 3 to 6 weeks after onset. Although no treatment is required, systemic antihistamines and topical steroids have been used to alleviate pruritus in symptomatic patients. Our patient was treated with triamcinolone cream 0.1% twice daily as well as oral diphenhydramine 25 mg every 6 hours as needed for associated pruritus. The eruption spontaneously resolved over the following 4 weeks.

Although the cause of APEC remains unknown, an infectious etiology has been presumed. The seasonal pattern, lack of efficacy of broad-spectrum antibiotics, frequently reported prodromal symptoms, and reports of familial cases suggest a viral etiology.¹ Additionally, the predilection to affect infants and young children as well as lack of recurrence in the same patient suggests that immunity may develop. Although no etiologic agent has been consistently detected, several reports have suggested a possible relationship to parvovirus B19.^7,8 Parainfluenzavirus 2, parainfluenzavirus 3, and adenovirus also have been isolated but may represent incidental viral infection.² An inoculation dermatosis from an arthropod bite also has been suggested, but this claim has not been substantiated.¹

The diagnosis often can be made on clinical features alone, and histopathologic evaluation is not required. Histologic features are nonspecific and include a superficial perivascular infiltrate of lymphocytes, often involving the dermal eccrine ducts without involvement of the secretory coils.^4,6 Mild lichenoid changes as well as spongiosis with exocytosis of lymphocytes into the acrosyringium also may be present.⁴ The clinical differential diagnosis of APEC includes allergic contact dermatitis, a nonspecific drug or viral eruption, atypical pityriasis rosea, miliaria, scabies, tinea corporis, and Gianotti-Crosti syndrome. Asymmetric periflexural exanthem of childhood lacks the peripheral scale present in tinea corporis or pityriasis rosea, but when an annular or reticular configuration predominates, a potassium hydroxide preparation of skin scrapings can exclude the presence of a dermatophyte. Similar to APEC, Gianotti-Crosti syndrome affects young children, is preceded by symptoms of a viral prodrome, and spontaneously resolves over several weeks. This condition is distinguished from APEC by the presence of papulovesicles located symmetrically on the face, buttocks, and extensor surface of the extremities, which largely spare the trunk. 

Asymmetric periflexural exanthem of childhood is a unique morbilliform eruption of infants and young children characterized by a stereotypical distribution and self-limited course. The cause of this syndrome remains unclear, but most authors suggest a viral etiology. Recognition of this entity and an ability to distinguish it from other common pediatric dermatoses is required to provide reassurance to parents and avoid unnecessary diagnostic procedures and treatments.

The Diagnosis: Asymmetric Periflexural Exanthem of Childhood (Unilateral Laterothoracic Exanthem)

Asymmetric periflexural exanthem of childhood (APEC), also known as unilateral laterothoracic exanthem, is a self-limited eruptive dermatosis that occurs most frequently in infants and young children. The term unilateral laterothoracic exanthem was first coined by Bodemer and de Prost¹ in 1992 due to its characteristic distribution. The eruption occurs in children aged 4 months to 10 years, with most cases presenting between 2 and 3 years of age.² Isolated cases also have been reported in adults.³ It affects girls more often than boys (2:1), and the majority of reported cases have occurred in white individuals. The disease is seen throughout Europe and North America, and seasonal variation has been noted with most cases occurring in late winter and early spring.^4,5

Fine erythematous macules coalescing to form morbilliform plaques with a reticulated pattern on the right axilla, flank, and chest (A). Unaffected contralateral left axilla and flank (B).

Clinically, APEC is characterized by its asymmetric localization and unilateral onset. In the majority of patients, the eruption presents as discrete erythematous papules that coalesce to form morbilliform plaques that may have reticular or annular configuration (Figure).⁴ The exanthem begins unilaterally near a flexural area, most commonly the axilla (75% of cases), and spreads centrifugally to the adjacent trunk and proximal extremity. There is no right or left dominance.^4,6 There is eventual involvement of the contralateral side in 70% of cases, but a unilateral predominance is maintained throughout the disease course.⁴ Rarely, the eruption may involve the face, genitals, and palmoplantar surfaces. As in our case, up to three-quarters of affected children report symptoms of an upper respiratory tract or gastrointestinal prodrome, including mild fever, diarrhea, and rhinitis.⁴ Accompanying regional lymphadenopathy has been reported in the majority of cases, and mild to moderate pruritus is not uncommon. The syndrome is self-limited, with spontaneous resolution commonly occurring 3 to 6 weeks after onset. Although no treatment is required, systemic antihistamines and topical steroids have been used to alleviate pruritus in symptomatic patients. Our patient was treated with triamcinolone cream 0.1% twice daily as well as oral diphenhydramine 25 mg every 6 hours as needed for associated pruritus. The eruption spontaneously resolved over the following 4 weeks.

Although the cause of APEC remains unknown, an infectious etiology has been presumed. The seasonal pattern, lack of efficacy of broad-spectrum antibiotics, frequently reported prodromal symptoms, and reports of familial cases suggest a viral etiology.¹ Additionally, the predilection to affect infants and young children as well as lack of recurrence in the same patient suggests that immunity may develop. Although no etiologic agent has been consistently detected, several reports have suggested a possible relationship to parvovirus B19.^7,8 Parainfluenzavirus 2, parainfluenzavirus 3, and adenovirus also have been isolated but may represent incidental viral infection.² An inoculation dermatosis from an arthropod bite also has been suggested, but this claim has not been substantiated.¹

The diagnosis often can be made on clinical features alone, and histopathologic evaluation is not required. Histologic features are nonspecific and include a superficial perivascular infiltrate of lymphocytes, often involving the dermal eccrine ducts without involvement of the secretory coils.^4,6 Mild lichenoid changes as well as spongiosis with exocytosis of lymphocytes into the acrosyringium also may be present.⁴ The clinical differential diagnosis of APEC includes allergic contact dermatitis, a nonspecific drug or viral eruption, atypical pityriasis rosea, miliaria, scabies, tinea corporis, and Gianotti-Crosti syndrome. Asymmetric periflexural exanthem of childhood lacks the peripheral scale present in tinea corporis or pityriasis rosea, but when an annular or reticular configuration predominates, a potassium hydroxide preparation of skin scrapings can exclude the presence of a dermatophyte. Similar to APEC, Gianotti-Crosti syndrome affects young children, is preceded by symptoms of a viral prodrome, and spontaneously resolves over several weeks. This condition is distinguished from APEC by the presence of papulovesicles located symmetrically on the face, buttocks, and extensor surface of the extremities, which largely spare the trunk. 

Asymmetric periflexural exanthem of childhood is a unique morbilliform eruption of infants and young children characterized by a stereotypical distribution and self-limited course. The cause of this syndrome remains unclear, but most authors suggest a viral etiology. Recognition of this entity and an ability to distinguish it from other common pediatric dermatoses is required to provide reassurance to parents and avoid unnecessary diagnostic procedures and treatments.

ANSWER
The radiograph shows that the distal femur is medially dislocated relative to the tibial plateau. In addition, the patella is laterally dislocated. No obvious fractures are evident. 

Such injuries are typically associated with significant ligament injuries, especially of the medial collateral ligament (MCL), lateral collateral ligament (LCL), and anterior cruciate ligament (ACL). Orthopedics was consulted for reduction of the dislocation, as well as further workup (including MRI of the knee).

ANSWER
The radiograph shows that the distal femur is medially dislocated relative to the tibial plateau. In addition, the patella is laterally dislocated. No obvious fractures are evident. 

Such injuries are typically associated with significant ligament injuries, especially of the medial collateral ligament (MCL), lateral collateral ligament (LCL), and anterior cruciate ligament (ACL). Orthopedics was consulted for reduction of the dislocation, as well as further workup (including MRI of the knee).

ANSWER
The radiograph shows that the distal femur is medially dislocated relative to the tibial plateau. In addition, the patella is laterally dislocated. No obvious fractures are evident. 

Such injuries are typically associated with significant ligament injuries, especially of the medial collateral ligament (MCL), lateral collateral ligament (LCL), and anterior cruciate ligament (ACL). Orthopedics was consulted for reduction of the dislocation, as well as further workup (including MRI of the knee).