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sources of infection
bacteria, fungi, virus
bacterial infection effect on microbes on the wound bed would be dependant on
type of bacteria, number of colony forming units/gram, host immune system
host resistance
ability of the host to mount an immune response in order to resist bacterial invasion or damage (most important factor in determining how severe an infection is)
virulence
quality of being extremely poisonous, infectious or damaging or the extent to which a disease or toxin possesses this quality
contamination
non-replicating bacteria with no effect on wound healing
colonization
replicating bacteria that have attached to the wound surface with no harm to the host and no effect on the wound healing process
critical colonization
presence of replicating bacteria with sufficient number to induce a host response and cause subtle clinical changes in the wound healing process
infection
movement of replicating bacteria that have invaded the surrounding tissue with visible effects in wound healing process in periwound tissues
sepsis
presence of replicating bacteria that produces a whole body inflammatory state termed systemic inflammatory response syndrome
local factors of host resistance
size, location and age of wound, necrotic tissue or foreign bodies, presence of scar, previous radiation, inadequate or improper topical treatments
systemic factors of host resistance
poorly controlled diabetes, inadequate vascular perfusion, edema, immunosuppressive drugs, malnutrition, alcohol, neutrophil
endogenous infections
invasion of indigenous, bacteria gets in from you're own skin
exogenous infections
contamination from microbial populations in the environment
clinical signs/symptoms of infection
pain, erythema, edema, heat, purulent exudate, discoloration, friability of granulation tissue, pocketing of wind
characteristics of inflammation
pain, erythema, edema, heat
treat an infection if
3 or more signs/symptoms noted
increasing pain
plasma derived mediators are activated near tiny, unmyelinated fibers (exception is neuropathy)
erythema
vasoactive mediators are produced in response to any damage to mast cells in connective tissue
purulent exudate
rich in WBCs, common in infections produced by strongly chemotactic bacteria
delayed healing
lack of progress toward wound closure and no decrease in wound size (should see healing in 2 weeks)
discoloration of granulation tissue
pale or dusky, excessive angiogenic responses and granulation tissue from invading micro-organisms
friable granulation tissue
excessive angiogenic response caused by heavy bioburden, bleeds spontaneously or with light pressure
pocketing at base of wound
wound base irregular maybe due to lack of granulation tissue around islands of infection
foul odor
usually due to gram-negative bacilli, always associated with presence of anaerobes
clinical presentation of systemic infection
fever, chills, hypotension, multiple organ failure, fatigue
treat superficial infections
topically with antimicrobial dressings
treat deep/systemic infections
systemically
if swabbing an infection
dont swab over hard eschar, use sterile swab, swab area of most dramatic infection after cleansing and debridement
cellulitis
inflammation of connective tissue of the skin from bacterial infection (any bacteria)
cellulitis spreads through either
lymphatics or blood (will start streaking)
clinical signs of cellulitis
pain, warmth, erythema, edema
cellulitis treatment
antibiotics, elevation, analgesics, compression (ASAP)
osteomyelitis
infection and inflammation of bone
order of imaging for suspected osteomyelitis
xray, MRI, and bone biopsy (gold standard)
if there is bone exposure at a wound
refer to imaging and wait for results before treating