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
drugs predispose to SSTI
immunosuppressants, SGLT2i
how should the sample be taken for culture?
- from deep in the wound after the surface cleansed
==> bc surface may be contaminated - from the base of a closed abscess where bacteria grow
- by curettage, rather than wound swab or irrigation
==> bc difficult to obtain representative samples from wound swabs
what culture is needed?
- cultures of pus, exudates or tissues from the wound
- blood culture (for severe cases with marked systemic sx of infection or immunocompromised pt)
what conditions are considered as purulent
furuncles, carbuncles, skin abscesses, purulent cellulitis
clinical presentaitons of skin abscess
collection of pus within the dermis and deeper skin tissues. manifest as painful, tender fluctuant and erythematous nodules
complications of cellulitis
more common in immunocompromised patients
- bacteremia, endocarditis, toxic shock, glomerulonephritis, lymphedema, osteomyelitis, necrotising soft-tissue infection
bc infection is usually caused by gram pos which likes to stick to heart, joint, spine & release toxins that cause accentuated response to go into sepsis & shock
pathogens need to cover for impetigo
staphylococci or streptococci, MSSA
toxin producing strain of S.aureus cause bullous
pathogens need to cover for ecthyma
group A streptococcus (S.pyogenes), MSSA
coverage for non-purulent cellulitis, erysipelas
mainly beta-hemolytic streptococcus (S.pyogenes), MSSA cover for moderate
Water exposure: aeromonas, vibrio vulnificus, pseudomonas aeruginosa
