L 70 Necrotizing soft tissue infections Flashcards
Types and pathogens of necrotizing cellulitis
2 anaerobic groups:
1) Clostridium anaerobic: Clostridium perfringens
2) Nonclostridial anaerobic:
Bacteroides, Peptostreptococcus
These are obligate anaerobes that are often mixed with facultative anaerobes like coliform bacilli, staph, strep
What are the colifrom bacteria?
Citrobacter
Enterobacter
E. Coli
Klebsiella
Signs and symptoms of Necrotizing Cellulitis
Thin, dark, sometimes foul smelling wound drainage and tissue gas
*Pain, swelling, and system toxicity
Crepitus skin
Sparing of deep fascia and muscles
What is Meleney’s Synergistic Gangrene
Rare infection of post-operative patients
Interaction between S. aureus and microaerophilic streptococci
Necrotizing Fasciitis general features
Can spread from the subQ tissues, goes along fascial planes, does not infect muscle, is not contagious
Describe Type I necrotizing fasciitis
Type I is polymicrobic
Includes at least 1 anaerobic species: Bacteroides, Clostridium, Peptostreptococcus (all normal microbiota)
Combined with one or more facultative anaerobic strep or members of enterobacteriaceae (PESSKEY Strains)
Two locations:
1) Cervical (face, neck, mediastinum): Fusobacterium, strep, Bacteroides, spirochetes
2) Perineum: Anaerobes (Bacteroides, Clostridium, Fusobacterium) & facultative anaerobes E.coli, klebsiella
Risk factors for type I necrotizing fasciitis
Surgery/Trauma to introduce the bacteria
Diabetes, peripheral vascular disease (lower extremities)
Neonates (abdomen, perineum)
Fournier’s Gangrene
Subtype of type I necrotizing fasciitis
A fasciitis of the genitalia
Type II necrotizing fasciitis
Monomicrobic or Streptococcal Gangrene
GABHS or
other beta-hemolytic strep
Alone or isolated with other species–S. aureus
Virulence factors in type II monomicrobic necrotizing fasciitis
GABHS having M-proteins 1 & 3
Causes of Type II necrotizing fasciitis
Can follow blunt trauma, bug bite, chickenpox, surgery, childbirth, IV drugs
Also hematogenous translocation
Other pathogens that can cause type II necrotizing fasciitis
Aeromonas hydrophilia – traumatic lesion in freshwater
Vibrio vulnificus – seawater injury
Type II necrotizing fasciitis risk factors
Patient often immunocompromised
No significant PMH
Any age group
History of skin injury: laceration, blunt trauma, surgery, burn, childbirth, IV drugs, varicella infection
Clinical manifestations overview for necrotizing fasciitis
Infects deeper tissues destroying muscle fascia and overlying subq
Spreads along muscle fascia because it has a poor blood supply and spares the muscle below
initially won’t see much, but patient will complain of pain out of proportion to manifestation
Rapid progression over several days
Skin changes color, skin breaks down and forms bullae
Pain disappears from destruction of nerves (cutaneous anesthesia) precedes the skin necrosis
Manifestations of an advanced infection in necrotizing fasciitis
Fever, tachycardia, systemic toxicity
If systemic=>altered mental state
Malaise, myalgia, diarrhea, anorexia, hypotension
Putrid odor only if anaerobic (type I) and not strep
Necrotizing Fasciitis diagnosis
Surgery only way to confirm presence and extent
Tissue biopsy can be useful, but requires time
In surgery, tissue is necrotic, fascia is swollen with dull gray to yellow-green color, easy separation along fascial planes
Necrotizing fasciitis treatment
Surgery debridement to remove all damaged tissue
Broad spectrum antibiotics
Clindamycin: very good at preventing enzyme production in the bacteria that are the toxins that cause the tissue damage (strep, staph, clostridium)
Use of sterile fly larvae
Useful to eat and remove dead tissue, secrete antimicrobial byproducts, eat/kill bacteria
Description and cause of spontaneous gangrenous myositis
Aggressive infection of skeletal muscle
Caused by Strep that is attracted to bruised or damaged skeletal muscle by the increased production of vimentin
Spontaneous gangrenous myositis manifestations
Fever, exquisit pain, tenderness
Swelling of affected muscle with induration (hardening)
Overlying skin initially uninvolved, later becomes erythematous, warm, petechiae, bullae, vesicles
Progresses rapidly to other muscle and soft tissue
Hypotension and renal failure precede cutaneous manifestations by 4-8 hours
Signs of STSS
Elevated serum creatinin kinase
NO gas formation in the tissues
Spontaneous gangrenous myositis diagnosis
Immediate surgery
Findings surgical specimens
Numerous gram (+) bac in muscle
Spontaneous gangrenous myositis treatment
Aggressive surgical debridement
Antibiotics–clindamycin
GAS gangrene causative agents
Also called Clostridial Myonecrosis
Caused by endorspore-forming anaerobic bacilli: Clostridium perfringens Type A (soil and human feces)
C. septicum–usually endogenous, cancer can be involved by releasing it from the gut
C. perfringens–usually exogenous, trauma or surgery
Initial progression of GAS gangrene
Short doubling time: 8-10 minutes
Develops
Toxins associated with gas gangrene
There are more than 20 virulence factors associated with clostridium, but ALPHA-Toxin (pohospholipase C, lecithinase?) is the major cause
Lyses lots of cell types
Triggers histamine release, platelet aggregation
Prevents extravasation of WBC’s
Don’t see PMNs in infected tissue
THETA-Toxin (Perfringolysin): causes direct vascular injury, cytolysis, hemolysis, may explain poor inflammatory response and absence of inflammatory cells
KAPPA-Toxin (collagenase): fascilitates necrosis and spread through tissue planes
Gas production in myonecrosis and GAS gangrene
Clostridia and other bac make in soluble H2 gas–useful to separate tissues and allow access to fresh tissue and nutrients, also collapses blood vessels to keep regions anaerobic
Myonecrosis clinical manifestations
Acute onset with sever pain at site of trauma/surgery
Pain from toxin mediated ischemia
Skin overlying the injury: Pale-bronze-purple/red, becomes tense & extensively tender, bullae clear, red, blue, purple
Rapid development of system toxicity: tachycardia, fever, multiple organ dysfunction syndrome, thin hemorrhagic exudate, sweet mousy smell (C. perfringens), (foul odor common with anaerobes)
Crepitus (not in type II necrotizing fasciitis)
Myonecrosis diagnosis
Definitive–surgery
Muscle tissue does not bleed, does not contract when stimulated, grossly edematous, my have re-blue to black coloration
*NO immune cell infiltration because of alpha-toxin preventing extravasation, and theta-toxin lyses any cells that do get to the tissue
Microscopic: gram-variable bacillis at site, gram (+) in culture
What does clostridium do on blood agar?
Has double zone of hemolysis:
beta-hemolysis of theta-toxin, and incomplete alpha-hemolysis of alpha-toxin
Treatment of traumatic myonecrosis
Surgical debridement
Maintain vascular integrity
Delay primary suturing to maintain oxygen exposure
Initiate broad spectrum antibiotics
For C. perfringens specific: combination IV penicillin, clindamycin, or tetracycline
Tetanus booster if appropriate
Non-Clostridial myonecrosis
Anaerobes:
Bacteroides fragilis
Peptostreptococcus
Aerobes:
G(+) S. aureus
Much better prognosis than clostridium caused
