NLE Integumentary & Skin Integrity — Burns and Dermatologic DisordersStudy Notes

A burn injury destroys the integumentary system's protective barrier, disrupting critical functions including thermoregulation, fluid balance, and infection prevention. The severity and prognosis of a burn depend primarily on the depth of tissue destruction. Burns are classified into five categories based on which skin layers are involved: **Superficial (First-Degree) Burns**: These burns involve only the epidermis, the outermost layer of skin. Clinical presentation includes erythema (redness), dry skin, pain, and blanching with pressure. There are NO blisters. Examples include typical sunburns. Healing occurs within 3–6 days without scarring, as the epidermis regenerates completely. Pain management typically requires only topical cooling measures and analgesics. **Superficial Partial-Thickness (Second-Degree) Burns**: These burns extend into the upper dermis. Key features are the presence of fluid-filled blisters, a moist and weeping red surface, severe pain (as nerve endings are largely intact), and blanching with pressure. These wounds are extremely painful because sensory nerves are stimulated by inflammatory mediators. Healing typically occurs within 2–3 weeks, usually without need for grafting, though scarring risk exists. Fluid loss through the moist surface is significant during the emergent phase. **Deep Partial-Thickness (Second-Degree) Burns**: These extend deeper into the dermis. The appearance ranges from red to waxy white, the surface is drier than superficial partial-thickness burns, pain is less severe (some nerve damage has occurred), and capillary refill is slower. These wounds often require skin grafting for optimal functional and cosmetic outcomes and carry a higher risk of hypertrophic scarring and contracture formation. Healing time is prolonged (3–8 weeks or longer). **Full-Thickness (Third-Degree) Burns**: These burn destroy the entire epidermis, dermis, and may extend into subcutaneous fat. The wound appearance is dry, leathery, inelastic, and charred or discolored (white, waxy, tan, brown, or black). Critically, full-thickness burns are PAINLESS in the center because all nerve endings are destroyed—this absence of pain is a diagnostic hallmark. The wound does NOT blanch with pressure. Skin grafting is mandatory because the skin cannot regenerate; autografting (use of the patient's own skin from unburned areas) is the permanent solution. **Fourth-Degree Burns**: These extend beyond skin into muscle, fascia, and bone. They appear completely charred and often require amputation of affected limbs. Mortality risk is extremely high. For NLE preparation, memorize this key principle: **Only partial-thickness and full-thickness burns (not superficial/first-degree burns) are counted when calculating total body surface area (TBSA) burned.** This is critical because TBSA determines fluid resuscitation needs via the Parkland formula.

Burns result from thermal, chemical, electrical, or radiation injury. Understanding the mechanism is crucial for appropriate management and anticipating complications. **Thermal Burns** (most common): Caused by flame, hot liquids (scalds), or direct contact with hot objects. In the Philippines, scalding accidents (cooking-related) and flame injuries (cooking fuel use, fireworks during celebrations) are prevalent. **Chemical Burns**: Caused by strong acids or alkalis that continue to damage tissue as long as the chemical is in contact with skin. Management requires immediate removal of the chemical—brush off dry powder chemicals first (without water), then flush with copious amounts of water or normal saline for at least 15–20 minutes. Chemical burns may be deeper than initially apparent because the chemical continues to penetrate. **Electrical Burns**: Cause deceptive injury patterns. The visible skin injury may be minimal, but internal tissue damage (from the current passing through the body) can be extensive and deep. Electrical current follows the path of least resistance through the body, potentially damaging the myocardium (cardiac muscle). All patients with electrical burns must be monitored for cardiac dysrhythmias via continuous ECG. Additionally, electrical current causes muscle destruction (rhabdomyolysis), releasing myoglobin into the bloodstream. Dark or cola-colored urine indicates myoglobinuria and carries a high risk of acute kidney injury (AKI). Aggressive fluid resuscitation beyond the Parkland formula (targeting urine output of 200–300 mL/hr) and urinary alkalinization (via sodium bicarbonate) are needed to prevent AKI. Watch serum potassium levels carefully, as rhabdomyolysis releases large amounts of potassium. **Radiation Burns**: Less common but occur in industrial or nuclear incidents. Cumulative exposure causes progressive damage. **Inhalation Injury**: This is the leading cause of early death in hospitalized burn patients and must be suspected based on clinical signs: - History of being in an enclosed space during fire - Facial burns or singed nasal hairs - Carbonaceous (sooty/black) sputum or nasal discharge - Hoarseness or stridor (indicating laryngeal edema) - Cough or dyspnea - Altered mental status Management: Provide 100% humidified oxygen immediately. Suspect carbon monoxide (CO) poisoning in enclosed-space fires—CO binds hemoglobin with 200× the affinity of oxygen, causing cellular hypoxia. Carboxyhemoglobin levels >20% are dangerous. Hyperbaric oxygen therapy accelerates CO elimination. Monitor for delayed pulmonary edema and airway obstruction (intubate early if signs of airway compromise develop, because swelling progresses rapidly and may make intubation impossible).

Accurate estimation of total body surface area (TBSA) burned is essential for calculating fluid resuscitation requirements and determining burn severity classification. The **Rule of Nines** is the rapid bedside method for adults. **Rule of Nines (Adult)**: - Head and neck: 9% (divided as 4.5% anterior + 4.5% posterior) - Each arm: 9% (4.5% anterior + 4.5% posterior per arm) - Anterior trunk (chest and abdomen): 18% - Posterior trunk (back): 18% - Each leg: 18% (9% anterior + 9% posterior per leg) - Perineum/genitalia: 1% Total: 100% These percentages are fixed and do not vary with patient size. When adding regions, remember that only partial-thickness and full-thickness burns are counted—superficial (first-degree) burns are excluded from TBSA calculation. **Special Populations**: In children, the Rule of Nines is inaccurate because a child's head is proportionally larger than an adult's (a child's head = approximately 18% of TBSA, whereas an adult's is 9%). The **Lund-Browder Chart** is the gold standard for pediatric TBSA estimation. This chart accounts for age-related differences in body proportions. **Palmar Method**: For small or scattered burns, the patient's palm (including fingers) is approximately 1% of their TBSA. This method is useful when burns are not in distinct anatomic regions. **Clinical Example for NLE**: A 70 kg, 35-year-old male sustains a burn to both arms, the entire anterior trunk, and the entire left leg from a house fire. Calculate TBSA: - Both arms: 9% + 9% = 18% - Anterior trunk: 18% - Left leg: 18% Total TBSA = 18% + 18% + 18% = 54% This 54% TBSA will be used in the Parkland formula to calculate fluid resuscitation.

The Parkland formula is the most widely used guideline for calculating fluid resuscitation in major burns. Severe burns cause massive fluid shifts from the intravascular space into the interstitium ("third spacing") due to increased capillary permeability from inflammatory mediators. Without adequate resuscitation, burn shock (hypovolemic shock) develops within hours. The Parkland formula guides initial therapy, but titration based on urine output is the gold standard for assessing adequacy. **The Parkland Formula**: **Total fluid (mL) for 24 hours = 4 mL × body weight (kg) × %TBSA burned** The fluid of choice is **Lactated Ringer's (LR) solution**—do NOT use normal saline alone (excessive sodium causes hyperchloremic acidosis) or hypotonic solutions (free water worsens cerebral edema). **Timing and Administration**: - **First 8 hours**: Give 50% of the total calculated volume, **calculated from the time of injury** (not from hospital arrival or IV insertion). - **Next 16 hours**: Give the remaining 50%. This timing is critical for NLE exams and clinical practice. If a burn occurs at 10:00 AM but the IV is not placed until 12:00 PM, the first-8-hour infusion must still be completed by 6:00 PM (8 hours post-injury), so the rate must be accelerated over the remaining 6 hours. **Worked Example**: 70 kg adult with 50% TBSA burns, injury time = 14:00 (2:00 PM). Total 24-hour fluid = 4 mL × 70 kg × 50 = **14,000 mL** First 8 hours (14:00–22:00, 2:00 PM–10:00 PM): 50% = 7,000 mL infused over 8 hours = **875 mL/hr** Second 16 hours (22:00 next day–14:00, 10:00 PM–2:00 PM): 50% = 7,000 mL infused over 16 hours = **437 mL/hr** **Assessing Adequacy of Resuscitation**: The Parkland formula is a **starting point**, not a fixed prescription. Titration is guided by **urine output**, which is the best indicator of tissue perfusion: - **Adults**: Target urine output = **0.5 mL/kg/hr** (approximately 30–50 mL/hr for an average adult) - **Children**: Target urine output = **1 mL/kg/hr** - **Electrical burns with rhabdomyolysis**: Target urine output = **200–300 mL/hr** (more aggressive) Other markers of adequate resuscitation include: - Mean arterial pressure (MAP) ≥65 mmHg - Clearing sensorium (improved mental status) - Absence of peripheral cyanosis - Capillary refill <2 seconds (in areas without burn) If urine output is **below target**, increase IV rate. If urine output is **above target**, decrease IV rate (to avoid fluid overload, which increases risk of pulmonary edema and compartment syndrome). A urinary catheter must be placed immediately to monitor hourly urine output accurately. **Special Considerations**: - **Circumferential burns** of the extremity can impede venous return and perfusion; an escharotomy (surgical incision of the eschar to allow expansion) may be needed. - **Inhalation injury** increases fluid requirements by 50% or more because additional fluid is lost through damaged respiratory mucosa. - Monitor **serum electrolytes** frequently during the emergent phase (hyperkalemia is a critical threat early; hypokalemia develops later during diuresis).

Burn injury progresses through three distinct clinical phases, each with different pathophysiology, priorities, and complications. Understanding these phases is essential for the NLE and for providing appropriate nursing care across the continuum. **EMERGENT (RESUSCITATIVE) PHASE: Onset to 24–48 hours** **Pathophysiology**: Immediately after a major burn, increased capillary permeability from inflammatory mediators (histamine, prostaglandins, cytokines) causes massive fluid shifts from the intravascular space into the interstitium ("third spacing"), creating edema. This results in **hypovolemia** (inadequate circulating volume) and **hemoconcentration** (blood becomes concentrated because fluid is lost). Cellular damage releases **potassium** into the bloodstream, causing **hyperkalemia**, while damaged cells trap **sodium** in edema fluid, causing **hyponatremia**. The greatest threat during this phase is **burn shock** (hypovolemic shock). **Nursing Priorities (Using Maslow's Hierarchy)**: 1. **Airway and breathing** (physiological safety): Assess for inhalation injury. If inhalation injury is suspected, provide 100% humidified oxygen immediately. Intubate early if signs of airway edema are present (hoarseness, stridor, difficulty swallowing) because laryngeal swelling can progress rapidly and compromise the airway. Delaying intubation risks losing a patent airway. 2. **Circulation and fluid resuscitation** (physiological safety): Establish two large-bore IV lines (14–16 gauge) and begin LR resuscitation using the Parkland formula. Insert an indwelling urinary catheter immediately to monitor hourly urine output—this is the most reliable indicator of tissue perfusion. Target urine output 0.5 mL/kg/hr in adults. Monitor vital signs, MAP, and sensorium. 3. **Pain management** (physiological safety): Give analgesia IV (not IM or SC) because during the emergent phase, peripheral vasoconstriction and edema make IM/SC absorption unreliable. Use IV opioids (morphine, fentanyl) titrated to effect. During dressing changes, provide analgesia 30 minutes before; consider sedation for burned patients requiring multiple painful procedures. 4. **Prevent complications from edema**: - **Circumferential burns**: Monitor distal circulation (pulses, color, sensation, temperature). If circulation is compromised, an **escharotomy** (surgical incision through the full-thickness burn eschar) may be needed to relieve constriction and restore blood flow. For circumferential chest/trunk burns, escharotomy prevents restrictive airway compression. - **Airway edema**: Position the patient upright (high Fowler's) to reduce laryngeal edema. Avoid neck hyperextension. 5. **Temperature management**: Keep the patient warm (use blankets, warm IV fluids) because large burns impair thermoregulation and cause hypothermia, which increases mortality. However, do NOT apply ice directly to burns (causes further tissue damage via vasoconstriction and hypothermia). 6. **GI management**: Keep the patient NPO initially because severe burns trigger paralytic ileus. Insert a nasogastric tube if extensive burns (>20% TBSA) to prevent gastric distention and aspiration. Monitor for **Curling's ulcer** (stress-related gastric ulcer)—give prophylactic H2 blockers (ranitidine) or proton pump inhibitors (omeprazole). 7. **Tetanus prophylaxis**: All burn wounds are tetanus-prone. Give tetanus toxoid or immunoglobulin as appropriate based on the patient's prior vaccination history. 8. **Psychosocial support**: Severe burns are psychologically traumatic. Provide reassurance, honest information, and family support. The fear and pain are overwhelming for the patient and family. **ACUTE PHASE: 48–72 hours until wound closure (days to weeks)** **Pathophysiology**: Capillary integrity begins to return as inflammation resolves. Fluid shifts back into the intravascular space (**diuresis**), and the risk shifts from hypovolemia to **fluid overload** and pulmonary edema. As potassium re-enters cells and is excreted in urine, **hypokalemia** develops. **Infection and sepsis** become the leading cause of death during this phase, as the destroyed skin barrier is lost and bacterial colonization occurs. **Nursing Priorities**: 1. **Wound management** (safety, physiological): - **Cleansing**: Daily gentle cleansing with mild soap and warm water or saline. Remove loose tissue and debris. - **Debridement**: Removal of necrotic tissue (eschar) to prevent bacterial overgrowth. May be done at bedside (tangential debridement with knife) or in the OR (surgical debridement). Enzymatic debridement products (collagenase, papain) accelerate removal of dead tissue. - **Topical antimicrobials**: Apply after cleansing. Common agents: - **Silver sulfadiazine (Silvadene)**: Broad-spectrum, painless application, but can cause transient leukopenia and is contraindicated in sulfa allergy and near-term pregnancy/newborns (can cause kernicterus). - **Mafenide acetate (Sulfamylon)**: Excellent eschar penetration (especially useful over cartilage/face), but PAINFUL on application and causes metabolic acidosis by inhibiting carbonic anhydrase—monitor arterial pH. - **Bacitracin**: Useful on face; allows visibility of the wound. - **Mupirocin**: For MRSA coverage if needed. - **Dressings**: Non-adherent dressings (gauze, hydrogels) with frequent changes (1–3 times daily) to prevent infection. Newer burn dressings (biological skin substitutes, synthetic dressings like Biobrane) reduce water loss and pain. - **Skin grafting**: Full-thickness burns require grafting once eschar is removed (usually 3–5 days post-injury or once the wound bed is clean). **Autografting** (patient's own skin from unburned areas) is the permanent solution. **Allograft** (cadaver skin) or **xenograft** (pig skin) serve as temporary biological dressings while waiting for autograft availability. **Cultured epithelial autografts** (CEA) from a small biopsy can cover large areas but require 2–3 weeks for culture. 2. **Infection prevention** (safety): - Use **strict aseptic technique** during wound care; hand hygiene is critical. - **Protective isolation** (private room, gloves, gowns) for extensive burns. - Monitor for **systemic signs of sepsis**: altered mental status (early sign in burns), fever or hypothermia (temperature instability), ileus, hyperglycemia, tachycardia, tachypnea. Burns commonly become colonized with **Pseudomonas, Staphylococcus aureus (including MRSA), and other gram-negatives**. - Blood cultures for fever >38.5°C; culture burn wound swabs if signs of infection. - **Do NOT give prophylactic systemic antibiotics**—this drives resistance. Use antibiotics only for documented infection (positive cultures). - Monitor the burn wound closely for signs of invasive infection (black or violaceous appearance, rapid eschar separation, hemorrhagic sublesions). 3. **Nutrition** (physiological, safety): - Severe burns dramatically increase metabolic rate (by 200% or more); provide **high-calorie, high-protein nutrition** to support healing, immune function, and prevent muscle catabolism. - Start **enteral nutrition early** (within 24–48 hours post-injury) via nasogastric or nasojejunal feeding to preserve GI integrity, prevent translocation of bacteria, and reduce infection risk. - Use specialized high-protein formulas (1.5–2.0 g protein/kg/day). - Provide micronutrients: **Vitamin C** (supports collagen synthesis), **Vitamin A** (supports epithelialization and immune function), **Zinc** (essential for wound healing). - Monitor serum albumin, prealbumin, and nitrogen balance; adjust intake as needed. 4. **Fluid and electrolyte management**: - Monitor for fluid overload now that diuresis begins. Reduce IV rate if urine output exceeds target. Watch for signs of pulmonary edema (crackles, dyspnea, pink frothy sputum). - Monitor **potassium closely**: hyperkalemia in first 24–48 hours, then hypokalemia; replace as needed. - Monitor other electrolytes (sodium, chloride, magnesium, calcium, phosphate) frequently; abnormalities impair cardiac function and wound healing. 5. **Positioning and splinting** (preventing contractures): - Position joints in **extension** (opposite of the flexion contracture position) to maintain ROM. - Use **splints** to maintain proper joint alignment, especially for neck, shoulders, elbows, wrists, hips, knees, and ankles. - Begin **early active range-of-motion exercise** as tolerated; PT/OT consultation is essential. - Contractures are THE major late complication of burns and are largely preventable with early positioning and therapy. 6. **Pain and anxiety management**: - Pain and anxiety persist throughout the acute phase and during dressing changes/PT. Use IV opioids, sedatives (midazolam), and non-pharmacologic approaches (breathing, distraction, music therapy). - Dressing changes are often the most painful part of burn care; plan analgesia 30–60 minutes before. - Anxiety about body image and function is common; provide reassurance and psychosocial support. **REHABILITATION PHASE: From wound closure onward (weeks to years)** **Pathophysiology**: Once the burn wound is closed (via grafting or epithelialization), the focus shifts from survival to restoring function and appearance. During this phase, the body remodels collagen in the scars, which can lead to hypertrophic scarring and contracture formation if not actively managed. Scar maturation continues for 12–24 months. **Nursing Priorities**: 1. **Contracture prevention and ROM** (physiological, safety): - Aggressive **active and passive range-of-motion exercise** to prevent joints from stiffening. - Continued **splinting** and positioning at night to maintain extensions. - PT/OT collaboration is crucial for ambulation training and functional recovery. - Contractures are difficult to reverse once formed; prevention is far superior to correction. 2. **Scar management**: - **Pressure garments** (compression sleeves, gloves, stockings, vests) worn 23 hours/day for months to years. These reduce blood flow to the scar, diminish collagen deposition, and flatten hypertrophic scars. Compliance is challenging because garments are hot and uncomfortable. - **Silicone gel sheeting** for localized scars. - **Laser therapy** (pulsed dye laser) to reduce scar vascularity and redness. - **Surgical scar revision** (Z-plasty, excision) for severe contractures or disfiguring scars. - **Topical scar treatments** (vitamin E, onion extract) have limited evidence but may help some patients. 3. **Psychosocial rehabilitation**: - **Body image disturbance** is common after extensive burns. The patient may grieve the loss of normal appearance and function. Provide counseling, support groups, and psychiatric referral if depression or PTSD develops. - **Return to work and school**: Gradual reintegration. Cosmetic camouflage techniques and clothing can improve confidence. - **Family reintegration**: Support family members who are also traumatized by the burn injury. - **Community resources**: Connect patients with burn survivor support organizations and resources. 4. **Itching and sensory disturbances**: - Itching is common during scar remodeling and can be severe. Manage with **emollients, antihistamines, and cool compresses**. Scratching delays healing and increases infection risk; teach the patient to resist scratching. - Some areas may have **hypersensitivity or numbness** depending on nerve damage. 5. **Monitoring for late complications**: - **Hypertrophic scarring and keloid formation**: More common in darker-skinned individuals and in areas of high tension. - **Joint contractures**: Monitor especially in hand burns (hand function is critical). - **Ectropion or entropion** (eyelid deformities) if facial burns are extensive; may require surgical correction. - **Hair loss** in the burn area due to destruction of hair follicles; permanent hair loss if follicles are destroyed. - **Pigmentation changes**: Hypopigmentation in healed burn areas is common and may gradually improve over months/years. Recommend sun protection.

Managing burns requires knowledge of specific medications used in the emergent, acute, and rehabilitation phases. **Topical Antimicrobials**: **Silver Sulfadiazine (Silvadene)** - Mechanism: Broad-spectrum antibacterial and antifungal; silver ions disrupt bacterial cell membranes and proteins. - Application: Apply 1/16-inch thick layer (about the thickness of a pencil line) once or twice daily after wound cleansing. Cover with a dressing or leave open to air. - Advantages: Painless application, broad-spectrum coverage, inexpensive, non-irritating. - Disadvantages: Can cause **transient leukopenia** (WBC count drops 2–3 days after starting, then recovers)—monitor CBC. Stains skin/clothing blue-gray. - Contraindications: **Sulfonamide allergy**, **pregnancy near term** (crosses placenta, sulfonamides displace bilirubin and cause kernicterus in newborns), **newborns** (especially <2 months old). - Use caution in patients with G6PD deficiency (risk of hemolysis). **Mafenide Acetate (Sulfamylon)** - Mechanism: Broad-spectrum coverage; penetrates eschar (unlike Silvadene, which doesn't penetrate well). - Application: Apply 1/16-inch thick layer once or twice daily; often used under dressing. - Advantages: **Excellent eschar penetration**, useful over cartilage (face, ears, nose) where eschar penetration is critical; allows wound visibility. - Disadvantages: **PAINFUL on application** (patients report burning pain that can last 20–30 minutes). Causes **metabolic acidosis** via inhibition of carbonic anhydrase (can develop within 24–48 hours of use)—monitor serum pH and HCO3. Can cause allergic reactions in sulfa-sensitive patients. - Monitor: Check ABG for metabolic acidosis; if pH <7.3, consider alternative agent or treatment for acidosis. - Contraindications: Same as Silvadene (sulfa allergy, pregnancy, newborns), and AVOID if patient is already acidotic. **Bacitracin** - Mechanism: Broad-spectrum; does not penetrate eschar significantly. - Application: Apply thin layer, often used on the face where visualization is important. - Advantages: Allows visibility, painless, inexpensive. - Disadvantages: No eschar penetration; can cause allergic contact dermatitis. - Best for: Superficial or small burns; face and eyelids (allows assessment of healing). **Antivirals**: **Acyclovir** (for herpes simplex or varicella-zoster (shingles) co-infection) - Mechanism: Inhibits viral DNA polymerase. - Dosing: Depends on indication and renal function; often 5 mg/kg IV Q8H for disseminated infection. - Monitor: Check senal function; accumulates in renal failure. Watch for **crystalline nephropathy** (especially if dehydrated)—ensure adequate hydration. **Systemic Antibiotics**: - **Do NOT use prophylactically**—this promotes resistant organisms. Use only for **documented infection** (positive wound or blood cultures). - Common burn wound pathogens: **Pseudomonas aeruginosa** (green/blue pigment, fruity odor), **Staphylococcus aureus** (including MRSA), **Acinetobacter**, **Klebsiella**, **E. coli**. - Empiric coverage for burn wound infection often includes: - **Fluoroquinolone** (e.g., ciprofloxacin) for gram-negative coverage. - **Beta-lactam** (e.g., piperacillin-tazobactam) for broader coverage. - **Vancomycin** if MRSA is suspected or confirmed. - Adjust antibiotics based on culture sensitivities. **Pain and Sedation**: **Morphine** - Mechanism: Mu-opioid agonist. - Route: **IV only** during emergent/acute phase (IM/SC absorption is unreliable due to peripheral vasoconstriction and edema). - Dosing: Titrate to effect; typically 5–15 mg IV Q4–6H or as continuous infusion. - Advantages: Potent analgesia, available, inexpensive. - Monitor: Watch for respiratory depression, hypotension, itching (opioid-induced), constipation. - Use in combination with anxiolytics and non-pharmacologic measures for dressing changes. **Fentanyl** - Mechanism: Mu-opioid agonist; 100× more potent than morphine. - Route: IV infusion or bolus; transdermal patches (avoid in acute burns—absorption unpredictable due to edema). - Advantages: Rapid onset, potent, less histamine release than morphine. - Monitor: Respiratory depression, hypotension. Risk of dependence with prolonged use. **Midazolam** - Mechanism: Benzodiazepine; anxiolytic and sedative. - Route: IV bolus or infusion. - Dosing: 0.03–0.1 mg/kg IV, can repeat Q5–15min; or infusion 0.5–2 mg/kg/hr. - Use: Often combined with opioids for dressing changes to reduce anxiety and procedural pain. Anterograde amnesia (patient won't remember the painful dressing change). - Monitor: Respiratory depression, hypotension, paradoxical agitation in some patients. - Reversal: Flumazenil (Romazicon) if overdose. **GI Prophylaxis**: **H2 Receptor Blockers (e.g., Ranitidine)** - Mechanism: Decrease gastric acid secretion. - Use: Prevent **Curling's ulcer** (stress-related gastric ulcer in burn patients). - Dosing: Ranitidine 50 mg IV Q6–8H or 300 mg PO BID. - Monitor: Adjust for renal impairment. **Proton Pump Inhibitors (e.g., Omeprazole, Pantoprazole)** - Mechanism: Inhibit gastric H+/K+ ATPase, more potent acid suppression than H2 blockers. - Use: Prevent Curling's ulcer; first-line in many burn centers. - Dosing: Omeprazole 20–40 mg PO QD or pantoprazole 40 mg IV Q12H. - Advantages: More effective than H2 blockers; once-daily dosing convenient. - Monitor: Long-term use may reduce vitamin B12 and magnesium absorption. **Tetanus Prophylaxis**: **Tetanus Toxoid** - Indicated for all burn wounds (considered tetanus-prone). - Dosing depends on prior vaccination history: - If fully vaccinated (3-dose series completed) and last booster <10 years ago: no dose needed. - If fully vaccinated but booster >10 years ago: give 1 dose Td or Tdap. - If incomplete series: complete the series. - If unknown history: assume incomplete and begin series. **Tetanus Immunoglobulin (TIG)** - Give if tetanus-prone wound AND no prior tetanus vaccination (or status unknown and insufficient time to vaccinate). - Dosing: 250–500 units IM or IV depending on wound severity. **Other Medications**: **Vitamins and Minerals** for healing: - **Vitamin C** (ascorbic acid): 500–1,000 mg BID–TID to support collagen synthesis. - **Vitamin A**: 5,000–10,000 IU daily to support epithelialization and immune function. - **Zinc**: 25–50 mg daily to support wound healing and immune function. - **Beta-carotene**: Antioxidant; supports healing. **Insulin** (for hyperglycemia): - Severe burns are hypermetabolic and cause insulin resistance. - Hyperglycemia impairs immune function and wound healing; maintain blood glucose 120–180 mg/dL if possible. - Use insulin infusion to titrate; transitions to SC insulin during rehabilitation phase.

While burns are acute emergencies, many patients present to clinics and hospitals with chronic dermatologic conditions. As an NLE-prepared nurse, you must recognize, manage, and teach about these common disorders. Using the nursing process and NANDA diagnoses, you will provide holistic skin care. **DERMATITIS (ECZEMA)** **Definition and Pathophysiology**: Dermatitis is acute or chronic **inflammation of the skin** causing erythema, pruritus, and scaling. There are several types: - **Contact Dermatitis**: Results from exposure to an irritant (mechanical, chemical, or phototoxic) or an allergen (delayed hypersensitivity reaction, Type IV). - *Irritant contact dermatitis*: From repeated exposure to irritants like soaps, detergents, solvents, water (hands, housewives). - *Allergic contact dermatitis*: From allergens like poison ivy, nickel (jewelry), latex, dyes, adhesives, cosmetics. Reaction develops 24–72 hours after exposure. - **Atopic Dermatitis (Eczema)**: A **chronic inflammatory disorder** strongly associated with genetic predisposition, allergy, and asthma (atopic triad). The skin barrier is defective, leading to dry, itchy, cracked skin prone to infection. **Clinical Presentation**: - Erythema, edema, vesicles (fluid-filled bumps), oozing, crusting (acute phase) - Lichenification (thickened, leathery skin), scaling, hyperpigmentation or hypopigmentation (chronic phase) - Severe **pruritus** (itching), sometimes worse at night, disrupts sleep - Distribution varies by type: - Contact dermatitis: only where exposure occurred (e.g., wrist for nickel watch, hands for chemicals) - Atopic dermatitis: face, hands, feet, flexural surfaces (inside elbows, behind knees), often widespread **Management**: 1. **Identify and avoid triggers** (NLE emphasis on prevention) - Contact dermatitis: Avoid the allergen/irritant. Wear gloves for wet work. Use skin barrier creams. - Atopic dermatitis: Triggers include harsh soaps, low humidity, stress, certain foods; avoid these. 2. **Emollients and moisturizers** (first-line treatment) - Apply immediately after bathing to damp skin to lock in moisture. - Examples: Cetaphil, CeraVe, Eucerin, plain petroleum jelly, coconut oil. - Thick creams/ointments are better than lotions (which contain water and evaporate). 3. **Topical corticosteroids** for acute flares - Potency varies (Class I = ultra-potent, Class VII = least potent). - For mild-to-moderate dermatitis: **hydrocortisone 1% or 2.5%** (Class V–VI). - For more severe dermatitis: **triamcinolone acetonide 0.1%** or stronger (Class II–IV). - Apply 1–2 times daily for 1–2 weeks; then taper as inflammation improves. - Caution: Prolonged use (>2–4 weeks) of potent steroids causes skin atrophy, striae, and telangiectasia; avoid using on face/neck without indication. - For atopic dermatitis, apply to active lesions; then emollients to entire body. 4. **Antihistamines** for itching - **First-generation antihistamines** (diphenhydramine, hydroxyzine): Sedating; useful if itching disrupts sleep. Give at bedtime. - **Second-generation antihistamines** (cetirizine, loratadine): Non-sedating; useful for daytime. - Topical antihistamine creams have limited efficacy. 5. **Systemic corticosteroids** (for severe cases only) - Oral prednisone (0.5–1 mg/kg/day, tapering over 1–2 weeks) if dermatitis is severe and widespread. - Short-term use only to avoid adrenal suppression and other side effects. 6. **Newer agents** for moderate-to-severe atopic dermatitis - **Topical calcineurin inhibitors** (tacrolimus, pimecrolimus): Non-steroidal; prevent skin atrophy. Used for face/sensitive areas. - **PDE4 inhibitors** (crisaborole): Topical; new agent for atopic dermatitis. - **Systemic immunosuppressants** (cyclosporine, azathioprine) for severe refractory cases. 7. **Phototherapy** - UVB phototherapy for widespread atopic dermatitis. - PUVA (psoralen + UVA) in some cases. 8. **Infection prevention** (critical nursing role) - Teach patient: **Avoid scratching** (breaks skin, invites bacterial infection). Trim nails short. Wear soft cotton gloves at night if scratching is severe. - Watch for signs of secondary **bacterial infection** (Staphylococcus aureus, Streptococcus): pustules, honey-colored crusts, fever, lymphadenitis. Treat with oral antibiotics (cephalexin, dicloxacillin, or topical mupirocin). **Nursing Diagnoses (NANDA)**: - **Impaired skin integrity** (r/t inflammation and broken skin) - **Acute pain/chronic pain** (r/t pruritus) - **Deficient knowledge** (r/t skin care and trigger avoidance) - **Risk for infection** (r/t scratching and broken skin) **Patient Teaching** (RA 9173 emphasis on health promotion): - Moisturize twice daily; use lukewarm water (not hot) for bathing. - Avoid harsh soaps; use fragrance-free, pH-balanced cleansers. - Identify and avoid personal triggers. - Treat flares promptly to prevent severe exacerbations. - Dermatitis is manageable but often lifelong; stress management and sleep help. **PSORIASIS** **Definition and Pathophysiology**: Psoriasis is a **chronic autoimmune inflammatory disorder** of the skin caused by accelerated epidermal cell turnover and T-cell-mediated inflammation. Genetic predisposition and environmental triggers (stress, infection, medications, trauma) precipitate flares. The condition is **NOT contagious**. **Clinical Presentation** (Classic features for NLE): - **Well-demarcated, raised, erythematous plaques** (sharply defined borders) - **Silvery-white micaceous (mica-like) scale** on the surface (most characteristic finding) - Common sites: **extensor surfaces** (elbows, knees, shins), **scalp** (thick white scale), **sacrum**, hands, feet - Auspitz sign: Remove scale and pinpoint bleeding occurs (due to thin suprapapillary epidermis) - Köbner phenomenon: Lesions appear at sites of trauma (scratches, surgical scars) - May have **nail involvement**: pitting, onycholysis (nail lifting), thickening - May have **arthritis** (psoriatic arthritis) affecting small joints, spine - Usually **NOT pruritic** (unlike dermatitis), though some patients itch - Severity ranges from limited plaques to erythroderma (>90% body surface involved; medical emergency due to fluid loss and thermoregulation failure) **Triggers**: - Stress (most common trigger for exacerbation) - Infection (streptococcal pharyngitis, HIV) - Medications (beta-blockers, NSAIDs, lithium, ACE inhibitors, antimalarials) - Trauma (Köbner phenomenon) - Climate changes (cold, dry weather often worsens) - Alcohol, smoking **Management**: 1. **Topical treatments** (first-line for limited psoriasis) - **Potent topical corticosteroids** (clobetasol propionate 0.05%, flucinonide): For plaques on body. Apply BID for 2–4 weeks; then taper. Avoid face/intertriginous areas (risk of atrophy). - **Vitamin D analogues** (calcipotriene cream/ointment): Effective for plaques; slow-acting (2–4 weeks for benefit). Apply BID. Can cause skin irritation; mix with corticosteroid to reduce irritation and improve efficacy. - **Retinoids** (tretinoin, tazarotene): Promote cell differentiation. Tazarotene 0.05–0.1% cream BID for plaques; teratogenic (avoid in pregnancy). - **Coal tar**: Traditional, inexpensive; smells bad, stains clothing. Apply at bedtime. Less popular now due to newer options. - **Anthralin (dithranol)**: Reduce inflammation and scaling. Can irritate skin; apply to plaques only, start low strength. - **Salicylic acid**: Helps remove scale; often combined with other agents. - **Emollients**: Keep skin hydrated; moisturize generously. 2. **Systemic treatments** (for moderate-to-severe psoriasis) - **Phototherapy** - UVB (narrowband, 311 nm preferred): 2–3 times/week for 8–12 weeks. Effective and relatively safe. - PUVA (psoralen + UVA): Oral psoralen, then UVA exposure. More effective than UVB but higher risk of photoaging and skin cancer (monitor for melanoma). - **Conventional systemic agents** (for widespread, severe psoriasis) - **Methotrexate**: Immunosuppressant; first-line systemic agent. Dosing 10–25 mg PO weekly or SC. Monitor CBC, LFTs, renal function (hepatotoxicity, bone marrow suppression). Teratogenic; avoid in pregnancy. Takes 4–8 weeks for benefit. - **Cyclosporine**: Immunosuppressant. Effective but can cause hypertension, renal dysfunction; monitor BP and creatinine. - **Acitretin** (retinoid): 25–50 mg daily for severe plaque psoriasis. Teratogenic; contraindicated in pregnancy. Monitor lipids and LFTs. - **Biologics** (TNF-α inhibitors, IL inhibitors): Highly effective for moderate-to-severe psoriasis - **TNF-α inhibitors**: Infliximab, etanercept, adalimumab. Reduce TNF-α, a key cytokine in psoriatic inflammation. - **IL-17 inhibitors**: Secukinumab, ixekizumab. Target IL-17, key driver of psoriasis. - **IL-23 inhibitors**: Risankizumab, guselkumab. Target IL-23. - Advantages: Very effective, rapid onset of action. - Monitoring: Risk of infections (TB reactivation for TNF inhibitors); screen for TB, hepatitis B before starting. Regular monitoring for opportunistic infections, monitor CBC. 3. **Treatment of triggers** - **Stress management**: Exercise, meditation, counseling, yoga, art therapy - **Infection treatment**: Treat strep throat promptly (start antibiotics) - **Medication review**: Change medications that worsen psoriasis (e.g., switch beta-blocker to another class) - **Lifestyle**: Stop smoking, limit alcohol, protect skin from trauma 4. **Special situations** - **Scalp psoriasis**: Use medicated shampoos (ketoconazole, zinc pyrithione, coal tar), topical corticosteroid lotions/solutions, vitamin D analogue solutions. Scalp psoriasis is notoriously difficult to treat. - **Psoriasis in skin folds (intertriginous)**: Use low-potency topical steroids (hydrocortisone 1%) to avoid atrophy. Calcineurin inhibitors are also safe here. - **Nail psoriasis**: Difficult to treat. Intralesional corticosteroids, topical agents, or systemic therapy if severe. - **Psoriatic arthritis**: NSAID or biologic therapy (TNF inhibitors, IL-17 inhibitors particularly effective). **Nursing Diagnoses (NANDA)**: - **Disturbed body image** (r/t visible lesions and chronic nature of disease) - **Deficient knowledge** (r/t disease process, triggers, and management) - **Risk for infection** (r/t open skin lesions and immunosuppressive therapy) - **Ineffective coping** (r/t chronic disease and psychosocial burden) **Patient Teaching** (NLE emphasis): - **Psoriasis is a lifelong condition with a remitting-relapsing course**; it is not curable, but highly manageable. - **NOT contagious**—assure patient and family. - Identify personal triggers (stress, infections, medications) and avoid when possible. - Stress management (exercise, meditation, support groups) is critical. - Adhere to prescribed topical and systemic treatments; benefits take weeks to appear. - Protect skin from trauma (Köbner phenomenon). - Moisturize regularly; avoid harsh soaps. - Seek treatment for systemic agents (methotrexate, biologics) requires regular lab monitoring; comply with monitoring. - Watch for signs of infection if on immunosuppressive therapy; report fever, cough, or other symptoms. - Sunlight may help (UVB), but avoid sunburn. - Join psoriasis support groups (normalize the experience, reduce isolation). **CELLULITIS** **Definition and Pathophysiology**: Cellulitis is an acute **bacterial infection of the dermis and subcutaneous tissues**, typically unilateral. It commonly results from **Streptococcus pyogenes** (Group A Streptococcus, GAS) or **Staphylococcus aureus** (including methicillin-resistant S. aureus, MRSA). The bacteria enter through a break in the skin (abrasion, cut, insect bite, ulcer, athlete's foot, surgical wound, or compromised skin integrity from dermatitis, edema, or venous insufficiency). **Clinical Presentation**: - **Localized erythema** (redness) with **poorly defined, diffuse borders** (unlike cellulitis, abscess has a well-demarcated central area and may fluctuate) - **Warmth** to palpation - **Edema** (swelling) - **Tenderness** to touch/palpation - Sometimes **systemic signs**: fever (>38.5°C), chills, malaise - **Lymphangitic streaking**: Red line extending from the infected area toward regional lymph nodes (indicates lymphatic involvement; sign of spreading infection) - **Regional lymphadenopathy**: Tender, enlarged lymph nodes draining the infected area - **Rapid progression** over 24–48 hours if untreated **Diagnosis**: - Clinical diagnosis based on presentation; cultures are NOT routinely obtained (cellulitis is not localized like abscess) - If systemic signs or rapid progression: **blood culture** (may grow organism) - **CBC**: WBC may be elevated (left shift indicates bacterial infection) - Ultrasound or MRI if diagnostic uncertainty (to rule out necrotizing fasciitis, abscess) **Risk Factors**: - **Diabetes mellitus** (impaired wound healing and immune function) - **Venous insufficiency** or **lymphedema** (impaired drainage) - **Skin barrier compromise**: dermatitis, fungal infection, trauma, surgical wound - **Immunosuppression**: HIV, chemotherapy, corticosteroids, organ transplant - **Extremes of age**: Young children, elderly - **Obesity** - **Previous cellulitis** (recurrence common) **Management**: 1. **Systemic antibiotics** (essential; IV for severe cases) - **Mild-to-moderate cellulitis** (outpatient, no systemic toxicity): - **Cephalexin** 500 mg PO QID for 7–10 days (covers GAS and non-MRSA Staph) - **Amoxicillin-clavulanate** (Augmentin) 500/125 mg PO TID for 7–10 days - **Dicloxacillin** 500 mg PO QID for 7–10 days - If **MRSA suspected/known**: **Trimethoprim-sulfamethoxazole (TMP-SMX)** 1–2 DS tablets PO BID or **doxycycline** 100 mg PO BID - **Severe cellulitis** (IV antibiotics, hospitalization if indicated): - **Cefazolin** 1–2 g IV Q6–8H (covers GAS and non-MRSA Staph) - **Cloxacillin** 1–2 g IV Q4–6H (similar spectrum) - If **MRSA suspected/confirmed**: **Vancomycin** 15–20 mg/kg IV Q8–12H (adjust for renal function) or **clindamycin** 600 mg IV Q6H - **Rapidly progressive or concerning features** (fever >39°C, rapid progression, immunocompromised): Hospitalize and start IV antibiotics. Consider necrotizing fasciitis (medical emergency). 2. **Supportive care** - **Elevation** of the affected limb above the heart (reduces edema, improves drainage) - **Warm compresses** to the area (promotes comfort and drainage) - **Analgesia** as needed (acetaminophen, NSAIDs, or stronger agents if severe) - **Rest**: Limit activity; ambulation on affected leg increases pain and swelling - Remove any **constrictive items** (tight clothing, jewelry, casts) that impair circulation 3. **Monitoring for progression and complications** - **Mark the borders** of erythema with a pen at initial visit (helps assess whether infection is spreading or resolving at follow-up) - **Follow-up assessment** in 24–48 hours; if erythema has spread beyond marked border, escalate treatment (consider IV antibiotics, imaging, hospitalization) - Watch for signs of **systemic spread**: fever, rising WBC, malaise, hypotension (progression to sepsis) - Watch for signs of **necrotizing fasciitis** (medical emergency): Severe pain out of proportion to skin findings, crepitus (gas in tissues), skin blistering/blackening, rapid progression, shock—requires immediate surgical consultation and debridement - Monitor for **compartment syndrome** (if cellulitis is circumferential or in a closed space): Pain with passive stretch of muscles in the compartment is an early sign; compartment pressure measurement may be needed; fasciotomy may be required - Watch for **abscess formation**: If a central area becomes fluctuant, drainage or incision and drainage (I&D) may be needed 4. **Identify and treat the source** - Look for the break in skin that allowed bacterial entry: abrasion, blister, surgical wound, dermatitis, fungal infection, ulcer - Treat underlying conditions (fungal infections, dermatitis, venous insufficiency) to prevent recurrence - Ensure **tetanus status** is current **Nursing Diagnoses (NANDA)**: - **Hyperthermia** (r/t bacterial infection and inflammatory response) - **Acute pain** (r/t inflammation and edema) - **Impaired skin integrity** (r/t infection and inflammation) - **Risk for infection spread** (r/t cellulitis) - **Deficient knowledge** (r/t antibiotic adherence, when to seek care) **Patient Teaching** (RA 9173 emphasis on prevention and management): - **Complete the full course of antibiotics** even if symptoms improve (incomplete treatment can lead to recurrence or resistance) - **Elevate the affected limb** above heart level to reduce swelling - Apply warm compresses for comfort - **Return immediately if**: Redness spreads, fever increases, new blisters or blackening appear, severe pain develops, or swelling worsens (signs of progression or necrotizing fasciitis) - **Prevent future cellulitis**: Keep skin clean and dry, moisturize to prevent cracks, treat any cuts/abrasions promptly, avoid walking barefoot if prone to athlete's foot, manage conditions like diabetes and venous insufficiency, and treat fungal/dermatologic conditions - **Proper foot care if diabetic** or if cellulitis is on the leg (inspect feet daily, keep clean and dry, wear proper footwear) - If recurrent cellulitis: Long-term low-dose antibiotic prophylaxis may be considered **HERPES ZOSTER (SHINGLES)** **Definition and Pathophysiology**: Herpes zoster (shingles) is **reactivation of latent varicella-zoster virus (VZV)** from the dorsal root ganglia, causing a painful vesicular rash in a **dermatomal distribution** (one or more dermatomes, typically unilateral). The virus lies dormant after primary varicella (chickenpox) infection and reactivates when immunity wanes (age, immunosuppression, stress, trauma). **Clinical Presentation** (prodrome → rash): - **Prodrome** (24–72 hours before rash): Burning, itching, or shooting pain in the affected dermatome; sometimes fever, malaise, headache - **Rash**: Begins as **erythematous macules** → **papules** → **clear vesicles on erythematous base** (fluid-filled blisters), described as "dew drops on rose petals" - **Distribution**: Follows a **single dermatome** (unilateral), commonly thoracic (chest) but can be cervical, lumbar, sacral, ophthalmic (V1 distribution—risk of eye involvement), facial (facial nerve, Ramsay Hunt syndrome if ear/facial involvement) - **Severity and spread**: Vesicles appear in crops over 3–5 days; new crops appear as older ones crust over - **Pain**: Severe **neuropathic pain** (burning, shooting), worse at night; may be more intense than the cutaneous findings - **Healing**: Crusts form within 7–10 days; heals in 2–4 weeks; leaves post-inflammatory hyperpigmentation (usually resolves in weeks to months) **Complications**: - **Post-herpetic neuralgia (PHN)**: Persistent pain after rash heals (most common complication, especially in elderly >60 years); can last months to years; very difficult to treat - **Secondary bacterial infection**: If patient scratches or breaks blisters - **Disseminated zoster**: VZV spreads beyond one or few dermatomes (suggests immunocompromise; concerning) - **Ophthalmic zoster** (V1): Risk of **corneal scarring, uveitis, vision loss**; requires ophthalmology referral - **Facial nerve involvement** (Ramsay Hunt syndrome): Facial paralysis, ear vesicles, hearing loss - **Meningitis or encephalitis**: Rare but serious **Management**: 1. **Antiviral therapy** (most important; started early for better outcomes) - **Acyclovir** 800 mg PO 5 times/day for 7–10 days (or 10–15 mg/kg IV Q8H if severe, disseminated, or immunocompromised) - **Valacyclovir** 1000 mg PO TID for 7 days (better bioavailability than acyclovir; more convenient) - **Famciclovir** 500 mg PO TID for 7 days (also good bioavailability) - **Efficacy**: Most effective if started within 72 hours of rash onset; reduces duration and severity of pain, decreases risk of PHN if given early - **Monitoring**: Check renal function; acyclovir can cause crystalline nephropathy (especially in dehydrated patients, elderly). Ensure adequate hydration. 2. **Pain management** (critical because pain can be severe) - **Acute neuropathic pain**: - **Topical agents**: Capsaicin cream (0.075%) applied 3–4 times daily to affected areas (depletes substance P; may help pain); **lidocaine patch** (5%) applied to affected area up to 12 hr/day (provides local anesthesia); **menthol** for cooling relief - **Systemic agents**: - **NSAIDs** (ibuprofen, naproxen) for 1–2 weeks during acute phase - **Opioids** (codeine, tramadol, morphine) if severe pain; titrate to effect; watch for dependence with prolonged use - **Adjuvant agents**: **Gabapentin** 300–3600 mg daily in divided doses (proven for neuropathic pain) or **pregabalin**; take 1–2 weeks to reach benefit - **Post-herpetic neuralgia** (if pain persists >1 month after rash heals): - **First-line**: Gabapentin or pregabalin (most evidence) - **Second-line**: **Tricyclic antidepressants** (amitriptyline 25–75 mg at bedtime) for neuropathic pain and sleep benefit - **Topical**: Lidocaine patch or capsaicin cream - **Specialized**: **Nerve blocks**, **transcutaneous electrical nerve stimulation (TENS)**, or **spinal cord stimulation** for severe refractory PHN 3. **Supportive care** - Keep lesions clean; avoid rupturing vesicles (risk of secondary infection) - **Loose, soft clothing** to avoid irritation - **Cool compresses** for comfort - **Elevation** if on extremity (reduces edema) - **Anti-itch measures**: **Antihistamines** (diphenhydramine, hydroxyzine), **cool baths** 4. **Infection control** (especially important in healthcare settings and around immunocompromised persons) - **Immunocompetent patients**: No special precautions needed (immunized persons are not at risk; non-immune children could contract varicella from exposure to vesicular fluid) - **Disseminated or severe immunocompromised zoster**: **Airborne and contact precautions** (zoster is less contagious than varicella, but disseminated zoster can transmit VZV) - **Avoid contact** with non-immune pregnant women (risk of congenital varicella), non-immune immunocompromised patients, and newborns 5. **Prevention of recurrence: Varicella-zoster vaccine** - **Recombinant zoster vaccine (RZV, Shingrix)**: Two doses, 2–6 months apart; efficacy >90% at preventing zoster and PHN; recommended for immunocompetent adults ≥50 years - **Live attenuated vaccine (Zostavax, mostly phased out)**: Single dose; older, less effective (~50–60%) but still available - **Post-zoster vaccination**: Can be given after zoster resolves (ideally 12 months later for recombinant vaccine) **Nursing Diagnoses (NANDA)**: - **Acute pain** (r/t herpetic inflammation and neuropathic pain) - **Chronic pain** (r/t post-herpetic neuralgia if applicable) - **Risk for infection** (r/t open vesicles) - **Deficient knowledge** (r/t antiviral therapy, prevention, and when to seek care) - **Social isolation** (r/t discomfort and infection control concerns) **Patient Teaching** (NLE emphasis): - **Take antivirals within 72 hours of rash onset** for best results; early treatment reduces pain duration and risk of PHN - Do **NOT scratch or rupture vesicles** (risk of secondary bacterial infection and scarring) - **Pain may persist after the rash heals** (post-herpetic neuralgia); early aggressive pain management helps prevent PHN - **Avoid contact** with people who have never had chickenpox and are not vaccinated (they could contract varicella) - **Avoid contact with immunocompromised persons** until vesicles have crusted over - **Watch for signs of complications**: Eye involvement (zoster ophthalmicus—seek ophthalmology evaluation immediately), facial paralysis (Ramsay Hunt—urgent evaluation), vision changes, severe headache, or stiff neck (meningitis—emergency) - **Get vaccinated** after zoster heals to reduce risk of recurrence (ask provider when safe to vaccinate) - **Pain management is important**: Use topical agents, systemic analgesics, and adjuvant drugs (gabapentin) as prescribed **OTHER SKIN INFECTIONS** **Impetigo** - **Definition**: Superficial bacterial skin infection, highly contagious, most common in children 2–5 years - **Causative organism**: Usually **Streptococcus pyogenes** (GAS) or **Staphylococcus aureus** (MRSA increasing) - **Clinical features**: **Honey-colored crusts** on intact or eroded skin, often on face, neck, extremities; may have minimal surrounding erythema - **Transmission**: Direct contact (skin-to-skin, through contaminated objects) - **Management**: - **Topical**: Mupirocin (Bactroban) ointment TID for localized impetigo (small, few lesions) - **Systemic**: Oral antibiotics for multiple lesions or if systemic signs: Cephalexin 500 mg QID, amoxicillin-clavulanate, or dicloxacillin for 7–10 days. If MRSA suspected: TMP-SMX or doxycycline - **Hygiene**: Gentle cleansing, non-adherent dressings, avoid scratching (prevents spread) - **Infection control**: Exclude from school/daycare until 24 hours of antibiotics completed and lesions are covered **Fungal Infections (Tinea, Candidiasis)** - **Tinea (Dermatophyte infections)** - Examples: Tinea pedis (athlete's foot), tinea corporis (ringworm), tinea cruris (jock itch), tinea capitis (scalp ringworm) - Features: Circular or annular (ring-shaped) lesions with central clearing, scaling, sometimes erythema; may be pruritic - Management: **Topical antifungals** (azoles like miconazole, clotrimazole; allylamines like terbinafine; benzyl alcohol) BID for 2–4 weeks. **Systemic antifungals** (terbinafine, fluconazole, griseofulvin) if extensive or unresponsive to topical therapy. - Prevention: Keep area dry (dry feet after bathing, between toes), wear breathable shoes/socks, avoid walking barefoot in public areas - **Candidiasis (Yeast infection)** - Most common is **Candida albicans** - Sites: Oral (thrush—white patches on tongue/mouth), vaginal (white discharge, itching, burning), skin folds (warm, moist areas) - Features: Erythema, maceration (white softened skin), sometimes pustules at borders - Risk factors: Diabetes, antibiotic use, immunosuppression, prolonged moisture - Management: **Topical antifungals** (miconazole, clotrimazole cream) BID for 1–2 weeks. **Systemic** (fluconazole, itraconazole) if extensive or resistant to topical therapy. - Prevention: Keep area dry, wear moisture-wicking underwear, avoid prolonged antibiotic use if possible (alters normal flora) **Bacterial Skin Infections Summary** | Condition | Organism | Features | Treatment | |-----------|----------|----------|----------| | Impetigo | GAS, MRSA | Honey-colored crusts, highly contagious | Topical mupirocin or systemic antibiotics | | Cellulitis | GAS, Staph | Diffuse erythema, poorly defined borders, systemic signs possible | Systemic antibiotics (oral or IV), elevation, warm compresses | | Abscess | Staph, GAS | Localized collection of pus, fluctuant central area, well-demarcated | Incision and drainage, systemic antibiotics if spreading | | Erysipelas | GAS | Sharply demarcated erythema, often facial, raised borders | Systemic antibiotics (penicillin-based) | **Viral Skin Infections Summary** | Condition | Virus | Features | Treatment | |-----------|-------|----------|----------| | Herpes simplex | HSV-1 or HSV-2 | Vesicular rash, often oral or genital, recurrent | Antivirals (acyclovir, valacyclovir) | | Herpes zoster | VZV | Dermatomal vesicular rash, one-sided, painful | Antivirals, analgesics, prevention with vaccine | | Warts | HPV | Hyperkeratotic papules, usually hands/feet | Salicylic acid, cryotherapy, laser, imiquimod | | Molluscum contagiosum | Molluscipoxvirus | Firm papules with central umbilication, contagious | Usually self-limited; topical treatments or removal if cosmetic concern | **Fungal Infections Summary** | Type | Common Sites | Organism | Features | Treatment | |------|--------------|----------|----------|----------| | Tinea pedis | Feet (spaces between toes) | Dermatophytes (T. rubrum) | Scaling, erythema, maceration, pruritis | Topical antifungals; systemic if extensive | | Tinea corporis | Body (arms, legs, trunk) | Dermatophytes | Ring-shaped (annular) lesions with central clearing | Topical antifungals; systemic if extensive | | Tinea capitis | Scalp | Dermatophytes (M. canis, T. tonsurans) | Scaling, patches of hair loss, may have purulent drainage | Systemic antifungals (terbinafine, griseofulvin) + topical shampoo | | Candidiasis | Oral, vaginal, skin folds | Candida albicans | Erythema, maceration, white patches (oral) or discharge (vaginal) | Topical azoles; systemic if extensive or resistant |

Burns and dermatologic disorders can lead to serious, life-threatening complications. As an NLE-prepared nurse, you must recognize early signs and intervene promptly. **BURN COMPLICATIONS** **Early (Emergent Phase) Complications**: 1. **Hypovolemic (Burn) Shock** - **Pathophysiology**: Massive third-spacing and fluid loss cause intravascular volume depletion. - **Signs**: Tachycardia, tachypnea, hypotension, altered mental status (confusion, agitation), weak peripheral pulses, cool extremities, oliguria (urine output <0.5 mL/kg/hr) - **Prevention/Management**: Aggressive fluid resuscitation per Parkland formula, monitoring urine output, IV access, vasopressors if hypotensive despite adequate fluids (suggests complications like sepsis or inhalation injury) 2. **Airway Obstruction and Inhalation Injury** - **Mechanisms**: - Direct thermal injury to upper airway (rare from hot air alone; water vapor causes more injury) - Inhalation of toxic gases (carbon monoxide, hydrogen cyanide, ammonia, aldehydes) from combustion - Laryngeal and pharyngeal edema from heat and inflammation - Smoke inhalation causing lower airway damage, bronchospasm, and pulmonary edema - **Signs of airway compromise**: Hoarseness, stridor, dyspnea, singed nasal hairs, carbonaceous sputum, facial burns, speaking in single words (tripod positioning) - **Early intervention**: Provide 100% humidified O₂, prepare for intubation, intubate early if signs of edema (do NOT delay—airway can close rapidly). Consider fiberoptic scope to assess airway. - **Complications**: Acute respiratory distress syndrome (ARDS), pulmonary edema, infection 3. **Cardiac Dysrhythmias** (especially with electrical burns) - **Pathophysiology**: Direct myocardial injury, hyperkalemia, acidosis, hypovolemia - **Dysrhythmias**: Ventricular fibrillation, asystole, PVCs, bradycardia - **Monitoring**: Continuous ECG for all electrical burn patients; frequent potassium checks - **Management**: ACLS, correct hyperkalemia, maintain euvolemia 4. **Compartment Syndrome** - **Pathophysiology**: Circumferential burn or deep burn causes edema within a confined fascial compartment, raising intracompartmental pressure and compromising circulation and tissue perfusion - **Signs** (pain out of proportion, 5 P's): **Pain** with passive stretch of muscles in the compartment (earliest, most sensitive sign), **Paresthesias** (tingling, numbness), **Pallor**, **Pulselessness**, **Paralysis** (late) - **Sites at risk**: Forearm, leg, hand, foot, trunk (especially chest with circumferential burns) - **Diagnosis**: Clinical (pain with passive stretch); confirm with compartment pressure measurement (>30 mmHg or within 30 mmHg of diastolic BP is concerning) - **Emergency management**: **Escharotomy** (surgical incision through the burned tissue to relieve constriction and allow fascial expansion) or **fasciotomy** (incision into the fascia itself). Delay increases risk of tissue necrosis and loss of limb. - **Nursing**: Monitor distal circulation (pulses, color, temperature, capillary refill), check for compartment syndrome signs hourly in first 48 hours **Mid-Phase (Acute Phase) Complications**: 5. **Infection and Sepsis** - **Pathophysiology**: Destroyed skin barrier loses protective function; burn wound becomes colonized with bacteria (especially gram-negatives like Pseudomonas and Acinetobacter, and Staphylococcus aureus/MRSA); progression to invasive infection and systemic sepsis - **Risk factors**: >20% TBSA, deep burns, immunosuppression, inhalation injury, prolonged hospitalization, central lines - **Signs of burn wound infection**: - Cellulitis beyond the burn margin (erythema, edema, warmth spreading into unburned skin) - **Change in wound appearance**: Black or violaceous eschar (vs. tan/white baseline), rapid eschar separation, hemorrhagic sublesions (suggest invasive infection) - Purulent drainage with odor - Eschar comes off prematurely - **Signs of sepsis in burn patients** (often subtle): - **Altered mental status** (often first sign in burns) - **Temperature instability** (fever OR hypothermia; temperature swings suggest sepsis) - **Ileus** (abdominal distention, absent bowel sounds, vomiting) - **Hyperglycemia** (even in non-diabetics; glucose >150 mg/dL in a non-diabetic suggests infection/stress) - Tachycardia, tachypnea, hypotension (later signs) - **Thrombocytopenia** (drop in platelet count) - **Diagnosis**: Blood cultures (positive culture = sepsis), wound swab culture (rapid identification), CBC (WBC elevated or decreased), lactate (elevated in sepsis), procalcitonin (elevated if bacterial infection) - **Management**: - **Aggressive wound debridement** (removes colonized tissue, reduces bacterial load) - **Topical antimicrobials** (Silvadene, Mafenide, bacitracin, mupirocin) - **Systemic antibiotics ONLY for documented infection** (do NOT use prophylactically). Empiric antibiotics for sepsis: Piperacillin-tazobactam or imipenem (broad gram-negative coverage) + vancomycin (gram-positive/MRSA coverage). Adjust based on cultures. - **Supportive care**: Fluid resuscitation, vasopressors if septic shock, nutritional support, infection control measures - **Prevention**: Strict asepsis, protective isolation for extensive burns, early wound coverage (grafting), nutritional support, early mobilization 6. **Acute Kidney Injury (AKI)** - **Pathophysiology**: - **Hypovolemic AKI**: Inadequate fluid resuscitation causes renal hypoperfusion and acute tubular necrosis - **Myoglobinuric AKI**: In electrical burns or crush injuries, rhabdomyolysis releases myoglobin → dark urine (myoglobinuria) → myoglobin precipitates in renal tubules → acute tubular necrosis - **Direct thermal injury to kidneys** (rare from thermal exposure alone) - **Signs**: Oliguria (urine output <0.5 mL/kg/hr), dark or cola-colored urine (myoglobinuria), rising BUN and creatinine, hyperkalemia (muscle breakdown releases potassium) - **Prevention/Management**: - **Adequate fluid resuscitation** with target urine output - **For myoglobinuria**: Target urine output 200–300 mL/hr (aggressive hydration to flush myoglobin), **urinary alkalinization** (sodium bicarbonate 50 mEq added to first IV bag, target urine pH >6.5; alkaline urine prevents myoglobin precipitation) - **Monitoring**: Urinalysis (myoglobin), serum creatinine, BUN, potassium, urine color, hourly urine output - **Treat hyperkalemia** (peaked T waves on ECG) with **calcium gluconate (cardiac stabilization), insulin + dextrose, sodium bicarbonate, beta-agonists, kayexalate, or dialysis if severe** - **Dialysis** may be needed if severe AKI with anuria 7. **Curling's Ulcer (Stress-Related Acute Gastritis/Ulcer)** - **Pathophysiology**: Severe stress from burn injury causes increased gastric acid and decreased mucosal protective mechanisms, leading to acute gastric ulceration - **Signs**: GI bleeding (hematemesis, melena), abdominal pain - **Prevention**: **Prophylactic H2 blockers or PPI** (must be given to ALL burn patients with >20% TBSA in the emergent phase) - **Management**: Continue prophylaxis, maintain NPO status until bowel sounds return, early enteral nutrition (protective), transfusion if significant GI bleeding 8. **Paralytic Ileus** - **Pathophysiology**: Severe burns cause sympathetic activation and inflammatory mediator release, impairing GI motility - **Signs**: Abdominal distention, absent or diminished bowel sounds, vomiting/nausea, constipation - **Management**: Keep NPO until ileus resolves (bowel sounds return), NG tube decompression if distended, early enteral nutrition (helps restore motility), avoid narcotics (worsen ileus; use non-opioid pain control if possible), mobilization **Late (Rehabilitation Phase) Complications**: 9. **Contractures** - **Pathophysiology**: Scar tissue contracts, shortening across joints and limiting range of motion - **Sites**: Most common in flexor surfaces (fingers, wrists, elbows, neck, knees, ankles) - **Impact**: Loss of function, disfigurement, inability to perform ADLs (e.g., contracture of fingers prevents gripping) - **Prevention** (THE MOST IMPORTANT STRATEGY): Early and aggressive positioning in extension, splinting, active ROM exercise starting in acute phase. Prevention is far superior to treatment. - **Management of existing contracture**: Serial splinting, aggressive PT (ROM), pressure garments, surgical release/Z-plasty if severe - **Nursing role**: Position joints in extension from day 1, apply splints, encourage PT compliance, educate patient on importance of exercises 10. **Hypertrophic Scarring** - **Pathophysiology**: Excessive collagen deposition and myofibroblast activity during wound remodeling - **Features**: Raised, red, thick, inelastic scar; may be itchy and restrict movement - **Risk factors**: Healing delayed >2–3 weeks (indicates deeper burn), darker skin types, location (joint areas, anterior chest) - **Prevention/Management**: Pressure garments (23 hrs/day, wears 6–24 months), silicone gel sheets, laser therapy (pulsed dye laser for vascularity), topical treatments (vitamin E, onion extract—limited evidence), scar massage, sun protection (UVA/UVB blockade) - **Timeline**: Scars continue to remodel for 12–24 months; patience and adherence to therapy are essential 11. **Other Late Complications**: - **Ectropion/Entropion** (eyelid deformities if facial burns): Surgical correction - **Contractures of eyelids**: Risk of corneal exposure and ulceration - **Alopecia** (hair loss): Permanent if hair follicles destroyed - **Pigmentation changes**: Hypopigmentation (very common in healed scars), hyperpigmentation; gradual improvement over months/years - **Psychological trauma**: PTSD, depression, anxiety, body image disturbance; address with counseling, support groups **DERMATOLOGIC COMPLICATIONS** 1. **Secondary Bacterial Infection** (especially with dermatitis, psoriasis, other inflammatory skin conditions) - **Mechanism**: Broken skin barrier from scratching, exudate, or inflammation allows bacterial colonization - **Common organisms**: Staphylococcus aureus, Streptococcus pyogenes - **Signs**: Pustules, purulent drainage, crusting, fever, lymphangitis - **Management**: Systemic antibiotics, topical antimicrobial (mupirocin), wound care, prevent scratching 2. **Spread/Dissemination** (cellulitis → necrotizing fasciitis; localized infection → systemic sepsis) - **Necrotizing fasciitis**: Medical emergency; rapidly progressive; requires immediate surgical consultation and debridement - **Prevention**: Timely antibiotic therapy, early recognition, aggressive wound care 3. **Abscess Formation** - **In cellulitis**: If not treated promptly, may localize and form a collection of pus (fluctuant area) - **Management**: Incision and drainage (I&D), systemic antibiotics 4. **Chronic/Recurrent Infections** - **Recurrent cellulitis**: Risk factors (diabetes, venous insufficiency, lymphedema); may require long-term low-dose antibiotic prophylaxis - **Chronic fungal infections**: Poor compliance, persistent moisture, immunosuppression; requires addressing underlying factors