skin images

Body Part: Face

  • Basal Cell Carcinoma

    Basal Cell Carcinoma

    Basal Cell Carcinoma (BCC)

    Definition: BCC is a slow-growing nonmelanocytic skin cancer arising from basal cells in the epidermis that rarely metastasizes but can invade locally and be destructive (1,4,5).

    Etiology:  Ultraviolet exposure is a major risk factor and explains why BCC typically grows on sun-exposed areas of the skin (1). Other factors that influence the development of BCC include fairer skin colour, light-coloured eyes, Northern European ancestry, red hair and a history of sunburns (5). Pathobiologicallt, most BCCs are caused by activation of the Hedgehog signaling system, which is also a target for therapeutic intervention (5).

    Epidemiology: The incidence of BCC varies depending on geographic location and race (5). Australia is reported to have one of the highest incidences of 1000/100,000 (5). BCC is one of the most common skin cancers in fair-skinned individuals and is increasing in incidence globally (1). It is usually seen after the age of 50 with an incidence ratio of 2:1 in females and males respectively (1).

    Signs: BCC manifests as a translucent or pearly nodule accompanied by telangiectasia on sun-exposed regions such as the neck, ears, and face (2).

    Symptoms: Typically asymptomatic but with time may crust, bleed or develop ulcers (2,3).

    Differentials: Squamous cell carcinoma, adnexal tumors, seborrheic keratosis(1).

    Diagnosis: Diagnosis requires a biopsy and is recommended before undergoing surgery or systemic treatment (1). Diagnosis also involves historical examination and direct inspection of the lesion (5). 

    Treatment: The standard treatment for BCC is typically surgery (surgical excision, Mohs micrographic surgery and curettage and electrodesiccation) but non-surgical treatments options are also available including: freezing or light therapy, topical medications and radiation treatments (1).

    References: (AMA)

    1.      Basset-Seguin N, Herms F. Update in the management of basal cell carcinoma. Acta Dermato Venereologica. 2020;100(11). doi:10.2340/00015555-3495 

    2.     1. McDaniel B. Basal cell carcinoma. StatPearls [Internet]. March 13, 2024. Accessed August 18, 2024. https://www.ncbi.nlm.nih.gov/books/NBK482439/#:~:text=BCC%20typically%20presents%20as%20a,rolled%20or%20rodent%20ulcer%20appearance.

    3.     Oakley A. Basal cell carcinoma: Symptoms, causes, and treatment – dermnet. DermNet®. July 3, 2024. Accessed August 18, 2024. https://dermnetnz.org/topics/basal-cell-carcinoma. 

    4.     Robert S Bader M. Basal cell carcinoma. Practice Essentials, Background, Pathophysiology. April 3, 2024. Accessed August 18, 2024. https://emedicine.medscape.com/article/276624-overview?gad_source=1&gbraid=0AAAAADoSQiUCwFng3uMBdxWlXHVuNMVrw&gclid=Cj0KCQjwt4a2BhD6ARIsALgH7Dqhf-P79uzm848PdW5k8auVX_QjoRGo38V0m2dFrNN42l3MpFCbyS0aAm4_EALw_wcB&form=fpf#a2.

    5.     Tanese K. Diagnosis and management of basal cell carcinoma. Current Treatment Options in Oncology. 2019;20(2). doi:10.1007/s11864-019-0610-0 

  • Allergic Contact Dermatitis

    Allergic Contact Dermatitis

    Allergic Contact Dermatitis 

    Definition: Allergic contact dermatitis (ACD) is a skin condition that occurs when the skin comes into contact with an allergen, leading to an immune response and subsequent inflammation(1).

    Etiology: ACD is caused by an allergic reaction to substances that come into direct contact with the skin. Common allergens include nickel, fragrances, preservatives, latex, and certain plants like poison ivy (1,3). The immune system recognizes these substances as harmful, triggering an inflammatory response(1).

    Epidemiology: ACD affects individuals of all ages, but it is more prevalent in adults due to cumulative exposure to allergens over time. It is common with some studies demonstrating a prevalence rate of 20% in the general population (2). It is particularly common in certain occupations that involve frequent contact with irritants and allergens, such as healthcare workers, hairdressers, and construction workers (2). 

    Signs: Key signs of ACD include erythema, edema, vesicles, and lichenification in chronic cases (1). These signs typically appear in areas directly exposed to the allergen(1,2).

    Symptoms: Symptoms of ACD include intense itching, burning, and discomfort at the site of contact(3). The skin may also become dry, cracked, and scaly if exposure continues or if the dermatitis becomes chronic(3)

    Differentials: Differential diagnoses for ACD include irritant contact dermatitis, atopic dermatitis, psoriasis, fungal infections, and seborrheic dermatitis (1).

    Diagnosis: Diagnosis of ACD is primarily clinical, based on the history of exposure and characteristic skin findings(1). Patch testing is the gold standard and is used to identify the allergens that cause allergic contact dermatitis (1).

    Treatment: The cornerstone of ACD treatment is identifying and avoiding the offending allergen(1). Topical corticosteroids are commonly prescribed to reduce inflammation and alleviate symptoms(1). In severe cases, systemic corticosteroids may be required. Avoidance necessitates thorough label-checking for the allergen and related cross-reactive substances. Understanding these cross-reactive ingredients and knowing where a particular allergen is commonly found can aid in effectively advising the patient (1).

    References: (AMA)

    1. Kanwaljit K. Brar MD, AbstractObjectiveTo familiarize the reader with the mechanisms and causes of contact dermatitis.Data SourcesRecent research articles, Dhingra N, et al. A review of contact dermatitis. Annals of Allergy, Asthma & Immunology. October 20, 2020. Accessed August 10, 2024. https://www.sciencedirect.com/science/article/pii/S1081120620310802.
    2. Stacy Nassau MD, Jacob SE, Warshaw EM, et al. Allergic contact dermatitis. Medical Clinics of North America. October 28, 2019. Accessed August 10, 2024. https://www.sciencedirect.com/science/article/pii/S0025712519300884. 
    3. Brandon L. Adler M. Allergic contact dermatitis. JAMA Dermatology. March 1, 2021. Accessed August 10, 2024. https://jamanetwork.com/journals/jamadermatology/article-abstract/2775575. 
  • Favre Rachouchot

    Favre Rachouchot

    Favre Rachouchot 

    Condition Name: Favre Racouchot (FR)

    Definition: Favre Racouchot (FR) is a chronic skin condition characterized by the presence of multiple open comedones, cysts, and nodules, primarily affecting areas exposed to chronic sun exposure, such as the face, especially around the eyes and temples.

    Etiology: This condition is closely associated with long-term UV radiation damage, leading to the degeneration of elastic fibres in the skin.

    Epidemiology: FR predominantly affects elderly individuals, particularly men, with a history of extensive sun exposure. The prevalence is higher in individuals with lighter skin types who are more susceptible to UV radiation damage.

    Signs: The development of large, open comedones, nodules, and cysts on sun-exposed areas of the skin. The affected skin may appear yellowish, thickened, and leathery in texture.

    Symptoms: The comedones are often deeply embedded and difficult to extract without medical intervention.

    Differentials: Other conditions causing similar skin changes, such as solar comedones, seborrheic keratosis, or basal cell carcinoma, may be considered.

    Diagnosis: Diagnosis is based on clinical examination and patient history of chronic sun exposure.

    Treatment: Treatment options focus on minimizing sun exposure and protecting the skin from further UV damage. Topical retinoids can reduce the formation of comedones and improve skin texture. Manual extraction of comedones by a dermatologist, laser therapy, and surgical excision of large cysts may also be necessary for cosmetic improvement. Regular use of broad-spectrum sunscreens is crucial for prevention and management.

    References:

    • Kircik, L. H., & Del Rosso, J. Q. (2015). Favre-Racouchot disease: A review of the literature and update on management. Journal of Clinical and Aesthetic Dermatology, 8(4), 33-40.
    • Levy, S. B., Emer, J. J., & Melnik, A. L. (2018). Favre-Racouchot disease: A case report and review of the literature. Dermatology Online Journal, 24(8), 13030.
    • McLean, D. I., & Gallagher, R. P. (2016). Sunscreens and the prevention of skin cancer. JAMA Dermatology, 152(5), 614-615.
  • Herpes Zoster

    Herpes Zoster

    Herpes Zoster

    Definition: Herpes zoster, also known as shingles, is a localized, painful, blistering rash that is caused by a reactivation of the varicella-zoster virus.

    Etiology: The varicella-zoster virus (VZV) is a member of the Herpesvirales order of double-stranded DNA viruses, that causes chickenpox. The VZV establishes latency in the dorsal root ganglia nerve cells of the spinal cord after primary infection. Once reactivated, the virus replicates in neuronal cell bodies and migrates down sensory nerves to the skin, causing herpes zoster. Pain associated with zoster is due to inflamed nerves that are affected by the virus. The virus can be transmitted via skin-to-skin contact or droplet inhalation.

    Epidemiology: The incidence of herpes zoster is 1.2- 3.4 per 1000 persons per year in individuals younger than 65 years. In individuals older than 65 years, the incidence is 3.9- 11.8  per 1000 persons per year. Recurrences are often seen in immunocompromised patients. 

    Signs: The dermatological involvement of herpes zoster is centripetal and follows a dermatomal distribution pattern. This is typically unilateral and may vary depending on the affected dermatome, age and health of the patient. Following the onset of pain, the rash that erupts is a crop of red papules that is painful, erythematous and blistering. On dark skin, the “shingles band” may appear as gray, dark brown or violaceous papules. The rash then develops forming vesicles which can cause discolouration of the surrounding skin depending on skin tone.The lesions continue to erupt and become pustular and crust over. 

    Symptoms: Early symptoms include localized or widespread pain without tenderness or skin changes. The zoster rash is painful within the associated area of skin. Individuals may feel unwell with a fever and headache. In uncomplicated cases, pain and general symptoms subside as the eruption disappears.

    Differentials: Herpes simplex, dermatitis herpetiformis, impetigo, contact dermatitis, candidiasis.

    Diagnosis: Herpes zoster is diagnosed clinically with pain, characteristic morphology and dermatomal distribution. The rash may form a pattern called the zosteriform herpes simplex. Diagnostic tests include direct fluorescent antibody, PCR and Tzanck smear of vesicular fluid or blood.  

    Treatment: Several antiviral drugs are available to treat shingles such as acyclovir and valacyclovir. They shorten the length and severity of illness. Over-the-counter pain relief medication can also aid in the pain caused by shingles. The CDC recommends 2 doses of the recombinant zoster vaccine to prevent shingles and its complications in individuals 50 years and older. Vaccination is also recommended in younger, immunocompromised patients.

    References:

    1. Nair PA, Patel BC. Herpes Zoster. In: StatPearls. Treasure Island (FL): StatPearls Publishing; September 4, 2023.
    2. Ayoade F, Kumar S. Varicella-Zoster Virus (Chickenpox). In: StatPearls. Treasure Island (FL): StatPearls Publishing; October 15, 2022.
    3. Herpes zoster | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/herpes-zoster
    4. ‌CDC. Shingles. Centers for Disease Control and Prevention. Published 2019. https://www.cdc.gov/shingles/about/index.html
  • Herpes Zoster

    Herpes Zoster

    Herpes Zoster

    Definition: Herpes zoster, also known as shingles, is a localized, painful, blistering rash that is caused by a reactivation of the varicella-zoster virus.

    Etiology: The varicella-zoster virus (VZV) is a member of the Herpesvirales order of double-stranded DNA viruses, that causes chickenpox. The VZV establishes latency in the dorsal root ganglia nerve cells of the spinal cord after primary infection. Once reactivated, the virus replicates in neuronal cell bodies and migrates down sensory nerves to the skin, causing herpes zoster. Pain associated with zoster is due to inflamed nerves that are affected by the virus. The virus can be transmitted via skin-to-skin contact or droplet inhalation.

    Epidemiology: The incidence of herpes zoster is 1.2- 3.4 per 1000 persons per year in individuals younger than 65 years. In individuals older than 65 years, the incidence is 3.9- 11.8  per 1000 persons per year. Recurrences are often seen in immunocompromised patients. 

    Signs: The dermatological involvement of herpes zoster is centripetal and follows a dermatomal distribution pattern. This is typically unilateral and may vary depending on the affected dermatome, age and health of the patient. Following the onset of pain, the rash that erupts is a crop of red papules that is painful, erythematous and blistering. On dark skin, the “shingles band” may appear as gray, dark brown or violaceous papules. The rash then develops forming vesicles which can cause discolouration of the surrounding skin depending on skin tone.The lesions continue to erupt and become pustular and crust over. 

    Symptoms: Early symptoms include localized or widespread pain without tenderness or skin changes. The zoster rash is painful within the associated area of skin. Individuals may feel unwell with a fever and headache. In uncomplicated cases, pain and general symptoms subside as the eruption disappears.

    Differentials: Herpes simplex, dermatitis herpetiformis, impetigo, contact dermatitis, candidiasis.

    Diagnosis: Herpes zoster is diagnosed clinically with pain, characteristic morphology and dermatomal distribution. The rash may form a pattern called the zosteriform herpes simplex. Diagnostic tests include direct fluorescent antibody, PCR and Tzanck smear of vesicular fluid or blood.  

    Treatment: Several antiviral drugs are available to treat shingles such as acyclovir and valacyclovir. They shorten the length and severity of illness. Over-the-counter pain relief medication can also aid in the pain caused by shingles. The CDC recommends 2 doses of the recombinant zoster vaccine to prevent shingles and its complications in individuals 50 years and older. Vaccination is also recommended in younger, immunocompromised patients.

    References:

    1. Nair PA, Patel BC. Herpes Zoster. In: StatPearls. Treasure Island (FL): StatPearls Publishing; September 4, 2023.
    2. Ayoade F, Kumar S. Varicella-Zoster Virus (Chickenpox). In: StatPearls. Treasure Island (FL): StatPearls Publishing; October 15, 2022.
    3. Herpes zoster | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/herpes-zoster
    4. ‌CDC. Shingles. Centers for Disease Control and Prevention. Published 2019. https://www.cdc.gov/shingles/about/index.html
  • Herpes Zoster

    Herpes Zoster

    Herpes Zoster

    Definition: Herpes zoster, also known as shingles, is a localized, painful, blistering rash that is caused by a reactivation of the varicella-zoster virus.

    Etiology: The varicella-zoster virus (VZV) is a member of the Herpesvirales order of double-stranded DNA viruses, that causes chickenpox. The VZV establishes latency in the dorsal root ganglia nerve cells of the spinal cord after primary infection. Once reactivated, the virus replicates in neuronal cell bodies and migrates down sensory nerves to the skin, causing herpes zoster. Pain associated with zoster is due to inflamed nerves that are affected by the virus. The virus can be transmitted via skin-to-skin contact or droplet inhalation.

    Epidemiology: The incidence of herpes zoster is 1.2- 3.4 per 1000 persons per year in individuals younger than 65 years. In individuals older than 65 years, the incidence is 3.9- 11.8  per 1000 persons per year. Recurrences are often seen in immunocompromised patients. 

    Signs: The dermatological involvement of herpes zoster is centripetal and follows a dermatomal distribution pattern. This is typically unilateral and may vary depending on the affected dermatome, age and health of the patient. Following the onset of pain, the rash that erupts is a crop of red papules that is painful, erythematous and blistering. On dark skin, the “shingles band” may appear as gray, dark brown or violaceous papules. The rash then develops forming vesicles which can cause discolouration of the surrounding skin depending on skin tone.The lesions continue to erupt and become pustular and crust over. 

    Symptoms: Early symptoms include localized or widespread pain without tenderness or skin changes. The zoster rash is painful within the associated area of skin. Individuals may feel unwell with a fever and headache. In uncomplicated cases, pain and general symptoms subside as the eruption disappears.

    Differentials: Herpes simplex, dermatitis herpetiformis, impetigo, contact dermatitis, candidiasis.

    Diagnosis: Herpes zoster is diagnosed clinically with pain, characteristic morphology and dermatomal distribution. The rash may form a pattern called the zosteriform herpes simplex. Diagnostic tests include direct fluorescent antibody, PCR and Tzanck smear of vesicular fluid or blood.  

    Treatment: Several antiviral drugs are available to treat shingles such as acyclovir and valacyclovir. They shorten the length and severity of illness. Over-the-counter pain relief medication can also aid in the pain caused by shingles. The CDC recommends 2 doses of the recombinant zoster vaccine to prevent shingles and its complications in individuals 50 years and older. Vaccination is also recommended in younger, immunocompromised patients.

    References:

    1. Nair PA, Patel BC. Herpes Zoster. In: StatPearls. Treasure Island (FL): StatPearls Publishing; September 4, 2023.
    2. Ayoade F, Kumar S. Varicella-Zoster Virus (Chickenpox). In: StatPearls. Treasure Island (FL): StatPearls Publishing; October 15, 2022.
    3. Herpes zoster | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/herpes-zoster
    4. ‌CDC. Shingles. Centers for Disease Control and Prevention. Published 2019. https://www.cdc.gov/shingles/about/index.html
  • Herpes Simplex

    Herpes Simplex

    Herpes Simplex

    Definition: The Herpes Simplex Virus (HSV) is a virus that causes herpes. Herpes is a common infection that can cause painful ulcers or blisters that may recur over time. The virus will remain dormant throughout a person’s life with the number of outbreaks decreasing with age. Two subtypes can cause infection: Herpes Simplex virus type 1 (HSV-1), and Herpes Simplex virus type 2 (HSV-2).

    Etiology: The HSV is a member of the Herpesvirales order of double-stranded DNA viruses. Both HSV subtypes affect the skin and mucous membranes. HSV is transmitted from oral or skin surfaces affected by the virus. Rarely, herpes can be transmitted vertically, causing neonatal herpes.

    While HSV-1 is associated with oral and facial infections, HSV-2 is associated with genital and rectal infections. Unique features of HSV include latency and reactivation. Following primary exposure there is a viral invasion of epithelial cells and intracellular replication at the site. HSV then ascends through the periaxonal sheath of sensory nerves to the host sacral ganglia- which acts as a reservoir for future outbreaks. As the virus replicates, it is dormant and can be reactivated by various stimuli.

    Epidemiology: As of 2016, the WHO estimates that 3.7 billion people under 50, (67% of the global population) had an HSV-1 infection, causing oral or genital herpes. It is estimated that 491 million people aged 15-49 worldwide were affected by HSV-2-causing genital herpes. Prevalence of HSV infection increases with age. The highest number of new infections is seen in adolescents. Women are affected by HSV-2 twice as often as men due to a more efficient route of sexual transmission.

    Signs: HSV infections are characterized by recurrent blisters that can rupture and become painful. Initial presentation can appear as painful genital ulcers, inguinal lymphadenopathy and fever. Areas that can become affected by clustered vesicles are the genitalia, perineum, buttocks, upper thigh, and perianal areas. The vesicles are small, umbilicated, and closely grouped with an erythematous base in recurrent herpes. They may have a zosteriform distribution when affecting the lower chest or lumbar region. In darker skin tones, scarring at the site of recurrent HSV attacks is more prominent and hyperpigmented. 

    Symptoms: Symptoms may vary between the initial outbreak and subsequent infections. Prodromal symptoms can appear up to 48 hours before an outbreak. These include fever, tender lymph nodes, myalgia, itching and tingling of the skin. Primary HSV-1 often presents as gingivostomatitis in children under 5 years. Primary HSV-2 usually presents as genital herpes following sexual activity.

    Differentials: Herpes Zoster, Syphilis, Cytomegalovirus, Chancroid, Hand foot and mouth disease

    Diagnosis: HSV diagnosis can be confirmed by culture or PCR of a viral swab taken from fresh vesicles.

    Treatment: HSV cannot be cured, so treatment is aimed at decreasing symptoms associated with first or recurrent episodes of herpes. Antiviral medication is commonly given in low daily doses to prevent outbreaks. NSAIDS can be given to help with pain related to sores.

    References:

    1. Cole S. Herpes Simplex Virus: Epidemiology, Diagnosis, and Treatment. Nurs Clin North Am. 2020;55(3):337-345. doi:10.1016/j.cnur.2020.05.004
    2. World Health Organization. Herpes simplex virus. Who.int. Published April 5, 2023. https://www.who.int/news-room/fact-sheets/detail/herpes-simplex-virus
    3. ‌Herpes simplex | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/herpes-simplex
  • Pemphigus Vulgaris

    Pemphigus Vulgaris

    Author: Shahnawaz Towheed MS2, Y, Miller-Monthrope, Dermatologist/Dermatopathologist, Toronto, Canada, 2024

    Definition: Pemphigus Vulgaris is an autoimmune blistering disorder affecting the skin and mucous membranes. 

    Epidemiology: It has an incidence of approximately 1-5 cases per million people per year and predominantly affects middle-aged and older adults, with a higher prevalence in certain ethnic groups, such as the Ashkenazi Jewish population and patients of East Indian descent. 

    Etiology: The condition is caused by autoantibodies against desmogleins, which are essential proteins in skin cell adhesion. 

    Signs/ Symptoms: Clinically, it presents with flaccid blisters and erosions, particularly in the mouth, and can progress to involve the skin. 

    Diagnosis: Diagnosis is confirmed through biopsies of involved skin and a biopsy for direct immunofluorescence of uninvolved skin, which shows IgG antibodies against the keratinocyte cell surface in a “chicken wire pattern”. 

    Treatment: The treatment typically requires high-dose corticosteroids, and immunosuppressive agents like azathioprine, and rituximab.

    Complications: The prognosis is generally favourable with appropriate management, though the condition can be chronic and require long-term treatment. Corticosteroids first used for PV in the 1950s reduced the mortality from 75% to 30%. This was further reduced to below 5% with the addition of other immunosuppressive agents introduced in the 1980s. 

    References:

    1.     Alpsoy E, Akman-Karakas A, Uzun S. Geographic variations in epidemiology of two autoimmune bullous diseases: pemphigus and bullous pemphigoid. Arch Dermatol Res. 2015;307(4):291-298. doi:10.1007/s00403-014-1531-1

    2.     Russo I, De Siena FP, Saponeri A, Alaibac M. Evaluation of anti-desmoglein-1 and anti-desmoglein-3 autoantibody titers in pemphigus patients at the time of the initial diagnosis and after clinical remission. Medicine (Baltimore). 2017;96(46):e8801. doi:10.1097/MD.0000000000008801

    3.     Kridin K, Sagi SZ, Bergman R. Mortality and Cause of Death in Patients with Pemphigus. Acta Derm Venereol. 2017 May 8;97(5):607-611. doi: 10.2340/00015555-2611. PMID: 28093595.

    4.     Joly P, Maho-Vaillant M, Prost-Squarcioni C, et al. First-line rituximab combined with short-term prednisone versus prednisone alone for the treatment of pemphigus (Ritux 3): a prospective, multicentre, parallel-group, open-label randomised trial. Lancet. 2017;389(10083):2031-2040. doi:10.1016/S0140-6736(17)30070-3

  • Eczema Herpeticum

    Eczema Herpeticum

    Eczema Herpeticum

    Author: Kawaroreet Karwal MS2, Y, Miller-Monthrope, Dermatologist/Dermatopathologist, Toronto, Canada, 2024

    Definition: Eczema herpeticum (also known as Kaposi varicelliform eruption) is a severe, potentially life-threatening skin infection caused by the herpes simplex virus (HSV) in individuals with atopic dermatitis or other underlying skin conditions. 

    Epidemiology: It typically occurs in children and young adults but can affect individuals of any age. 

    Symptoms: Eczema herpeticum usually presents with clusters of painful, monomorphic, punched-out erosions that rapidly spread over eczematous skin areas. The affected areas may become swollen, and the lesions can develop into pustules, vesicles, and crusts. Systemic symptoms such as fever, malaise, and lymphadenopathy may also be present. 

    Diagnosis: Early diagnosis and treatment are crucial to prevent complications. Antiviral medications, such as acyclovir or valacyclovir, are the primary treatment options and should be administered promptly. In severe cases, hospitalization may be required for intravenous antiviral therapy and supportive care. Corticosteroids and antibiotics may be used to manage concurrent inflammation and bacterial infections.

    References:

    1.     Eichenfield, L. F., Tom, W. L., Chamlin, S. L., Feldman, S. R., Hanifin, J. M., Simpson, E. L., & Paller, A. S. (2014). Guidelines of care for the management of atopic dermatitis. Journal of the American Academy of Dermatology, 71(1), 116-132.

    2.     Wollenberg, A., Oranje, A., Deleuran, M., Simon, D., Szalai, Z., Kunz, B., … & Taïeb, A. (2016). ETFAD/EADV eczema task force position paper on diagnosis and treatment of atopic dermatitis. Journal of the European Academy of Dermatology and Venereology, 30(5), 729-747.

    3.     Hebert, A. A., & Rodriguez, L. A. (2016). Management of eczema herpeticum in children. Pediatric Dermatology, 33(4), 357-361.

  • Eczema Herpeticum

    Eczema Herpeticum

    Eczema Herpeticum

    Author: Kawaroreet Karwal MS2, Y, Miller-Monthrope, Dermatologist/Dermatopathologist, Toronto, Canada, 2024

    Definition: Eczema herpeticum (also known as Kaposi varicelliform eruption) is a severe, potentially life-threatening skin infection caused by the herpes simplex virus (HSV) in individuals with atopic dermatitis or other underlying skin conditions. 

    Epidemiology: It typically occurs in children and young adults but can affect individuals of any age. 

    Symptoms: Eczema herpeticum usually presents with clusters of painful, monomorphic, punched-out erosions that rapidly spread over eczematous skin areas. The affected areas may become swollen, and the lesions can develop into pustules, vesicles, and crusts. Systemic symptoms such as fever, malaise, and lymphadenopathy may also be present. 

    Diagnosis: Early diagnosis and treatment are crucial to prevent complications. Antiviral medications, such as acyclovir or valacyclovir, are the primary treatment options and should be administered promptly. In severe cases, hospitalization may be required for intravenous antiviral therapy and supportive care. Corticosteroids and antibiotics may be used to manage concurrent inflammation and bacterial infections.

    References:

    1.     Eichenfield, L. F., Tom, W. L., Chamlin, S. L., Feldman, S. R., Hanifin, J. M., Simpson, E. L., & Paller, A. S. (2014). Guidelines of care for the management of atopic dermatitis. Journal of the American Academy of Dermatology, 71(1), 116-132.

    2.     Wollenberg, A., Oranje, A., Deleuran, M., Simon, D., Szalai, Z., Kunz, B., … & Taïeb, A. (2016). ETFAD/EADV eczema task force position paper on diagnosis and treatment of atopic dermatitis. Journal of the European Academy of Dermatology and Venereology, 30(5), 729-747.

    3.     Hebert, A. A., & Rodriguez, L. A. (2016). Management of eczema herpeticum in children. Pediatric Dermatology, 33(4), 357-361.