Skin and soft tissue inflammation and infections Notes


Osmosis High-Yield Notes

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Pressure ulcer


Acne vulgaris




Hidradenitis suppurativa


Necrotizing fasciitis

NOTES NOTES SKIN & SOFT TISSUE INFLAMMATION & INFECTIONS GENERALLY, WHAT ARE THEY? PATHOLOGY & CAUSES DIAGNOSIS ▪ Inflammation of epidermis, dermis, underlying tissues LAB RESULTS CAUSES OTHER DIAGNOSTICS ▪ Infections, autoimmune response RISK FACTORS ▪ ▪ ▪ ▪ ▪ Impaired skin barrier Pressure Friction Exposure to infectious agents Immunosuppression COMPLICATIONS ▪ Infection ▫ Local or systemic disease ▪ Tissue cultures, Gram stain ▪ Mostly clinical, based on presentation TREATMENT MEDICATIONS ▪ Infections: antimicrobials OTHER INTERVENTIONS ▪ Dressings, ointments ▪ Cryotherapy ▪ Curettage SIGNS & SYMPTOMS ▪ See individual disorders OSMOSIS.ORG 43
ACNE VULGARIS PATHOLOGY & CAUSES ▪ Common inflammatory skin disorder affecting hair follicles, sebaceous glands ▪ May involve comedones, papules, pustules, cysts, scars ▪ Especially affects individuals who are ▫ Biologically male, with hormonal disorders producing androgens (e.g. polycystic ovarian syndrome), adolescent ▫ Symptoms decrease with age TYPES Mild ▪ Occasional, comedones, inflammatory papules, pustules ▪ Infection ▫ Follicle colonization by Propionibacterium acnes ▪ Medications ▫ Lithium, glucocorticoids, anabolic steroids ▪ Polycystic ovarian syndrome ▪ Stress COMPLICATIONS ▪ Cosmetic ▫ Scars, hyperpigmentation, pyogenic granulomas, osteoma cutis ▪ Psychiatric ▫ Low self esteem, depression Moderate ▪ Multiple pustules, nodules occur on trunk Severe ▪ Cystic, large nodules predominant, with persistent involvement of trunk; scarring CAUSES ▪ Androgen stimulates sebaceous follicles to overproduce sebum → follicles become blocked ▪ Hyperkeratinization of epithelium → accumulation → follicular blocking → debris accumulates further → skin follicles rupture ▪ Propionibacterium acnes replicates within follicle → releases lipase → sebum converted to free fatty acids → release of cytokines → inflammation RISK FACTORS ▪ Genetic predisposition ▪ Oil-based skin products ▪ Hormonal imbalance 44 OSMOSIS.ORG Figure 8.1 Acne vulgaris affecting the face of an adolescent male.
Chapter 8 Skin & Soft Tissue Inflammation & Infections SIGNS & SYMPTOMS ▪ Papules, pustules, painful nodules (cysts) on face, neck, chest, back ▪ Closed comedones ▪ Erythema DIAGNOSIS ▪ In case of comedonal acne, use azelaic acid, salicylic acid as anti-inflammatory, antibacterial, antiproliferative agent Mild to moderate ▪ Benzoyl peroxide, retinoid ▪ Add topical antibiotic (clindamycin) for synergistic effect with benzoyl peroxide Severe ▪ Oral isotretinoin decreases sebum production, bacterial proliferation, inflammation ▪ Avoid using tetracycline due to sun sensitivity OTHER DIAGNOSTICS ▪ Clinical presentation TREATMENT OTHER INTERVENTIONS MEDICATIONS ▪ Target sebum production, inflammation, bacterial/follicular proliferation Mild ▪ Benzoyl peroxide treats Propionibacterium acnes ▪ Add topical retinoids to prevent follicular proliferation ▪ Clean skin with gentle agents ▪ Comedones extraction ▪ Pigmentation ▫ Topical retinoid, azelaic acid, chemical peels ▫ Photodynamic treatment with lasers (removes superficial layers of skin) ▫ Dermabrasion (treatment of scars; may irritate skin) CELLULITIS PATHOLOGY & CAUSES ▪ Non-necrotizing inflammation of dermis, subcutaneous tissue, typically caused by streptococci (S. aureus, S. pyogenes); usually unilateral ▪ Skin breach: trauma; dry, fissuring skin; ulcers → bacteria invade skin, subcutaneous tissue ▪ Common locations: face, legs; may affect arms ▪ Other locations: causes vary ▫ Orbital cellulitis: originates from trauma, sinuses, hematogenous spread ▫ Abdominal wall cellulitis: morbid obesity causes bacteria to enter skin sores ▫ Buccal cellulitis: spread from tooth infection ▫ Perianal cellulitis: affects all demographics TYPES ▪ Purulent ▫ Furuncles (inflamed follicles), carbuncles (accumulation of furuncles), abscesses, cysts ▪ Non-purulent ▫ Superficial cellulitis, erysipelas OSMOSIS.ORG 45
RISK FACTORS ▪ Skin inflammation ▫ Abrasion: wounds, eczema, radiation, broken skin between toes ▪ Lowered immunity ▫ Diabetes mellitus, alcohol abuse, HIV, older age ▪ Skin infection ▫ Tinea, impetigo, varicella, rash ▪ Edema ▫ Lymphatic obstruction, venous insufficiency ▪ Obesity DIAGNOSIS DIAGNOSTIC IMAGING Ultrasound ▪ Subcutaneous fat separates into lobules ▫ Cobblestone appearance COMPLICATIONS ▪ Recurrence, abscess formation, necrotizing fasciitis, osteomyelitis, sepsis SIGNS & SYMPTOMS ▪ Fever, chills ▪ Localized inflammation ▫ Swelling ▫ Warmth ▫ Erythema with unclear borders (contrast to erysipelas—clear demarcations) ▫ Often painful ▪ Enlarged lymph nodes ▪ Purulent cellulitis associated with S. aureus infection Figure 8.2 An ultrasound scan of the right lower limb demonstrating the cobblestone appearance of subcutaneous edema, in this case secondary to cellulitis. LAB RESULTS ▪ Complete blood count (CBC) ▫ ↑ inflammatory markers: ↑ C-reactive protein (CRP), ↑ erythrocyte sedimentation rate (ESR), ↑ WBC count ▪ Wound, blood cultures ▫ Identify causative microbe OTHER DIAGNOSTICS ▪ Clinical presentation ▫ Spreading inflammation of skin/ subcutaneous tissues TREATMENT MEDICATIONS Figure 8.3 An individual with cellulitis of the left leg. ▪ Antibiotics: second generation penicillins, first generation cephalosporins; vancomycin for MRSA OTHER INTERVENTIONS ▪ Immobilization, elevation, dressings ▪ Drain abscess 46 OSMOSIS.ORG
Chapter 8 Skin & Soft Tissue Inflammation & Infections ERYSIPELAS PATHOLOGY & CAUSES ▪ Acute, non-necrotizing infection of upper dermis, superficial lymphatics; usually unilateral ▪ Well-defined demarcation between normal, infected tissue; non-purulent ▪ Usually caused by streptococci; most often Streptococcus pyogenes ▪ Elevated, warm, painful rash called “forest fire rash” (because it’s reddest at border) ▪ Vesicles may be present; may be bright, salmon red ▪ Inflammation of regional lymph nodes, lymphangitis in chronic infection RISK FACTORS ▪ Very young/old age ▪ Breaks in skin ▫ Abrasions, trauma, eczema, radiation, bites ▪ Lowered immunity ▫ Diabetes mellitus, alcohol abuse, HIV, older age ▪ Skin infection ▫ Tinea, impetigo, varicella, rash ▪ Edema ▫ Lymphatic obstruction, venous insufficiency ▪ Obesity COMPLICATIONS ▪ Lymphedema due to impaired lymphatic drainage ▪ Necrosis ▪ If spread hematogenously to other areas ▫ Arthritis, osteomyelitis, necrotizing fasciitis, glomerulonephritis SIGNS & SYMPTOMS ▪ Initially, general infection symptoms ▫ Fever, chills, headache, fatigue ▪ Lesions ▫ Mostly on legs, but may be found on face, arms, fingers, toes Figure 8.4 Erysipelas affecting the face of an elderly individual. DIAGNOSIS LAB RESULTS ▪ Blood test ▫ CBC: ↑ CRP, ↑ ESR, ↑ WBCs; antistreptolysin titer O shows streptococcal involvement ▪ Wound, blood culture OTHER DIAGNOSTICS ▪ Clinical presentation OSMOSIS.ORG 47
TREATMENT MEDICATIONS ▪ Antibiotics: oral penicillins/macrolides, vancomycin for MRSA, intravenous (IV) route in severe infection FOLLICULITIS PATHOLOGY & CAUSES ▪ Hair follicle inflammation (pyoderma), usually infectious cause ▪ May also be due to persistent trauma (mechanical folliculitis) ▪ Pathogen enters hair follicle → inflammatory inflammatory response → infection causes a perifollicular infiltrate of lymphocytes, neutrophils, macrophages → pustule formation CAUSES ▪ Bacterial ▫ S. aureus, Pseudomonas aeruginosa (hot-tub folliculitis) ▪ Viral ▫ Herpes simplex virus (HSV) ▪ Fungal ▫ Tinea barbae ▪ Rarely ▫ Autoimmune; oily skin in factory workers RISK FACTORS ▪ Swimming pools, hot tubs ▪ Shaving against hair growth, tight clothes causing friction, profuse sweating (hyperhidrosis) ▪ Use of antibiotics, acne medication, topical corticosteroids ▪ Upper respiratory presence of S. aureus 48 OSMOSIS.ORG COMPLICATIONS ▪ Recurrence ▪ Furunculosis ▫ Deep infection of hair follicle → evolves into swollen nodule, may coalesce into carbuncles SIGNS & SYMPTOMS ▪ Many small pustules, papules in areas of hair growth (e.g. face, legs, arms, back) ▫ Typical in groin, armpits ▫ Gram-negative infections more common on the face (areas of acne) ▫ Methicillin resistant S. aureus (MRSA) more common on the front trunk ▪ Itching, redness; often tender ▪ Does not appear in areas without hair growth (palms of hands, soles of feet) ▪ Sycosis vulgaris ▫ Multiple pustules on chin, upper lip; caused by S. aureus infection after shaving DIAGNOSIS LAB RESULTS ▪ Gram stain, wound culture performed for treatment-resistant individuals ▪ Skin biopsy ▫ Differentiation from other skin disorders in persistent folliculitis
Chapter 8 Skin & Soft Tissue Inflammation & Infections OTHER DIAGNOSTICS ▪ History ▫ Risk behavior/predisposition ▪ Clinical presentation TREATMENT MEDICATIONS ▪ Topical antibiotics: mupirocin, clindamycin ▪ Oral antibiotics: tetracycline, cephalosporin ▫ Used in extensive involvement ▪ MRSA treatment: trimethoprim/ sulfamethoxazole, clindamycin, tetracycline ▪ Fungal treatment: fluconazole, itraconazole ▪ Viral treatment: acyclovir, valacyclovir, famciclovir Figure 8.5 The clinical appearance of folliculitis. OTHER INTERVENTIONS ▪ May resolve spontaneously ▪ Warm compress with antiseptic use ▪ Loose fitting clothing; avoiding shaving HIDRADENITIS SUPPURATIVA PATHOLOGY & CAUSES ▪ Chronic, pus-producing dermatological disorder ▫ AKA acne inversa ▪ Dysfunctional hair follicles/apocrine sweat glands → pore clogging → inflammation → painful abscesses CAUSES Environmental ▪ Skin/clothes friction, hormonal changes, sweating, humidity Genetic ▪ Apocrine gland dysfunction, cellular disorders RISK FACTORS ▪ Obesity, tight clothes, smoking, deodorant use, shaving ▪ More common for biologically-female individuals COMPLICATIONS ▪ Scarring, bacterial infection, interstitial keratitis, sinus formation, fistula formation; squamous cell carcinoma (chronic lesions); depression SIGNS & SYMPTOMS ▪ Red inflamed areas, painful bumps that drain with pus ▪ Presence of double comedones ▪ Mostly in axilla, groin, under breasts OSMOSIS.ORG 49
DIAGNOSIS TREATMENT OTHER DIAGNOSTICS MEDICATIONS Clinical presentation ▪ Sartorius/Hurley’s staging systems (determines severity; guides treatment) ▫ Stage I: solitary/multiple isolated abscess formation without scarring/ sinus tracts ▫ Stage II: recurrent abscesses; lesions may be single/multiple, widely separated; sinus tract formation ▫ Stage III: diffuse, regional involvement across; multiple interconnected sinus tracts, abscesses ▪ Corticosteroids, anti-androgen medication, oral antibiotics, tumor necrosis factor (TNF) inhibitors to ↓ inflammation SURGERY ▪ Incision, drainage; sinus tract opening OTHER INTERVENTIONS ▪ Clean affected area ▪ Laser treatments remove lesions, scarring Behavioral ▪ Smoking cessation, weight loss IMPETIGO PATHOLOGY & CAUSES ▪ Highly infectious skin infection; affects superficial epidermis ▫ Commonly affects children ▫ Skin-to-skin spread possible ▪ Contact with carrier → pathogen enters intact/non-intact skin → incubation → lesion formation, spread over body through scratching ▪ Commonly caused by S. aureus, S. pyogenes TYPES ▪ Nonbullous ▪ Bullous ▪ Ecthyma RISK FACTORS ▪ Higher incidence in warm, humid climates ▪ Eczema, HSV, diabetes mellitus, malnutrition ▪ School, daycare 50 OSMOSIS.ORG COMPLICATIONS ▪ Cellulitis, poststreptococcal glomerulonephritis SIGNS & SYMPTOMS ▪ Nonbullous ▫ Most common ▫ Red bump → blister → blisters rupture, ooze, form crusts → characteristic yellow scab formation ▪ Bullous ▫ Bullae on limbs, trunk ▫ Not painful ▫ Ruptured bullae become covered with thin, brown crust ▪ Ecthyma ▫ Deeper nonbullous impetigo appears on limbs ▫ Painful ▫ Evolves into yellow scabs ▪ Fever (rare); blisters may be painful, itchy
Chapter 8 Skin & Soft Tissue Inflammation & Infections DIAGNOSIS LAB RESULTS ▪ Lesion culture ▫ Identify pathogen, adjust treatment OTHER DIAGNOSTICS ▪ History ▪ Physical exam TREATMENT MEDICATIONS ▪ Topical antibiotic ▪ Penicillins ▪ In case of MRSA, use trimethoprim/ sulfamethoxazole OTHER INTERVENTIONS ▪ Clean with antiseptic to prevent spreading ▪ Topical antibiotic ▫ Penicillins ▫ In case of MRSA use trimethoprim/ sulfamethoxazole Figure 8.6 Impetigo on the back of the neck of an adult male. NECROTIZING FASCIITIS PATHOLOGY & CAUSES ▪ Potentially life-threatening infection ▫ Progressive destruction of deep soft tissue (subcutaneous fat, muscle fascia) ▪ Bacteria spread via subcutaneous tissue → release exotoxins → tissue destruction spreads along fascial planes TYPES Type I: polymicrobial ▪ Causes: combination of aerobic, anaerobic bacteria ▫ Most common anaerobes: Bacteroides, Clostridium, Peptostreptococcus ▫ Enterobacteriaceae: Escherichia coli, Klebsiella, Proteus, Enterobacter ▫ Facultative anaerobic streptococci ▪ Common sites ▫ Perineum (Fournier’s gangrene): impaired gastrointestinal/urethral mucosal integrity → spreads to anterior abdominal wall; gluteal muscles; scrotum, penis (in biological male); labia (in biological female) ▫ Cervical (head, neck): impaired oropharynx mucosa (often related to dental/odontogenic infection) → spreads to face, neck, mediastinum OSMOSIS.ORG 51
Type II: monomicrobial ▪ Causes: Group A Streptococcus, other beta-hemolytic streptococci, Staphylococcus aureus Type III: saltwater infection ▪ Cause: Vibrio vulnificus ▪ Rare Type IV: fungal infection RISK FACTORS ▪ Immunosuppression ▫ HIV, diabetes, cirrhosis, corticosteroid use ▪ Peripheral vascular disease ▪ Trauma ▫ Injury, surgery ▪ IV drug abuse ▪ Childbirth ▪ Exposure of open wound to fresh/salt water, swimming pools, hot tubs ▪ Ludwig’s angina (submandibular region infection) ▪ Lemierre syndrome (septic thrombophlebitis located in jugular vein) COMPLICATIONS ▪ Shock ▪ Organ failure ▪ Potentially fatal SIGNS & SYMPTOMS Overlying skin ▪ May appear normal initially ▪ Later ▫ Warmth, erythema/violet/purple (violaceous), woody induration, edema, necrosis ▪ Bullae; may fill with serosanguinous fluid ▪ Subcutaneous emphysema (if infection with anaerobes) Systemic findings ▪ Pain ▫ Often out of proportion to exam findings ▪ Fever ▪ ↑ pulse ▪ ↓ perfusion (motling, pallor, altered level of consciousness) ▪ Hemodynamic instability (↓ BP) DIAGNOSIS DIAGNOSTIC IMAGING CT scan ▪ Subcutaneous gas visualized in fascial planes LAB RESULTS Blood ▪ ↑ WBCs, left shift; ↑ creatine phosphokinase; ↓ hemoglobin, ↑ glucose, ↓ sodium Urine ▪ Proteinuria Gram stain, cultures of skin ▪ Debrided tissue identifies organism(s) Figure 8.7 Necrotizing fasciitis on the left leg. The dark areas represent progression to necrosis. 52 OSMOSIS.ORG OTHER DIAGNOSTICS ▪ Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score ▫ Score = 6: ↑ suspicion of necrotizing fasciitis ▫ Score = 8: strongly predictive
Chapter 8 Skin & Soft Tissue Inflammation & Infections Figure 8.9 A histological section of subcutaneous tissue in a case of necrotizing fasciitis showing an inflammatory infiltrate in the fascia leading to necrosis. TREATMENT MEDICATIONS Figure 8.8 A CT scan in the coronal plane demonstrating the presence of gas in the fascial planes of the leg, consistent with a diagnosis of necrotizing fasciitis. ▪ Empiric IV antibiotics ▫ Carbapenem/beta-lactam-betalactamase inhibitor + vancomycin/ linezolid + clindamycin ▪ Hemodynamic support ▫ Fluids, vasopressors SURGERY ▪ Direct surgical examination of skin, subcutaneous tissue, fascial planes, muscle → debridement of all devitalized, necrotic tissue ▪ Fasciotomy OTHER INTERVENTIONS ▪ Hyperbaric oxygen OSMOSIS.ORG 53
ONYCHOMYCOSIS PATHOLOGY & CAUSES ▪ Chronic fungal infection ▫ Nail bed, matrix, plate of toes/fingers ▪ Infection spread by direct contact from people, animals, soil, fomites (upholstery, hairbrushes, hats) ▪ Causative agents ▫ Dermatophytes (tinea unguium): most commonly Trichophyton rubrum ▫ Nondermatophyte molds: Aspergillus spp. ▫ Yeasts: most commonly Candida albicans ▪ Dermatophyte hyphae penetrate stratum corneum of skin, nails → manufacture keratinolytic proteases → invade living cells ▪ Spores of nondermatophyte (e.g. Aspergillus) lodge under nail/at lateral nail folds → colonization, spread toward cuticle Candida spp. → infect soft tissue around nail, penetrate nail plate TYPES Mixed pattern ▪ Combination of other types RISK FACTORS ↑ age Biological male > female Communal showers, swimming pools Contributory/predisposing factors ↑ warmth, humidity Occlusive footwear Occupational ▫ Jobs that involve frequent hand washing; dishwashers, housekeepers ▪ Immunocompromised state (HIV, diabetes) ▪ Living with others affected by onychomycosis ▪ Chronic mucocutaneous fungal infection ▪ ▪ ▪ ▪ ▪ ▪ ▪ COMPLICATIONS ▪ ▪ ▪ ▪ Pain ↑ risk of bacterial coinfection, cellulitis Nail disfigurement Recurrence Distal lateral subungual ▪ Initially affects distal corner of nail; eventually spreads toward cuticle ▪ Most common Proximal subungual ▪ Affects nail plate near cuticle; extends distally ▪ Sign of severely immunocompromised state White superficial ▪ Affects nail surface; may spread to cover entire nail Endonyx ▪ Affects interior of nail plate Total dystrophic ▪ Nail plate is completely destroyed 54 OSMOSIS.ORG Figure 8.10 Onychomycosis of the toe nails.
Chapter 8 Skin & Soft Tissue Inflammation & Infections TREATMENT SIGNS & SYMPTOMS ▪ Distal lateral subungual ▫ Yellow, brown, white discoloration; subungual hyperkeratosis; mild inflammation; onycholysis ▪ Proximal subungual ▫ Diffuse patches/transverse striate of white to yellow patches on nail plate ▪ Endonyx ▫ Discoloration, onycholysis ▪ White superficial ▫ Soft white spots on nail surface ▪ Total dystrophic ▫ Keratotic debris on thick, rigid nail bed ▪ Other associated features ▫ Coexisting tinea pedis infection (common) ▫ Chronic paronychia (proximal/lateral fold inflammation) ▫ Dermatophytoma (linear, yellow/white band of dermatophyte hyphae) ▫ Fungal melanonychia (black/brown discoloration; caused by pigmentproducing molds, fungi) MEDICATIONS ▪ Topical triazole ▫ Efinaconazole ▪ Systemic ▫ Terbinafine (dermatophyte infections); itraconazole (yeast, non-dermatophyte infections) ▪ Coexisting tinea capitis ▫ Griseofulvin ▪ Keratolytic (urea) ▫ Reduces nail thickening SURGERY ▪ Nail removal in some cases (nail avulsion) OTHER INTERVENTIONS ▪ Laser (Nd:YAG) ▪ Photodynamic therapy DIAGNOSIS LAB RESULTS ▪ Potassium hydroxide (KOH) microscopy ▫ Identifies fungal elements (e.g. fungal hyphae, pseudohyphae, yeast) ▪ Histopathological analysis using periodic acid-Schiff (PAS) stain ▫ Identifies fungal elements ▪ Fungal culture (e.g. dermatophyte test medium/DTM) ▫ Identifies organism OTHER DIAGNOSTICS ▪ History, physical examination with characteristic findings OSMOSIS.ORG 55
PRESSURE ULCER PATHOLOGY & CAUSES ▪ Localized skin, underlying-tissue injury ▫ Caused by unrelieved pressure/pressure in combination with friction, shearing forces ▪ AKA bedsores/decubitus ▪ Blood flow diminishes ▫ Pressure → ischemia → necrosis ▪ Bony prominences most commonly affected ▫ Sacrum, heels, hips, elbows RISK FACTORS ▪ Reduced mobility ▫ Chronic/acute disease (e.g. hip fracture, stroke, Parkinson disease) ▫ Central/peripheral neural damage, altered level of consciousness, advanced age ▪ Reduced perfusion ▫ Atherosclerosis, peripheral vascular disease, hypotension, smoking ▪ Factors affecting skin structure ▫ Malnutrition, protein deficiency, skin moisture (incontinence, sweating) ▪ Diabetes mellitus STAGING ▪ Stage I: nonblanchable erythema; skin intact, localized ▪ Stage II: partial thickness dermis loss; red wound bed; serum-filled blister; no skin sloughing ▪ Stage III: full thickness tissue loss; visible subcutaneous fat; raised wound edges (epibole); skin sloughs ▪ Stage IV: full thickness tissue loss; bone, muscle, tendon exposed; raised wound edges; skin sloughs/eschar formation 56 OSMOSIS.ORG ▪ Unstageable: if filled with sloughed skin, scabs; diagnosis difficult ▪ Deep tissue injury: nonblanchable erythema, skin separation; no skin disruption COMPLICATIONS ▪ Biofilm formation on wound → inflammation → delayed healing → wound dehiscence ▪ Wound, bone, joint infection; sepsis; fistulas; gangrene ▪ Malignant transformation rare SIGNS & SYMPTOMS ▪ Ulceration (skin in contact with underlying surface) ▪ Fever, foul odor (if complicated by infection) ▪ May be painful DIAGNOSIS LAB RESULTS ▪ Swab culture ▫ May help determine treatment in healing-resistant ulcers OTHER DIAGNOSTICS ▪ Clinical presentation TREATMENT MEDICATIONS ▪ Topical sulfadiazine cream OTHER INTERVENTIONS ▪ Debridement of biofilm, dressing replacement, negative pressure therapy
Chapter 8 Skin & Soft Tissue Inflammation & Infections Prevention ▪ If bedridden, reposition at least every two hours (reduces chance of ulcer development) ▪ Use of special mattresses ROSACEA PATHOLOGY & CAUSES ▪ Chronic inflammatory cutaneous disorder ▫ Usually affects face (may extend to neck, upper chest, ears) ▫ Ocular involvement: dry, burning, itching, foreign-body sensation ▪ Typical onset: 30–50 years ▪ Defining features ▫ Persistent central facial erythema; intensity may be intermittent ▫ Phymatous changes (irregular, nodular skin), usually affecting nose (biologically-male > biologically-female individuals) ▪ Hyperactive vascular response, may extend to eyes (ocular rosacea) ▪ Triggered by warm weather, alcohol, certain foods, sun, stress CAUSES ▪ Unknown ▪ May be innate immune system dysfunction; response to bacteria, UV → chronic inflammation COMPLICATIONS ▪ Skin thickening, scarring, rhinophyma, ocular rosacea (blepharitis) RISK FACTORS ▪ Genetic predisposition ▪ More common in biologically-female individuals, especially of Celtic/NorthernEuropean descent SIGNS & SYMPTOMS ▪ Telangiectasia with erythema, papules, pustules ▪ Flushing Characteristics of different types ▪ Papulopustular ▫ Similar to acne, no comedones ▪ Phymatous ▫ Thick oily skin; mostly on nose, in biologically-male individuals ▪ Ocular (common) ▫ Conjunctivitis, keratitis, tearing, burning, telangiectasias ▪ Granulomatous ▫ Papules around eyes, cheeks ▪ Pediatric (rare) ▫ Never phymatous ▪ Neurogenic ▫ Pain, neurologic symptoms DIAGNOSIS OTHER DIAGNOSTICS ▪ History; clinical exam with characteristic findings TREATMENT MEDICATIONS ▪ Antibiotic (topical metronidazole) ▪ Topical azelaic acid ▪ Oral doxycycline OSMOSIS.ORG 57
OTHER INTERVENTIONS ▪ Avoid exacerbating factors (e.g. spicy food, alcohol, sun, stress) ▪ Regular sunscreen use ▪ Laser therapy ▫ Telangiectasia ablation STAPHYLOCOCCAL SCALDED SKIN SYNDROME (SSS) PATHOLOGY & CAUSES ▪ Infectious, superficial skin disorder ▫ Skin blistering, desquamation ▪ AKA Ritter’s disease CAUSES ▪ S. aureus produces epidermolytic exotoxin → enters skin → breaks down desmosomes between cells → peeling skin COMPLICATIONS ▪ Cellulitis, sepsis RISK FACTORS ▪ ▪ ▪ ▪ S. aureus infection Immunocompromised state Immature renal function/kidney disease Affects children < six years SIGNS & SYMPTOMS ▪ Tender erythema with large desquamation areas, moist patches ▪ Nikolsky sign: skin peels at gentle touch ▪ Fever, malaise, appetite loss 58 OSMOSIS.ORG DIAGNOSIS DIAGNOSTIC IMAGING Chest X-ray ▪ Check for pneumonia as infectious cause; lobar infiltrates LAB RESULTS Biopsy ▪ Epidermal splitting in stratum granulosum near skin surface Blood culture ▪ S. aureus OTHER DIAGNOSTICS ▪ Clinical presentation TREATMENT MEDICATIONS ▪ Antibiotics

Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Skin and soft tissue inflammation and infections essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Skin and soft tissue inflammation and infections by visiting the associated Learn Page.