Lesson 9: Wounds Caused By Disease Process Flashcards
Viral Lesions
Painful vesicular rash with progression to discrete shallow ulcers
- Herpes simplex: oral + perianal lesions
- Herpes zoster: lesions follow path of dermatome and is unilateral
Diagnostic
- Viral culture of wet lesions
Treatment
- Antiviral agents
Topical options
- Need to protect nerve endings, absorb drainage, and prevent trauma
- Silicone adhesive foam
- Glycerin-based gels
- Zinc oxide-based ointments
Fungal Lesions
Maculopapular rash with solid center which thins at periphery with distinct satellite lesions
- Itchy and tender
Diagnostics
- Based on clinical findings
- Definitive: skin scrapings and stain under microscope
Treatment
- Systemic is multiple sites of infection
- Ketoconazole or fluconazole
- Topical options
— Azole and nystatin for 14 days
— Cream/ointment vs powder (based on affected areas)
— Burrow’s solution if rash is itchy
Tinea Lesions
- Fungal infection like ringworm or jock itch
- Rash intense at periphery and clears towards center
Diagnostics
- Clinical presentation and skin scrapings
Treatment
- Azole products +/- systemic supports
Folliculitis
Pustular lesions caused by damage to hair follicle +/- obstruction of sweat gland
Treatment
- Atraumatic hair removal
- Cleansing with antibacterial soap
- Topical antibiotics prn
Cellulitis
Invasive infection of the dermis and subcutaneous tissue
- Caused by staph or strep
Sign/symptoms
- Pain
- Edema
- Erythema
- Induration
- Vesicle/bulla formation
lymphedema
Treatment
- Systemic antibiotics
- Topical antibiotics only if wound is open/unroofed
- If not, moist wound healing
CA-MRSA
Community-acquired MRSA (genetically different than hospital MRSA)
- Contagious and spreads easily
- Daycares, gyms, locker rooms, prisons, etc
- Can escalate to pneumonia and sepsis
Signs/symptoms
- Tenderness, erythema, indurated lesions
- Purulent center
Treatment
- I+D of purulent fluid
- Antibiotic coverage
- Dressing coverage on all 4 sides
Staphylococcal Scalded Skin Syndrome
Rare infection, usually limited to children <5 years old
- Heals in < 1 week
- Exfoliation of large skin surfaces due to presence of staph aureus
- Begins as vesicular rash → bullae formation → massive skin sloughing
Treatment
- Antibiotics
- Nonadherent dressings
- Topical antimicrobials
Impetigo Contagiosum
- Caused by Strep A or Strep B
- Vesicles that rupture to form red, denuded lesions with yellow crusts
- Usually seen in children and on face/limbs
Treatment
- Hand hygiene and standard infection control measures
- Mupirocin PRN
Hidradenitis Suppurativa
Chronic infection/inflammation of apocrine sweat glands and hair follicles
- Lesions usually in axilla, perineum, or areola
Risk factors
- Family history
- Females > males
- Black individuals
- Smokers
- Hyperhidrosis
Present as tender nodules with malodorous drainage
Treatment
- I+D of lesions
- Antibiotic coverage
- Pain management
- Smoking cessation
Necrotizing Fasciitis - Type 1
Most common
- Common in trunk and perineum
- Associated with breaks in skin
Pathology
- Aerobes deplete oxygen levels → facilitates anaerobic growth
- Causes massive tissue breakdown
Presentation
- Erythema
- edema
- induration,
- fever
- chills
- Pain out of proportion to injury
Necrotizing Fasciitis - Type 2
Common on head and neck
- May be no break in skin
- NSAID use as kid is risk factor
Pathology
- Tissue breakdown via bacterial enzymes and toxins
- Surface proteins protect organisms against phagocytosis
- Toxins cause release of inflammatory cytokines
- Inactivates T-cell receptors
Presentation
- Patchy blisters, discoloration of skin
- Indistinct margins
- Patient is increasingly ill with possible altered mental status
Necrotizing Fasciitis - Type 3
Single organism (vibrio vulfinicus found in saltwater)
Presentation
- Eschar-like plaques
- Wounds may be numb d/t nerve destruction
- Crepitus
- hemorrhagic bullae with foul smelling drainage
Spider Bites
- Fairly uncommon
Characteristic
- Full thickness lesions that become necrotic
- Intense erythematous halo with bluish discoloration
- Pain and itching, fever, nausea
- Possible thrombocytopenia
Management
- Moist wound healing
- Anti-inflammatory agents
Bullous Lesions
Damage to anchoring fibers within skin that attach - skin to surrounding tissues and each other
- Results in separation of skin layers with blister formation with minimal trauma
Characteristics
- Partial thickness
- Will heal without a scar
- Possible hyperpigmentation
Causes
- Congenital disease
- Autoimmune conditions
- Allergic reaction that targets anchoring fibers
Management
- Low friction + shear support surfaces
- Nonadherent dressings with silicone or petrolatum contact layer
- Anti-inflammatory agents
- Plasmapheresis
- Gene therapy
- Bilayer skin products
- Genetic counselling
Cutaneous Malignant Lesions
Solid tumor that invades skin
- Usually associated with advanced disease
Management issues
- Necrosis
- Exudate management
— AMD + absorptive dressing
— Alginate or AMD foam
- Bleeding
— Alginates or silver for surface bleeding
— Hemostatic dressings with nonadherent dressing
- Infection
— Monitor for cellulitis
- Body image
— Conceal tumor and manage odor
— Topical Flagyl
— Dakins-soaked gauze
— Odor-proof ostomy pouch
Radiation-Induced Skin Damage
Clinical presentation
- Hyperpigmentation
- Dry desquamation vs wet desquamation
- Dry: dry, flakey, shedding skin
- Wet: total loss of epidermis with partial thickness injury
Staging
- Stage 1
— Inflammation
— Erythema
— Slight edema
— Dry desquamation
- Stage 2
— Brisk erythema
— Patchy moist desquamation
— Stage 3
— Extensive moist desquamation
- Stage 4
— Deep dermal damage
— Causes full thickness wound
— Loss of epidermal appendages
Prevention
- Routine hygiene
- Minimize trauma
- Routine use of approved emollients
- Topical steroids to reduce inflammation
Management
- Continued prevention where applicable
- Moist wound healing
- Non-adhesive or silicone foams
- Hydrocolloids
- Gels
Osteoradionecrosis
Damage to blood vessels and fibroblasts in affected area
- Causes chronic ischemia, dermal fibrosis, and failure to thrive
- Need high levels of preventative care
Management
- HBOT
- Surgical flap/excision
Graft vs Host Disease
Patient receiving allogenic blood/bone marrow transplant
- Allogenic: blood/bone marrow from donor
- Autologous: patient self-donates
Phases
- Conditioning
- Transplant
- Pre-engraftment (waiting for donated products to start working)
- Engraftment (once cells start working)
Risks
- Histocompatibility
- Age >40
- History of multiple blood transfusions
Acute vs chronic
- Acute GVHD occurs in 1st 100 days post-transplant
— Moist desquamation
— Systemic therapy with immunosuppressants
- Chronic GVHD is >100 days post-transplant
— Xerosis, sclerosis, erythema, ulcers
— Systemic therapy with immunosuppressants
Extravasation Injuries
Tissue damage due to leakage of irritant drugs into tissue
Management
- Initial
— D/c infusion and aspirate residuals
— Administer antidote if applicable
- Moist wound healing
- Plastic consult if tendon, joint, or bone affected
Burns - Zones
Central: devitalized tissue/zone of coagulation
Stasis zone: just outside the central zone
- May survive with fluid resuscitation or prevention of infection
Hyperemia zone: outermost zone (equivalent to 1st degree burn)
Burns - Epidermal Stage
Epidermal
- No skin loss
- Red, hot, and painful
- Heals in 3-4 days
- Not counted in the Total Burn Score
Burns - Partial Thickness
- Pale, dry, and non-blanchable
- Heals in 3 weeks with moist wound healing
- May blister with minor trauma post-3 months
- Due to reduced cohesion between epidermis and dermis
Burns - Full Thickness
- Extension through dermis to involve subcutaneous or deeper tissue
- Subcutaneous thermal = dry, waxy, and white
- Deep dermal = brown, dry, and leathery
- Scald thermal = dry, cherry red
- Treat with early excision and grafting to prevent infection
Burns - Emergent Phase
Emergent phase
- Fluid resuscitation
- Early wound management
- Cleaning
- Assessment
- Deroofing large blisters
- Escharotomy PRN
