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164 Cards in this Set

  • Front
  • Back
what causes the inflammation in an infection
-result of vasodilation which allows greater blood flow
-also result of increased WBC to the area (pus)
post-op infections (no implant)
-Staph aureus (if pt had hx of MRSA, MRSA should be suspected)
post op infection (with implant)
staph epidermis or coagulase negative staph (large majority are M resistant)
-NOTE: SA is coag positive whiich gives it its virulence
puncture wound OM
pseudomonas aeruginosa
celllulitis following a puncture wound
staph and strept
infected ulcer in DM pt
staph aureus and group B streptococcus(aka strept agalactiae)
clinical signs/symptoms of infection
-lumps of stiffness behind the knees or in the groin
-red streaking (lymphangitis)
does HIV infection have an impact on presentation of LE bacterial infections
no, bc most of the immune alterations in HIV invovlves T cells and therfore response to fingal, viral and parasitic infections may be altered
what bacteria should be covered with all IVDA infections
-MRSA and P.aeruginosa
-SBA should also be ruled out
which abx shouldnt be used with alcohol bc they have disulfirim (Antabuse) reaction of nausea, vomit, tachycardia
-bactrim, flagyl
how is cellulitis diagnosed
-redness (rubor)
-swelling (tumor)
-pain (dolor)
-heat (calor)
-loss of fxn
list some non-infectious inflammatory conditions that can mimic infectious cellulitis
-chronic indurated celulitis(venous)
-acute trauma
-post surgical changes
into what nodes do infections of the foot and leg drain to
-popliteal and inguinal nodes
when is an intermittant fever seen
-in abscesses; which intermittantly see the blood, MC in LE infections
list the drugs that can cause fever
differ sepsis from bacteremia
-bacteremia is presence of bacteria in the blood, sepsis is clinically significant and presents with symptoms
clincical signs of sepsis
-fever (>38 C, 100.4)
-change in mental status
-inc resp rate (>20)
-leukocytosis (<12,000)
how many days should you wait for normalization of WBC with abx tx before switching tx options
-3 days
what is ANC and what level should it be
-absolute neutrophil count
-if <1000, pt should be isolated to prevent exogenous infection
normal ESR
<17 mm/hr in males
<25 mm/hr in females
normal CRP
<1 mg/L
>10 in inflammation
serum creatinine should be monitored in all parenteral abx pts because it is the best index of renal fxn and thus abx excretion, what is N
0.8-1.4 in males
0.6-1.2 in females
what tests are in LFT (liver fxn tests)
list 2 abx metabolized in the liver and thus should be given with LFT
if you order a gram stain of LE infection; what are the most likely results
-gram positive (except in the rare cases of gonococci septic arthritis)
Gram Stain results:
G pos (blue) cocci in grape clusters
Gram Stain results:
G pos (blue) cocci in chains
Gram Stain results:
G pos (blue) rods in chinese characters
Gram Stain results:
G pos (blue) rods with raquet shape
Gram Stain results:
G neg (red) curved rod
on gram stain; in addition to organisms, what else would be present in an infection
-white cells (mainly PMN's)
if gram stain reveals a large number of organisms differing in morphology and culture report only isolates a few, what should be suspected
-anerobic bacteria
what is the Levine method
-cleanse the wound bed or debride
-roll swab in 1cm square area while applying enough pressure to the swab to express fluid from the wound
what do acid fast smears test for
(to be thorough you can order gram stain, aerobic, anaerobicc, fungal and acid fast)
clinical hints that suggest resolution of an infection
-decrease in the amount and anger of cellulitis
-presence of skin wrinkles seen with decreased edema
-appearance of a band of peeling skin, centered around the area of original cellulitis
-post inflammatory hyperpigmentation of a violet color in area of previous cellulitis - may be present for more then one year and isnt warm, so dont confuse with cellulitis
if a pt presents with cellulitis and no opening or drainage, should you aspirate the edge to get a culture
NO. can cause deep spread of the infection and also results in poor recovery of the organism
MC cause of celulitis
-strept and staph
Oral tx for staph/strept cellulitis
-augmentin (amox/clav)
-Penicillinase resistant PCN (cloxacillin, dicloxicillan)
-doxy if MRSA is suspected
parenteral (IV) for staph/strept cellulitis
-ancef (1st gen cephalosporin)
-Augmentin, Pip/tazo
-nafcillan, oxacillin
pathognomonic for CA-MRSA
-pt got a spider or insect bite, but never saw the insect
-agressive spreading abscess
ID masceration, itching and cellulitis over distal foot, red fluorescence under Woods.
Dx, gram stain and Tx
-erythrasma (gram + bacilli)
Tx: oral erythromycin
Honey colored crusts with yellow creamy drainage. Gram stain, Dx, Tx?
-Group A strept, SA, MRSA
-G pos cocci in chains and clusters
-Mupirocin topical or topical retapamulin- latter is effective against MRSA
punched out lesions with greenish yellow crusts with surrounding erythema
-caused by strept
cellulitis with sharply demarcated geographic borders, raised border
-form of cellulitis that involves lymphatic blockage
-group A strept
necrotizing fascitis: bacteria and clinical presentation
-pain out of proportion
-swab can be passed easily b/w tissue planes
-Group A, beta hemolytic strept
Gas gangrene: MC organism and tx
-tense bulla with brown red drainage
-Pen G + Clinda
-or Ertapenem
-or imipenem/cilistain
-anything with g neg coverage
OM types based on etiology
-hematogenous spread
-direct extension or contiguous
-OM secondary to vascular insufficiency
Anatomic stages of OM
-medullary (mc in hematogenous)
-superficial (only outer cortex)
-localized (at least one cortex through into the medullary canal)
-diffuse (more then one cortex is involved plus medullary- bone is unstable)
clinical signs suggestive of OM
-mushy crumbly bone on probing
-purulence inside a bone
-pinpoint swelling, pain or redness over a bone w/o sinus opening
-presence of sinus tract
-scars over the area suggesting a healed sinus
-ulcer greater then 2 cm
lab findings of OM
ESR >70
-elevated WBC
imaging gold std for OM
plain film signs of OM
-cortical breaking
-periosteal elevation-caused by pus breaking through cortex
-lysis and lucency of bone
-brodie abscess in chronic OM
order of imaging for OM
-plain film
-bone scan
very good bone penetration and coverage for staph OM
why is dead space management used in open wounds and fractures
-prevent the collection of fluid that may harbor bacteria
excessive lavage pressure can cause tissue damage and implant organisms deeper in the wound; what pressure should be used
60 psi; which is equivalent to 30 mL syringe with 19 gauge needle
-pressure is more imp than any additives to the water (abx, etc)
what is the "grandfathered" method for deciding when to close a wound
-after 3 negative cultures
what clinical criteria should be met before a wound is closed
-no SOI (no area of red, hot, swollen or pain)
-no purulent drainage
-no odor
-granular appearance of wound bed
-staph epi on wound cultures is not a contraindication to closure
treatment for foot puncture wound (nail)
-amox/calvulanic acid 500 or 875 bid
-clinda 300 mg tid
-cephalexin 500 bid-qid
-levofloxacin 500 qid (includes pseudomonas coverage)
bacteria found in puncture wounds in marine environment
-P. aeruginosa
-mycobacterium marinum
how can a stingray puncture be treated
-this is not bacterial
-the venom is heat labile, so soat in hot water for 30-60 minutes
how does mycobacterium marinum found in pools and freshwater present in the LE
-bluish purple nodules that may drain and ulcerate
why are cat bites more llikely to become infected than dog bites
-cats have deeper punctures
what is your window of tx for bite wounds to prevent infection
-with in 12 hours
with in how many hours should a bite wound be irrigated and debrided if you are going to primary close it
-with in 12 hours
-after 12 hours, leave the wound open
drugs of first choice for bite wounds
-any beta lactamase inhibitor compound (amox/clav, pip/tazo, ticarcillin/clav, ampicillin sulbactam)
why is cefazolin commonly used in traumatic fxs and surgery
-long half life
-good staph coverage
-some gram neg coverage
wound less then 1 cm (puncture wound)
Gustillo Anderson 1
wound 1- 10 cm with soft tissue coverage
Gustillo Anderson 2
Gustillo Anderson 3
greater then 10 cm
A: with soft tissue coverage
B: with periosteal stripping
C: with vascualr damage
gustill anderson 1 tx
gram positive coverage with cephalosporin
gustillo anderson 2 tx
gram pos coverage with cephalosporin, add gram neg coverage with aminoglycoside such as gentamycin (or you can use a newer quinolone or ES cephalosporin - rocephin)
according to lavery, what % of DM ulcers become infected
5 yr and 50% with relation to DM amps
-5 yr survival of one leg amp is 50%
-pts with 1 limb amp have 50% chance of 2nd limb amp in 5 years
triad of factors for DM foot infection
list the 3 neuropathys of DM and their role in ulceration
-sensory neuropathy
-motor neuropathy (muscle wasting, imbalance of flexors, dorsal dislocations, claw toes, pseudo-cavus, dorsal dislocation of fat pad)
-autonomic neuropathy: impaired sweating, xerosis, sympathetic failure causes vasodilation adn AV shunting causing decreased perfusion, edema
what effect does hyperglycemia have on the immune system
-decreases chemotaxis to site of infection
-decrease phagocytosis
American Diabetes Assoc with regards to DM and PAD
In DM the occulsive disease:
-more widespread and multisegmental
-occurs at earlier age
-is more frequent
-progresses to more advanced stages
-presents with more distal involvement
-presents with moer gangrene
-tends to be bilateral
-affects men and women equally
which abx should be avoided in DM because of impaired renal fxn in LT DM
6 grades of ulcers primarily based on depth
Mantra of DM ulcers
what is excessive hyperkeratosis around a wound edge a sign of
-excessive WB and/or pressure
Biofilm over the granulation tissue of a wound does not indicate infection, however what 2 organisms commonly form biofilms
-staph and pseudomonas
normal flora in ulcers (flora in non-infected ulcers)
-staph epi
-p mirabilis
-p aeruginosa
clincial presentation of MILDLY infected ulcers
-lack of healthy granulation (pink instead of red) base
-necrosis, eschar formation
-red, swollen, heat
-purulent drainage
-less then 2cm of erythema from wound edge
bacteria of mild infections
-SA, Group B strept (strept agalactiae)
TX for mild infected ulcers (<2cm erythema around wound, >2 SOI, no systemic signs)
-debride and offload
-oral abx
-Augmentin 875 bid
-Keflex 500 mg tid
-clinda 300 mg bid
clinical presentation of MODERATE infected ulcer
1 or more of these symptoms:
-cellulitis >2 cm from wound edge
-lymph streaking
-spread anywhere beneath the superficial fascia
-no systemic SOI
bacteria of MODERATE infections
-Group B strept
-Gram pos anaerobes (Pepto)
-Gram neg aerobes (Ecoli, proteus, enterobacter, pseudomonas
-gram neg anaerobes (B fragilis, bacteroides
which group of abx have good bioavialiability orally and parenterally
Tx for moderate infections
-debride and offload
-IV abx
-Pip/tazo (Zosyn) 3.375 q6
-linezolid (zyvox) 600 mg q12
-Ertapenem (Invanz) 1 g q24
MRSA coverage for moderate DM infections
-Linezolid 600 mg q12
-vanco 1 g IV q12
-daptomycin 4mg/kg IV q24
-tigecycline 100 mg IV, tehn 50 mg q12
clinical signs of SEVERE foot infection
-local wound and systemic signs are present (F/C/N/V/tachy/hypotension)
tx for SEVERE infections
-hospitalization and IV abx (same as moderate)
Pip/tazo (Zosyn) 3.375 q6
-linezolid (zyvox) 600 mg q12
-Ertapenem (Invanz) 1 g q24
MC areas for arterial ulcers
-distal toes
-medial side of 1st met head
-lateral side of 5th met head
Clinical symptoms/signs of arterial ulcers
-worse at night
-relieved with dependency
-necrotic bases with eschar
-remain stable for long periods or until vascular intervention
what is post-bypass hyperemic flush
-occurs after revascularization in arterial ulcer
-may be confused with infection (arterial ulcers are rarely infected)
Tx for arterial ulcers
-not usually debrided
-topical enzymes for breaking down eschar
DM are 4-5 times more likely to get fungal infection, why is it imp to treat these
-ID tinea leads to masceration that can lead to secondary bacterial infection
-the anatomy of the webspaces allows infection to spread via many tendons that insert near the webspaces
when should surgical prophylactic abx be given
-sx lasting longer then 2 hours
-sx on immunocompromised pts (DM, CA, RA, HIV)
-trauma sx
-implant sx
most common post-op pathogen
implant infections are MC caused by
-staph epidermis
-is often MRSE
-can take up to 1 year from sx to show up
what is the dosage time for pre-op oral, IV, muscular injections of prophylactic abx
-oral should be given 1 hour before incision
-45 minutes for IM route
-IV should be given before tourniquet inflation
how many days of post op abx is suggested to decrease infection rate
3-5 days
why is cefazolin used for preop abx (ancef)
-long half life to last in cases around 2 hours
-covers staph and some gram negs
if in a hospital with high MRSA or implant surgery (activity against coag neg staph) what pre-op abx should be used
-1 g begun 1 hour before sx and infused over that hour
what is the alternaative for PCN allergic pts (cant use ancef) or beta lactam allergic pts (cant use vanco)
clinda 600-900 mg IV
why shouldnt cipro be used in surgery prophy
-doesnt cover staph well
newer quinolones are just as bioavailable in their oral as their IV form; give example
levofloxacin (levaquin)
what are the current guidelines for pre-op abx (who gets them)
-all pts during the first two years after a joint replacement
-immune compromised pts
-pts with comorbidities (previous joint infections, malnutrition, hemophillia, HIV, DM, CA)
what was the first FDA approved topical therapy for onychomycosis
ciclopirox 8% lacquer (penlac)
-broad spectrum effective against fungus, yeast, molds and some g pos, g negs
name the three dermatophytes that cause human fungal infections
MC causes of tinea pedis
T rubrum
T mentagrophytes
E floccosum
what pathogen is most likely to cause ID infection
C. albicans
explain the phrase "gram neg tinea"
-fungus breaks down the ID tissue which leads to secondary bacterial infection by pseudomonas and proteus
name 3 predisposing factors for tinea pedis in pts
-genetics (some lack the genetics in T cells to fight dermatophytes)
-environment (pts who work in wet shoes etc)
-anatomic occlusion (pts with lack of room b/w their toes)
fungus of skin and nail unit: fungus produces hyperkeratosis that builds up under the nail plate and lifts it up
DSO- distal subungual
name the 3 types of onychomycosis and describe them
-DSO; thickened nails with peri nail involvement
-WSO: white superficial with out nail thickening
-Proximal white onychomycosis: common in HIV and immune compromised
best oral drug for onychomycosis
Terbinifine (lamisil)
when culture material is gathered on a swab, what should be ordered
-Gram stain with culture and sensitivity
what is the time frame on gram stain
-24 hours
what is the time frame on a complete culture report (what bacteria are present)
48 hours
what are 2 methods for determining sensitivity of bacteria
-Kirby Bauer disc diffusion (qualitative)
-MIC with microdilution (quantitative)
abx can killa by "concentration dependent killing" or "time dependent killing"; list examples of each
-as concentration increases above MIC, so does killing (quinolones, aminoglycosides)
-minimal increase in rate of healing above MIC (PCN, ceph)
what happens when a G6PD pts take sulfonamides
how are most abx cleared from the body
-the kidneys
-so renal pts should have the dose adjusted or time interval b/w doses altered
liver metabolized abx
clinda, erythromycin, chloramphenicol
abx associated with ototoxicity; which are reversible
-aminoglycosides (gentamycin) and erythromycin, vancomycin
-erythromycin is reversible
-vanco ototoxicity was thought to be related to impurities
why should aminoglycosides always be administered over 30 minute period and never in a bolus
-due to their NM blockade and affect ACh uptake and release
abx that cause nephrotoxicity
-PCN and cephs
abx that are liver toxic
-erythromycin (reversible)
what abx can cause neutropenia (WBC drop)
-sulfonamides can cause agranulocytosis
-beta lactams (augmentin, cillins, cephs)
although this abx is rarely used in the foot; can be used for gram pos cocci in chains, OM where strept is only pahtogen, septic arthritis in young individual where gonococcus is suspected
Penicillin G
SA (not MRSA) infection
-nafcillin, cloxacillin, dicloxacillin
first choice for staph - methicillin sensitive
antistaph oral (cephalosporin)
IV for non MRSA staph
oral for strept
same as staph (cephs)
-keflex, ceftin, omnicef, cefzil
oral for staph (MRSA)
Zyvox (linezolid), bactrim, mino/doxy
IV for staph (MRSA)
drug for VRE
linezolid (zyvox) - oral and IV
oral drug for enterococcus (not VRE)
IV for enterococcus (not VRE)
oral for ecoli
cephalosporin (similar to staph and strept coverage) or quinolone
IV for ecoli
oral for pseudomonas
anti anaerobic agents
-metronidazole (flagyl)
anti gram positive abx
-synercid (quinupristin/dalfopristin)
-zyvox (linezolid)
-cubicin (daptomycin)
-tygacil (tigecycline)
aerobic gram pos cocci
-staph is clusters
-strept is chains
aerobic gram pos cocci enterococci
-enterococci (E. faecalis)
-found in gut
anerobic gram pos cocci
gram pos bacilli
-clostridium tetani
- c perfringens
gram neg cocci
neisseria gonorrhea
neisseria meningitides
anerobic gram neg rods
aerobic gram neg rods
enterobacteriacea; citrobacter, enterobacter, ecoli, klebsiella, proteus, salmonella, serratia, pseudomonas
greatest cause of steven johnson reaction
sulfa drugs
later generation tetracyclines can be used for CA-MRSA; list them and the dose
-100 mg q12 po
If there is an "S" next to Clinda, can you use clinda?
no, look at the macrolide line usually represented by erythromycin. If it is resistant to erythromycin, cant use clinda.
what is the MIC creep for vanco
-in the past MRSA strains could be inhibited by 0.5 micrograms, it is now creeping to 1 and even 2
-if greater then 2, choose another drug
only oral drug for MRSA soft tissue infections
Zyvox - linezolid
4 FDA approved abx for MRSA
-linezolid (zyvox); only oral
-daptomycin (cubicin)
-tigecycline (tygacil)
how does celulitis and erysipelas differ
-cellulitis has a less demarcated borders
-erysipelas is a form of cellulitis, but the lesion is indurated, scarlet red and often complicated by lymphangitis
-erysipelas is more superficial then cellulitis
hypotension is a SOI, what is considered hypotensive
-systolic <90 20mmHg below baseline
SSI (surgical site infections)-fever or clinical evidence of soft tissue infection with in the first 48 hours after a surgery (usually they show 5 days-2 wks); which bacteria are implicated with an infection this early post op
S pyogenes