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75 Cards in this Set
- Front
- Back
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What is necrotizing fasciitis, what is myonecrosis |
nec fasciitis- superficial and deep fascia is directly affected. Myonecrosis- mm affected
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Is NF contagious
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nope, but there are group occurances
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Type I vs type II NF
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type I- polymicrobial, type II- monomicrobial
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Tell me a little about type I NF
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4-6 microbes, both aerobic and anerobic so damage is synergistic. S aureus, E coli, Pseudomonas, strepto, bacteroides, clostridium, peptostreotococcus, prevetella
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What are the facultative anerobes associated with type I NF
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S aureus, e coli, Pseudomonas, streptococcus milleri, GAS, vibrio vulnificus (salf water contamination)
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What are the anerobes associated with type I NF
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bacteroides, clostridium, prevotella, peptostreptococcus
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What are some risk factors for type I NF
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surgery, trauma, DM
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On what parts of the body are type I NF common
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trunk, abdomen, perineum
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Your pt who underwent appendectomy recently presents with an abdominal abcess with several microbes, where might the damage be?
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Superficial and deep fascia. This is type I NF. Can also be on trunk or perineum
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What is Fourniers Gangrene?
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NF of genitalia, subtype of Type I NF
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What is the subtype of NF type I that affects the genitalia
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Fourniers Gangrene
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Tell me about type II NF
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one microbe! GABHS, GAS. Has M1/3 protein. No hx of exposure, can follow microabraisions, blunt trauma, bug bite, chicken pox, IV drug use, surgery
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What type of NF can occur with out a clear hx of infection
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type II the mono infection. Can be a microabraision or like a bug bite
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Does type I or II NF occur as part of strep toxic shock (STSS)
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type II, mono infection. GABHS. Or with NO initial signs of shock or organ failure
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What are the risk factors for type II NF
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NONE! It happens to healthy ppl w/o hx of exposure. Contract to type I which was exposure, trauma, surgery, and host debilitation
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What is the KEY to the initial presentation of NF
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pain is OUT OF PROPORTION to clinical findings. Skin from RED, purple, Blue. Facial planes are hard
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Your pt is a healthy 25 yo male who is crying like a baby but you don’t really see anything other than some red skin and its hard to palpate facial planes. What can be the problem
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NF- skin changes from red to purple to blue
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What infection has skin change from red to purple to blue
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NF
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What infection has initial pain out of proportion to clinical findings
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NF
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With NF we know the person will have super pain, and red, purple blue skin changes as well as hard fascial planes. How else might they present
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bullae, systemic toxicity, type I can have gas in tissue (crepitance), smelly if anerobic (GAS as in type II wont smell)
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Do we treat NF ASAP or wait for labs
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ASAP!
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If you have a skin infection that responds to AB what are you thinking, what about if it does NOT respond to AB
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cellulitis- responds to AB NF- wont respond to AB, needs surgical resection first
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Ok so we have our healthy male who is crying like a babe and has red, purple, blue skin changes and hard facial planes. He does NOT respond to AB, should we biopsy
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YES! Determine extent of infection, and ID the microbe. Sounds like NF
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Eew, what does NF look like in surgery
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swollen, necrotic, yellow green fascia. NO true pus, brownish exudates. Undermining of surrounding tissue. Separation of necrotic tissue along facial plane
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What infection has no tru pus but has some brownish exudates
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NF
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How is NF treated
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debridement. Surgery to remove all necrotic tissue. Cut into facial planes to expose all damge including gas bubbles
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What is the AB tx for Type I and II NF
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I- recall polymicrobial infection: ampicillin, clinamycin, metronidazole II- single microbe (GABHS often) clindamycin, penicillin G, Vancomycin
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Is hyperbaric oxygen therapy used for NF
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ya but its controversy, done after surgical resection
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What are some of the unusual tx for NF
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hyperbaric Oxygen, maggots
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Tell me about maggot therapy and tx of NF
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sterile larvae placed in wound, they secrete antimicrobial products, they breakdown and consume dead tissue, they eat/kill bacteria
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Is NF pretty bad
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ya! Death in 1-4 days. Overall morbidity/mortality is 70-80%, this includes the genital NF- Fournier gangrene
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What are some complications associated with NF
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Endotoxin shock from gram – infection, Cutaneous gangrene and myonecrosis, DIC, TS-STSS, bacteremia
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What is deeper necrotizing infections (DNI)
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type III NF, myonecrosis, life threatening. Caused by clostridium or GAS
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What is type III NF
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its deeper, included mm. life threatening. Caused by clostridium or GAS
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How can myonecrosis as seen in type III NF develop
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develops contiguously from area of trauma or hematogenously from GI. Often caused by clostridium or GAS
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What is spontaneous gangrenous myositis
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it’s a type of DNI (deep necrotizing infection). Its RARE but deadly.
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Ok so spontaneous gangrenous myositis is the rare DNI that progresses fast and is deadly. Who does it affect and how
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enters men and women of all ages who are healthy through abraision/blunt trauma. There is NO increased risk
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Why is spontaneous gangrenous myositis scary
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its fast progression, deadly and infects healthy ppl of all ages w/o any risk. But its rare so that is good
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Vementin is important in what infection
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spontaneous gangrenous myositis. A strain or previous injury upregulates vimentin which increases adherence of GAS to mm
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Whats the deal with NSAIDS and spontaneous gangrenous myositis
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don’t take them. It masks signs and delays dx
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What are the clinical manifestations of spontaneous gangrenous myositis
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fever, pain, tenderness, doard like induration of mm, skin is red, hot, bullea, vesicles etc (sounds like NF II) but there is NO gas formation!
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Is there gas formation in NF or spontaneous gangrenous myositis
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NF
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How is spontaneous gangrenous myositis made
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histopath, take them to surgery and get it out! Degeneration of mm fibers, LOTS OF GRANULOCYTES, lots of gram + streptococci
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Your pt was not looking good so you took them in for surgery and biopsied mm, it showed mm degeneration/necrosis, granulocytes nad gram + streptococci. What are you suspicious of
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spontaneous gangrenous myositis. Tc with surgery and clindimycin but still like 80% die
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Whats the tx for spontaneous gangrenous myositis
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surgery, clindimycin, hyperbaric oxygen, immunotherapy (not maggots as was seen in NF)
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Why use clindamycin for spontaneous gangrenous myositis
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not affected by size of innoculum, suppresses protein synthesis, inhibits M protein synthesis and facilitates phagocytosis! All good things for this really nasty disease!
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What is clostridial myonecrosis
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it’s a deep infection caused by clostridium- gram +, ANEROBIC, endospore forming. Divides VERY fast, gas gangrene
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What bug is responsible for the gas gangrene
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clostridium perfringens A, its gram +, endosprore forming, anerobic. Doubles very fast. Found in soil and poo
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Tell me about clostridium perfringes type A
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causes clostridial myonecrosis, its anerobic, gram +, endospore forming- looks like tennis racquet, FAST doubling time
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Clostridium perfringens type A causes what
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gangrene, also cellulitis and fasciitis W/O myonecrosis. Clostridium is found in soil and feces
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Other than C perfringens what other C species cause skin infections
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C septicum- more prominent, endogenous. C histolyticum
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Clostridial myonecrosis occurs when
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usually about a day after an injury, it then doubles really fast! It enters vegetative cells or spores during the initial insult
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Whats the dif btwn traumatic and spontaneous gangrene
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Traumatic (surgical): not super lethal, direct inoculation of wound- surgery, car accident, IV drug use Spontaneous: Hematogenous spread from GI, associated with cancer. C septicum, endogenous
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What type of clostridial gas gangrene is from and endogenous infection
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nonspontaneous- its from hematogenous spread from GI, associated with cancer. C septicum
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What is responsible for the damage caused by clostridium perfringens
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exotoxins: a toxin, Phospholipase C, Lecithinase- destroys membranes
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Tell me about the a toxin and phospholipase C that is seen in c perfringens .
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lyses RBC, myocytes, fibroblasts, platelets, WBC. Also decreases force of cardiac contraction. Releases histamine platelet aggregation thrombus
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Why is there a poor host inflammatory response with a clostridium infection
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theta toxin destroys PMN. Also causes direct vascular injury. Contrast this to the alpha toxin which lyses RBC, WBC, decreases heart contractility, and triggers histamine release
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What does the kappa toxin of clostridium infections cause
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collagenase, helps necrosis spread
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What are the 3 main toxins associated with clostridium
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a- WBC/RBC lysis, decrease heart contractility, release histamine. Theta- PMN destruction. Kappa- collagenase
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Tell me about the gas formation in clostridia infection
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makes H2 gas. Gas seperates tissue and allows access to fresh tissue, breaks BV to keep the area of infection ANEROBIC
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Can clostridium survive in oxygen
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ya its anerobic but is tolerant to some O2. Recall it has that H2 gas formation that helps keep it anerobic by destroying BV
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Where on the body do we see most clostridial infection, what is the initiating event
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extremities, after surgery or trauma
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Is it common to have bacteremia with clostridial infections
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NO! its rare
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What are some systemic finding with clostridia infections
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not bacteremia, shock, DIC, CO decreases. PMN killed
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What infection changes colors from pale to red to bronze and has bullea
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clostridium
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What is the skin color change with clostridial infection
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pale, red, bronze
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What bacteria has a sweet mousy smell
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clostridium
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Does it take a while for a clostridial infection to get bad
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nope, fast onset. Pain gets worse and worse. Low grade fever, toxemia, tachycardia. Can get shocky. Sweet mousy smell
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Is crepitance (gas pockets) dx of clostridium infection
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nope, other infections cause gas formation
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If you biopsy a skin infection and there are NO inflammatory cells, what infection might you suspect
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costridial. Pale-red-bronze. AFTER surgery/trauma. FAST onset. Gas formation. Alpha, theta, kappa toxins
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What is known about the hemolytic property of clostridial infection
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double zone of hemolysis
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Whats the tx for clostridial infection
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surgery defridement, delay suture to allow O2, AB, hyperbaric O2, amputation
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Whats the mortality for clostridial infection? What about nonslostridial myonecrosis
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30% w/tx 100% w/o tx. Non clostridial: MUCH better prognosis
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What bugs cause nonclostridial myonecrosis
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bacteroides, peptostreptococcus (aneroebs), s aureus (aerobe). Better prognosis than the clostridial myonecrosis
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What are the 3 thigns maggots do to help treat skin infection
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1. Debride wound by dissolving necrotic tissue. 2. Kill bacteria 3. Stim wound healing
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