The cause of acne is multifactorial. Diet isn’t believed to be a precipitating factor. Possible causes of acne include increased activity of sebaceous glands and blockage of the pilosebaceous ducts (hair follicles).

Factors that may predispose a patient to acne include:

♦ cobalt irradiation

♦ cosmetics

♦ drugs, including androgens, bromides, corticosteroids, corticotropin (ACTH), halothane, iodides, isoniazid (Laniazid), lithium (Eskalith), phenytoin (Dilantin), striadril (Stri-Vectin SD), and trimethadione

♦ emotional stress

♦ exposure to greases, heavy oils, or tars

♦ heredity

♦ hormonal contraceptive use (Many women experience acne flare-up during their first few menses after starting or discontinuing hormonal contraceptives.)

♦ hormones (A decreased estrogen level or an increased testosterone level can exacerbate acne outbreaks.)

♦ hyperalimentation

♦ trauma or rubbing from tight clothing

♦ tropical climate.

There are two types of acne: inflammatory, in which the hair follicle is blocked by sebum, causing bacteria to grow and eventually rupture the follicle; and noninflammatory, in which the follicle doesn’t rupture but remains dilated. (See Understanding acne, page 560.)

The acne plug may appear as:

♦ a closed comedo, or whitehead (may be protruding from the follicle and covered by the epidermis)

♦ an open comedo, or blackhead (protruding from the follicle and not covered by the epidermis; melanin or pigment of the follicle causes the black color).

Rupture or leakage of an enlarged plug into the epidermis produces inflammation, characteristic acne pustules, papules or, in severe forms, acne cysts or abscesses (chronic, recurring lesions producing acne scars).

In women, signs and symptoms may include increased severity just before or during menstruation when the estrogen level is at its lowest. Additionally, an increased testosterone level, which occurs in both males and females during puberty, may also trigger an acne outbreak.

♦ Acne conglobata

♦ Scarring (when acne is severe)

♦ Impaired self-esteem

♦ Abscesses or secondary bacterial infections

Diagnosis of acne vulgaris is confirmed by characteristic acne lesions, especially in adolescents.

Topical treatment for noninflammatory acne includes the application of retinoic acid (tretinoin) on open and closed comedones. For inflammatory acne, an antibacterial such as benzoyl peroxide is effective. Topical and systemic antibiotics and systemic retinoids help reduce the effects of acne.

Systemic therapy consists primarily of:

♦ an antibiotic, usually tetracycline, to decrease bacterial growth (Dosage is reduced for longterm maintenance when the acne in remission.)

♦ oral isotretinoin (Accutane) to inhibit sebaceous gland function and keratinization (A 16- to 20-week course of isotretinoin is limited to patients with severe papulopustular or cystic acne not responding to conventional therapy because of its severe adverse effects. Also, because this drug is known to cause birth defects, the manufacturer, with U.S. Food and Drug Administration approval, recommends the following precautions: pregnancy testing before dispensing; dispensing only a 30-day supply, repeat pregnancy testing throughout the treatment period, effective contraception during treatment, and informed consent. Finally, because of the drug’s effects on the liver, a serum triglyceride level should be drawn before and periodically during treatment.)

♦ for females, estrogens to inhibit androgen activity

♦ other treatments, including intralesional and oral corticosteroids, vitamin A and zinc supplements, exposure to ultraviolet light (although not when the patient is using a photosensitizing agent such as tretinoin), cryotherapy, and surgery.

The main focus of your care is teaching about the disorder, its treatment, and its prevention.

♦ Check the patient’s drug history because certain medications, such as hormonal contraceptives, may cause an acne flare-up.

♦ Try to identify predisposing factors that may be eliminated or modified.

♦ Try to identify eruption patterns (seasonal or monthly).

♦ Explain the causes of acne to the patient and his family. Make sure they understand that the prescribed treatment is more likely to improve acne than a strict diet and fanatical scrubbing with soap and water. Provide written instructions regarding treatment.

♦ Describe the importance of not picking lesions and practicing good personal hygiene to prevent secondary infections.

♦ Instruct the patient receiving tretinoin to apply it at least 30 minutes after washing his face and at least 1 hour before bedtime. Warn against using it around the eyes or lips. After treatments, the skin should look pink and dry. If it appears red or starts to peel, the preparation may have to be weakened or applied less often. Advise the patient to avoid exposure to sunlight or to use a sunscreen. If the prescribed regimen includes tretinoin and benzoyl peroxide, avoid skin irritation by using one preparation in the morning and the other at night.

♦ Instruct the patient to take tetracycline on an empty stomach and not to take it with an antacid or milk because both have metallic ions, and tetracycline interacts with these ions and is then poorly absorbed.

♦ Tell the patient who is taking isotretinoin to avoid vitamin A supplements, which can worsen any adverse reactions. Also, teach the patient how to deal with the dry skin and mucous membranes that usually occur during treatment. Tell the female patient about the severe risk of teratogenicity. Monitor liver enzyme and lipid levels.

♦ Inform the patient that acne takes a long time to clear—even years for complete resolution. Encourage continued local skin care even after
acne clears. Explain the adverse effects of all drugs.

♦ Pay special attention to the patient’s perception of his physical appearance, and offer emotional support.

More than 75% of all burn injuries and those that result in death are preventable.

Thermal burns, the most common type, typically result from:

♦ automobile accidents

♦ clothes that have caught on fire

♦ improper handling of firecrackers and gasoline

♦ kitchen and scalding accidents (such as a child climbing on top of a stove or grabbing a hot iron)

♦ parental abuse (of children or elderly people)

♦ playing with matches

♦ residential fires.

Chemical burns result from contact, ingestion, inhalation, or injection of acids, alkalis, or vesicants.

Electrical burns usually result from contact with faulty electrical wiring or high-voltage power lines. Sometimes young children chew electrical cords.

Friction or abrasion burns occur when the skin rubs harshly against a coarse surface.

Sunburn results from excessive exposure to sunlight. Sunlamp use may also result in burns.

The injuring agent denatures cellular proteins. Some cells die because of traumatic or ischemic necrosis. Loss of collagen cross-linking also occurs with denaturation, creating abnormal osmotic and hydrostatic pressure gradients, which cause the movement of intravascular fluid into interstitial spaces. Cellular injury triggers the release of mediators of inflammation, contributing to local and, in the case of major burns, systemic increases in capillary permeability. Specific pathophysiologic events depend on the cause and classification of the burn. (See Classifications of burns.)

Signs and symptoms depend on the type of burn and may include:

♦ localized pain and erythema, usually without blisters in the first 24 hours, caused by injury from direct or indirect contact with a burn source (first-degree burn)

♦ chills, headache, localized edema, and nausea and vomiting (more severe first-degree burn)

♦ thin-walled, fluid-filled blisters appearing within minutes of the injury, with mild to moderate edema and pain (second-degree superficial partial-thickness burn)

♦ white, waxy appearance to damaged area (second-degree deep partial-thickness burn)

♦ white, brown, or black leathery tissue and visible thrombosed vessels due to destruction of skin elasticity (dorsum of hand most common site of thrombosed veins), without blisters (third-degree burn)

♦ silver-colored, raised area, usually at the site of electrical contact (electrical burn)

♦ singed nasal hairs, mucosal burns, voice changes, coughing, wheezing, soot in mouth or nose, and darkened sputum (with smoke inhalation and pulmonary damage).

♦ Infection (signs and symptoms including fever, increased pain, redness, swelling, drainage, pus, lymphadenopathy, and red streaks from the burn site)

♦ Dehydration (signs and symptoms including thirst, dry skin, dizziness, headache, lightheadedness, and decreased urine output)

♦ Loss of function (burns to face, hands, feet, and genitalia)

♦ Total occlusion of circulation in extremity (due to edema from circumferential burns)

♦ Airway obstruction (neck burns) or restricted respiratory expansion (chest burns)

♦ Pulmonary injury (from smoke inhalation or pulmonary embolism)

♦ Acute respiratory distress syndrome (due to left-sided heart failure or a myocardial infarction)

♦ Greater damage than indicated by the surface burn (electrical and chemical burns) or internal tissue damage along the conduction pathway (electrical burns)

♦ Cardiac arrhythmias (due to electrical shock and fluid shifts)

♦ Hypotension, secondary to shock or hypovolemia

♦ Stroke, heart attack, or pulmonary embolism (due to formation of blood clots resulting from slower blood flow)

♦ Burn shock (due to fluid shifts out of the vascular compartments, possibly leading to kidney damage and renal failure)

♦ Peptic ulcer disease or ileus (due to decreased blood supply in the abdominal area)

♦ Disseminated intravascular coagulation (more severe burn states)

♦ Added pain, depression, and financial burden (due to psychological component of disfigurement)

Diagnosis involves determining the size and classifying the wound. The following methods are used to determine size:

♦ percentage of BSA covered by the burn using the rule of nines chart

♦ Lund-Browder chart (more accurate because it allows BSA changes with age); correlation of the burn’s depth and size to estimate its severity. (See Using the Rule of Nines and the Lund-Browder chart, pages 566 and 567.)

Major burns are classified as:

♦ third-degree burns over more than 10% of BSA

♦ second-degree burns over more than 25% of adult BSA (over 20% in children)

♦ burns of hands, face, feet, or genitalia

♦ burns complicated by fractures or respiratory damage

♦ electrical burns

♦ all burns in poor-risk patients. Moderate burns are classified as:

♦ third-degree burns over 2% to 10% of BSA

♦ second-degree burns over 15% to 25% of adult BSA (10% to 20% in children). Minor burns are classified as:

♦ third-degree burns over less than 2% of BSA

♦ second-degree burns over less than 15% of adult BSA (10% in children).

Initial burn treatments are based on the type of burn and may include:

♦ immersing the burned area in cool water (55°F [12.8°C]) or applying cool compresses (minor burns)

♦ administering pain medication, as needed, or an anti-inflammatory

♦ covering the area with an antimicrobial and a nonstick bulky dressing (after debridement); prophylactic tetanus injection as needed

♦ not disturbing blisters or dead skin (increases risk of infection)

♦ preventing hypoxia by maintaining an open airway; assessing airway, breathing, and circulation; checking for smoke inhalation immediately when the patient presents; assisting with endotracheal intubation; and giving 100% oxygen (first immediate treatment for moderate and major burns)

♦ controlling active bleeding

♦ covering partial-thickness burns over 30% of BSA or full-thickness burns over 5% of BSA with a clean, dry, sterile bedsheet (because of drastic reduction in body temperature, don’t cover large burns with saline-soaked dressings)

♦ removing smoldering clothing (first soaking the clothing in saline solution if it’s stuck to the patient’s skin), rings, and other constricting items

♦ 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)

♦ antimicrobial therapy (all patients with major burns)

♦ correction of electrolyte imbalances, transfusion and replacement blood products as indicated by laboratory results, and dialysis for renal failure or myoglobinuria

♦ closely monitoring intake and output, frequently checking vital signs (every 15 minutes), possibly inserting an indwelling urinary catheter

♦ nasogastric tube to decompress the stomach and avoid aspiration of stomach contents

♦ irrigating the wound with copious amounts of normal saline solution (chemical burns)

♦ surgical intervention, including skin grafts and more thorough surgical cleaning (major burns).

♦ Don’t treat the burn wound for a patient being transferred to a specialty facility within 4 hours. Maintain airway, breathing, and circulation. Wrap the patient in a sterile sheet and blanket for warmth, elevate the burned extremity, and prepare the patient for transport. Upon discharge or during prolonged care:

♦ Ensure increased caloric intake due to increased metabolic rate to promote healing and recovery.

♦ Give the patient complete discharge instructions, teaching him what he needs to know about home care; stress the importance of keeping the dressing clean and dry, elevating the burned extremity for the first 24 hours, and having the wound rechecked in 1 to 2 days. Also
stress the importance of taking pain medication as needed, especially before dressing changes.

Possible causes of cellulitis are bacterial and fungal infections, commonly group A streptococcus and Staphylococcus aureus.

As the offending organism invades the compromised area, it overwhelms the defensive cells
(neutrophils, eosinophils, basophils, and mast cells) that break down the cellular components, which normally contain and localize the inflammation. As cellulitis progresses, the organism invades tissue around the initial wound site.