Milia

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Overview:

Milia are small, superficial, harmless cysts commonly seen across all ages. The term milia refers to multiple lesions, while milium a single lesion. These cysts originate either from the infundibulum of hair follicles or from eccrine ducts. When found in oral cavity, they arise from minor salivary gland ducts. 

 

Clinical Features:

Milia present as firm, white to yellow papules measuring 1-2 mm in diameter. The face, particularly the eyelids, is the most frequently affected area. Several clinical types of milia exist:

Neonatal milia:

Affect approximately 40-50% of newborn, these lesions may appear in clusters on the nose, scalp, or inside the mouth. They usually resolve spontaneously within the first few weeks of life.

Primary milia in children and adults: 

These commonly occur on the eyelids, cheek, forehead, and genitalia. 

Juvenile milia:

These may be linked to inherited genetic conditions. 

Milia en plaque: 

A rare variant appears as a multiple milia within erythematous edematous plaque, most often located postauricular area.

Traumatic milia:

These develop at sites of skin injury, such as thermal burns or blistering rashes. They originate from eccrine sweat ducts.

Drug-induced Milia:

Certain topical medications, including corticosteroids and hydroquinone, have been associated with the development of milia. 

 

Diagnosis: 

The diagnosis is primarily clinical and is based on the characteristic appearance of the lesions. In rare or uncertain cases, a skin biopsy may be performed to confirm diagnosis.

 

Histopathology:

On histological examination, milia are identified as small epidermoid cysts with stratified squamous epithelial lining and a granular layer.  The cyst cavity contains laminated keratin. 

 

Treatment:

Milia are benign and often resolve spontaneously within few months. In newborns, milia resolve within 4 weeks of life. For cosmetic reasons or in persistent cases, individual milia may be removed by incising the overlying epidermis using needle, lancet, or scalpel, followed by expressing the cyst contents. Other treatment options include:

  • Laser ablation
  • Electrodesiccation.
  • Topical retinoids – beneficial in cases of multiple milia. 

 

Done by: 

Layan Alshehri, Medical Intern 

Revised by: 

Naif Alshehri, Medical Intern

Resources:

Bolognia 5th Edition 

DermNet

 

Cherry Angiomas

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Definition

Cherry angiomas are benign vascular skin lesions characterized by capillary proliferation within the dermis. Clinically known as Campbell de Morgan spots, these papular lesions are among the most common acquired cutaneous vascular proliferations. Though typically asymptomatic, their appearance can be cosmetically concerning. In rare instances, eruptive forms may be associated with systemic conditions.

 

Epidemiology

Cherry angiomas are extremely common, especially with increasing age. They usually start to appear in adulthood most often after the age of 30 and gradually become more numerous over time.

  • By the age of 60, most people will have at least one.
  • By 75 years old, around 75% of individuals are affected.

They occur equally in men and women, and affect all ethnic groups, although they tend to be more visible in lighter skin tones. There may also be a genetic tendency, as some people have a family history of similar lesions.

Rarely, sudden onset of numerous lesions (eruptive cherry angiomas) has been reported in association with internal malignancy or during pregnancy.

 

Etiology and Pathogenesis

Exact cause is not fully known, but several factors are linked:

  1. Hormonal factors

– More common during pregnancy

– May shrink after delivery

– Linked to high prolactin levels in some cases

  1. Genetic mutations

Changes in certain genes like GNAQ, GNA11, and GNA14, Also sometimes seen in HRAS and KRAS genes. These genes are involved in blood vessel growth.

  1. Possibly minor trauma or skin irritation:

May trigger development in some cases.

  1. Not caused by cancer, but may rarely appear alongside internal tumors or systemic diseases

 

Clinical Features

Cherry angiomas present as firm, dome-shaped papules ranging from red to blue or purple in color, typically measuring 1–10 mm in diameter. They are usually multiple and randomly distributed across the trunk and extremities, sparing mucous membranes, hands, and feet. The lesions are asymptomatic but may bleed if traumatized. In thrombosed angiomas, the surface may appear blackish, though dermoscopy can help reveal the underlying vascular hue.

 

Diagnosis

Diagnosis is primarily clinical, supported by characteristic dermoscopic features, such as red to purple lacunae in a lobular or “red clod” pattern. Histological evaluation, when necessary, reveals dilated venules within a thickened papillary dermis with intervening collagen bundles. Cherry angiomas should be distinguished from petechiae and glomeruloid hemangiomas, particularly when multiple lesions erupt suddenly or there is suspicion of systemic disease.

 

Management

Cherry angiomas are benign and generally require no treatment unless they are symptomatic, subject to recurrent trauma, or cosmetically undesirable. When removal is indicated, options include:

– Laser therapy (e.g., pulsed dye laser)

– Electrosurgery

– Cryotherapy

– Shave excision

Recurrence following treatment is uncommon, and procedures are typically well-tolerated.

 

Written by: 

Raneem Alahmadi, Medical Intern.

Revised by: 

 Naif Alshehri, Medical Intern

Resources:

Bolognia 5th edition

Dermnet

Squamous Cell Carcinoma (cSCC)

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Background

Cutaneous squamous cell carcinoma (cSCC) is the second most common form of skin cancer, arising from the malignant transformation of keratinocytes in the epidermis. It accounts for approximately 20% of all non-melanoma skin cancers. While many cases are low-risk and treatable with local therapies, cSCC has a greater potential for local tissue invasion and distant metastasis than basal cell carcinoma. The increasing incidence of cSCC globally reflects rising ultraviolet (UV) exposure, an aging population, and a growing number of immunosuppressed individuals.

 

Etiology and Risk Factors

The principal etiological factor in cSCC is cumulative exposure to ultraviolet radiation, particularly UVB, which induces DNA damage and mutations in tumor suppressor genes. Additional risk factors include chronic immunosuppression, such as that seen in transplant recipients or patients with HIV/AIDS, which significantly elevates both incidence and aggressiveness of disease. Environmental exposures, including arsenic and ionizing radiation, also contribute to carcinogenesis. Chronic wounds, burns, or inflammatory skin conditions can evolve into cSCC through a process known as Marjolin ulceration. Moreover, infection with certain subtypes of human papillomavirus (HPV), particularly in mucosal or periungual lesions, is implicated in some cases. Genetic conditions like xeroderma pigmentosum, which impair DNA repair, further increase susceptibility.

 

Clinical Features

cSCC most commonly presents as a firm, erythematous papule, plaque, or nodule with a scaly or crusted surface, often located on sun-exposed areas such as the face, ears, scalp, neck, and dorsal hands. Lesions may ulcerate, become tender, or bleed. Growth is often gradual but can be rapid in aggressive variants. High-risk lesions may exhibit perineural symptoms, such as pain, numbness, or tingling, indicating possible nerve involvement. The clinical appearance can mimic benign conditions such as actinic keratoses or keratoacanthomas, underscoring the importance of biopsy in suspicious cases.

 

Diagnosis

Diagnosis of cSCC relies on histopathological confirmation through skin biopsy. A punch, shave, or excisional biopsy is typically performed, depending on lesion size and location. Histologically, cSCC is characterized by atypical keratinocytes extending into the dermis with varying degrees of differentiation. Poorly differentiated tumors may lose characteristic squamous features and be more challenging to diagnose. In cases where metastasis is suspected—such as with large, deeply invasive tumors or those in high-risk anatomical locations—imaging studies like ultrasound, CT, or MRI may be indicated. Sentinel lymph node biopsy may be considered in select cases.

 

Management

Treatment decisions are guided by tumor size, location, depth of invasion, histologic differentiation, and patient comorbidities. Surgical excision with histologically clear margins remains the standard of care for most cases of cSCC. Mohs micrographic surgery offers the highest cure rates and maximal tissue preservation, making it the treatment of choice for high-risk or cosmetically sensitive areas. For patients who are not surgical candidates, radiation therapy may be used as primary or adjuvant treatment. In situ lesions may be managed with topical therapies such as 5-fluorouracil or imiquimod, while advanced or metastatic cSCC may require systemic therapies, including immune checkpoint inhibitors like cemiplimab. 

 

Prognosis and Prevention

The prognosis of cSCC is generally favorable, with cure rates exceeding 90% for low-risk lesions treated appropriately. However, features such as tumor diameter >2 cm, depth >2 mm, perineural invasion, and poor differentiation are associated with increased risk of recurrence or metastasis. Preventive strategies include sun protection through regular use of broad-spectrum sunscreen, protective clothing, and avoidance of peak UV exposure. Patients with actinic keratoses or a history of cSCC should undergo regular dermatologic surveillance to detect early lesions.

 

Written by: 

Dr Renad AlKanaan

Revised by: 

Naif Alshehri, Medical Intern

References:

Dermnet

UpToDate

Bolognia 5th Edition

Basal cell carcinoma (BCC)

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Definition and Epidemiology:

Basal cell carcinoma (BCC) is a common skin cancer arising from the basal layer of epidermis and its appendages. These tumors have been referred to as “epitheliomas” because of their low metastatic potential. However, the term carcinoma is appropriate, since they are locally invasive, aggressive, and destructive of skin and the surrounding structures including bone. Estimates of the incidence of BCC are imprecise since there is no cancer registry that collects data on BCC. The American Cancer society estimates that in 2012, 5.4 million cases of nonmelanoma skin cancers (NMSCs) were diagnosed in 3.3 million people, of which approximately 8 in 10 cases would have been BCC.

 

Risk factors:

  • BCC is particularly common in Caucasians; it is very uncommon in darker-skinned populations.
  • The incidence in men is 30 percent higher than in women, particularly with the superficial type.
  • The incidence of BCC increases with age; persons aged 55 to 75 have about a 100-fold higher incidence of BCC than those younger than 20.
  • Exposure to UV light.
  • Chronic arsenic exposure
  • Radiation therapy
  • Long term immunosuppressive therapy
  • Basal cell nevus syndrome.

 

Clinical features:

Approximately 70 percent of BCCs occur on the face, consistent with the etiologic role of solar radiation. Fifteen percent present on the trunk, and only rarely is BCC diagnosed on areas like the penis, vulva, or perianal skin.

The clinical presentation of BCC can be divided into three groups, based upon lesion histopathology: nodular, superficial, and morpheaform.

Nodular: Nodular BCCs, which represent about 60 percent of cases, typically present on the face as a pink or flesh-colored papule. The lesion usually has a pearly or translucent quality and a telangiectatic vessel is frequently seen within the papule. The papule may often be described as having a “rolled” border, where the periphery is more raised than the middle. Ulceration is frequent, and the term “rodent ulcer” refers to these ulcerated nodular BCCs.

Superficial: About 30 percent of BCCs are superficial BCCs. For unclear reasons, men have a higher incidence of superficial BCC than do women. 

Superficial BCCs most commonly occur on the trunk, and typically present as slightly scaly, non-firm macules, patches, or thin plaques light red to pink in color. The center of the lesion sometimes exhibits an atrophic appearance and the periphery may be rimmed with fine translucent papules. A shiny quality may be evident when a superficial BCC is illuminated. 

Morpheaform: Morpheaform or sclerosing BCCs constitute 5 to 10 percent of BCCs. These lesions are typically smooth, flesh-colored, or very lightly erythematous papules or plaques that are frequently atrophic; they usually have a firm or indurated quality with ill-defined borders.

 

Diagnosis:

Clinicians who are familiar with the clinical manifestations of BCC are often able to make the diagnosis based upon clinical examination. Even so, a skin biopsy is usually performed to provide histologic confirmation of the diagnosis.

 

Treatment:

The treatment for a BCC depends on its type, size and location, the number to be treated, patient factors, and the preference or expertise of the doctor. Most BCCs are treated surgically. Long-term follow-up is recommended to check for new lesions and recurrence; the latter may be unnecessary if histology has reported wide clear margins.

Treatment options include:

  • Excision biopsy
  • Mohs micrographically controlled surgery involves examining carefully marked excised tissue under the microscope, layer by layer, to ensure complete excision.
  • Superficial skin surgery comprises shave, curettage, and electrocautery. It is a rapid technique using local anaesthesia and does not require sutures.
  • Cryotherapy is the treatment of a superficial skin lesion by freezing it, usually with liquid nitrogen.
  • Photodynamic therapy (PDT) refers to a technique in which BCC is treated with a photosensitising chemical, and exposed to light several hours later.
  • Topical imiquimod
  • Topical 5-Fluorouracil
  • Radiotherapy

 

Written by: 

Bandar Alharbi, Medical Intern.

Revised by: 

Naif Alshehri, Medical Intern.

Resources:

UTD

Dermnet

Mayo clinic

Kaposi Sarcoma

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Definition:

Kaposi sarcoma (KS) is a vascular neoplasm first described in 1872 by Moritz Kaposi as “idiopathic multiple pigmented sarcoma of the skin.” Historically, it was seen primarily in elderly men of Mediterranean, Eastern European, or Ashkenazi descent. Although sporadically observed in organ transplant recipients and in African populations, KS gained major attention during the AIDS epidemic as a defining illness. All clinical forms of KS are associated with human herpesvirus 8 (HHV-8), also known as Kaposi sarcoma-associated herpesvirus (KSHV).

 

Epidemiology:

KS manifests in four clinical variants:

  • Classic KS: Primarily affects elderly men of Mediterranean or Eastern European descent; typically slow-growing and indolent.
  • African endemic KS: Common among children and adults in Sub-Saharan Africa; includes aggressive lymphadenopathic forms.
  • Iatrogenic KS: Occurs in immunosuppressed individuals, especially post-organ transplantation or with chronic immunosuppressive therapies (e.g., corticosteroids, calcineurin inhibitors). Lesions may regress upon reduction of immunosuppression.
  • AIDS-related (epidemic) KS: Predominantly affects individuals with HIV/AIDS. It was particularly prevalent in the 1980s but has declined with the advent of highly active antiretroviral therapy (HAART).

 

Etiology:

KS originates from endothelial cells of blood vessels and lymphatics, though the exact lineage remains mixed. HHV-8 infection plays a central role by altering endothelial cells, promoting lymphangiogenic and mesenchymal features through endothelial to mesenchymal transition. The virus encodes homologs of cellular genes that stimulate proliferation, inhibit apoptosis, and promote angiogenesis. Immunosuppression, cytokine release, and chronic inflammation further contribute to tumor development. Transmission of HHV-8 occurs primarily through saliva but can also involve sexual and possibly arthropod vectors. The virus may remain latent and reactivate under conditions of immune dysfunction.

 

Clinical Features:

  • Classic KS: Presents as slowly enlarging, pink to red-violet macules on the lower extremities that may evolve into plaques or nodules. Lesions can be unilateral initially but often become multifocal over time.
  • AIDS-related KS: Characterized by widespread, violaceous plaques and nodules affecting the skin, mucous membranes, gastrointestinal tract, and lymph nodes. Lesions can worsen during immune reconstitution inflammatory syndrome (IRIS).
  • Iatrogenic KS: Typically resolves with reduction of immunosuppressive therapy.
  • African endemic KS: Manifests in nodular, florid, infiltrative, or lymphadenopathic forms, with the lymphadenopathic type primarily affecting children. Lymphedema and visceral involvement (oral cavity, gastrointestinal tract, lungs) are common in advanced disease.

 

Diagnosis:

Diagnosis is clinical but confirmed by histopathology showing spindle-shaped endothelial cells, slit-like vascular spaces, and HHV-8 positivity by immunohistochemistry or PCR.

 

Management:

Management depends on the clinical variant and disease extent:

  • HIV-associated KS: Initiation of HAART is critical and often leads to lesion regression.
  • Localized disease: Options include cryotherapy, radiotherapy, or intralesional chemotherapy.
  • Extensive disease: Systemic chemotherapy (liposomal doxorubicin, paclitaxel) is indicated.
  • Iatrogenic KS: Reduction or modification of immunosuppressive therapy may lead to lesion regression.

 

Written by: 

Raneem Alahmadi, Medical Intern.

Revised by: 

Naif Alshehri, Medical Intern

Resources:

Bolognia 5th edition

Dermnet

Erythema Dyschromicum Perstans

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Background

Ashy dermatosis, also known as erythema dyschromicum perstans (EDP), is a rare, chronic, idiopathic skin disorder characterized by the gradual appearance of bluish-gray to slate-colored macules and patches. It primarily affects individuals with darker skin phototypes (Fitzpatrick III–VI), particularly those from Latin America, Asia, and the Middle East. The condition is more commonly seen in young adults, but it can affect individuals of all ages. The term “ashy” refers to the gray color of the lesions, which gives the skin a dusky or dirty appearance.

Etiology

The exact cause of ashy dermatosis remains unknown, making it a diagnosis of exclusion. Several hypotheses have been proposed, including a delayed-type hypersensitivity reaction or cell-mediated immune response targeting basal keratinocytes. Histopathological findings often resemble a lichenoid tissue reaction, further supporting this theory.

There have been occasional associations with infections (e.g., hepatitis C), medications (e.g., proton pump inhibitors, antibiotics, and antiepileptics), and autoimmune conditions. However, these associations are not consistent and are often anecdotal.

Clinical Features

Ashy dermatosis typically begins with the insidious onset of slate-gray or bluish macules, which may be preceded by a faint erythematous border in early lesions. The patches are usually symmetrical, with a predilection for the trunk, neck, arms, and face. Lesions are non-scaly, non-itchy, and may gradually enlarge over time, coalescing into larger patches.The disease course is chronic and can persist for years.

Diagnosis

The diagnosis of ashy dermatosis is clinical, supported by histopathological examination when necessary to rule out mimickers. Skin biopsy typically shows interface dermatitis with basal cell vacuolization, melanin incontinence, and a perivascular lymphocytic infiltrate in the superficial dermis. However, these findings are not pathognomonic.

Dermoscopy may aid in identifying gray-blue dots and globules corresponding to dermal melanin. Differential diagnoses include lichen planus pigmentosus, post-inflammatory hyperpigmentation, macular amyloidosis, and drug-induced pigmentation. Careful clinical history and distribution of lesions help in differentiation.

Management

Treatment of ashy dermatosis is often challenging, as the condition tends to be resistant to therapy and cosmetically distressing for patients. There is no universally effective treatment, and management focuses on patient education, psychosocial support, and trial of medications with anecdotal or limited evidence.

Topical corticosteroids, calcineurin inhibitors (e.g., tacrolimus), and systemic agents such as clofazimine, dapsone, and isotretinoin have been tried with variable success. Some reports suggest that Q-switched lasers may provide pigment improvement, though recurrence is common. Sun protection is recommended as a general skincare measure, although sun exposure is not a known trigger.

Prognosis and Prevention

Ashy dermatosis is a benign condition without systemic involvement, but its chronicity and cosmetic impact can lead to psychological distress. Lesions may stabilize over time but often persist indefinitely. There is no established method for prevention, and recurrence after treatment is common.

 

Written by: 

Dr Renad AlKanaan

Revised by: 

Naif Alshehri, Medical Intern

References:

Dermnet

UpToDate

Bolognia 5th Edition

Picture Reference:

Bolognia 5th Edition

Hand, Foot, and Mouth Disease (HFMD)

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Background

Hand, Foot, and Mouth Disease (HFMD) is a common, self-limiting viral infection primarily affecting children under five years old. Characterized by a distinctive rash and oral lesions, HFMD occurs worldwide, with increased incidence during late summer and early autumn. 

 

Etiology

HFMD is predominantly caused by coxsackievirus A16 and enterovirus 71, both members of the Enterovirus genus. Transmission occurs through direct contact with nasal secretions, saliva, blister fluid, or stool of infected individuals. The virus can also spread via respiratory droplets or contaminated surfaces, making it highly contagious, especially in childcare settings. 

 

Clinical Features

After an incubation period of 3 to 5 days, initial symptoms include fever, malaise, and sore throat. Within a few days, painful oral lesions develop, appearing as red macules that progress to vesicles and ulcers, commonly located on the tongue, gums, and inside of the cheeks. Simultaneously or shortly after, a non-itchy rash emerges on the palms, soles, and sometimes the buttocks, presenting as red macules or vesicles. These skin lesions are typically not painful. 

 

Diagnosis

Diagnosis is primarily clinical, based on the characteristic presentation of oral ulcers and a distinctive rash on the hands and feet. Laboratory tests are generally not required but may be used in atypical cases or when complications arise. The preferred confirmatory test is polymerase chain reaction (PCR), which can detect enteroviruses from throat swabs, stool samples, or vesicle fluid. Serologic tests and viral culture are rarely performed due to limited clinical utility and slow turnaround times.

 

Management

Treatment focuses on symptomatic relief, as HFMD is self-limiting and typically resolves within 7 to 10 days. Recommended measures include:

  • Pain Relief: Administering acetaminophen or ibuprofen to alleviate fever and discomfort.
  • Hydration: Encouraging fluid intake to prevent dehydration, especially in children with painful oral lesions.
  • Topical Treatments: Using mouthwashes or sprays to reduce oral discomfort.

Antiviral medications are not indicated, and antibiotics are ineffective unless a secondary bacterial infection develops. 

 

Prevention

Preventative strategies focus on limiting the spread of the virus:

  • Hygiene Practices: Regular handwashing with soap and water, especially after diaper changes or using the toilet.
  • Cleaning: Disinfecting contaminated surfaces and objects, such as toys and doorknobs.
  • Isolation: Keeping infected individuals, particularly children, away from school or daycare during the acute phase of the illness to reduce transmission.

Currently, no vaccines are available for HFMD, making these preventive measures crucial. 

 

Prognosis

HFMD generally has an excellent prognosis, with most individuals recovering fully without complications. However, rare severe manifestations can occur, especially with enterovirus 71 infections, including neurological complications like aseptic meningitis or encephalitis. Prompt medical attention is essential if neurological symptoms or signs of dehydration arise.

In conclusion, Hand, Foot, and Mouth Disease is a common viral illness with distinctive clinical features. Understanding its etiology, clinical presentation, and management strategies is vital for effective care and prevention. 

 

Written by: 

Dr Renad AlKanaan

Revised by: 

Naif Alshehri, Medical Intern

References:

Dermnet

UpToDate

Bolognia 5th Edition

Chickenpox

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Introduction and Epidemiology:

Chickenpox is a highly contagious viral infection that causes an acute fever and blistered rash, mainly in children. Varicella virus is the etiologic agent of chickenpox. Varicella zoster virus has a worldwide distribution and 98% of the adult population is seropositive.  In  the  pre-vaccine  era,  90%  of  children  <10  years  of  age developed varicella and ~4 million cases occurred annually in the US, with large outbreaks during the winter and spring. Since the introduction of the varicella vaccine in 1995, the overall incidence of varicella has  decreased  by  ~85%,  with  evidence  of  herd  immunity.

 

Pathogenesis:

Airborne  droplets  are  the  usual  route  of  transmission  of  varicella, although direct contact with vesicular fluid is another mode of spread, and the incubation period is 11–20 days. Varicella is extremely contagious,  and  80–90%  of  susceptible  household  contacts  develop  a  clinically  evident  infection.  The  affected  individual  is  infectious  from  1–2 days before skin lesions appear until all the vesicles have crusted.

 

Clinical features:

A  prodrome  of  mild  fever,  malaise,  and  myalgia  may  occur,  especially in  adults.  This  is  followed  by  an  eruption  of  pruritic,  erythematous macules  and  papules,  which  starts  on  the  scalp  and  face,  and  then spreads to the trunk and extremities. Lesions rapidly evolve over 12 hours into 1–3 mm clear vesicles surrounded by narrow red halos (“dew drops on a rose petal”). The number of vesicles varies from only  a  few  to  several  hundred,  and  there  is  often  involvement  of  the oral mucosa. Sparing of the distal and lower extremities is common. Older vesicles evolve to form pustules and crusts, with individual lesions healing within 7–10 days. The presence of lesions in all stages of development is a hallmark of varicella. The  disease  course  is  usually  self-limited  and  benign  in  healthy children. Secondary  bacterial  infection  of  the  skin  with  subsequent  scarring  is the most common complication. CNS sequelae are uncommon ( <1 per 1000  cases)  and  may  include  encephalitis  and  acute  cerebellar  ataxia. Reye  syndrome  which  consists  of  encephalitis  plus  fatty  liver  is  now rare  due  to  avoidance  of  aspirin  in  children  with  varicella.  Varicella in  adolescents  and  adults  is  often  more  severe  than  in  children,  with an  increased  number  of  skin  lesions.

 

Diagnosis:

A clinical diagnosis can usually be made based upon the history, including previous varicella or vaccine administration, and physical examination.  A  Tzanck  smear,  PCR  or  DFA  can  assist  in  quickly  confirming the diagnosis.

 

Treatment:

Varicella in immunocompetent children can be treated symptomatically with  antipyretics  (e.g.  acetaminophen),  antihistamines,  calamine lotion,  and  tepid  baths.  If  started  within  24–72  hours  after  the  onset of  the  cutaneous  eruption,  acyclovir  has  been  shown  to  decrease  the duration and severity of varicella. Oral acyclovir and valacyclovir are FDA-approved for the treatment of varicella in children (2–17 years of age) while acyclovir is approved for adults. These antiviral  agents  are  recommended  for  varicella  in  healthy  adolescents  and adults  as  well  as  in  children  with  chronic  cutaneous  or  pulmonary disorders  and  in  those  receiving  chronic  salicylate  therapy,  inhaled corticosteroids,  or  intermittent  oral  corticosteroids.  However,  routine antiviral  therapy  is  not  recommended  for  otherwise  healthy  children with varicella due to the self-limited disease course and modest benefits of  treatment.

 

Written by: 

Bandar Alharbi, Medical Intern

Revised by: 

Naif Alshehri, Medical Intern

Resources:

Bolognia 5th edition

Dermnet

MOH 

Congenital Dermal Melanocytosis

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Definition:

Congenital Dermal Melanocytosis, commonly known as Mongolian spots, is a congenital dermal pigmentation that appears as blue-grey patches on the skin, typically affecting the lower back and buttocks of newborns. It is a benign form of birthmark caused by the presence of melanocytes in the dermis.

 

Epidemiology:

Dermal melanocytosis is usually present at birth or develops within the first few weeks of life. In most cases, the lesions regress during early childhood, though persistence into adulthood has been documented, with a prevalence of 4% in Japanese males aged 18–22 years.

The incidence of dermal melanocytosis varies significantly based on ethnicity, occurring in nearly 100% of Malaysian, Mongolian, Japanese, Chinese, and Korean newborns; 87% of Bolivian Indigenous populations; 65% of Black individuals in Brazil; 17% of White individuals in Bolivia; and only 1.5% of White persons in Brazil. These variations suggest a genetic influence on the persistence of dermal melanocytes. Histologically, traces of dermal melanocytosis have been found in the presacral area of all newborns, regardless of race.

 

Etiology:

The characteristic blue-grey color of dermal melanocytosis results from the presence of melanin-producing melanocytes in the middle to lower dermis. During fetal development, melanocytes appear in the dermis around the 10th week of gestation and typically migrate to the epidermis or undergo apoptosis. However, in certain areas—such as the sacral region, scalp, and distal extremities—some melanocytes remain in the dermis, leading to persistent pigmentation.

The bluish appearance is due to the Tyndall effect, in which shorter wavelengths (blue and violet) are more likely to be scattered and reflected than longer wavelengths (red, orange, and yellow), giving the lesions their characteristic coloration.

 

Clinical Features:

Lumbosacral dermal melanocytosis typically presents as bluish-grey macular patches on the sacrococcygeal, lumbar, and gluteal regions. The patches can be round, oval, or irregular in shape, ranging in size from a few centimeters to over 20 cm. While they are usually limited to less than 5% of the body surface area, extrasacral variants can involve other areas such as the back, limbs, or face.

The affected skin remains unchanged apart from the pigmentation—there is no thickening, textural alteration, or other skin abnormalities. Persistent or extensive dermal melanocytosis may be associated with phakomatosis cesioflammea or phakomatosis cesiomarmorata, warranting further evaluation in such cases.

 

Diagnosis:

The diagnosis of dermal melanocytosis is clinical, based on the characteristic appearance and location of the lesions. No further testing is typically required unless an associated condition is suspected.

 

Management:

Dermal melanocytosis is a benign condition that usually fades spontaneously by the age of four. No treatment is necessary in most cases. However, in instances where lesions persist into adulthood, cosmetic camouflage or laser therapy (such as those used for nevus of Ota) may be considered for aesthetic reasons.

 

Written by: 

Raneem Alahmadi, Medical Intern

Revised by: 

 Naif Alshehri, Medical Intern

Resources:

Bolognia 5th edition

Dermnet

 

Impetigo

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Overview:

Impetigo is the most common bacterial skin infection in children. It is a highly contagious superficial infection primarily caused by the Staphylococcus aureus and, less commonly, Streptococcus pyogenes. The condition can present in two forms: non-bullous and bullous impetigo.

 

Epidemiology:

  • Primarily affects children <6 years of age. 
  • Highly contagious and spreads through direct contact with an infected individual or contaminated objects (fomites). 

Predisposing factors: 

Several factors increase the risk of developing impetigo, including:

  • Environmental factors: Warm temperature and high humidity 
  • Poor hygiene 
  • Underlying skin conditions: Atopic dermatitis, scabies, and chicken pox.
  • Skin trauma: Lacerations, insect bites, and burns.

 

Pathogenesis:

Infection occurs when bacteria enter through minor skin breaks, such as scratches, trauma, or other skin infections. Disruption of the skin barrier allows bacterial adherence and invasion, leading to infection.

 

Clinical features:

Non-Bullous Impetigo (Most common form):

Lesion characteristics:

  • Commonly appears on the face (especially around the nose and mouth) and extremities.
  • Initially presents as a single erythematous macule, which evolves into vesicle or pustule.
  • Later develops into superficial erosions covered by characteristic honey-colored yellow crusts.
  • Minimal or no surrounding erythema.

Bullous Impetigo:

Lesion characteristics:

  • Affects the face, trunk, buttocks, axillae, and extremities.
  • Begins as small vesicles that enlarge into superfecial Bullae.
  • In late stages, bullae become flaccid and transparent, then ruptures to leave scale with no thick crust.
  • More likely to be associated  with systemic symptoms.

 

Diagnosis:

  • Impetigo is primarily a clinical diagnosis.
  • A skin swab culture (from the exudate beneath crusts or fluid from an intact bullae) may be performed for confirmation.
  • Approximately 50% of patients may have leukocytosis.

 

Treatment:

General Measures:

  • Cleanse the affected area and remove crusts.
  • Maintain proper hand hygiene.

Topical Antibiotics:

For healthy patients with few lesions and no systemic symptoms, the following topical treatments are recommended:

Mupirocin, retapamulin, or ozenoxacin.

Oral Antibiotics:

Systemic antibiotic therapy is required in the following situations: 

  • Bullous impetigo 
  • Widespread non-bullous impetigo 
  • Failure to respond to topical treatment 
  • High risk of complications 
  • Presence of comorbidities 

First line oral antibiotic: flucloxacillin

Prevention:

  • Avoid touching affected areas.
  • Practice regular hand hygiene.
  • Refrain from sharing personal items, such as towels and clothing.
  • Change and wash clothing and bedding daily in hot water.
  • Avoid close contact with others.

 

Done by:

Layan Alshehri, Medical Intern 

Revised by:

Naif Alshehri, Medical Intern

Resources:

Bolognia 5th Edition

DermNet

Reactive perforating collagenosis

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Definition

Reactive perforating dermatoses are characterized by the transepidermal elimination of dermal connective tissue through the epidermis. 

Reactive perforating collagenosis (RPC) is a form of perforating dermatosis involving the extrusion of altered collagen fibers. RPC can be inherited or acquired, with inherited cases often triggered by trauma or cold exposure. 

The acquired form is more common and frequently associated with systemic conditions such as diabetes mellitus or chronic kidney disease, particularly in patients undergoing dialysis, where pruritus-induced trauma exacerbates the condition.

 

Epidemiology : 

RPC occurs globally without a clear racial predilection. The inherited form is rare and often familial, with onset typically in infancy or early childhood. It may follow either an autosomal dominant or autosomal recessive inheritance pattern. In contrast, the acquired form is more prevalent and usually develops later in life, showing a higher incidence in women with a female-to-male ratio of approximately 3:1. Acquired RPC is strongly associated with chronic systemic illnesses such as diabetes and chronic kidney disease,

 

Etiology

The exact pathogenesis of RPC remains uncertain, but key factors include:

  1. Inherited Form:

 – Linked to genetic abnormalities in collagen structure, leading to focal damage and extrusion through the epidermis.

 – Triggers such as trauma or cold weather often exacerbate the condition.

  1. Acquired Form:

 – Associated with microvascular insufficiency and elevated plasma fibronectin levels, commonly seen in diabetes and chronic kidney disease.

 – Abnormal glycosylation of collagen types I and III in diabetes may alter collagen fibers, contributing to their extrusion.

 – Superficial trauma, scratching, and cold exposure lead to epidermal thinning and necrobiosis in susceptible patients.

 

Clinical Features

RPC typically manifests as a papulonodular mucocutaneous disorder. Lesions appear as red-brown umbilicated papules or nodules with a central keratotic plug and an erythematous halo. The size of the lesions can range from a few millimeters to 10 mm, though rare giant forms measuring up to 10 cm have been reported.

 Lesions are intensely pruritic but are rarely painful or tender. Inherited RPC often affects the hands, elbows, and knees, while the acquired form commonly involves the legs. In both forms, the distribution is generally symmetrical, and lesions may appear more widely scattered or even generalized. A hallmark feature of RPC is the Koebner phenomenon, where new lesions develop in response to trauma or scratching. Lesions typically resolve spontaneously within 6 to 10 weeks, though they may leave post-inflammatory hyperpigmentation or scarring.

 

Diagnosis 

Diagnosis is primarily clinical, based on characteristic lesions and associated systemic conditions.

 – Dermoscopy: May reveal central keratotic plugs and erythematous halos.

 – Skin Biopsy: Multiple biopsies are often required to confirm the histopathological findings, including transepidermal elimination of altered collagen.

 

Management

The management of RPC can be challenging, particularly in the acquired form, as it often involves addressing both the skin lesions and any underlying systemic conditions. Treatment typically focuses on reducing pruritus, minimizing trauma, and promoting lesion healing.

– Topical Treatments:

  • Corticosteroids: Superpotent formulations under occlusion can reduce inflammation.
  • Retinoids: Topical agents like tretinoin may aid in reducing keratotic plugging.
  • Emollients: Improve skin hydration and barrier function.

– Systemic Therapies:

  • Antihistamines: Sedating antihistamines help alleviate itching and improve sleep.
  • Oral Retinoids: Acitretin can reduce lesion severity.
  • Allopurinol: May be considered for refractory cases.

– Procedural Interventions:

  • Intralesional Corticosteroids
  • Cryotherapy or Curettage

– Phototherapy:

  • Broadband or Narrowband UVB: Particularly beneficial for patients with chronic kidney disease, as it can relieve pruritus and improve skin lesions.

– Lifestyle Modifications:

  • Avoid scratching and trauma to the skin to prevent exacerbations. Optimize management of systemic diseases like diabetes and renal dysfunction.

 

 

Written by: 

Raneem Alahmadi, Medical Intern.

Revised by: 

Naif Alshehri, Medical Intern.

Resources:

Bolognia 5th edition

Dermnet

Scabies

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Overview:

Scabies is a contagious skin infestation caused by Sarcoptes scabiei var. hominis mite. It leads to severe pruritus and skin lesions due to the mite burrowing into the epidermis. 

 

Epidemiology:

Scabies is a widespread condition affecting individuals of all ages, ethnicities, and socioeconomic groups. Factors contribute to its spread:

  • Overcrowded living conditions 
  • Delayed diagnosis and treatment 
  • Limited public awareness 
  • Poor hygiene 

Transmission can be through direct skin to skin contact, and indirectly through contaminated objects (fomites). 

A severe form of scabies, crusted scabies (Norwegian scabies), occurs in immunocompromised individuals, and is highly contagious. 

 

Pathogenesis:

The Incubation period varies:

  • First time infestation: symptoms appear within 2 to 6 weeks, 
  • Reinfestation: symptoms develop faster,  within 24 to 48 hours. 

Scabies mites can survive outside the human body for up to 3 days. However, in crusted scabies, mites can survive up to 7 days. 

 

Clinical features:

Itching (pruritus):

  • Often severe and worse at night or with hot showers. 
  • It can be the first symptom before visible skin lesions appear.

Lesions distribution and appearance: 

  • Lesions present as small erythematous papules with varying degree of excoriations. 
  • Other possible lesions include nodules and vesicles.  
  • Symmetrically affects interdigital web spaces of the hands, wrists, axillae, waist, ankles, feet, and buttocks. 
  • The face and scalp are typically spared, except in infants, elderly, immunocompromised patients, and in crusted scabies cases.
  • Burrows is a pathognomonic sign, representing the tunnels created by female mites as they lay eggs. Burrows appear as grayish-white, thread like lines, measuring 1 to 10 mm in length. 
  • Crusted scabies has a widespread involvement of thick scaling and crusting.

 

Diagnosis:

Diagnosis is clinically, based on history and physical examination. Can be confirmed using diagnostic methods include:

  • Dermoscopy allows visualization of mites and eggs. 
  • Skin scraping and microscopy using mineral oil preparation. 

 

Treatment:

First line treatment: Topical Permethrin 5%

  • Applied from head to toe in infants and elderly. In other age groups, face and scalp are excluded from treatment. Applied overnight for 8 to 12 hours on day 1 and 8. 

Environmental and Preventive Measures:

  • Clothing, bedding, and towels should be washed in hot water and dried in high heat or sealed in a bag for 7 to 10 days. 
  • All close contacts, even asymptomatic, must be treated in the same way. 

Post-Treatment: 

  • After successful treatment, pruritus and skin lesions may persist for 2 to 4 weeks, this is called post scabetic pruritus. 

Oral ivermectin is an option for treatment failures, outbreaks, or non-adherence, with a repeat dose after two weeks. Other alternatives include 25% benzyl benzoate or 0.5% malathion lotion.

 

Done by:

Layan AlShehri, Medical Intern 

Revised by: 

Naif Alshehri, Medical Intern

Resources:

Bolognia 5th Edition. 

DermNet