Skin and Soft Tissue Infection Flashcards
classification of SSTI by layers of skin
epidermis - impetigo
dermis - ecthyma & erysipelas
hair follicles: furuncles & carbuncles
subcutaneous fat and deep dermis: cellulitis
fascia: necrotizing fascilitis
muscle: myositis
clinical presentation of impetigo
localised superficial infection characterised by pustules or vesicles which then ruptured to form crusts or bullae on an erythematous base
located at the face & extremities
clinical presentation of ecthyma
deeper variant of impetigo begins as vesicles/pustules –> evolve to become ulcers.
- pruitis is common.
clinical presentation of erysipelas
superficial infection of the upper dermis involving the lymphatics. characterised by tender erythematous plaque with well-demarcated borders
common on face & lower extremities
clinical presentation of furuncles & carbuncles
infection of hair follicles with associated small subcutaneous abscess
carbuncle: a cluster of furuncles
clinical presentation of cellulitis
acute infection involving deep dermis and subcutaneous fat
- almost unilateral
- common on lower extremities
mimickers of cellulitis:
deep venous thrombosis, calciphylaxis, stasis dermatitis, hematoma, erythema migrans
the function of the skin
act as physical, chemical and immunological barriers against infection
- chemical: maintain acidic environment to keep microbial load low & regulate desquamation to keep transient bacteria low & sebaceous secretion inhibit growth of bacteria and fungi
- immunological: part of innate immunity & produce anti-microbial peptides to kill pathogens & normal skin commensal prevents colonisation and overgrowth of more pathogenic strains
pathophysiology of SSTI
majority results from the disruption of normal host defences –> lead to overgrowth and invasion of pathogenic micro-organisms
risk factors of SSTI
- disruption of the skin barrier via
- traumatic & non-traumatic
- reduced venous & lymphatic drainage due to obesity, saphenous venectomy, chronic venous insufficiency
- peripheral artery disease
- age
- physical environment (pH, soap and detergent use, humidity & moisture) - medical conditions: (DM, cirrhosis, neutropenia, HIV)
3 drugs: immunosuppressive agents & SGLT2i - history of cellulitis
prevention of SSTI:
- good care to maintain skin integrity
- identity and treat predisposing factors at the time of initial diagnosis to decrease the risk of occurrence
- acute traumatic wounds should be copiously irrigated & remove foreign objects & debride devitalised tissue
when culture is needed for SSTI?
mild and superficial infections no need (eg. impetigo, ecthyma)
What can lead to disruption of the skin barrier
- traumatic injury
- non-traumatic
- reduced venous and lymphatic drainage
- peripheral artery disease
- advanced age
- physical environment (eg. pH, soap, detergent, moisture, urine, feces, sweat, chronic wound fluid)
what are some conditions can lead to a reduced venous & lymphatic drainage
saphenous venectomy, obesity, chronic venous insufficiency
conditions predispose to SSTI
diabetes, cirrhosis, neutropenia, HIV, history of cellulitis