Skin Disorders
ACNE
Acne is an inflammatory disease of the pilosebaceous units (hair follicles). It occurs on areas of the body that have sebaceous glands, such as the face, neck, chest, back, and shoulders, and is associated with a high rate of sebum secretion. When sebum blocks a hair follicle, one of two types of acne develops. In inflammatory acne, bacterial growth in the blocked follicle leads to inflammation and eventual rupture of the follicle. In noninflammatory acne, the follicle remains dilated by accumulating secretions but does not rupture.
AGE ALERT
Acne occurs in both males and females. Acne vulgaris develops in 80% to 90% of adolescents or young adults, primarily between ages 15 and 18, although the lesions can appear as early as age 8 or into the late 20s.Causes
Multifactorial — diet not believed to be a factor
Predisposing Factors
Heredity
Androgen stimulation
Certain drugs, including corticosteroids, corticotropin, androgens, iodides, bromides, trimethadione, phenytoin, isoniazid, lithium, and halothane
Exposure to heavy oils, greases, tars, and cosmetics
Cobalt irradiation
Hyperalimentation
Trauma, skin occlusion, or pressure
Emotional stress
Hormonal contraceptive use (may exacerbate acne in some women)
Pathophysiology
Androgens stimulate sebaceous gland growth, sebum production, and shedding of the epithelial cells that line sebaceous follicles. The stimulated follicles become dilated, and sebum and keratin from the epithelial cells form a plug that seals the follicle, creating a favorable environment for bacterial growth. The bacteria, usually Propionibacterium acnes or Staphylococcus epidermidis, are normal skin flora that secrete lipase. This enzyme converts sebum to free fatty acids, which provoke inflammation and formation of open or closed comedones that may rupture and cause a foreign body response resulting in the formation of papules, nodules, or pustules. Rupture and inflammation may lead to scarring.
COMPLICATIONS
Infection
Gross inflammation
Abscess
Scars
Hyperpigmentation
Signs and Symptoms
Closed comedo, or whitehead does not protrude from follicle, covered by epidermis
Open comedo, or blackhead protrudes from the follicle, not covered by epidermis; black color caused by melanin or pigment of the follicle
Rupture or leakage of comedo into the epidermis:
inflammation
pustules, papules
in severe forms, cysts or abscesses (chronic, recurring lesions producing acne scars)
Diagnostic Test Results
No test for acne vulgaris exists other than visualization of acne lesions to confirm diagnosis.
Treatment
Gentle cleaning with a sponge to dislodge superficial comedones
Recommend using the 2016 treatment regimen from American Academy of Dermatology (Zaenglein, A. L., Pathy, A. L., Schlosser, B. J., Alikhan, A., Baldwin, H. E., Berson D. S., … Bhushan, R. (2016). Guidelines of care for the management of acne vulgaris. American Academy of Dermatology, 74(5), 945.)
Topical Agents for Mild Acne
Antibacterial agents, such as benzoyl peroxide gels (2%, 5%, or 10%), clindamycin, or erythromycin
Keratolytic Agents
Dry and peel the skin to open blocked follicles and release sebum
Benzoyl peroxide, tretinoin
Systemic Therapy for Moderate to Severe Acne
Tetracycline or minocycline
Oral isotretinoin to inhibit sebaceous gland function and abnormal keratinization; has severe adverse effects, which limit its use to patients with severe papulopustular or cystic acne not responding to conventional therapy
For females, antiandrogens — birth control pills, such as norgestimate and ethinyl estradiol, or spironolactone
ATOPIC DERMATITIS
Atopic dermatitis (also called atopic or infantile eczema) is a chronic or recurrent inflammatory skin disease. It is commonly associated with other atopic diseases, such as bronchial asthma and allergic rhinitis. Atopic dermatitis is genetically transmitted.
AGE ALERT
Atopic dermatitis commonly develops in infants and toddlers between ages 1 month and 1 year, usually in those with a strong family history of atopic disease. These children can develop atopic dermatitis in infancy, then subsequent allergic rhinitis and asthma in later childhood is known as the atopic march.Typically, atopic dermatitis flares and subsides repeatedly before finally resolving during adolescence, but it can persist into adulthood.
Causes
The exact etiology is unknown. A genetic predisposition is likely, with a complex relationship between genetic and environmental factors.
Possible Contributing Factors
Studies are showing that second hand tobacco smoke exposure is a contributing factor
Food allergy, especially eggs, peanuts, milk, or wheat
Infection
Chemical irritants
Extremes of temperature and humidity
Psychological stress or strong emotions
Pathophysiology
The allergic mechanism of hypersensitivity results in a release of inflammatory mediators through sensitized antibodies of the immunoglobulin IgE class. Histamine and other cytokines induce acute inflammation. Abnormally dry skin and a decreased threshold for itching set up the “itch-scratch-itch” cycle, which eventually causes lesions (excoriations, lichenification).
COMPLICATIONS
Sleep difficulties
Secondary infection
Scars
Signs and Symptoms
Erythematous areas on excessively dry skin; in children, typically on the forehead, cheeks, and extensor surfaces of the arms and legs; in adults, at flexion points (antecubital fossa, popliteal area, and neck), infants spares the diaper area (this is important to note as some parents confuse eczema and diaper rash)
Edema, crusting, scaling caused by pruritus and scratching
Multiple areas of dry, scaly skin, with white dermatographism, blanching, and lichenification with chronic atrophic lesions
Infantile form presents as red skin with tiny vesicles, especially on the face (sparing the mouth); possible development of wet crusts and fissures
In blacks, follicular eczema common, appearing as discrete follicular papules involving hair follicles in the affected area
Pinkish, swollen upper eyelid and double fold under lower lid
Viral, fungal, or bacterial infections and ocular disorders possible secondary conditions
Diagnostic Test Results
Blood tests reveal eosinophilia and elevated IgE levels.
Treatment
Important to control the itch to promote healing and prevent infection
Eliminating allergens and avoiding irritants (strong soaps, cleansers, and other chemicals), extreme temperature changes, and other precipitating factors
Preventing excessive dryness of the skin (critical to successful therapy) by maintaining adequate fluid intake, taking tepid baths, and humidifying air recommend including bleach baths recommend including soak and seal therapy (wet wraps)
Topical tar preparations in a lubricating base (contraindicated for intensely inflamed or open lesions)
Topical corticosteroid ointment, hydrocortisone 1% especially after bathing, to alleviate inflammation; moisturizing cream between steroid doses to help retain moisture
Topical doxepin hydrochloride
Topical immunomodulators, such as tacrolimus and pimecrolimus
Systemic antihistamines such as diphenhydramine
Systemic corticosteroid therapy for severe disease only
Ultraviolet B or psoralens plus ultraviolet A therapy
In severe adult-onset disease, cyclosporine A, if other treatments fail
Antibiotics, if skin culture positive for bacteria
 APPEARANCE OF ATOPIC DERMATITIS |
CLINICAL TIP
MORGAN’S LINEIn children with atopic dermatitis, severe pruritus with recurrent rubbing leads to characteristic pink pigmentation and swelling of the upper eyelid and a double fold under the lower lid (Morgan’s line, Dennie’s sign, or mongolian fold).
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BURNS
Burns are the third leading cause of accidental death in the United States.
Causes
Thermal: residential fires, automobile accidents, playing with matches, improper handling of firecrackers, scalds caused by kitchen, or bathroom accidents
Chemical: contact, ingestion, inhalation, or injection of acids, alkalis, or vesicants
Electrical: contact with faulty electrical wiring, electrical cords, or high-voltage power lines
Friction or abrasion
Ultraviolet radiation: sunburn
Pathophysiology
The injuring agent denatures all cellular proteins. Some cells die because of traumatic or ischemic necrosis. Denaturation disrupts collagen cross-links in connective tissue. The consequent abnormal osmotic and hydrostatic pressure gradients force intravascular fluid into interstitial spaces. Cellular injury triggers the release of mediators of inflammation, further contributing to local or systemic increases in capillary permeability.
Burns are classified according to their depth and size.
First-degree burns. Localized injury to or destruction of epidermis by direct or indirect contact. The barrier function of the skin remains intact.
Second-degree superficial partial-thickness burns. Destruction of epidermis and some of the upper area of the dermis. The barrier function of the skin is lost.
Second-degree deep partial-thickness burns. Destruction of epidermis and more of the dermis.
Third- and fourth-degree burns. Affect every body system and organ. A third-degree burn extends through the epidermis and dermis and into the subcutaneous tissue layer; a fourth-degree burn damages muscle, bone, and interstitial tissues. Within hours, fluids and protein shift from capillary to interstitial spaces, causing edema.
COMPLICATIONS
Sepsis
Respiratory complications
Hypovolemic shock and multisystem organ dysfunction
Anemia
Malnutrition
Infection
Deep burns can cause bone and joint limitations
Signs and Symptoms
First-degree burn: localized pain and erythema, usually without blisters in the first 24 hours
More severe first-degree burn: chills, headache, localized edema, nausea, and vomiting
Second-degree superficial partial-thickness burn: thinwalled, fluid-filled blisters that appear within minutes of injury; mild to moderate edema; pain
Second-degree deep partial-thickness burn: white, waxy appearance of damaged area, edema, and pain (or may be nonpainful)
Third- and fourth-degree burns: white, brown, or black leathery tissue; visible thrombosed vessels; no blisters
Electrical burn: silver-colored, raised area, usually at the site of electrical contact (damage to underlying tissue can occur even with intact epidermis)
Smoke inhalation and pulmonary damage: singed nasal hairs, mucosal burns, voice changes, coughing, wheezing, soot in mouth or nose, darkened sputum
Total burn surface area (BSA) may be estimated quickly using the Rule of Nines, in which an adult patient’s body parts are assigned percentages based on the number 9. The Lund-Browder classification reference allows more precise assessment by assigning specific percentages to an infant or child’s body parts and accounts for burn thickness and age differences.
Minor Burns
Third-degree burns on less than 2% of BSA
Second-degree burns on less than 15% of adult BSA (less than 10% in children)
All first-degree burns
Moderate Burns
Third-degree burns on 2% to 10% of BSA
Second-degree burns on 15% to 25% of adult BSA (10% to 20% in children)
Major Burns
Third-degree burns on more than 10% of BSA
Second-degree burns on more than 25% of adult BSA (more than 20% in children)
Burns of hands, face, feet, or genitalia
Burns complicated by fractures or respiratory damage
Electrical burns and burns in poor-risk patients
Diagnostic Test Results
Arterial blood gas levels show evidence of smoke inhalation; they may also show decreased alveolar function and hypoxia.
Complete blood count reveals decreased hemoglobin level and hematocrit if blood loss occurs.
Blood chemistries show abnormal electrolytes from fluid loss and shifts, increased blood urea nitrogen with fluid loss, and decreased glucose in children due to limited glycogen storage.
Urinalysis shows myoglobinuria and hemoglobinuria.
Other blood tests detect increased carboxyhemoglobin.
Electrocardiogram shows ischemia, injury, or arrhythmias, especially in electrical burns.
Fiber-optic bronchoscopy reveals edema of the airways.
Treatment
Minor burns: immersion of burned area in cool water (55°F [12.8°C]) or application of cool compresses
Immediate treatment for moderate and major burns: maintain an open airway, endotracheal intubation, 100% oxygen
Immediate I.V. therapy to prevent hypovolemic shock and maintain cardiac output (lactated Ringer’s solution or a fluid replacement formula; additional I.V. lines may be needed)
Partial-thickness burns over 30% of BSA or full-thickness burns over 5% of BSA: cover patient with a clean, dry, sterile bed sheet to help preserve body temperature; don’t cover large burns with saline-soaked dressings
Debridement followed by application of antimicrobial and nonstick bulky dressing; tetanus prophylaxis if needed
Fragments of necrotic blisters may increase the risk of infection and limit the contact of topical antimicrobial agents to the burn wound
Pain or anti-inflammatory medication as needed
Major burns: systemic antimicrobial therapy
 CLASSIFICATION OF BURNS BY DEPTH OF INJURY |
CLINICAL TIP
ESTIMATING THE EXTENT OF BURNS
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CELLULITIS
Cellulitis is an acute, spreading infection of the dermis or subcutaneous layer of the skin. It may follow damage to the skin, such as a bite or wound. As the cellulitis spreads, fever, erythema, and lymphangitis may occur. Persons with a chronic illness, such as diabetes mellitus immunodeficiency, or Peripheral artery disease contributing health problems, such as diabetes, immunodeficiency, or impaired circulation, have an increased risk for cellulitis. If treated promptly, the prognosis is usually good.
AGE ALERT
Cellulitis of the lower extremity is more likely to develop into thrombophlebitis in an elderly patient. Orbital cellulitis, especially in children, may require hospitalization and I.V. antibiotics because of the increased risk of spread to intracranial structures, such as in thin bones and numerous openings in the bone.Causes
Bacterial infections, commonly with group A beta-hemolytic streptococcus or Staphylococcus aureus
In patients with diabetes or decreased immune function: Escherichia coli, Proteus mirabilis, Acinetobacter, Enterobacter, Pseudomonas aeruginosa, Pasteurella multocida, Vibrio vulnificus, Mycobacterium fortuitum complex, and Cryptococcus neoformans
In children, less commonly caused by pneumococci and Neisseria meningitidis group B (periorbital)
Pathophysiology
After the organisms enter the tissue spaces and planes of cleavage, hyaluronidases break down the ground substances composed of polysaccharides, while fibrinolysins digest fibrin barriers and lecithinases destroy cell membranes. This overwhelms the normal cells of defense (neutrophils, eosinophils, basophils, and mast cells) that normally contain and localize inflammation, and cellular debris accumulates.
COMPLICATIONS
Bacteremia
Necrotizing fasciitis
Lymphangitis
Meningitis (in facial cellulitis)
Signs and Symptoms
Classic signs: erythema and edema due to inflammatory response, usually well-demarcated
Pain at site and possibly in surrounding area
Fever and warmth
Regional lymphadenopathy or lymphangitis
Diagnostic Test Results
The diagnosis of cellulitis is based upon clinical manifestations. White blood cell count shows mild leukocytosis with a shift to the left.
Erythrocyte sedimentation rate is mildly elevated.
Culture and gram stain results of fluid from abscesses and bulla are positive for the offending organism.
Using the “Touch” preparation, potassium hydroxide is applied to a microscope slide containing a skin lesion specimen that detects the presence of yeast or mycelial forms of fungus.
Treatment
Oral or I.V. penicillinase-resistant penicillin (drug of choice for initial treatment) unless the patient has known penicillin allergy; antifungal medications if needed
Antibiotic selection for treatment depends on the clinical presentation of purulent or nonpurulent cellulitis.
Alternative antibiotics based on culture and sensitivity results
Warm soaks to the site to help relieve pain and decrease edema by increasing vasodilation
Pain medication as needed
Elevation of infected extremity
Surgical drainage or debridement for abscess formation
 PHASES OF ACUTE INFLAMMATORY RESPONSE |
CLINICAL TIP
RECOGNIZING CELLULITISThe classic signs of cellulitis, a spreading soft tissue infection, are erythema and edema surrounding the initial wound. The tissue is warm to the touch.
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CONTACT DERMATITIS
Contact dermatitis commonly appears as a sharply demarcated inflammation of the skin that results from contact with an irritating chemical or atopic allergen (a substance that produces an allergic reaction in the skin). It can also appear as an irritation of the skin that results from contact with concentrated substances to which the skin is sensitized, such as perfumes, soaps, chemicals, or metals and alloys (such as nickel used in jewelry). Localized inflammatory skin resulting from exposure of a wide range of chemical or physical agents.
Causes
Mild Irritants
Chronic exposure to detergents or solvents
