Unit 12B Skin Infection & Burns
DISORDERS OF SKIN INTEGRITY AND FUNCTION
self study: sweat gland → apocrine, skin variation and patient ed for dark skinned patients
Chapter 52
Primary Skin Disorders
Definition: Primary skin disorders encompass various conditions affecting the skin directly.
Categories of Primary Skin Disorders:
- Disorders of pigmentation
- Infectious processes
- Acne and rosacea
- Allergic and hypersensitivity dermatoses
- Papulosquamous dermatoses
- Arthropod infestations
Pigmentary Skin Disorders
Overview: Pigmentary skin disorders involve the melanocytes, which are responsible for the production of melanin.
Types of Pigmentary Disorders:
- Absence of melanin production: Examples include vitiligo and albinism.
- Increased melanin or other pigments: Examples include congenital dermal melanocytosis (formerly known as Mongolian blue spots) and melasma.Emotional Impact: All types can lead to significant emotional distress, including anxiety and depression.
Vitiligo
Definition: A pigmentary disorder characterized by the loss of skin color in patches; affects individuals of all skin colors and ages.
Onset Age: Approximately 50% of cases begin before age 20.
Gender Comparison: The condition affects females and males equally.
Social Concerns: More visible in individuals with darker skin, making it a social issue.
Etiology: The exact cause is unknown but theories suggest:
1. Autoimmune mechanism: Loss of melanocytes leads to depigmented patches.
2. Genetics: Family history may play a role.
3. Acquired Factors: Stress or physical trauma can precipitate the condition.Additional Factors:
- High serum homocysteine levels: May contribute to the destruction of melanocytes.
- Associated Conditions: Includes hypothyroidism, Graves disease, Addison's disease, pernicious anemia, diabetes mellitus, and melanoma.
Clinical Manifestations:
Lesions: Sudden appearance of white patches on skin, smooth borders, located commonly on the face, axillae, neck, or extremities.
Sizes of Patches: Range from small macules to large areas; large macules are more common.
Coloration of Depigmented Areas: Appears white, pale, or grayish-blue.
Mechanisms in Affected Areas:
1. Melanocytes that no longer produce melanin.
2. No functioning melanocytes present.
3. Very few functioning melanocytes.Ultraviolet Sensitivity: Affected areas are prone to sunburn and tend to enlarge over time.
Types of Vitiligo
Vitiligo A:
- Later onset in life; higher frequency.
- White patches are symmetrical with discrete borders and slowly progressives cover hands, face, and body folds.Vitiligo B:
- Earlier onset; segmental form.
- White patches are asymmetrical and can occur anywhere on the body.
Albinism
Definition: Congenital genetic disorder characterized by a complete or partial absence of pigment in the skin, hair, and eyes.
Prevalence: Affects individuals of all races; over 10 types identified.
Appearance: Individuals present with pale skin, white or yellow hair, and light-colored or pink eyes.
Common Type: Recessively inherited oculocutaneous albinism results from a normal number of melanocytes but with little to no tyrosinase, the enzyme necessary for melanin production.
Ocular Problems: Individuals may experience:
- Extreme light sensitivity
- Refractive errors
- Foveal hypoplasia
- Nystagmus
Melasma
Definition: A dermatological disorder characterized by the appearance of darkened macules on the face.
Demographics: More commonly seen in females, especially during pregnancy or while using hormonal contraception.
Resolution: Often resolves after childbirth or discontinuing hormonal use and exacerbates with sun exposure.
Popular Among: Individuals with darker skin tones, especially those from Asia, India, the Caribbean, and Central and South America.
Infectious Processes
Overview
Vulnerability: Skin is susceptible to invasion by various potentially infectious microorganisms such as fungi, bacteria, and viruses.
Defense Mechanisms: Skin flora, sebum, immune responses, and other protective mechanisms typically prevent infections.
Infection Factors: Likelihood of infection depends on the virulence of the infecting agent and the immune capability of the host.
Superficial Fungal Infections → common
Definition: Fungi are free-living, saprophytic organisms; many strains are part of normal skin flora.
Classification:
- Two types of fungi: Yeasts and Molds.
- Yeasts: Grow as single cells, reproduce asexually (e.g., Candida albicans).
- Molds: Form long filaments known as hyphae.Infections: Fungal (mycotic skin infections) can be superficial (most common) or deep.
- Superficial Mycoses: Includes tinea or ringworm, affecting only the keratinized tissue of skin, hair, and nails.
- Deep Fungal Infections: Involve the epidermis, dermis, and subcutis, especially concerning in immunocompromised patients.
Pathogenesis of Superficial Mycoses
Mechanism: Fungi feed on dead keratinized epidermal cells and secrete enzymes that digest keratin, leading to skin, nail, and hair breaking, and other related conditions.
Specific Tinea Infections:
- Tinea Corporis: Ringworm affecting the body
- Tinea Faciale: Affects the face and neck.
- Tinea Capitis: Affects the scalp.
- Tinea Manus: Affects the hands.
- Tinea Pedalis: Affects the feet.
- Tinea Unguium: Affects the nails.
- Tinea Cruris: Affects the genital area.Tinea Corporis (Ringworm of the Body):
- Common etiological agent is M. canis.
- More prevalent in children than adults.
- Transmission: Typically from contact with infected pets or children→ KNOW THIS
- Clinical Manifestation: Lesions appear as circular or oval patches on exposed skin: - -trunk, limbs, back, or buttocks
- Symptoms: May include pruritus, mild burning sensation, and erythema.

> Note: Describing a dermatophytic skin infection characterized by erythematous, pruritic, annular lesions with raised borders and central clearing.
Bacterial Infections
Overview
Normal Flora: Bacteria are a component of normal skin flora; most are non-pathogenic.
Pathogenicity: Skin infections can manifest when pathogenic bacteria invade, leading to superficial or systemic conditions.
Classification:
- Primary Infections: e.g., impetigo and ecthyma (superficial).
- Secondary Infections: Involve deeper cutaneous infections, such as infected ulcers.
- Diagnosis: Generally based on cultures from the site of infection.
Impetigo
Definition: A common, superficial bacterial infection predominantly seen in young children (2-5), caused by Staphylococcus or group A beta-hemolytic streptococci.
Age Group: Most prevalent among infants and young children, adults can get it
Seasonal Incidence: Higher incidence during warm months or in warm, moist climates.
Clinical Manifestations:
- Lesions can present as small vesicles or pustules, or as large bullae, particularly on the face.
- Lesions eventually rupture, leading to a denuded area that excretes serous fluid, forming a honey-colored crust.
- Pruritus often accompanies these lesions, sometimes leading to excoriation and the potential for further infection.
> Note: Characteristic vesicles or bullae rupture to create a honey-colored crust.
Complications: Although rare, untreated streptococcal impetigo may lead to poststreptococcal glomerulonephritis.
Treatment: Topical or systemic antibiotics depending on infection extent.
Bullous Impetigo
Definition: A variant of impetigo primarily due to Staphylococcus aureus.
Population Affected: Common in children, but typically not contaminated by streptococci.
Presentation: Thin bullae erupt, coalesce, and can appear anywhere on the body, predominantly affecting the face.
Ecthyma
Definition: A more severe, ulcerative form of impetigo.
Etiology: Often secondary to minor trauma; caused by group A beta-hemolytic streptococci, S. aureus, or Pseudomonas.
Areas Affected: Commonly found on buttocks and thighs in children.
Clinical Features: Develops similarly to impetigo but can result in ulcerations and scarring.
Symptoms: There may be a low-grade fever with extensive ecthyma, indicating systemic spread.
Treatment: Often involves systemic antibiotics.
Viral Infections
Overview
Definition: Viruses are intracellular pathogens that depend on host cells for reproduction.
Structure: They consist of a DNA or RNA core encased in a protein coat.
Skin Lesions: Viruses, particularly DNA viruses, invade keratinocytes, reproduce, and can lead to cell proliferation or death.
Increased Viral Infections: Notable rise attributed to increased corticosteroid use, alterations in skin flora from antibiotics, leading to a reduction in bacterial infections but an increase in viral infections.
Verrucae (Warts)
Definition: Common benign papillomas caused by human papillomavirus (HPV).
Transmission: Spread via direct contact or autoinoculation.
Classification by Morphology and Location:
- Variations based on anatomical location and HPV type, with over 80 HPV types
- Common Warts (verrucae vulgaris): Typically seen on hands dorsal side (top)Verruca plana (flat warts): common on the face/hands dorsal (Top)
Verruca plantaris/palmaris: found on palms/soles of feet.
Immune Response: Warts often resolve spontaneously as immunity against the virus develops, which can take several months to years.
Herpes Simplex
Definition: Caused by the herpes simplex virus (HSV), leading to skin and mucous membrane infections (cold sores, fever blisters).
Types of HSV:
- HSV-1: Primarily spreads via respiratory droplets; associated with oropharyngeal infections, contracted in childhoodprimary and recurrent
- HSV-2: Associated with genital infections.
- Increase in Transmission Risk: HSV-1 genital infections and HSV-2 oral infections are becoming increasingly common.
HSV1 Primary Clinical Features:
- Fever, sore throat, painful vesicles, and ulcers in oral mucosa.
- Most severe primary infections are common in early childhood (1-5 years).
- After the initial infection, HSV remains latent in the trigeminal and other dorsal root ganglia, with recurrent symptoms generally less severe and localized.
- Reactivation Triggers: Stress, menses, hormonal changes, injury, and UV exposure.üRecurrent or secondary HSV-1 lesions usually begin with a burning or tingling sensation, the prodrome
üUmbilicated vesicles and erythema follow, progressing to pustules, ulcers, and crusts before healing (see Fig. 52.9)
§HSV-1 lesions are most common on the lips, face, mouth, nasal septum, and nose
oWhen a lesion is active, HSV-1 is shed, with the associated risk of virus transmission to others
- Healing Duration: Typically takes 10-14 days with pain and lesions healing gradually.
Herpes Zoster (Shingles)
Definition: Characterized by acute, localized vesicular rash over a dermatomal segment of skin, affecting approximately 10-20% of the population.
Etiology: Caused by reactivation of the varicella-zoster virus from previous chickenpox infection, lying dormant in sensory dorsal root ganglia
Reactivated virus travels from the ganglia to the skin on the corresponding dermatome
Demographics: More common in > 60 older adults but can occur at any age.
Clinical Manifestations:
- Lesions typically preceded by a prodrome of burning pain, tingling, and extreme sensitivity in affected dermatome.Most frequently affected dermatomes: thoracic, cervical, trigeminal, and lumbosacral
- Rash develops into vesicular eruptions (rash/exanthem), unilaterally, and usually thoracicBurning and tingling in the area affected by the rash, and extreme sensitivity to touch
New groups of vesicles erupt for up to 3-5 days along the nerve pathway
•Vesicles dry off, form crusts, and eventually fall off
- Symptoms may be mistaken for other conditions.
- Typically clears in 2-3 weeks.
Complication: Postherpetic neuralgia (pain > 1-3 months post-rash).
- Prevalence of Neuralgia: More common in > 60 older adults.Vaccination: Zoster vaccine (Zostavax) recommended to prevent or lessen severity of herpes zoster, with the expectation of increased incidence due to an aging population.
Skin Damage from Ultraviolet Radiation
Overview
Role of Skin: The skin acts as a barrier against harmful UV rays.
Consequences: Exposure can lead to skin cancers, early aging, and other skin disorders.
Types of UV Radiation: measured by nanometers
- UVC: Shortest wavelength; does not penetrate the earth’s atmosphere but harmful.
- UVB: Known as “sunburn rays”; responsible for photoaging, pigment changes, and skin dryness
- UVA: Includes short-wave and long-wave types; associated with skin alterations and present in tanning beds.
- Source: (Hight, 2024, p. 1537)
Effects of UV Radiation
Acute Effects: Immediate effects from UVA and UVB exposure include erythema, skin pigmentation changes, and injury to Keratinocytes and Langerhans cells.
- UVA-Induced Erythema: Occurs immediately while fading within hours (heat load).
- UVB-Induced Erythema: Has a delayed response, peaking 6-24 hours post exposure.Tanning Response: Tanning occurs through increased melanocyte activity, which provides some protection against further UV exposure.
- However, tanning from UVA exposure offers limited protection compared to UVB exposure.
Chronic Damage and Carcinogenic Effects
Long-term Damage: UVB exposure leads to reactive oxygen species generation and damages melanin, leading to photoaging.
Solar Elastosis: Characterized by abnormal elastotic material accumulation in the upper dermis, leading to skin thickening and loss of elasticity, causing deep, coarse wrinkles.
Carcinogenesis: Both UVA and UVB are carcinogenic, with UVA potentially more damaging due to its ability to penetrate deeply.
§UVA → less sunburn: present year-round during all daylight hours; penetrate deeper and → greater keratinocyte damage (where skin cancers arise)—in contrast to UVB varying by season, location, and time of day
Thermal Injuries
Overview
Statistics: Approximately 490,000 individuals in the US require medical care for thermal injuries annually; 40,000 require hospitalization.
Consequences of Thermal Injury: Thermal injuries result in significant integumentary tissue loss, exposing individuals to environmental pathogens, leading to:
1. Loss of body fluids
2. Temperature regulation issues
3. Compromised immune system response
4. Increased metabolic and reparative demands for recovery
Sources of Burns
Types of Burns:
- Flame Burns: From direct fire exposure.
- Scald Burns: Resulting from hot liquids; significant in children—may be indicative of child abuse.
- Chemical Burns: Often due to industrial agents in occupational settings.
- Electrical Burns: Generally more extensive due to internal damage.
- Other Sources: Lightning, electromagnetic, and ionizing radiation can also lead to skin burns.
Classification of Burns
Types Based on Depth of Involvement:
- First-Degree Burns: Only the outer layers of the epidermis affected.
- Second-Degree Burns: Involves the dermis and epidermis.
- Third-Degree Burns: Extends deeper, affecting subcutaneous tissue.
First-Degree Burns
Description: Superficial partial-thickness burns affecting only the outer skin layer.
Appearance and Symptoms: Red or pink, dry, and painful with no blister formation (e.g., mild sunburn).
Skin maintains its ability to function as a water vapor and bacterial barrier
Healing Time: Typically heals in 3-10 days without requiring extensive treatment, although certain populations may require additional care.
Healing→ managing pain, hydrate
Extensive first-degree burns in infants, older adults, and immunocompromised individuals may require additional care
Second-Degree Burns → very common
Partial Thickness: Involve the epidermis and varying depths of the dermis.
Characteristics: Painful, moist, red, and blistered appearance.
Sensitive to temperature changes, air exposure, and touch
Healing Process: Usually 7-21 days; blisters help retain moisture and promote healing.
oMain goal of treatment: prevent microbial colonization of the wound
oSecond-degree partial thickness burns heal in ≈ 7-21 days → KNOW THIS
Full Thickness: Involving the entire epidermis and dermis
Can be very painful because the pain sensors remain intact
Appearance: mottled pink, with red or waxy white areas covered with blisters and edema
•Blisters resemble flat, waxy, or dry tissue paper rather than the bullous blisters seen in second-degree partial-thickness burns
Healing: Timeframe can extend longer than one month, typically leads to scar formation.
Third-Degree Burns → full thickness
Description: Extend deeply into the subcutaneous tissue, potentially involving muscle and bone.
Appearance: Can be waxy white or yellow to tan to deep brown, deep red or black; with hard and leathery skin.
Severe edema
Pain Sensation: Typically absent due to destroyed nerve endings, wider than 1.5 inches →requires skin grafts for extensive damage.
Regeneration: Slower healing process, resulting in significant scarring.
Systemic Complications Associated with Burns
Overview
Response Magnitude: The systemic response correlates with the injury extent, usually plateauing when around 60% of the body is affected.
Associated Complications: Include infection, hemodynamic instability, respiratory dysfunction, hypermetabolic response, and multiple-organ dysfunction
Hemodynamic Instability
Initial Effects: Immediate injury leads to fluid loss and hypovolemic shock, known as burn shock, especially in major burns.
Relevant Concerns: Need for immediate prompt medical intervention includes addressing cardiovascular concerns due to electrical burns or internal damage.
oElectrical injuries → burns can → cardiac arrhythmias requiring immediate attention
Respiratory System Dysfunction
Causes of Injury: Inhalation of smoke and possible thermal injury from burns can damage respiratory passages.
Signs of Injury: Hoarseness, drooling, coughing, and respiratory distress usually present after 24-48 hours after sustaining burns.
Potential Outcomes: Conditions may include pneumonia, pulmonary embolism, or pneumothorax.
Hypermetabolic Response
Increased Needs: The stress associated with burns raises metabolic rates and nutrient requirements for recovery and thermoregulation.
Hormonal Changes: Elevated secretion of catecholamines and cortisol to maintain physiological balance, peaking in the post-burn state.
Metabolic Features: Increased oxygen consumption, glucose utilization, and fat and protein wasting occur as part of this response.
Burn shock → impaired function of vital organs
oAffected individuals may experience renal, GI tract, and nervous system impairment
Sepsis
Primary Concern: Significant risk factor in burn injuries—greater susceptibility to bacterial infections due to compromised skin barrier.
Sources of Infection: Affected individuals may experience infections from various sources including pneumonia, urinary tract infections, and invasive medical procedures due to loss of skin integrity.