Deep tissue infections Flashcards
Necrotizing fascitis?
extensive tissue destruction
thrombosis of blood vessels
abundant bacteria spreading through fascial plains
in early stages relatively few acute inflammatory cells
necrotizing fascitis from simple cellulitis?
pain out of proportion to the clinical appearance of affected skin
identify those at increased risk(diabetes, abnormal peripheral circulation, trauma wounds, surgical incisions)
high fever
toxic appearance
Type 1 necrotizing fascitis?
diabtes mellitus, abdominal surgery, perineal infections
mixed infection
Type 2 necrotizing fascitis?
Grp A streptococcus (flesh eating strain)
-Aeromonas hydrophilia and Vibrio vulnificus
Type 1 necrotizing fasciitis?
clinically resembles gas gangrene
significant gas formation
copiuos seropurulent exudate occurs 3-4 days afer injury
unpleasant sour odor
if muscles involved, react to stimulation
diagnose type 1?
gram stain- numerous strep, pleomorphic gram neg rods with many polys
culture usually mixed
mixed culture in type 1?
anaerobic strep
group A strep or S. aureues
often enteric bacteria and bacteroides
diagnostic criteria of NF?
leukocytosis with a left shift (increase in the numer of immature white blood cells) elevated sedimentation rate elevated creatinine phosphokinase hypocalcemia hypoalbuminemia
Therapy of NF?
meticulous debridement
large does of antibiotics (penicillin and aminoglycoside)
Type 2 necrotizing fascitis etiology?
Grp A streptococcus (flesh eating strain due to high amt of lipase enzyme, secrete superantigens)
rapid progression
resembles clostridial gas gangrene but not gas formation
Diagnosis type 2 NF?
gram stain and culture of infected tissue
lab tests: lecuocytosis, ESR, creatinine phosphotase, electrolyte imbalance
Xray or MRI ck for gas (no gas with S. pyogenes NF)
Histo: incisional or fascial biopsy
Treat type 2?
surgical debridement with prompt antimicrobial therapy (penicllin G)
Aeromonas hydrophilia myonecrosis?
motile gram neg rods, fresh water, oxidase pos
rapid progression
resembles clostridial gas gangrene
bacteremia is frequently present
Treatment Aeromonas hydrophilia myonecrosis?
surgical debriedement and prompt anitmicrobial therapy (fluoroquinolone, amioglucosides, or trimeth/sulfa)
Gas gangrene (clostridial myonecrosis)?
rapidly progressive, life threatening, toxemic infection of subcutaneous tissue and skeletal due to clostridia
usually due to traumatic injury
Patholophysiology Gas gangrene (clostridial myonecrosis)?
most often caused by Clostridium perfringens, others include C. novyi, C. septicum, C. hitslyticum
infections have very low level host inflammation (purulence is often absent, due to effect of the toxins)
most damage due to alpha and theta toxins
Predisposing factors Gas gangrene (clostridial myonecrosis)?
accidental trauma injury with compound fracture
penetrating war wounds
surgical wounds
artery insufficiency in an extremity
clinical findings Gas gangrene (clostridial myonecrosis)?
incubation period usually 2-3 days but may be as short as 6-8 hours
excruciating pain with rapid increasing intensity
patient appears ill with a rapid pulse and falling BP, shock and renal failure may follow
process is rapid and often fatal
appearance Gas gangrene (clostridial myonecrosis)?
wound has peculiar foul odor
gas bubbles may be visible in the discharge, crepitus is usually present
skin around wound is usually swollen and white, yellowish discolor
blebs contain sero-sanguineous fluid develop in overlying skin and areas of green black cutaneous necrosis appear
involved m undergoes rapid disintegration and fails to contact upon stimulation
fulminant cases occur rapidly
Diagnose Gas gangrene (clostridial myonecrosis)?
gram stain of exudate or aspiration of bled reveal large gram pos rods but few polymorpholeukocytes
Clostridium perfringens isolated
Therapy Gas gangrene (clostridial myonecrosis)?
emergency surgery to carry out appropriate debridement
DOC: peniciilin G and clindamycin
Hyperbaric oxygen
Spontaneous, non traumatic gas gangrene?
Clostridium septicum
assoc with colon cancer, diverticulitis, and GI surgery
Clinical presentation Spontaneous, non traumatic gas gangrene?
bacteremia, pain, fever
Treatment Spontaneous, non traumatic gas gangrene?
similar to traumatic gas gangrene
Myalgias?
prominant features of a variety of viral infections and intracellular bacterial infection
actual cause is unknown but is likely do to an immunological response- some evidence of direct invasion
Muscle degeration assoc with infection at another site?
catabolism of the skeletal m, weakness and muscle wasting
acute phase response to sepsis and trauma
central role played by IL-1 and TNF which leads to increased synthesis in muscle cell lysosomes
Macrophages- IL-1 and TNF- prostaglandin E2- muscle protease