Photo Rounds

The FP diagnosed this patient with probable condyloma acuminata but was also concerned about the possibility of other sexually transmitted infections (STIs). He ordered a rapid plasma reagin (RPR) and a human immunodeficiency virus (HIV) test.

A Pap smear was also performed using liquid-based technology to include screening for gonorrhea and chlamydia. While condyloma lata (secondary syphilis) was considered in the differential diagnosis, the verrucous appearance of the lesions pointed to condyloma acuminata from human papillomavirus (HPV).

The RPR came back positive for syphilis with a titer of 1:32. The confirmatory serologic test for syphilis was also positive. The remaining STI screening tests were negative, including the HIV test. The patient remembered having a nonhealing sore on her labia about 2 months ago that healed on its own, making this most likely a case of early latent syphilis.

For the syphilis, the FP treated the patient with a single intramuscular injection in the buttocks of 2.4 million units of benzathine penicillin G. The patient was told to follow up in 6 months for a repeat RPR.

The physician offered treatment for the condyloma acuminata on the first visit. The patient chose to have cryotherapy, which was performed with liquid nitrogen and a cryo-gun. Only one freeze thaw cycle was performed, as the patient found it too painful to have a second cycle. An appointment was made to repeat the cryotherapy in 4 weeks. While the patient was interested in using topical imiquimod, she did not have health insurance and could not afford it.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ, Usatine R. Genital warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:759-765.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed this patient with probable condyloma acuminata but was also concerned about the possibility of other sexually transmitted infections (STIs). He ordered a rapid plasma reagin (RPR) and a human immunodeficiency virus (HIV) test.

A Pap smear was also performed using liquid-based technology to include screening for gonorrhea and chlamydia. While condyloma lata (secondary syphilis) was considered in the differential diagnosis, the verrucous appearance of the lesions pointed to condyloma acuminata from human papillomavirus (HPV).

The RPR came back positive for syphilis with a titer of 1:32. The confirmatory serologic test for syphilis was also positive. The remaining STI screening tests were negative, including the HIV test. The patient remembered having a nonhealing sore on her labia about 2 months ago that healed on its own, making this most likely a case of early latent syphilis.

For the syphilis, the FP treated the patient with a single intramuscular injection in the buttocks of 2.4 million units of benzathine penicillin G. The patient was told to follow up in 6 months for a repeat RPR.

The physician offered treatment for the condyloma acuminata on the first visit. The patient chose to have cryotherapy, which was performed with liquid nitrogen and a cryo-gun. Only one freeze thaw cycle was performed, as the patient found it too painful to have a second cycle. An appointment was made to repeat the cryotherapy in 4 weeks. While the patient was interested in using topical imiquimod, she did not have health insurance and could not afford it.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ, Usatine R. Genital warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:759-765.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed this patient with probable condyloma acuminata but was also concerned about the possibility of other sexually transmitted infections (STIs). He ordered a rapid plasma reagin (RPR) and a human immunodeficiency virus (HIV) test.

A Pap smear was also performed using liquid-based technology to include screening for gonorrhea and chlamydia. While condyloma lata (secondary syphilis) was considered in the differential diagnosis, the verrucous appearance of the lesions pointed to condyloma acuminata from human papillomavirus (HPV).

The RPR came back positive for syphilis with a titer of 1:32. The confirmatory serologic test for syphilis was also positive. The remaining STI screening tests were negative, including the HIV test. The patient remembered having a nonhealing sore on her labia about 2 months ago that healed on its own, making this most likely a case of early latent syphilis.

For the syphilis, the FP treated the patient with a single intramuscular injection in the buttocks of 2.4 million units of benzathine penicillin G. The patient was told to follow up in 6 months for a repeat RPR.

The physician offered treatment for the condyloma acuminata on the first visit. The patient chose to have cryotherapy, which was performed with liquid nitrogen and a cryo-gun. Only one freeze thaw cycle was performed, as the patient found it too painful to have a second cycle. An appointment was made to repeat the cryotherapy in 4 weeks. While the patient was interested in using topical imiquimod, she did not have health insurance and could not afford it.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ, Usatine R. Genital warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:759-765.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

While the lesions appeared verrucous and cauliflower-like, this seemed an unusual place for condyloma. So the FP performed a shave biopsy out of concern that this could be a benign tumor. The results came back as human papillomavirus (HPV)-related condyloma.

In addition to the growths that were seen under the pannus, there was also intertrigo in that area. Intertrigo is a nonspecific term for a rash in an intertriginous area. Erythema seen between skin folds is the tip-off to intertrigo. The most common causes of intertrigo are fungal infections and irritation that come from sweating and the rubbing together of skin. Another cause of an erythematous rash in an intertriginous area is inverse psoriasis.

The FP performed a potassium hydroxide (KOH) preparation by scraping the erythematous area with a microscope slide and looking at the specimen under the microscope. The KOH was negative and the diagnosis was determined to be nonspecific intertrigo related to obesity. The FP told the patient to try to keep the area dry and to try some over-the-counter 1% hydrocortisone cream for the inflammation and irritation.

Pannus condylomas are uncommon—but not rare—in this age of increasing obesity. While they are secondary to HPV, they are not necessarily sexually transmitted HPV types. Based on the patient’s sexual history, the FP did not recommend screening for sexually transmitted infections.

On the initial visit, the FP counseled the patient about the importance of weight loss for good health and hygiene. The patient chose cryotherapy for treatment of the growths. While the patient held the pannus up, the FP sprayed the condyloma with liquid nitrogen using a cryo-gun. The patient chose to have a second freeze-thaw cycle and was scheduled for a follow-up visit in 3 to 4 weeks.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ, Usatine R. Genital warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:759-765.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

While the lesions appeared verrucous and cauliflower-like, this seemed an unusual place for condyloma. So the FP performed a shave biopsy out of concern that this could be a benign tumor. The results came back as human papillomavirus (HPV)-related condyloma.

In addition to the growths that were seen under the pannus, there was also intertrigo in that area. Intertrigo is a nonspecific term for a rash in an intertriginous area. Erythema seen between skin folds is the tip-off to intertrigo. The most common causes of intertrigo are fungal infections and irritation that come from sweating and the rubbing together of skin. Another cause of an erythematous rash in an intertriginous area is inverse psoriasis.

The FP performed a potassium hydroxide (KOH) preparation by scraping the erythematous area with a microscope slide and looking at the specimen under the microscope. The KOH was negative and the diagnosis was determined to be nonspecific intertrigo related to obesity. The FP told the patient to try to keep the area dry and to try some over-the-counter 1% hydrocortisone cream for the inflammation and irritation.

Pannus condylomas are uncommon—but not rare—in this age of increasing obesity. While they are secondary to HPV, they are not necessarily sexually transmitted HPV types. Based on the patient’s sexual history, the FP did not recommend screening for sexually transmitted infections.

On the initial visit, the FP counseled the patient about the importance of weight loss for good health and hygiene. The patient chose cryotherapy for treatment of the growths. While the patient held the pannus up, the FP sprayed the condyloma with liquid nitrogen using a cryo-gun. The patient chose to have a second freeze-thaw cycle and was scheduled for a follow-up visit in 3 to 4 weeks.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ, Usatine R. Genital warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:759-765.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

While the lesions appeared verrucous and cauliflower-like, this seemed an unusual place for condyloma. So the FP performed a shave biopsy out of concern that this could be a benign tumor. The results came back as human papillomavirus (HPV)-related condyloma.

In addition to the growths that were seen under the pannus, there was also intertrigo in that area. Intertrigo is a nonspecific term for a rash in an intertriginous area. Erythema seen between skin folds is the tip-off to intertrigo. The most common causes of intertrigo are fungal infections and irritation that come from sweating and the rubbing together of skin. Another cause of an erythematous rash in an intertriginous area is inverse psoriasis.

The FP performed a potassium hydroxide (KOH) preparation by scraping the erythematous area with a microscope slide and looking at the specimen under the microscope. The KOH was negative and the diagnosis was determined to be nonspecific intertrigo related to obesity. The FP told the patient to try to keep the area dry and to try some over-the-counter 1% hydrocortisone cream for the inflammation and irritation.

Pannus condylomas are uncommon—but not rare—in this age of increasing obesity. While they are secondary to HPV, they are not necessarily sexually transmitted HPV types. Based on the patient’s sexual history, the FP did not recommend screening for sexually transmitted infections.

On the initial visit, the FP counseled the patient about the importance of weight loss for good health and hygiene. The patient chose cryotherapy for treatment of the growths. While the patient held the pannus up, the FP sprayed the condyloma with liquid nitrogen using a cryo-gun. The patient chose to have a second freeze-thaw cycle and was scheduled for a follow-up visit in 3 to 4 weeks.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ, Usatine R. Genital warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:759-765.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

At first, the FP considered the diagnosis of seborrheic keratosis, as the lesions were verrucous and pigmented. But after asking to see the patient’s genital area, the FP made the diagnosis of condyloma acuminata.

This is a good example of how seeing the whole picture beyond what the patient shows you can lead to a more accurate diagnosis. Verrucous lesions on the penis are usually condyloma acuminata, but it is important to know that condyloma can spread up the abdomen and onto the upper thighs, as was seen in this case. The lesions can also be hyperpigmented in people of color. If any doubts remain, a shave biopsy of one of the abdominal lesions would prove the diagnosis of condyloma by demonstrating human papillomavirus (HPV) changes histologically.

In this case, the FP discussed the risk of other sexually transmitted infections with the patient. Syphilis and human immunodeficiency virus tests were ordered, and both turned out to be negative.

The patient chose cryotherapy as a treatment option and the lesions were frozen with liquid nitrogen using a standard cryo-gun and a 1 mm halo, creating an appropriate freeze ball for each lesion. The patient tolerated the procedure well and was willing to have a second freeze thaw cycle for a more rapid treatment response. The FP suggested a follow-up visit in 3 to 4 weeks for a second round of cryotherapy. The patient indicated that he would be willing to try topical imiquimod after the next visit if the cryotherapy didn’t fully work.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ, Usatine R. Genital warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:759-765.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

At first, the FP considered the diagnosis of seborrheic keratosis, as the lesions were verrucous and pigmented. But after asking to see the patient’s genital area, the FP made the diagnosis of condyloma acuminata.

This is a good example of how seeing the whole picture beyond what the patient shows you can lead to a more accurate diagnosis. Verrucous lesions on the penis are usually condyloma acuminata, but it is important to know that condyloma can spread up the abdomen and onto the upper thighs, as was seen in this case. The lesions can also be hyperpigmented in people of color. If any doubts remain, a shave biopsy of one of the abdominal lesions would prove the diagnosis of condyloma by demonstrating human papillomavirus (HPV) changes histologically.

In this case, the FP discussed the risk of other sexually transmitted infections with the patient. Syphilis and human immunodeficiency virus tests were ordered, and both turned out to be negative.

The patient chose cryotherapy as a treatment option and the lesions were frozen with liquid nitrogen using a standard cryo-gun and a 1 mm halo, creating an appropriate freeze ball for each lesion. The patient tolerated the procedure well and was willing to have a second freeze thaw cycle for a more rapid treatment response. The FP suggested a follow-up visit in 3 to 4 weeks for a second round of cryotherapy. The patient indicated that he would be willing to try topical imiquimod after the next visit if the cryotherapy didn’t fully work.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ, Usatine R. Genital warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:759-765.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

At first, the FP considered the diagnosis of seborrheic keratosis, as the lesions were verrucous and pigmented. But after asking to see the patient’s genital area, the FP made the diagnosis of condyloma acuminata.

This is a good example of how seeing the whole picture beyond what the patient shows you can lead to a more accurate diagnosis. Verrucous lesions on the penis are usually condyloma acuminata, but it is important to know that condyloma can spread up the abdomen and onto the upper thighs, as was seen in this case. The lesions can also be hyperpigmented in people of color. If any doubts remain, a shave biopsy of one of the abdominal lesions would prove the diagnosis of condyloma by demonstrating human papillomavirus (HPV) changes histologically.

In this case, the FP discussed the risk of other sexually transmitted infections with the patient. Syphilis and human immunodeficiency virus tests were ordered, and both turned out to be negative.

The patient chose cryotherapy as a treatment option and the lesions were frozen with liquid nitrogen using a standard cryo-gun and a 1 mm halo, creating an appropriate freeze ball for each lesion. The patient tolerated the procedure well and was willing to have a second freeze thaw cycle for a more rapid treatment response. The FP suggested a follow-up visit in 3 to 4 weeks for a second round of cryotherapy. The patient indicated that he would be willing to try topical imiquimod after the next visit if the cryotherapy didn’t fully work.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ, Usatine R. Genital warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:759-765.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed this patient with condyloma acuminata, also known as genital warts. The warts were well-keratinized since the patient was circumcised and the warts were not under foreskin. Genital warts found in the moist area under the foreskin of uncircumcised men tend to look more cauliflower-like.

Genital warts are caused by human papillomavirus infection, which encompasses a family of primarily sexually transmitted double-stranded DNA viruses. The incubation period after exposure ranges from 3 weeks to 8 months.

Anogenital warts are the most common viral sexually transmitted disease (STD) in the United States. There are approximately one million new cases of genital warts per year in the United States. Most infections are transient and clear up within 2 years, but some infections persist and recur, causing a great deal of distress for patients.

The diagnosis is usually clinical. Genital warts are typically asymptomatic and present as flesh-colored, exophytic lesions on the genitalia, including the penis, vulva, vagina, scrotum, perineum, and perianal skin. External warts can appear as small bumps, or they may be flat, verrucous, or pedunculated.

The FP discussed the patient’s history of unsafe sex and recommended that he receive screening for other STDs. The patient did not believe he had human immunodeficiency virus (HIV), but was willing to be tested for it and for syphilis. He denied any urethral discharge or burning on urination, but wanted to be screened for gonorrhea and chlamydia, as well. The FP ordered blood tests for syphilis and HIV and a urine screen for gonorrhea and chlamydia which were all negative.

After discussing treatment options, the patient opted to pursue cryotherapy. The FP sprayed the condyloma with liquid nitrogen using a freeze/thaw/freeze cycle and offered the patient a prescription for imiquimod cream. However, the patient preferred to return for additional cryotherapy. A follow-up appointment was set for 3 weeks.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ, Usatine R. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:759-765.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed this patient with condyloma acuminata, also known as genital warts. The warts were well-keratinized since the patient was circumcised and the warts were not under foreskin. Genital warts found in the moist area under the foreskin of uncircumcised men tend to look more cauliflower-like.

Genital warts are caused by human papillomavirus infection, which encompasses a family of primarily sexually transmitted double-stranded DNA viruses. The incubation period after exposure ranges from 3 weeks to 8 months.

Anogenital warts are the most common viral sexually transmitted disease (STD) in the United States. There are approximately one million new cases of genital warts per year in the United States. Most infections are transient and clear up within 2 years, but some infections persist and recur, causing a great deal of distress for patients.

The diagnosis is usually clinical. Genital warts are typically asymptomatic and present as flesh-colored, exophytic lesions on the genitalia, including the penis, vulva, vagina, scrotum, perineum, and perianal skin. External warts can appear as small bumps, or they may be flat, verrucous, or pedunculated.

The FP discussed the patient’s history of unsafe sex and recommended that he receive screening for other STDs. The patient did not believe he had human immunodeficiency virus (HIV), but was willing to be tested for it and for syphilis. He denied any urethral discharge or burning on urination, but wanted to be screened for gonorrhea and chlamydia, as well. The FP ordered blood tests for syphilis and HIV and a urine screen for gonorrhea and chlamydia which were all negative.

After discussing treatment options, the patient opted to pursue cryotherapy. The FP sprayed the condyloma with liquid nitrogen using a freeze/thaw/freeze cycle and offered the patient a prescription for imiquimod cream. However, the patient preferred to return for additional cryotherapy. A follow-up appointment was set for 3 weeks.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ, Usatine R. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:759-765.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed this patient with condyloma acuminata, also known as genital warts. The warts were well-keratinized since the patient was circumcised and the warts were not under foreskin. Genital warts found in the moist area under the foreskin of uncircumcised men tend to look more cauliflower-like.

Genital warts are caused by human papillomavirus infection, which encompasses a family of primarily sexually transmitted double-stranded DNA viruses. The incubation period after exposure ranges from 3 weeks to 8 months.

Anogenital warts are the most common viral sexually transmitted disease (STD) in the United States. There are approximately one million new cases of genital warts per year in the United States. Most infections are transient and clear up within 2 years, but some infections persist and recur, causing a great deal of distress for patients.

The diagnosis is usually clinical. Genital warts are typically asymptomatic and present as flesh-colored, exophytic lesions on the genitalia, including the penis, vulva, vagina, scrotum, perineum, and perianal skin. External warts can appear as small bumps, or they may be flat, verrucous, or pedunculated.

The FP discussed the patient’s history of unsafe sex and recommended that he receive screening for other STDs. The patient did not believe he had human immunodeficiency virus (HIV), but was willing to be tested for it and for syphilis. He denied any urethral discharge or burning on urination, but wanted to be screened for gonorrhea and chlamydia, as well. The FP ordered blood tests for syphilis and HIV and a urine screen for gonorrhea and chlamydia which were all negative.

After discussing treatment options, the patient opted to pursue cryotherapy. The FP sprayed the condyloma with liquid nitrogen using a freeze/thaw/freeze cycle and offered the patient a prescription for imiquimod cream. However, the patient preferred to return for additional cryotherapy. A follow-up appointment was set for 3 weeks.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ, Usatine R. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:759-765.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

A 2-year-old boy with atopic dermatitis developed a flare of his eczema after having a bath with mint-scented soap. His mother treated the flare with over-the-counter topical hydrocortisone cream. Two to 3 days later, he developed grouped vesicles on the right side of his neck. Three days after that, he developed a painful generalized vesicular eruption all over his body.

The boy was admitted to a hospital for supportive care and empiric antibiotics, but was discharged when no bacterial infection was found. The patient’s mother was instructed to follow up with his primary care provider in the next 2 weeks.

Three days after his hospitalization, the eruption on the young boy’s body spread and he was uncomfortable. He was brought to our hospital’s pediatric clinic, where physicians examined him and decided to transfer him to the university hospital for further evaluation.

On exam, the boy was afebrile, but uncomfortable and irritable. Diffuse heme-crusted and punched-out erosions covered about 90% of his body (FIGURE). His mucous membranes were not involved. Underneath the heme-crusted erosions, there were lichenified pink plaques on the antecubital fossae, popliteal fossae, periocular face, and buttocks. The patient’s right dorsal foot had a small vesicle; all other vesicles on his body had crusted over.

The patient’s family indicated that the child had received the varicella vaccine without incident at 12 months of age. He had no history of travel, no contact with sick individuals, and no exposure to pets or other animals.

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

Diagnosis: Eczema herpeticum

Eczema herpeticum (EH) was suspected based on the appearance of the lesions. A Tzanck smear came back positive for multinucleated giant cells and a herpes simplex virus (HSV) amplified probe came back positive for HSV-1—confirming the diagnosis.

EH—also known as Kaposi varicelliform eruption—is a superficial generalized viral infection (typically caused by HSV-1; HSV-2 is less common). The infection commonly occurs in patients with underlying atopic dermatitis, but may also occur in those with Darier disease, pemphigus, burns, and other conditions that disrupt the skin barrier. Other viruses, such as Coxsackie virus, can also cause EH. Eczema vaccinatum is a variant that may occur after smallpox vaccination.¹ EH occurs more often in infants and children than in adults,² and is a potentially life-threatening dermatologic emergency.

Eczema herpeticum occurs more often in infants and children than in adults, and is a potentially life-threatening emergency.

Who’s at risk? Patients with underlying chronic skin conditions such as eczema may have impaired cell-mediated immunity, making them more susceptible to a viral infection like EH.¹ In addition, treatment of underlying chronic skin conditions with immunosuppressive therapies often increases susceptibility to superimposed infection.¹ (In this case, the patient’s parents had treated an eczema flare with a topical hydrocortisone cream.) Lastly, increased risk may be associated with mutations in the gene encoding filaggrin.²

Areas affected. EH typically appears in areas of pre-existing dermatitis as monomorphic, discrete, 2- to 3-mm, punched-out, heme-crusted erosions with scalloped borders.² The erosions initially appear as vesicles or pustules, which may appear concurrently with the erosions. The erosions can coalesce to form larger lesions.³ Fever, malaise, and lymphadenopathy may also be present.^2,3

4 factors differentiate EH from other conditions

The differential for eczema herpeticum includes impetigo, bullous impetigo, shingles, chicken pox, scabies, pustular psoriasis, bullous pemphigoid, drug hypersensitivity reactions, and exacerbation of a primary dermatosis or skin condition.^1,4

EH may be differentiated from these by its location, its development in the setting of pre-existing dermatitis, its response to antiviral medications, and the results of laboratory testing. Because of the vast differential, physicians must maintain a high index of suspicion for EH, particularly when a patient with a pre-existing skin condition presents with acute onset cutaneous pain.³

Perform a Tzanck smear to diagnose the underlying infection

If EH is suspected, treatment must be initiated immediately.³ (In our patient’s case, he was started on intravenous acyclovir 10 mg/kg every 8 hours.)

Once treatment is underway, a Tzanck smear of the vesicle base can be performed at the patient’s bedside to narrow the cause of the infection to HSV or varicella zoster virus (VZV). Multinucleated giant keratinocytes (as in our patient’s case) are diagnostic for one of the herpes viruses; concurrent inflammatory cells are also to be expected in an inflammatory skin condition but by themselves are not diagnostic of herpes.

If available in the laboratory, direct fluorescent antibody testing can differentiate between HSV and VZV. Alternatively, a nucleic acid amplified probe test may be used to provide a quick and specific result. The most specific test is a viral culture, but it lacks sensitivity and usually requires 2 to 5 daysfor results.² A bacterial skin swab and blood culture should also be considered to direct antibiotic therapy if superinfection has occurred.

Antivirals and antibiotics should be given until lesions heal

Patients with EH should be admitted to the hospital for at least 24 to 48 hours of intravenous acyclovir.⁴ Antivirals—oral or intravenous—should be given for 10 to 14 days or until all mucocutaneous lesions are healed. Recommended dosing for acyclovir is 15 mg/kg (up to 400 mg) by mouth 3 to 5 times per day or, if severe, 5 mg/kg (if ≥12 years of age) to 10 mg/kg (if <12 years of age) intravenously every 8 hours.² Patients should also receive a 3- to 6-month suppressive course of oral acyclovir, valacyclovir, or famciclovir.⁴

Intravenous antibiotics should also be considered, pending the results of bacterial skin swabs and a blood culture, as the skin of patients with atopic dermatitis is colonized with staphylococcus 90% of the time.⁴

Potential complications. Bacterial sepsis resulting from superinfection and disseminated HSV, although extremely rare, is the main cause of death associated with EH.³ One case in the literature described a 43-year-old woman with extensive EH superimposed on atopic dermatitis, disseminated HSV, and Pseudomonas aeruginosa septicemia. Despite treatment with intravenous acyclovir and antibiotics in a burn center intensive care unit, the patient experienced septic shock and disseminated intravascular coagulation with progression to multiorgan failure and death.³

Our patient’s antiviral regimen was transitioned to a 14-day course of oral acyclovir, which he completed. Topical steroids and an immunosuppressant (tacrolimus ointment) were applied concurrently. He was subsequently prescribed a 6-month suppressive course of acyclovir and was scheduled for follow-up at an outpatient dermatology clinic to discuss resuming therapy for atopic dermatitis.

CORRESPONDENCE
Sahand Rahnama-Moghadam, MD, 7323 Snowden Road #1205, San Antonio, TX 78240; [email protected].

A 2-year-old boy with atopic dermatitis developed a flare of his eczema after having a bath with mint-scented soap. His mother treated the flare with over-the-counter topical hydrocortisone cream. Two to 3 days later, he developed grouped vesicles on the right side of his neck. Three days after that, he developed a painful generalized vesicular eruption all over his body.

The boy was admitted to a hospital for supportive care and empiric antibiotics, but was discharged when no bacterial infection was found. The patient’s mother was instructed to follow up with his primary care provider in the next 2 weeks.

Three days after his hospitalization, the eruption on the young boy’s body spread and he was uncomfortable. He was brought to our hospital’s pediatric clinic, where physicians examined him and decided to transfer him to the university hospital for further evaluation.

On exam, the boy was afebrile, but uncomfortable and irritable. Diffuse heme-crusted and punched-out erosions covered about 90% of his body (FIGURE). His mucous membranes were not involved. Underneath the heme-crusted erosions, there were lichenified pink plaques on the antecubital fossae, popliteal fossae, periocular face, and buttocks. The patient’s right dorsal foot had a small vesicle; all other vesicles on his body had crusted over.

The patient’s family indicated that the child had received the varicella vaccine without incident at 12 months of age. He had no history of travel, no contact with sick individuals, and no exposure to pets or other animals.

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

Diagnosis: Eczema herpeticum

Eczema herpeticum (EH) was suspected based on the appearance of the lesions. A Tzanck smear came back positive for multinucleated giant cells and a herpes simplex virus (HSV) amplified probe came back positive for HSV-1—confirming the diagnosis.

EH—also known as Kaposi varicelliform eruption—is a superficial generalized viral infection (typically caused by HSV-1; HSV-2 is less common). The infection commonly occurs in patients with underlying atopic dermatitis, but may also occur in those with Darier disease, pemphigus, burns, and other conditions that disrupt the skin barrier. Other viruses, such as Coxsackie virus, can also cause EH. Eczema vaccinatum is a variant that may occur after smallpox vaccination.¹ EH occurs more often in infants and children than in adults,² and is a potentially life-threatening dermatologic emergency.

Eczema herpeticum occurs more often in infants and children than in adults, and is a potentially life-threatening emergency.

Who’s at risk? Patients with underlying chronic skin conditions such as eczema may have impaired cell-mediated immunity, making them more susceptible to a viral infection like EH.¹ In addition, treatment of underlying chronic skin conditions with immunosuppressive therapies often increases susceptibility to superimposed infection.¹ (In this case, the patient’s parents had treated an eczema flare with a topical hydrocortisone cream.) Lastly, increased risk may be associated with mutations in the gene encoding filaggrin.²

Areas affected. EH typically appears in areas of pre-existing dermatitis as monomorphic, discrete, 2- to 3-mm, punched-out, heme-crusted erosions with scalloped borders.² The erosions initially appear as vesicles or pustules, which may appear concurrently with the erosions. The erosions can coalesce to form larger lesions.³ Fever, malaise, and lymphadenopathy may also be present.^2,3

4 factors differentiate EH from other conditions

The differential for eczema herpeticum includes impetigo, bullous impetigo, shingles, chicken pox, scabies, pustular psoriasis, bullous pemphigoid, drug hypersensitivity reactions, and exacerbation of a primary dermatosis or skin condition.^1,4

EH may be differentiated from these by its location, its development in the setting of pre-existing dermatitis, its response to antiviral medications, and the results of laboratory testing. Because of the vast differential, physicians must maintain a high index of suspicion for EH, particularly when a patient with a pre-existing skin condition presents with acute onset cutaneous pain.³

Perform a Tzanck smear to diagnose the underlying infection

If EH is suspected, treatment must be initiated immediately.³ (In our patient’s case, he was started on intravenous acyclovir 10 mg/kg every 8 hours.)

Once treatment is underway, a Tzanck smear of the vesicle base can be performed at the patient’s bedside to narrow the cause of the infection to HSV or varicella zoster virus (VZV). Multinucleated giant keratinocytes (as in our patient’s case) are diagnostic for one of the herpes viruses; concurrent inflammatory cells are also to be expected in an inflammatory skin condition but by themselves are not diagnostic of herpes.

If available in the laboratory, direct fluorescent antibody testing can differentiate between HSV and VZV. Alternatively, a nucleic acid amplified probe test may be used to provide a quick and specific result. The most specific test is a viral culture, but it lacks sensitivity and usually requires 2 to 5 daysfor results.² A bacterial skin swab and blood culture should also be considered to direct antibiotic therapy if superinfection has occurred.

Antivirals and antibiotics should be given until lesions heal

Patients with EH should be admitted to the hospital for at least 24 to 48 hours of intravenous acyclovir.⁴ Antivirals—oral or intravenous—should be given for 10 to 14 days or until all mucocutaneous lesions are healed. Recommended dosing for acyclovir is 15 mg/kg (up to 400 mg) by mouth 3 to 5 times per day or, if severe, 5 mg/kg (if ≥12 years of age) to 10 mg/kg (if <12 years of age) intravenously every 8 hours.² Patients should also receive a 3- to 6-month suppressive course of oral acyclovir, valacyclovir, or famciclovir.⁴

Intravenous antibiotics should also be considered, pending the results of bacterial skin swabs and a blood culture, as the skin of patients with atopic dermatitis is colonized with staphylococcus 90% of the time.⁴

Potential complications. Bacterial sepsis resulting from superinfection and disseminated HSV, although extremely rare, is the main cause of death associated with EH.³ One case in the literature described a 43-year-old woman with extensive EH superimposed on atopic dermatitis, disseminated HSV, and Pseudomonas aeruginosa septicemia. Despite treatment with intravenous acyclovir and antibiotics in a burn center intensive care unit, the patient experienced septic shock and disseminated intravascular coagulation with progression to multiorgan failure and death.³

Our patient’s antiviral regimen was transitioned to a 14-day course of oral acyclovir, which he completed. Topical steroids and an immunosuppressant (tacrolimus ointment) were applied concurrently. He was subsequently prescribed a 6-month suppressive course of acyclovir and was scheduled for follow-up at an outpatient dermatology clinic to discuss resuming therapy for atopic dermatitis.

CORRESPONDENCE
Sahand Rahnama-Moghadam, MD, 7323 Snowden Road #1205, San Antonio, TX 78240; [email protected].

A 2-year-old boy with atopic dermatitis developed a flare of his eczema after having a bath with mint-scented soap. His mother treated the flare with over-the-counter topical hydrocortisone cream. Two to 3 days later, he developed grouped vesicles on the right side of his neck. Three days after that, he developed a painful generalized vesicular eruption all over his body.

The boy was admitted to a hospital for supportive care and empiric antibiotics, but was discharged when no bacterial infection was found. The patient’s mother was instructed to follow up with his primary care provider in the next 2 weeks.

Three days after his hospitalization, the eruption on the young boy’s body spread and he was uncomfortable. He was brought to our hospital’s pediatric clinic, where physicians examined him and decided to transfer him to the university hospital for further evaluation.

On exam, the boy was afebrile, but uncomfortable and irritable. Diffuse heme-crusted and punched-out erosions covered about 90% of his body (FIGURE). His mucous membranes were not involved. Underneath the heme-crusted erosions, there were lichenified pink plaques on the antecubital fossae, popliteal fossae, periocular face, and buttocks. The patient’s right dorsal foot had a small vesicle; all other vesicles on his body had crusted over.

The patient’s family indicated that the child had received the varicella vaccine without incident at 12 months of age. He had no history of travel, no contact with sick individuals, and no exposure to pets or other animals.

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

Diagnosis: Eczema herpeticum

Eczema herpeticum (EH) was suspected based on the appearance of the lesions. A Tzanck smear came back positive for multinucleated giant cells and a herpes simplex virus (HSV) amplified probe came back positive for HSV-1—confirming the diagnosis.

EH—also known as Kaposi varicelliform eruption—is a superficial generalized viral infection (typically caused by HSV-1; HSV-2 is less common). The infection commonly occurs in patients with underlying atopic dermatitis, but may also occur in those with Darier disease, pemphigus, burns, and other conditions that disrupt the skin barrier. Other viruses, such as Coxsackie virus, can also cause EH. Eczema vaccinatum is a variant that may occur after smallpox vaccination.¹ EH occurs more often in infants and children than in adults,² and is a potentially life-threatening dermatologic emergency.

Eczema herpeticum occurs more often in infants and children than in adults, and is a potentially life-threatening emergency.

Who’s at risk? Patients with underlying chronic skin conditions such as eczema may have impaired cell-mediated immunity, making them more susceptible to a viral infection like EH.¹ In addition, treatment of underlying chronic skin conditions with immunosuppressive therapies often increases susceptibility to superimposed infection.¹ (In this case, the patient’s parents had treated an eczema flare with a topical hydrocortisone cream.) Lastly, increased risk may be associated with mutations in the gene encoding filaggrin.²

Areas affected. EH typically appears in areas of pre-existing dermatitis as monomorphic, discrete, 2- to 3-mm, punched-out, heme-crusted erosions with scalloped borders.² The erosions initially appear as vesicles or pustules, which may appear concurrently with the erosions. The erosions can coalesce to form larger lesions.³ Fever, malaise, and lymphadenopathy may also be present.^2,3

4 factors differentiate EH from other conditions

The differential for eczema herpeticum includes impetigo, bullous impetigo, shingles, chicken pox, scabies, pustular psoriasis, bullous pemphigoid, drug hypersensitivity reactions, and exacerbation of a primary dermatosis or skin condition.^1,4

EH may be differentiated from these by its location, its development in the setting of pre-existing dermatitis, its response to antiviral medications, and the results of laboratory testing. Because of the vast differential, physicians must maintain a high index of suspicion for EH, particularly when a patient with a pre-existing skin condition presents with acute onset cutaneous pain.³

Perform a Tzanck smear to diagnose the underlying infection

If EH is suspected, treatment must be initiated immediately.³ (In our patient’s case, he was started on intravenous acyclovir 10 mg/kg every 8 hours.)

Once treatment is underway, a Tzanck smear of the vesicle base can be performed at the patient’s bedside to narrow the cause of the infection to HSV or varicella zoster virus (VZV). Multinucleated giant keratinocytes (as in our patient’s case) are diagnostic for one of the herpes viruses; concurrent inflammatory cells are also to be expected in an inflammatory skin condition but by themselves are not diagnostic of herpes.

If available in the laboratory, direct fluorescent antibody testing can differentiate between HSV and VZV. Alternatively, a nucleic acid amplified probe test may be used to provide a quick and specific result. The most specific test is a viral culture, but it lacks sensitivity and usually requires 2 to 5 daysfor results.² A bacterial skin swab and blood culture should also be considered to direct antibiotic therapy if superinfection has occurred.

Antivirals and antibiotics should be given until lesions heal

Patients with EH should be admitted to the hospital for at least 24 to 48 hours of intravenous acyclovir.⁴ Antivirals—oral or intravenous—should be given for 10 to 14 days or until all mucocutaneous lesions are healed. Recommended dosing for acyclovir is 15 mg/kg (up to 400 mg) by mouth 3 to 5 times per day or, if severe, 5 mg/kg (if ≥12 years of age) to 10 mg/kg (if <12 years of age) intravenously every 8 hours.² Patients should also receive a 3- to 6-month suppressive course of oral acyclovir, valacyclovir, or famciclovir.⁴

Intravenous antibiotics should also be considered, pending the results of bacterial skin swabs and a blood culture, as the skin of patients with atopic dermatitis is colonized with staphylococcus 90% of the time.⁴

Potential complications. Bacterial sepsis resulting from superinfection and disseminated HSV, although extremely rare, is the main cause of death associated with EH.³ One case in the literature described a 43-year-old woman with extensive EH superimposed on atopic dermatitis, disseminated HSV, and Pseudomonas aeruginosa septicemia. Despite treatment with intravenous acyclovir and antibiotics in a burn center intensive care unit, the patient experienced septic shock and disseminated intravascular coagulation with progression to multiorgan failure and death.³

Our patient’s antiviral regimen was transitioned to a 14-day course of oral acyclovir, which he completed. Topical steroids and an immunosuppressant (tacrolimus ointment) were applied concurrently. He was subsequently prescribed a 6-month suppressive course of acyclovir and was scheduled for follow-up at an outpatient dermatology clinic to discuss resuming therapy for atopic dermatitis.

CORRESPONDENCE
Sahand Rahnama-Moghadam, MD, 7323 Snowden Road #1205, San Antonio, TX 78240; [email protected].

A biopsy was performed and direct immunofluorescence came back negative. This, along with the patient’s history of diabetes, led us to diagnose bullosis diabeticorum.

This condition, also known as bullous disease of diabetes, is characterized by abrupt development of noninflammatory bullae on acral areas in patients with diabetes. The skin appears normal except for the bullae. Bullosis diabeticorum occurs in just .5% of patients with diabetes and is twice as common in men as it is in women.

The etiology of bullosis diabeticorum is unknown. The acral location suggests that trauma may be a contributing factor. Although electron microscopy has suggested an abnormality in anchoring fibrils, this cellular change does not fully explain the development of multiple blisters at varying sites. Glycemic control is not thought to play a role.

The distribution of lesions and the presence—or absence—of systemic symptoms goes a long way toward narrowing the differential of blistering diseases. The presence of generalized blistering and systemic symptoms would suggest conditions related to medication exposure, such as Stevens-Johnson syndrome or toxic epidermal necrolysis; infectious etiologies (eg, staphylococcal scalded skin syndrome); autoimmune causes; or underlying malignancy. Generalized blistering in the absence of systemic symptoms would support diagnoses such as bullous impetigo and pemphigoid.

Lesion distribution provides important clues, too. Sun exposure-related causes typically leave lesions on the hands and forearms, not just the toes. A dermatomal distribution would suggest herpes zoster. A linear distribution of blisters argues for contact dermatitis.

A diagnosis of bullosis diabeticorum can be made when biopsy with immunofluorescence excludes other histologically similar entities such as epidermolysis bullosa, noninflammatory bullous pemphigoid, and porphyria cutanea tarda. And while immunofluorescence findings are typically negative, elevated levels of immunoglobulin M and C3 have, on occasion, been reported. Cultures are warranted only if a secondary infection is suspected.

The bullae of this condition spontaneously resolve over several weeks without treatment, but tend to recur. The lesions typically heal without significant scarring, although they may have a darker pigmentation after the first occurrence. Treatment may be warranted if a patient develops a secondary infection.

In our patient’s case, the bullae resolved within 2 weeks without treatment, although mild hyperpigmentation remained.

Adapted from: Mims L, Savage A, Chessman A. Blisters on an elderly woman's toes. J Fam Pract. 2014;63:273-274.

A biopsy was performed and direct immunofluorescence came back negative. This, along with the patient’s history of diabetes, led us to diagnose bullosis diabeticorum.

This condition, also known as bullous disease of diabetes, is characterized by abrupt development of noninflammatory bullae on acral areas in patients with diabetes. The skin appears normal except for the bullae. Bullosis diabeticorum occurs in just .5% of patients with diabetes and is twice as common in men as it is in women.

The etiology of bullosis diabeticorum is unknown. The acral location suggests that trauma may be a contributing factor. Although electron microscopy has suggested an abnormality in anchoring fibrils, this cellular change does not fully explain the development of multiple blisters at varying sites. Glycemic control is not thought to play a role.

The distribution of lesions and the presence—or absence—of systemic symptoms goes a long way toward narrowing the differential of blistering diseases. The presence of generalized blistering and systemic symptoms would suggest conditions related to medication exposure, such as Stevens-Johnson syndrome or toxic epidermal necrolysis; infectious etiologies (eg, staphylococcal scalded skin syndrome); autoimmune causes; or underlying malignancy. Generalized blistering in the absence of systemic symptoms would support diagnoses such as bullous impetigo and pemphigoid.

Lesion distribution provides important clues, too. Sun exposure-related causes typically leave lesions on the hands and forearms, not just the toes. A dermatomal distribution would suggest herpes zoster. A linear distribution of blisters argues for contact dermatitis.

A diagnosis of bullosis diabeticorum can be made when biopsy with immunofluorescence excludes other histologically similar entities such as epidermolysis bullosa, noninflammatory bullous pemphigoid, and porphyria cutanea tarda. And while immunofluorescence findings are typically negative, elevated levels of immunoglobulin M and C3 have, on occasion, been reported. Cultures are warranted only if a secondary infection is suspected.

The bullae of this condition spontaneously resolve over several weeks without treatment, but tend to recur. The lesions typically heal without significant scarring, although they may have a darker pigmentation after the first occurrence. Treatment may be warranted if a patient develops a secondary infection.

In our patient’s case, the bullae resolved within 2 weeks without treatment, although mild hyperpigmentation remained.

Adapted from: Mims L, Savage A, Chessman A. Blisters on an elderly woman's toes. J Fam Pract. 2014;63:273-274.

A biopsy was performed and direct immunofluorescence came back negative. This, along with the patient’s history of diabetes, led us to diagnose bullosis diabeticorum.

This condition, also known as bullous disease of diabetes, is characterized by abrupt development of noninflammatory bullae on acral areas in patients with diabetes. The skin appears normal except for the bullae. Bullosis diabeticorum occurs in just .5% of patients with diabetes and is twice as common in men as it is in women.

The etiology of bullosis diabeticorum is unknown. The acral location suggests that trauma may be a contributing factor. Although electron microscopy has suggested an abnormality in anchoring fibrils, this cellular change does not fully explain the development of multiple blisters at varying sites. Glycemic control is not thought to play a role.

The distribution of lesions and the presence—or absence—of systemic symptoms goes a long way toward narrowing the differential of blistering diseases. The presence of generalized blistering and systemic symptoms would suggest conditions related to medication exposure, such as Stevens-Johnson syndrome or toxic epidermal necrolysis; infectious etiologies (eg, staphylococcal scalded skin syndrome); autoimmune causes; or underlying malignancy. Generalized blistering in the absence of systemic symptoms would support diagnoses such as bullous impetigo and pemphigoid.

Lesion distribution provides important clues, too. Sun exposure-related causes typically leave lesions on the hands and forearms, not just the toes. A dermatomal distribution would suggest herpes zoster. A linear distribution of blisters argues for contact dermatitis.

A diagnosis of bullosis diabeticorum can be made when biopsy with immunofluorescence excludes other histologically similar entities such as epidermolysis bullosa, noninflammatory bullous pemphigoid, and porphyria cutanea tarda. And while immunofluorescence findings are typically negative, elevated levels of immunoglobulin M and C3 have, on occasion, been reported. Cultures are warranted only if a secondary infection is suspected.

The bullae of this condition spontaneously resolve over several weeks without treatment, but tend to recur. The lesions typically heal without significant scarring, although they may have a darker pigmentation after the first occurrence. Treatment may be warranted if a patient develops a secondary infection.

In our patient’s case, the bullae resolved within 2 weeks without treatment, although mild hyperpigmentation remained.

Adapted from: Mims L, Savage A, Chessman A. Blisters on an elderly woman's toes. J Fam Pract. 2014;63:273-274.

A 31-year-old incarcerated man sought care for one crusted ulcer and one adjacent open ulcer with granulation tissue on his left malleolus. The ulcers were caused by chronic venous insufficiency—the result of previous trauma to the ankle. Concerned that the ulcers would become infected, the physician prescribed one double-strength tablet twice a day of trimethoprim-sulfamethoxazole (TMP-SMX). The patient took 2 doses of the antibiotic and one dose of naproxen.

When the patient awoke the next morning, he had a generalized skin eruption on his chin, trunk, buttocks, glans penis, and extremities (FIGURE). The rash began as red edematous plaques that became itchy and painful with dark, violaceous dusky centers surrounded by redness. The patient was treated with topical hydrocortisone 2.5% twice a day and oral diphenhydramine 25 mg followed by 50 mg, but the rash didn’t improve.

The patient was transported to the local emergency department where physicians noted that the patient had about 30 to 40 well-demarcated papules and plaques of various sizes that were haphazardly located over the patient’s chin, chest, back, upper and lower extremities, and genitalia. There was one lesion on the chest with central vesiculation. There were no lesions on the mucous membranes of his eyes, ears, nose, mouth, or anus.

The patient, whose vital signs were within normal limits, was empirically treated with one dose of methylprednisolone (125 mg intravenous [IV]) and started on IV piperacillin-tazobactam and vancomycin. Lab work revealed no elevation in his white blood cell count, creatinine, liver function enzymes, or C-reactive protein.

The patient subsequently revealed that he’d had a similar experience a year earlier after being treated with TMP-SMX for cellulitis. He noted that during the previous episode, the lesions were located on the exact same areas of his glans penis and chin.

Diagnosis: Disseminated fixed-drug eruption

The diagnosis was based on the morphologic characteristics of the eruption and the patient’s history of similar lesions that appeared in the exact same initial locations (chin and glans penis) following previous treatment with TMP-SMX.

A fixed-drug eruption is an adverse cutaneous reaction to a drug that is defined by a dusky red or violaceous macule, which evolves into a patch, and eventually, an edematous plaque. Fixed-drug eruptions are typically solitary, but may be generalized (as was the case with our patient).

The pathophysiology of the disease involves resident intra-epidermal CD8+ T-cells resembling effector memory T-cells. These T-cells are increased in number at the dermoepidermal junction of normal appearing skin; their aberrant activation leads to an inflammatory response, stimulating tissue destruction and formation of the classic fixed-drug lesion.¹

The diagnosis is usually made based on a history of similar lesions recurring at the same location in response to a specific drug² and the classic physical exam findings of well-demarcated, edematous, and violaceous plaques. To confirm a fixed-drug eruption in the case of clinical equipoise, a skin biopsy may be performed.

Classic histologic findings of a fixed-drug eruption include:

• band-like lichenoid lymphocytic infiltrates with vacuolar changes at the dermoepidermal junction,
• mixed cellular infiltrates, including eosinophils, throughout the dermis and occasional superficial and deep mixed cellular perivascular infiltrates, and
• abundant melanophages suggesting pigment incontinence.

There are several reports of similar TMP-SMX–induced generalized fixed-drug eruptions in the literature.³ One study of 64 cases of fixed-drug eruption found that TMP-SMX was the most common offender, causing 75% of fixed-drug eruption cases; naproxen sodium came in second with 12.5%.³ Other common culprits include the antipyretic metamizole and other pyrazolone derivatives such as tetracycline, metronidazole, ciprofloxacin, and phenytoin sodium.⁴ There is evidence supporting a correlation between the offending drug and the subsequent site of reaction; TMP-SMX is associated with mucosal junction and genital involvement.^4,5 This finding may aid physicians in the investigation of provoking agents.

Distinguish fixed-drug eruptions from serious bullous diseases

Fixed-drug eruptions occasionally exhibit bullae and erosions and must be differentiated from more serious generalized bullous diseases, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). The differential diagnosis also includes erythema multiforme, early bullous drug eruption, and bullous arthropod assault, which may leave similar hyperpigmented patches. Fixed-drug eruptions can be distinguished by the lack of simultaneous involvement of 2 mucosal surfaces, lack of generalized desquamation, and normal vital signs and lab values, including white blood cell count and erythrocyte sedimentation rate/C-reactive protein.

A subset of fixed-drug eruption, generalized bullous fixed-drug eruption (which has been defined as blistering on >10% of the body’s surface area at 3 different anatomic sites), may be particularly hard to distinguish from SJS and TEN. Generalized bullous fixed-drug eruption generally has a shorter latency period than SJS or TEN (usually <3 days compared to 7-10 days) and has less mucosal involvement.⁶

Symptomatic therapy includes antihistamines, glucocorticoid ointment

Management of a disseminated fixed-drug eruption requires a thorough history to identify the causative agent (including over-the-counter drugs, herbals, topicals, and eye drops). Most patients are asymptomatic, but some (like our patient) are symptomatic and experience generalized pruritus, cutaneous burning, and/or pain. Symptomatic therapy includes oral antihistamines and potent topical glucocorticoid ointment for non-eroded lesions. Additionally, if not medically contraindicated, oral steroids may be used for generalized or extremely painful mucosal lesions at a dose of 0.5 mg/kg daily for 3 to 5 days. Be advised, however, that these therapies are based on case report level data.²

Local wound care of eroded lesions includes keeping the site moist with a bland emollient and bandaging. The inciting agent must be added to the patient’s allergy list and avoided in the future. In equivocal cases, it is prudent to admit the patient for observation to ensure that the eruption is not a nascent SJS or TEN eruption.

Our patient was admitted to the observation unit overnight to monitor for the appearance of systemic symptoms and to assess the evolution of the rash for further mucosal involvement that could have indicated SJS. Upon reassessment the next day, his older lesions had evolved into vesiculated and necrotic areas as per the natural history of severe fixed-drug eruption.

He was prescribed prednisone 40 mg/d for 3 days to help with local inflammation, pain, and itching. TMP-SMX was added to his allergy list and he was given local wound care instructions. He was told to return if he developed any systemic symptoms.

CORRESPONDENCE
Jackie Bucher, MD, 7733 Louis Pasteur Drive Apt. 209, San Antonio, TX 78229; [email protected].

A 31-year-old incarcerated man sought care for one crusted ulcer and one adjacent open ulcer with granulation tissue on his left malleolus. The ulcers were caused by chronic venous insufficiency—the result of previous trauma to the ankle. Concerned that the ulcers would become infected, the physician prescribed one double-strength tablet twice a day of trimethoprim-sulfamethoxazole (TMP-SMX). The patient took 2 doses of the antibiotic and one dose of naproxen.

When the patient awoke the next morning, he had a generalized skin eruption on his chin, trunk, buttocks, glans penis, and extremities (FIGURE). The rash began as red edematous plaques that became itchy and painful with dark, violaceous dusky centers surrounded by redness. The patient was treated with topical hydrocortisone 2.5% twice a day and oral diphenhydramine 25 mg followed by 50 mg, but the rash didn’t improve.

The patient was transported to the local emergency department where physicians noted that the patient had about 30 to 40 well-demarcated papules and plaques of various sizes that were haphazardly located over the patient’s chin, chest, back, upper and lower extremities, and genitalia. There was one lesion on the chest with central vesiculation. There were no lesions on the mucous membranes of his eyes, ears, nose, mouth, or anus.

The patient, whose vital signs were within normal limits, was empirically treated with one dose of methylprednisolone (125 mg intravenous [IV]) and started on IV piperacillin-tazobactam and vancomycin. Lab work revealed no elevation in his white blood cell count, creatinine, liver function enzymes, or C-reactive protein.

The patient subsequently revealed that he’d had a similar experience a year earlier after being treated with TMP-SMX for cellulitis. He noted that during the previous episode, the lesions were located on the exact same areas of his glans penis and chin.

Diagnosis: Disseminated fixed-drug eruption

The diagnosis was based on the morphologic characteristics of the eruption and the patient’s history of similar lesions that appeared in the exact same initial locations (chin and glans penis) following previous treatment with TMP-SMX.

A fixed-drug eruption is an adverse cutaneous reaction to a drug that is defined by a dusky red or violaceous macule, which evolves into a patch, and eventually, an edematous plaque. Fixed-drug eruptions are typically solitary, but may be generalized (as was the case with our patient).

The pathophysiology of the disease involves resident intra-epidermal CD8+ T-cells resembling effector memory T-cells. These T-cells are increased in number at the dermoepidermal junction of normal appearing skin; their aberrant activation leads to an inflammatory response, stimulating tissue destruction and formation of the classic fixed-drug lesion.¹

The diagnosis is usually made based on a history of similar lesions recurring at the same location in response to a specific drug² and the classic physical exam findings of well-demarcated, edematous, and violaceous plaques. To confirm a fixed-drug eruption in the case of clinical equipoise, a skin biopsy may be performed.

Classic histologic findings of a fixed-drug eruption include:

• band-like lichenoid lymphocytic infiltrates with vacuolar changes at the dermoepidermal junction,
• mixed cellular infiltrates, including eosinophils, throughout the dermis and occasional superficial and deep mixed cellular perivascular infiltrates, and
• abundant melanophages suggesting pigment incontinence.

There are several reports of similar TMP-SMX–induced generalized fixed-drug eruptions in the literature.³ One study of 64 cases of fixed-drug eruption found that TMP-SMX was the most common offender, causing 75% of fixed-drug eruption cases; naproxen sodium came in second with 12.5%.³ Other common culprits include the antipyretic metamizole and other pyrazolone derivatives such as tetracycline, metronidazole, ciprofloxacin, and phenytoin sodium.⁴ There is evidence supporting a correlation between the offending drug and the subsequent site of reaction; TMP-SMX is associated with mucosal junction and genital involvement.^4,5 This finding may aid physicians in the investigation of provoking agents.

Distinguish fixed-drug eruptions from serious bullous diseases

Fixed-drug eruptions occasionally exhibit bullae and erosions and must be differentiated from more serious generalized bullous diseases, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). The differential diagnosis also includes erythema multiforme, early bullous drug eruption, and bullous arthropod assault, which may leave similar hyperpigmented patches. Fixed-drug eruptions can be distinguished by the lack of simultaneous involvement of 2 mucosal surfaces, lack of generalized desquamation, and normal vital signs and lab values, including white blood cell count and erythrocyte sedimentation rate/C-reactive protein.

A subset of fixed-drug eruption, generalized bullous fixed-drug eruption (which has been defined as blistering on >10% of the body’s surface area at 3 different anatomic sites), may be particularly hard to distinguish from SJS and TEN. Generalized bullous fixed-drug eruption generally has a shorter latency period than SJS or TEN (usually <3 days compared to 7-10 days) and has less mucosal involvement.⁶

Symptomatic therapy includes antihistamines, glucocorticoid ointment

Management of a disseminated fixed-drug eruption requires a thorough history to identify the causative agent (including over-the-counter drugs, herbals, topicals, and eye drops). Most patients are asymptomatic, but some (like our patient) are symptomatic and experience generalized pruritus, cutaneous burning, and/or pain. Symptomatic therapy includes oral antihistamines and potent topical glucocorticoid ointment for non-eroded lesions. Additionally, if not medically contraindicated, oral steroids may be used for generalized or extremely painful mucosal lesions at a dose of 0.5 mg/kg daily for 3 to 5 days. Be advised, however, that these therapies are based on case report level data.²

Local wound care of eroded lesions includes keeping the site moist with a bland emollient and bandaging. The inciting agent must be added to the patient’s allergy list and avoided in the future. In equivocal cases, it is prudent to admit the patient for observation to ensure that the eruption is not a nascent SJS or TEN eruption.

Our patient was admitted to the observation unit overnight to monitor for the appearance of systemic symptoms and to assess the evolution of the rash for further mucosal involvement that could have indicated SJS. Upon reassessment the next day, his older lesions had evolved into vesiculated and necrotic areas as per the natural history of severe fixed-drug eruption.

He was prescribed prednisone 40 mg/d for 3 days to help with local inflammation, pain, and itching. TMP-SMX was added to his allergy list and he was given local wound care instructions. He was told to return if he developed any systemic symptoms.

CORRESPONDENCE
Jackie Bucher, MD, 7733 Louis Pasteur Drive Apt. 209, San Antonio, TX 78229; [email protected].

A 31-year-old incarcerated man sought care for one crusted ulcer and one adjacent open ulcer with granulation tissue on his left malleolus. The ulcers were caused by chronic venous insufficiency—the result of previous trauma to the ankle. Concerned that the ulcers would become infected, the physician prescribed one double-strength tablet twice a day of trimethoprim-sulfamethoxazole (TMP-SMX). The patient took 2 doses of the antibiotic and one dose of naproxen.

When the patient awoke the next morning, he had a generalized skin eruption on his chin, trunk, buttocks, glans penis, and extremities (FIGURE). The rash began as red edematous plaques that became itchy and painful with dark, violaceous dusky centers surrounded by redness. The patient was treated with topical hydrocortisone 2.5% twice a day and oral diphenhydramine 25 mg followed by 50 mg, but the rash didn’t improve.

The patient was transported to the local emergency department where physicians noted that the patient had about 30 to 40 well-demarcated papules and plaques of various sizes that were haphazardly located over the patient’s chin, chest, back, upper and lower extremities, and genitalia. There was one lesion on the chest with central vesiculation. There were no lesions on the mucous membranes of his eyes, ears, nose, mouth, or anus.

The patient, whose vital signs were within normal limits, was empirically treated with one dose of methylprednisolone (125 mg intravenous [IV]) and started on IV piperacillin-tazobactam and vancomycin. Lab work revealed no elevation in his white blood cell count, creatinine, liver function enzymes, or C-reactive protein.

The patient subsequently revealed that he’d had a similar experience a year earlier after being treated with TMP-SMX for cellulitis. He noted that during the previous episode, the lesions were located on the exact same areas of his glans penis and chin.

Diagnosis: Disseminated fixed-drug eruption

The diagnosis was based on the morphologic characteristics of the eruption and the patient’s history of similar lesions that appeared in the exact same initial locations (chin and glans penis) following previous treatment with TMP-SMX.

A fixed-drug eruption is an adverse cutaneous reaction to a drug that is defined by a dusky red or violaceous macule, which evolves into a patch, and eventually, an edematous plaque. Fixed-drug eruptions are typically solitary, but may be generalized (as was the case with our patient).

The pathophysiology of the disease involves resident intra-epidermal CD8+ T-cells resembling effector memory T-cells. These T-cells are increased in number at the dermoepidermal junction of normal appearing skin; their aberrant activation leads to an inflammatory response, stimulating tissue destruction and formation of the classic fixed-drug lesion.¹

The diagnosis is usually made based on a history of similar lesions recurring at the same location in response to a specific drug² and the classic physical exam findings of well-demarcated, edematous, and violaceous plaques. To confirm a fixed-drug eruption in the case of clinical equipoise, a skin biopsy may be performed.

Classic histologic findings of a fixed-drug eruption include:

• band-like lichenoid lymphocytic infiltrates with vacuolar changes at the dermoepidermal junction,
• mixed cellular infiltrates, including eosinophils, throughout the dermis and occasional superficial and deep mixed cellular perivascular infiltrates, and
• abundant melanophages suggesting pigment incontinence.

There are several reports of similar TMP-SMX–induced generalized fixed-drug eruptions in the literature.³ One study of 64 cases of fixed-drug eruption found that TMP-SMX was the most common offender, causing 75% of fixed-drug eruption cases; naproxen sodium came in second with 12.5%.³ Other common culprits include the antipyretic metamizole and other pyrazolone derivatives such as tetracycline, metronidazole, ciprofloxacin, and phenytoin sodium.⁴ There is evidence supporting a correlation between the offending drug and the subsequent site of reaction; TMP-SMX is associated with mucosal junction and genital involvement.^4,5 This finding may aid physicians in the investigation of provoking agents.

Distinguish fixed-drug eruptions from serious bullous diseases

Fixed-drug eruptions occasionally exhibit bullae and erosions and must be differentiated from more serious generalized bullous diseases, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). The differential diagnosis also includes erythema multiforme, early bullous drug eruption, and bullous arthropod assault, which may leave similar hyperpigmented patches. Fixed-drug eruptions can be distinguished by the lack of simultaneous involvement of 2 mucosal surfaces, lack of generalized desquamation, and normal vital signs and lab values, including white blood cell count and erythrocyte sedimentation rate/C-reactive protein.

A subset of fixed-drug eruption, generalized bullous fixed-drug eruption (which has been defined as blistering on >10% of the body’s surface area at 3 different anatomic sites), may be particularly hard to distinguish from SJS and TEN. Generalized bullous fixed-drug eruption generally has a shorter latency period than SJS or TEN (usually <3 days compared to 7-10 days) and has less mucosal involvement.⁶

Symptomatic therapy includes antihistamines, glucocorticoid ointment

Management of a disseminated fixed-drug eruption requires a thorough history to identify the causative agent (including over-the-counter drugs, herbals, topicals, and eye drops). Most patients are asymptomatic, but some (like our patient) are symptomatic and experience generalized pruritus, cutaneous burning, and/or pain. Symptomatic therapy includes oral antihistamines and potent topical glucocorticoid ointment for non-eroded lesions. Additionally, if not medically contraindicated, oral steroids may be used for generalized or extremely painful mucosal lesions at a dose of 0.5 mg/kg daily for 3 to 5 days. Be advised, however, that these therapies are based on case report level data.²

Local wound care of eroded lesions includes keeping the site moist with a bland emollient and bandaging. The inciting agent must be added to the patient’s allergy list and avoided in the future. In equivocal cases, it is prudent to admit the patient for observation to ensure that the eruption is not a nascent SJS or TEN eruption.

Our patient was admitted to the observation unit overnight to monitor for the appearance of systemic symptoms and to assess the evolution of the rash for further mucosal involvement that could have indicated SJS. Upon reassessment the next day, his older lesions had evolved into vesiculated and necrotic areas as per the natural history of severe fixed-drug eruption.

He was prescribed prednisone 40 mg/d for 3 days to help with local inflammation, pain, and itching. TMP-SMX was added to his allergy list and he was given local wound care instructions. He was told to return if he developed any systemic symptoms.

CORRESPONDENCE
Jackie Bucher, MD, 7733 Louis Pasteur Drive Apt. 209, San Antonio, TX 78229; [email protected].

The FP diagnosed flat warts based on their typical appearance and location. Flat warts are frequently found on the face and neck and can easily be spread when men shave their beards or women shave their legs. Flat warts can also occur on the face of young children.

The FP suggested cryotherapy for the largest warts and prescribed topical imiquimod (3 times per week) for home use. The FP suggested that the patient wait 2 weeks before starting the imiquimod to allow the cryotherapy to do its work and for any blistering or irritation to subside. A follow-up appointment was set for 6 weeks.

At the follow-up visit, there was little improvement and the patient wanted to try an alternative therapy. The risks and benefits of Candida antigen intralesional injection were discussed and the patient decided to proceed with this approach. Intralesional injections with Candida antigen induce a localized, cell-mediated, and human papillomavirus (HPV)-specific response that may target the injected wart as well as more distant warts. This method has moderate effectiveness (60% cure rates) for treatment of recalcitrant warts. The Candida antigen must be diluted before use, and 0.1 to 0.3 mL should be injected into the largest warts using a 30-gauge needle (up to 1 mL per treatment). Warn patients to expect itching in the area, burning, or peeling, and repeat the procedure every 4 weeks with up to 3 treatments or until warts are gone.

For this patient, the Candida antigen was diluted with normal saline (0.25 mL of generic Candida antigen with 0.75 mL of normal saline). The mixture was injected with a 30-gauge needle into approximately 10 of the largest flat warts. One month later, all of the flat warts were gone.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Flat warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:755-758.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed flat warts based on their typical appearance and location. Flat warts are frequently found on the face and neck and can easily be spread when men shave their beards or women shave their legs. Flat warts can also occur on the face of young children.

The FP suggested cryotherapy for the largest warts and prescribed topical imiquimod (3 times per week) for home use. The FP suggested that the patient wait 2 weeks before starting the imiquimod to allow the cryotherapy to do its work and for any blistering or irritation to subside. A follow-up appointment was set for 6 weeks.

At the follow-up visit, there was little improvement and the patient wanted to try an alternative therapy. The risks and benefits of Candida antigen intralesional injection were discussed and the patient decided to proceed with this approach. Intralesional injections with Candida antigen induce a localized, cell-mediated, and human papillomavirus (HPV)-specific response that may target the injected wart as well as more distant warts. This method has moderate effectiveness (60% cure rates) for treatment of recalcitrant warts. The Candida antigen must be diluted before use, and 0.1 to 0.3 mL should be injected into the largest warts using a 30-gauge needle (up to 1 mL per treatment). Warn patients to expect itching in the area, burning, or peeling, and repeat the procedure every 4 weeks with up to 3 treatments or until warts are gone.

For this patient, the Candida antigen was diluted with normal saline (0.25 mL of generic Candida antigen with 0.75 mL of normal saline). The mixture was injected with a 30-gauge needle into approximately 10 of the largest flat warts. One month later, all of the flat warts were gone.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Flat warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:755-758.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed flat warts based on their typical appearance and location. Flat warts are frequently found on the face and neck and can easily be spread when men shave their beards or women shave their legs. Flat warts can also occur on the face of young children.

The FP suggested cryotherapy for the largest warts and prescribed topical imiquimod (3 times per week) for home use. The FP suggested that the patient wait 2 weeks before starting the imiquimod to allow the cryotherapy to do its work and for any blistering or irritation to subside. A follow-up appointment was set for 6 weeks.

At the follow-up visit, there was little improvement and the patient wanted to try an alternative therapy. The risks and benefits of Candida antigen intralesional injection were discussed and the patient decided to proceed with this approach. Intralesional injections with Candida antigen induce a localized, cell-mediated, and human papillomavirus (HPV)-specific response that may target the injected wart as well as more distant warts. This method has moderate effectiveness (60% cure rates) for treatment of recalcitrant warts. The Candida antigen must be diluted before use, and 0.1 to 0.3 mL should be injected into the largest warts using a 30-gauge needle (up to 1 mL per treatment). Warn patients to expect itching in the area, burning, or peeling, and repeat the procedure every 4 weeks with up to 3 treatments or until warts are gone.

For this patient, the Candida antigen was diluted with normal saline (0.25 mL of generic Candida antigen with 0.75 mL of normal saline). The mixture was injected with a 30-gauge needle into approximately 10 of the largest flat warts. One month later, all of the flat warts were gone.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Flat warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:755-758.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed this patient with common warts. While any child can develop a large cluster of warts, the FP decided to ask more about the family’s health in case this was a sign of immunosuppression. The mother acknowledged that she was positive for human immunodeficiency virus (HIV) and that the father had passed away from acquired immune deficiency syndrome (AIDS). She consented to HIV testing for her son and he tested positive. Unfortunately, the mother did not have antiretroviral therapy during her pregnancy with this child.

While there were resources within the village for HIV treatment, there were no resources for wart treatment. Because the child could receive treatment for HIV, the warts could resolve on their own as his immune system improved. Even immunocompetent children will often see their warts completely disappear over time.

In settings with greater resources, typical treatments for common warts include: cryotherapy, topical salicylic acid, topical cantharidin, topical imiquimod, and intralesional immunotherapy. Intralesional immunotherapy can be performed with Candida antigens, the measles, mumps, and rubella vaccine, and a purified protein derivative (as used for tuberculosis testing). Other less commonly used treatments include lasers, photodynamic therapy, contact immunotherapy, hypnosis, oral cimetidine, duct tape, and surgery.

The reason there are so many treatments is that no single treatment works well enough in most cases. Based on a Cochrane review, the strongest evidence supports topical salicylic acid and cryotherapy.¹ Immunosuppressed patients can sometimes have the most recalcitrant warts, but treatment of the immune system, along with typical treatment options, can still be successful.

1. Gibbs S, Harvey I, Sterling JC, et al. Local treatments for cutaneous warts. Cochrane Database Syst Rev. 2001;(2):CD001781.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Common warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:749-754.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed this patient with common warts. While any child can develop a large cluster of warts, the FP decided to ask more about the family’s health in case this was a sign of immunosuppression. The mother acknowledged that she was positive for human immunodeficiency virus (HIV) and that the father had passed away from acquired immune deficiency syndrome (AIDS). She consented to HIV testing for her son and he tested positive. Unfortunately, the mother did not have antiretroviral therapy during her pregnancy with this child.

While there were resources within the village for HIV treatment, there were no resources for wart treatment. Because the child could receive treatment for HIV, the warts could resolve on their own as his immune system improved. Even immunocompetent children will often see their warts completely disappear over time.

In settings with greater resources, typical treatments for common warts include: cryotherapy, topical salicylic acid, topical cantharidin, topical imiquimod, and intralesional immunotherapy. Intralesional immunotherapy can be performed with Candida antigens, the measles, mumps, and rubella vaccine, and a purified protein derivative (as used for tuberculosis testing). Other less commonly used treatments include lasers, photodynamic therapy, contact immunotherapy, hypnosis, oral cimetidine, duct tape, and surgery.

The reason there are so many treatments is that no single treatment works well enough in most cases. Based on a Cochrane review, the strongest evidence supports topical salicylic acid and cryotherapy.¹ Immunosuppressed patients can sometimes have the most recalcitrant warts, but treatment of the immune system, along with typical treatment options, can still be successful.

1. Gibbs S, Harvey I, Sterling JC, et al. Local treatments for cutaneous warts. Cochrane Database Syst Rev. 2001;(2):CD001781.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Common warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:749-754.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed this patient with common warts. While any child can develop a large cluster of warts, the FP decided to ask more about the family’s health in case this was a sign of immunosuppression. The mother acknowledged that she was positive for human immunodeficiency virus (HIV) and that the father had passed away from acquired immune deficiency syndrome (AIDS). She consented to HIV testing for her son and he tested positive. Unfortunately, the mother did not have antiretroviral therapy during her pregnancy with this child.

While there were resources within the village for HIV treatment, there were no resources for wart treatment. Because the child could receive treatment for HIV, the warts could resolve on their own as his immune system improved. Even immunocompetent children will often see their warts completely disappear over time.

In settings with greater resources, typical treatments for common warts include: cryotherapy, topical salicylic acid, topical cantharidin, topical imiquimod, and intralesional immunotherapy. Intralesional immunotherapy can be performed with Candida antigens, the measles, mumps, and rubella vaccine, and a purified protein derivative (as used for tuberculosis testing). Other less commonly used treatments include lasers, photodynamic therapy, contact immunotherapy, hypnosis, oral cimetidine, duct tape, and surgery.

The reason there are so many treatments is that no single treatment works well enough in most cases. Based on a Cochrane review, the strongest evidence supports topical salicylic acid and cryotherapy.¹ Immunosuppressed patients can sometimes have the most recalcitrant warts, but treatment of the immune system, along with typical treatment options, can still be successful.

1. Gibbs S, Harvey I, Sterling JC, et al. Local treatments for cutaneous warts. Cochrane Database Syst Rev. 2001;(2):CD001781.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Common warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:749-754.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed molluscum contagiosum because a few of the papules had central umbilication. While she noticed that many papules did not have central umbilication, she was aware that not all molluscum lesions would have this feature. Pearly papules are classic for molluscum, even when central umbilication is not visible.

Children with atopic dermatitis are more prone to molluscum infections and frequently get them in areas that have been, or presently are, involved with atopic dermatitis. In this case, the child had antecubital involvement with her atopic dermatitis (although her skin was relatively normal at the time). The altered barrier function found in atopic individuals makes them more prone to various viral and bacterial super infections, including molluscum, herpes, and bacterial impetigo.

In immunocompetent patients, lesions usually spontaneously resolve within 8 to 12 months. In a minority of cases, disease persists for a few years. Children do not have to be kept out of day care or school for this condition, even though it is somewhat contagious. Like warts, keeping kids out of school or day care is not useful to prevent the spread of disease and is not practical on a societal level.

The FP discussed cryotherapy with the mother and child, but the girl was not willing to allow it due to her fear of the pain. Other options included watch and wait, topical salicylic acid, tretinoin, and imiquimod—although none of these have been approved by the Food and Drug Administration. Cantharidin had also been used previously in this office, but it was not available because regulations have made it very difficult to obtain. Imiquimod is not suggested for children younger than 12; therefore, this costly medicine would not be covered by insurance.

The mother requested a prescription for tretinoin and stated that if the insurance would not cover it, she would go with over-the-counter salicylic acid. The FP wrote a prescription for 0.025% tretinoin cream to be applied daily and said to stop using it if irritation became too bothersome. Follow-up was to be done as needed, but was not completed.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Molluscum contagiosum. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:743-748.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed molluscum contagiosum because a few of the papules had central umbilication. While she noticed that many papules did not have central umbilication, she was aware that not all molluscum lesions would have this feature. Pearly papules are classic for molluscum, even when central umbilication is not visible.

Children with atopic dermatitis are more prone to molluscum infections and frequently get them in areas that have been, or presently are, involved with atopic dermatitis. In this case, the child had antecubital involvement with her atopic dermatitis (although her skin was relatively normal at the time). The altered barrier function found in atopic individuals makes them more prone to various viral and bacterial super infections, including molluscum, herpes, and bacterial impetigo.

In immunocompetent patients, lesions usually spontaneously resolve within 8 to 12 months. In a minority of cases, disease persists for a few years. Children do not have to be kept out of day care or school for this condition, even though it is somewhat contagious. Like warts, keeping kids out of school or day care is not useful to prevent the spread of disease and is not practical on a societal level.

The FP discussed cryotherapy with the mother and child, but the girl was not willing to allow it due to her fear of the pain. Other options included watch and wait, topical salicylic acid, tretinoin, and imiquimod—although none of these have been approved by the Food and Drug Administration. Cantharidin had also been used previously in this office, but it was not available because regulations have made it very difficult to obtain. Imiquimod is not suggested for children younger than 12; therefore, this costly medicine would not be covered by insurance.

The mother requested a prescription for tretinoin and stated that if the insurance would not cover it, she would go with over-the-counter salicylic acid. The FP wrote a prescription for 0.025% tretinoin cream to be applied daily and said to stop using it if irritation became too bothersome. Follow-up was to be done as needed, but was not completed.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Molluscum contagiosum. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:743-748.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed molluscum contagiosum because a few of the papules had central umbilication. While she noticed that many papules did not have central umbilication, she was aware that not all molluscum lesions would have this feature. Pearly papules are classic for molluscum, even when central umbilication is not visible.

Children with atopic dermatitis are more prone to molluscum infections and frequently get them in areas that have been, or presently are, involved with atopic dermatitis. In this case, the child had antecubital involvement with her atopic dermatitis (although her skin was relatively normal at the time). The altered barrier function found in atopic individuals makes them more prone to various viral and bacterial super infections, including molluscum, herpes, and bacterial impetigo.

In immunocompetent patients, lesions usually spontaneously resolve within 8 to 12 months. In a minority of cases, disease persists for a few years. Children do not have to be kept out of day care or school for this condition, even though it is somewhat contagious. Like warts, keeping kids out of school or day care is not useful to prevent the spread of disease and is not practical on a societal level.

The FP discussed cryotherapy with the mother and child, but the girl was not willing to allow it due to her fear of the pain. Other options included watch and wait, topical salicylic acid, tretinoin, and imiquimod—although none of these have been approved by the Food and Drug Administration. Cantharidin had also been used previously in this office, but it was not available because regulations have made it very difficult to obtain. Imiquimod is not suggested for children younger than 12; therefore, this costly medicine would not be covered by insurance.

The mother requested a prescription for tretinoin and stated that if the insurance would not cover it, she would go with over-the-counter salicylic acid. The FP wrote a prescription for 0.025% tretinoin cream to be applied daily and said to stop using it if irritation became too bothersome. Follow-up was to be done as needed, but was not completed.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Molluscum contagiosum. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:743-748.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com