This information is derived from the following lectures by Jerry Shapiro MD, FAAD: Management of Hair Loss Disorders in 2023, and Alopecia Areata Ritlecitinib: What I Do. 

Alopecia Areata. This is our algorithm. If someone is more than ten-years-old, we look at the disease severity. If it's more than 50% scalp involvement, we'll use JAK inhibitors, plus or minus intralesional corticosteroids. We may add oral minoxidil. And then if all that doesn't work, we'll use topical immunotherapy or squaric acid dibutyl ester. If they have less than 50% scalp involvement, if it's rapidly progressing, we'll go to a JAK inhibitor.

If it's stable, we'll use topical steroids, intralesional steroids, oral minoxidil, topical immunotherapy as well. If someone is less than ten-years-old, topical corticosteroids as well as topical 5% minoxidil. In addition to the oldest approval for AA which is baricitinib, we have ritlecitinib, Litfulo (now FDA approved for patients 12 years and older) and deuruxolitinib (Leqselvi) in patients 18 yrs and older. While there are no controlled trials switching between the three commercially available JAKinibs for AA in patients who experience treatment failure with one treatment, that strategy could potentially be successful. Alternatively, in severe AA patients (SALT > 95%), a study using 20 mg/d of prednisone tapered over 3 months  in conjunction with baricitinib 4 mg resulted in a significant improvement  with almost 90% of patients experiencing nearly complete hair regrowth in the 8 patients studied. 

When we're looking at how much of the scalp is involved, we do a SALT score. We do a percentage of the scalp that's involved. If it's more than 50% of the scalp, then they are candidates for JAK inhibitors. Good candidates are those between age (12) and 50, have >6 months of AA and have failed prior treatment. No comorbidities, SALT more than 50, active disease, no major organ system dysfunction, no history of thromboembolic events. Bad candidates are over aged 50, whether they have viral reactivation, for instance of herpes simplex or, or zoster infections, coronary events, thrombosis, immunizations, malignancy, hepatic impairment or renal impairment, they are not good candidates.

Prior to starting, we check their CBC. We check their liver enzymes. We do a lipid panel as well. We do QuantiFERON Gold for TB as well as hepatitis panel, and pregnancy testing. Twelve weeks after starting, we'll do the lipid panel making sure that everything is okay with their triglycerides. This is the kind of chart prior to starting what we order, 12 weeks after starting, yearly monitoring. If there are any abnormalities, we stop it, wait till it goes back to normal, then restart it again.

Keep in mind that when we use these medications (JAKs), we may use them with other things like injections. We published this in the British Journal of Dermatology. We also have used baricitinib 4mg a day, with injection 2.5mg per cc to the scalp, and low dose oral minoxidil being used as well. So, that would be another regimen one might use. This was a patient who was on tofacitinib, and then we added injections to this patient, and you can see the remarkable growth that he had of his scalp as well as his, his eyebrows as well.

Now, how do we down titrate? After one year, you might want to go from 4mg to 2mg, and you did see some people did get worse, but most did better. This data suggests the down titration from 4mg to 2mg is possible. What if you stop the medication cold turkey? They do poorly. 

Visible light is a part of the electromagnetic spectrum that is visible to the human eye. It includes wavelengths ranging from approximately 380 to 740 nanometers and comprises 45 to 50% of the sunlight reaching the surface of the earth. Visible light has long been regarded to be without significant biologic effects on the skin. Now, through multiple studies, we know that visible light has a photobiologic effect on the skin, which varies tremendously based on the wavelength.

EXPLANATION
While visible light is generally well-tolerated by the skin and does not cause ionization or damage on the cellular level like ultraviolet (UV) radiation, it can still have effects on the skin. Below are some of main areas of concern.

Skin Pigmentation:
Visible light plays a role in the pigmentation of the skin. Chronic exposure to visible light can contribute to skin pigmentation, and it may exacerbate existing pigmentation conditions, such as melasma and post-inflammatory hyperpigmentation.
Photoaging:
Long-term exposure to visible light, especially in combination with other environmental factors like UV radiation, may contribute to the process of photoaging. Photoaging involves the development of fine lines, wrinkles, and changes in skin texture over time.
Wavelength-Specific Effects:
Different wavelengths within the visible light spectrum can have varying effects on the skin. For example, blue light (wavelengths around 400-500 nm) has been a topic of interest due to its potential impact on skin health. Some studies suggest that blue light, particularly in the higher energy range, may contribute to oxidative stress and skin damage.
Protection Mechanisms:
The skin has natural defense mechanisms to protect against the potential harmful effects of visible light, including antioxidant systems that help neutralize free radicals generated by light exposure.
Phototherapy:
Visible light is also used therapeutically in certain dermatological procedures, such as photodynamic therapy (PDT). In PDT, a photosensitizing agent is applied to the skin, and then visible light is used to activate the agent to treat specific skin conditions, including certain types of skin cancer.

SUMMARY
It's important to note that the effects of visible light on the skin are complex, and research in this area is ongoing. While some studies suggest potential concerns, more research is needed to fully understand the impact of visible light on skin health. Additionally, protective measures, such as broad-spectrum sunscreens and antioxidant-rich skin care products, are recommended to mitigate potential damage from various wavelengths of light, including visible light.

Learn more in Dr. Henry W. Lim's lecture Effects of UV and Visible Light.

Image credit: NASA, Public domain, via Wikimedia Commons

Image credit: William Anderson, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons

“Fish tank granuloma” caused by Mycobacterium marinum is by far the most common.

Explanation

Fish tank granuloma, also known as “fish tank granuloma” or “swimming pool granuloma”, is a skin infection caused by Mycobacterium marinum. This is a type of bacteria commonly found in aquatic environments including fish tanks. People can acquire this infection when they come into contact with contaminated water, objects in fish tanks, or swimming pools.

Fish tank granuloma is generally a localized and self-limiting infection, but appropriate medical treatment is essential to prevent complications and promote healing.

“Fish Tank Granuloma”

Causative Agent: 
M. marinum
 
Transmission:
Transmission typically occurs through direct contact of the skin with contaminated water or surfaces in aquatic environments. The bacteria can enter the skin through cuts, abrasions, or puncture wounds.

Clinical Presentation:
Fish tank granuloma usually presents as a localized skin nodule or ulcer at the site of entry. The affected area may become red, swollen, and tender. The lesion may progress over time, and multiple nodules may develop.
Sporotrichoid pattern or ascending nodules that go from the original site to the closest regional lymph node are characteristic. 

Time of Onset:
Symptoms may appear several weeks to months after exposure to contaminated water. The delayed onset is characteristic of M. marinum infections.

Location of Lesions:
Common sites for lesions include the hands, fingers, and arms, as these areas are more likely to come into direct contact with contaminated water.

Risk Factors 

• Personal home aquarium owners
• Professionals who clean aquariums
• Marine biologists
• Anglers and workers exposed to saltwater fish
• Immunocompromised patients (HIV/AIDS)

·     How do you confirm the diagnosis of atypical mycobacteria?

• Biopsy: The diagnosis is often based upon histology in a general sense. Sarcoidal or suppurative granulomas will be seen.
• Acid Fast Stain of exudate or tissue may be positive, but will not identify the species.

• Diagnosis is often based on clinical presentation, history of exposure to contaminated water, and laboratory tests. 
• Skin biopsy and culture may be performed to confirm the presence of M. marinum.

Treatment:

• Antibiotic therapy is the primary treatment for fish tank granuloma. The choice of antibiotics may include doxycycline, minocycline, or clarithromycin. It may need to be continued for an extended duration due to the slow growth of the bacteria. Monotherapy may be adequate if the infection is mild or limited to a single nodule.
• M. marinum does not like heat.  So, thermotherapy, which can be accomplished with a heating pad on high for 10 to 15 minutes three times a day, has been employed.
• If severe infection or multiple nodules, specific anti-organism and antimicrobial may be prescribed. Minocycline or clarithromycin + Ethambutol.

Prevention:

To prevent fish tank granuloma, individuals should practice good wound care, avoiding exposure of cuts or wounds to contaminated water. Additionally, maintaining proper hygiene in aquariums and swimming pools, including regular cleaning and proper disinfection, can reduce the risk of infection.

Learn more in Dr. Matthew J. Zirwas' lecture Granuloma Annulare. 

References

Image credit: https://www.wikihow.pet/ 

Image credit: www.blogsport.com

Image credit: Acid Fast Stain www.quizlet.com

T. indotineae (genotype VIII of Trichophyton mentagrophytes) is a rapidly emerging and drug-resistant dermatophytosis.  

Explanation 

Most dermatophyte infections in North America are caused by T. Rubrum and T. mentagrophytes. 

This species has been identified in the US since 2017.  It has been associated with severe, recalcitrant infections and Terbinafine resistance.  Cañete-Gibas et al (2023), summarize the results of fungal speciation performed on North American dermatophyte isolates received at a fungal diagnostic reference laboratory. Terbinafine resistance was noted in a significant number of infections with T. indotineae.  T. rubrum, T. interdigitale, T. mentagrophytes, and T. verrucosum. It is important to be aware of new species in our region and to practice good antimicrobial stewardship. 

Learn more about Trichophyton indotineae in Dr. Aditya K. Gupta's lecture Dermatophyte Fungal. 

References

Lockhart, S. R., Smith, D. J., & Gold, J. A. W. (2023). Trichophyton indotineae and other terbinafine-resistant dermatophytes in North America. Journal of clinical microbiology, 61(12), e0090323. https://doi.org/10.1128/jcm.00903-23

Cañete-Gibas, C. F., Mele, J., Patterson, H. P., Sanders, C. J., Ferrer, D., Garcia, V., Fan, H., David, M., & Wiederhold, N. P. (2023). Terbinafine-Resistant Dermatophytes and the Presence of Trichophyton indotineae in North America. Journal of clinical microbiology, 61(8), e0056223. https://doi.org/10.1128/jcm.00562-23

Xie W, Kong X, Zheng H, et al. Rapid Emergence of Recalcitrant Dermatophytosis by a Cluster of Multidrug-Resistant Trichophyton indotineae, China. Br J Dermatol. Published online January 5, 2024. doi:10.1093/bjd/ljae00

Image credit: Sammandi, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons

Yes. Treatment should be guided by phenotype for the best results.

Explanation

The pathophysiology of rosacea is based on inflammation and angiogenesis. Many factors can trigger these physiological responses including UV exposure, increased bacteria on the skin, demodex mites, hormones, exercise, heat, spices, and stress. Historically, rosacea has been divided into clinical subtypes, but recent therapeutic research has shown that a treatment algorithm based on phenotype is best. The four main phenotypes are:

·      Telangiectasias and flushing

·      Background erythema

·      Papules and pustules

·      Ocular disease

The chart below shows the treatment options for each phenotype. It is important to note that phenotypes can overlap, and anyone with ocular disease should have a comprehensive ophthalmology examination.

Additionally, it is important to differentiate the patient’s type of facial redness, which can guide therapeutics and optimize patient outcomes.

Learn more about rosacea in Dr. Hilary Baldwin's lecture Rosacea.

Pseudoscleroderma is a term that is sometimes used to describe conditions or situations that mimic or resemble scleroderma (systemic sclerosis) but are not autoimmune variants.  It's important to note that pseudoscleroderma is not a specific medical diagnosis but rather a descriptive term. 

Explanation

It is important to differentiate between true systemic sclerosis (scleroderma) and conditions that may resemble it. Systemic sclerosis is an autoimmune connective tissue disorder characterized by widespread fibrosis, vascular changes, and involvement of multiple organs.

Scleroderma-like disorders: Some autoimmune or rheumatic conditions may present with skin changes resembling scleroderma but do not meet the criteria for systemic sclerosis. Conditions that may be referred to as pseudo scleroderma include:

Eosinophilic fasciitis:
Eosinophilic fasciitis is a rare disorder characterized by inflammation and thickening of the fascia (connective tissue beneath the skin). It can cause symptoms similar to scleroderma, including skin tightening and joint pain. However, eosinophilic fasciitis is distinct from systemic sclerosis.

Scleredema:
Scleredema is a condition characterized by thickening and hardening of the skin, particularly in the upper back and neck. It may be associated with infections or other underlying conditions. Scleredema can resemble scleroderma, but it has different pathophysiology.

Medication-induced fibrosis:
Certain medications or drug reactions may lead to skin changes that mimic scleroderma. For example, exposure to bleomycin, a chemotherapy drug, can cause scleroderma-like skin changes.

Morphea-like changes:
Morphea is a localized form of scleroderma that involves thickening and hardening of the skin. Some conditions or injuries may lead to morphea-like changes in the skin without systemic involvement.

Learn more in Dr. Richard D. Sontheimer's lecture Skin Changes of Autoimmune Scleroderma and Vasculitis. 

References

image credit: https://creativecommons.org/licenses/by-sa/4.0/  

Innate immunity and adaptive immunity are two components of the immune system that work together to defend the body against pathogens such as bacteria, viruses, and other foreign substances.

Ecthyma is a deeper version of impetigo where the wound/infection extends into the dermis resulting in an ulceration.

EXPLANATION:

Impetigo

• Impetigo is a highly contagious superficial skin infection that is most common in children 2-5 years old but can be present at all ages. 
• There are typically two forms: bullous and non-bullous.

       Non-Bullous Impetigo                                 Bullous Impetigo

• 70-80% of impetigo cases are caused by S. aureus and the rest are caused by beta-hemolytic Streptococci.
• Non-bullous lesions are usually shallow erosions on the face or extremities with a honey-colored crust.
• Bullous lesions are usually on the trunk or extremities and start with a vesicle/bulla that progresses to a crusted erosion. 
• Blistering is due to S. aureus that produces exfoliative toxin A, which reduces cellular adhesion by attacking desmoglein 1.

Ecthyma

• Ecthyma is an ulcerative pyoderma of the skin well known to be caused by Group A beta-hemolytic Streptococci. Concomitant Staphylococcus aureus (S. aureus) is often isolated from lesional skin. On occasion, S. aureus alone has been isolated.
• It is characterized by the formation of adherent crusts, beneath which is an ulceration in the dermis.
• Poor hygiene and repeated trauma are key elements.
• Culture can be done to confirm the diagnosis and the organism involved.
• Start treatment while waiting for culture results based on suspected diagnosis.
• Always consider other differential diagnoses, such as bullous drug eruption, bullous insect bite, tinea, or HSV.

Learn more in Dr. Ted Rosen's lecture Impetigo. 

Vasculitis and vasculopathy are terms related to disorders affecting blood vessels, but they refer to distinct conditions with different underlying mechanisms and characteristics. 

• In addition to a full body skin exam, make sure to evaluate the patient’s past medical history or diagnoses that might be relevant. Illnesses like a recent stroke, Parkinson's disease, or kidney disease can cause severe pruritus. 
• Determine if itch is generalized or localized.
• Assess the patient for a rash that may have accompanied the itch. What does the morphology or distribution suggest?
• If there is no primary eruption, assess the patient for secondary skin lesions or changes. Linear or round erosions may be present or scarring if they have healed.
• Inquire about other household members or contacts that are also experiencing pruritus. 

Explanation:

• Any adult who presents with a new onset, pruritic, non-specific rash should have empiric treatment for scabies strongly considered.
• If after a review of systems, H&P, medications, and travel history, there is no suspected cause, consider the following labs:
  
  • CBC, comprehensive metabolic panel (AST/ALT/BUN/Cr)
  • Liver function studies
  • IgE (atopy)
  • Gliadin, tissue transglutaminase (celiac)
  • HIV, Hepatitis B, and Hepatitis C screening labs
  • Stool for ova and parasites if patient has traveled or has GI symptoms
  • Consider biopsy if there is a primary lesion or patch testing if appropriate
• Initiate a low allergenicity skin care routine including gentle cleansers, moisturizers, and topical steroids if indicated.
• Have the patient follow-up in one week for reassessment and review of lab results. 

 Learn more in Dr. Matthew J. Zirwas' lecture Managing the Itchy Patient. 

Syringoma and trichoepithelioma are both benign skin tumors, but they arise from different types of skin cells and have distinct clinical and histological features. 

Syringoma:

Cell Origin: Syringomas arise from eccrine sweat glands, which are found throughout the skin.
Location: They are commonly found in the lower eyelids, although they can occur in other areas of the face and body.
Clinical Features:

• Typically, they present as small, firm, skin-colored or yellowish papules usually 1 mm to 3 mm in diameter.
• They often occur in clusters and may be symmetrically distributed.
• Histologically, syringomas show ductal structures consisting of small tubules or cystic spaces lined by two layers of epithelial cells. The stroma surrounding the ductal structures may contain fibrous tissue. 
• Some individuals may have multiple syringomas as part of a genetic condition known as familial syringoma.

Trichoepithelioma:

Cell Origin: Trichoepitheliomas arise from hair follicles, specifically the outer root sheath cells.
Location: They are commonly found on the face, particularly on the central face, but can occur elsewhere.
Clinical Features:

• Small, skin-colored or slightly pink papules or nodules.
• Usually, a few millimeters to a centimeter in diameter.
• May be solitary or occur in clusters.
• Histologically, trichoepitheliomas exhibit islands of basaloid cells surrounding a fibrous stroma. Trichoepitheliomas may show differentiation toward hair follicle structures, including the formation of hair papillae and hair shafts.
• May be associated with Brooke-Spiegler syndrome, an inherited condition characterized by the development of multiple skin tumors, including cylindromas.
  

Distinguishing Features:

• Location: Syringomas are more commonly found around the eyes, while trichoepitheliomas are frequently located on the central face.
• Histological Features: The histological examination is crucial for differentiation, as syringomas exhibit ductal structures from sweat glands, while trichoepitheliomas show differentiation toward hair follicle structures.

In summary, syringomas and trichoepitheliomas are benign skin tumors that arise from different skin structures (sweat glands and hair follicles, respectively), and they have distinct clinical and histological features. The location, appearance, and microscopic characteristics are key factors in differentiating between the two conditions.

Learn more in Dr. George Martin's lecture Uncommon Benign Tumors.

Image credit:  Margaret Bobonich

Treatment for varicella exposure during pregnancy will depend on the mother’s immune status and gestation.

Explanation

• Varicella-Zoster Immune Status:
  • If the pregnant woman is known to be immune to varicella (either through documented vaccination or a history of previous infection), she is considered protected, and no specific intervention is typically necessary.
• Varicella-Zoster Immune Globulin (VariZIG):
  • If the pregnant woman is not immune and has been exposed to varicella, administration of varicella-zoster immune globulin (VariZIG) may be considered.
  • VariZIG is a blood product that contains antibodies against the varicella-zoster virus. It can provide passive immunity and may help prevent or reduce the severity of varicella infection. VariZIG is most effective when administered within 96 hours (preferably within 72 hours) of exposure.
• Varicella Vaccine:
  • If the pregnant woman is not immune and has not received the varicella vaccine, administration of the varicella vaccine within 72 hours of exposure may be considered in some cases. However, the use of the varicella vaccine during pregnancy is generally avoided due to theoretical concerns about the live attenuated virus in the vaccine. Pregnant women are usually advised to wait until after delivery to receive the varicella vaccine.
• Antiviral Medications:
  • Antiviral medications, such as acyclovir, may be considered for pregnant women who develop varicella, especially if the infection is severe or involves complications. Antiviral therapy is generally recommended for pregnant women with varicella pneumonia or other severe manifestations.
  • Because disease can be severe in adults and pregnant women, acyclovir or valacyclovir is usually recommended, starting within 24-48 hours of rash onset. Oral therapy is usually sufficient.
  • Patients who are immunocompromised and neonates require more aggressive therapy. Intravenous acyclovir and IM VZIG are often utilized. 

Monitoring and Fetal Assessment:

• Pregnant women who have been exposed to varicella should be monitored for signs and symptoms of infection. Fetal well-being may be assessed through ultrasound and other appropriate measures.
• It's important for pregnant women to seek prompt medical evaluation and guidance if they have been exposed to varicella, as the timing of interventions is crucial. Healthcare providers will assess the individual circumstances and make recommendations based on the specific situation.
• Additionally, pregnant women should discuss their varicella immune status and vaccination history with their healthcare provider during prenatal care. In some cases, postpartum vaccination may be recommended for women who are not immune to varicella.

Learn more about varicella in Dr. Sheila Friedlander's lecture Varicella. 

References

Sile B, Brown KE, Gower C, et al. Effectiveness of oral aciclovir in preventing maternal chickenpox: A comparison with VZIG. J Infect. 2022;85(2):147–151. https://doi.org/10.1016/j.jinf.2022.05.037

Cuerden C, Gower C, Brown K, et al. PEPtalk 3: oral aciclovir is equivalent to varicella zoster immunoglobulin as postexposure prophylaxis against chickenpox in children with cancer - results of a multicentre UK evaluation. Arch Dis Child. 2022 Jul 8:archdischild-2022-324396. https://doi.org/10.1136/archdischild-2022-324396

Image credit: Nowforever, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons 

Answer:

Time-Limited Therapy with Venetoclax:

• Benefits:
  
  • Fixed Duration: Venetoclax, particularly when combined with Obinutuzumab, offers the advantage of a fixed-duration therapy, usually one year. This means that patients can achieve remission and stop therapy, avoiding long-term side effects and the burden of continuous treatment.
  • Durable Remission: Clinical trials such as CLL14 have shown that Venetoclax-based regimens can provide durable remissions, with many patients remaining progression-free for years after completing therapy.
  • Reduced Long-term Toxicity: Because treatment is not continuous, the risks associated with long-term drug exposure, such as cumulative toxicity and secondary malignancies, are minimized.
  • Cost-Effective: Time-limited therapy can be more cost-effective, reducing the financial burden on patients and the healthcare system by avoiding prolonged use of expensive drugs.
• Challenges:
  
  • Monitoring for Tumor Lysis Syndrome: Venetoclax carries a risk of tumor lysis syndrome (TLS), particularly during the initial dose ramp-up. This requires close monitoring and prophylactic measures, which can be logistically challenging.
  • Relapse and Retreatment: While many patients achieve long-lasting remissions, relapse can occur, necessitating retreatment. The long-term efficacy of retreatment with Venetoclax after initial use is still being studied.
  • Patient Selection: Not all patients may be suitable for Venetoclax-based therapy, especially those with very high tumor burden or certain high-risk genetic features, where continuous therapy might be preferred.

Continuous BTK Inhibitor Therapy:

• Benefits:
  
  • Simplicity and Consistency: Continuous therapy with BTK inhibitors like Ibrutinib or Acalabrutinib provides consistent disease control with an established safety profile and requires less frequent monitoring than Venetoclax.
  • High-Risk Patients: BTK inhibitors are particularly effective in patients with high-risk cytogenetic abnormalities, offering a reliable option for long-term disease management.
  • Ease of Use: Oral administration and the absence of infusion-related reactions make BTK inhibitors convenient for patients, contributing to better adherence.
• Challenges:
  
  • Long-term Toxicity: Continuous use of BTK inhibitors can lead to cumulative toxicity, including cardiovascular issues such as atrial fibrillation and hypertension, which can limit long-term tolerability.
  • Cost and Compliance: Continuous therapy can be expensive over time, with ongoing costs potentially impacting patient compliance and overall healthcare expenditure.
  • Resistance Development: Over time, some patients may develop resistance to BTK inhibitors, necessitating a switch to alternative therapies.

Rationale:

• The choice between time-limited Venetoclax-based therapy and continuous BTK inhibitor therapy should be individualized based on patient factors, disease characteristics, and patient preferences. Time-limited therapy is appealing for its fixed duration and reduced long-term toxicity, while continuous BTK inhibitor therapy provides a stable, long-term treatment option, particularly for high-risk patients. Both approaches have their merits, and ongoing clinical trials will further refine their roles in CLL management.

Image credit: MS 365

Yes, topical timolol may be effective for the treatment of a pyogenic granuloma, but the results can vary.

Explanation

Several studies have examined the efficacy and safety of timolol solution for the treatment of pyogenic granulomas. It may have some utility in treating early lesions or shrinking the size of lesions before removal with surgical means. The response is usually slow and may take months.

Other treatment modalities for pyogenic granuloma include electrocautery or silver nitrate application, cryotherapy, surgical excision, and intralesional cryotherapy. Interestingly, case reports have shown that the novel use of table salt applied to the lesion can be very effective.

Learn more in Dr. Vikash S. Oza's lecture Lumps and Bumps. 

You may find these recent studies useful:

Daruwalla SB, Dhurat RS. A pinch of salt is all it takes! The novel use of table salt for the effective treatment of pyogenic  granuloma. J Am Acad Dermatol. 2020;83(2):e107-e108. doi:10.1016/j.jaad.2019.12.013

Lopez-Bernal T, Aranegui B. RF - FTopical Timolol in Dermatology. FR - Usos de timolol tópico en Dermatología. Actas Dermosifiliogr. 2023;114(4):334-335. doi:10.1016/j.ad.2021.09.014

Patra AC, Sil A, Ahmed SS, et al. Effectiveness and safety of 0.5% timolol solution in the treatment of pyogenic granuloma: A randomized, double-blind and placebo-controlled study. Indian J Dermatol Venereol Leprol. 2022;88(4):500-508. doi:10.25259/IJDVL_565_20

Although a precise diagnosis based on clinical findings remains imperfect, four-fifths of the malignant lesions in children can be recognized based on these risk factors or warning signs:  

Worrisome history or clinical presentation:

• Onset as a neonate
• Really rapid, progressive, consistent growth is always concerning
• A nodule that is growing and ulcerates is one of the most important warning signs
• Poorly circumscribed lesions (benign lesions are usually well-circumscribed)
• A lesion that is affixed deep into the tissues
• Immunocompromised patient
• A firm mass and those greater than 3 cm in diameter

Consider these clinical signs and symptoms during your evaluation of a child with a lesion. If none of the risk factors above are present, the likelihood that a worrisome bump exists is probably low. 

Learn more in Dr. Vikash S. Oza's lecture Lumps and Bumps. 

References
Knight PJ, Reiner CB. Superficial lumps in children: what, when, and why? Pediatrics. 1983;72(2):147–153.

Explanation

While some keloids and hypertrophic scars may be similar in appearance, it is important to clinically distinguish between the two to guide treatment and prevent future occurrences. Keloids and hypertrophic scars have a different physiological basis.

• Hypertrophic scars develop from excess type III collagen bundles and do not extend beyond the extent of the injury.
• Keloids, however, develop from excess Type I and Type III collagen and will extend beyond the injured areas.
• Keloids also tend to have an irregular and firmer shape.
• Keloids also have a genetic predisposition and can even have a delayed onset.

Learn more about Keloids in Dr. Hilary Baldwin's course Keloids and Hypertophic Scars.

No

EXPLANATION

Furuncles or boils are infections involving the deep portion of the hair follicle. They begin as hard, red, and painful nodules and develop into large lumps that can burst, releasing purulent content. It can look like a volcano getting ready to erupt. Furuncles are almost always infected with Staphylococcus aureus, either MSSA or MRSA.

RISK FACTORS AND COMPLICATIONS

Risk factors for furuncles include poor hygiene, compromised immune function, diabetes, obesity, and close contact with carriers of Staphylococcus aureus. These factors can also increase the likelihood of recurrence.

Complications can arise from untreated or severe furuncles. Individuals can develop cellulitis, abscess formation, and systemic infection. Timely treatment, good hygiene, and addressing underlying risk factors can prevent complications.

Associated conditions, such as diabetes, immune system disorders, and obesity, may compromise the body's ability to fight infections.

TREATMENT

Primary therapeutic approach

The primary approach to a furuncle is INCISION AND DRAINAGE (I&D). Needle aspiration is not effective. Also, frequent warm water or warm saline compresses and analgesics can be used as needed.

Antibiotic therapy

Systemic antibiotics are NOT usually necessary in furuncles meeting the following criteria:

• Single, small furuncle (<2 cm) with no prior failure of I&D alone
• No surrounding cellulitis or lymphangitis
• No systemic toxicity
• No immune suppression
• No medical device implanted (prosthetic joint); no endocarditis risk
• No risk of transmission (contact sports, military)

Systemic antibiotics, which cover MRSA, ARE indicated in patients with: 

• Serious signs and symptoms of systemic toxicity like fever (which could also lead to sepsis)
• Large lesions >2 cm or previous failed I&D
• Progressive erythema surrounding the lesion >5 cm ring 
• Regional lymphadenopathy
• A history of immune suppression, implanted devices, risk for endocarditis, or diabetes
• High risk of transmission

****Parenteral drugs (e.g., vancomycin) should be considered in patients with sepsis, severe toxicity, inability to swallow pills, neutropenia, chemotherapy, implanted medical devices, perianal or vulvar furuncles, or prosthetic heart valves. 

PRECAUTIONS

Prevention of Spread

Care should be taken to avoid the spread especially in shared living spaces. While furunculosis itself is not highly contagious, the bacteria (Staphylococcus aureus) can be transmitted. Individuals should practice good hygiene, avoid sharing personal items, and keep wounds covered.

Diabetes

Diabetic patients may require more aggressive management due to impaired immune function. Glycemic control is crucial to prevent complications and improve healing.

Learn more in Dr. Ted Rosen's lecture Furunculosis.

References