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Med School > Sepsis > Flashcards

Sepsis Flashcards

1
Q

Definition of Sepsis

A
  • symptoms due to infection which results in organ dysfunction or failure
  • dysregulated host response, NOT necessarily just a blood stream infection
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2
Q

Pathophysiology of Sepsis/ Septic Shock

A
  • bacteria Ag trigger macrophages to release cyto/chemokines –> vasodilation and increased vascular permeability –> migration into tissue
  • DIC (systemic activation of coagulation cascade), widespread endothelial damage (edema), microcirculatory dysfunction, lower contractility, tissue hypoxia and damage/ death
  • cytokine storm of TNF, IL-1, IL-6
  • initially hyper-inflammatory but can also progress to hypo-inflammatory with cell-exhaustion and high risk of secondary infection
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3
Q

Minor Differentiations Between:
Systemic Inflammatory Response Syndrome (SIRS)
Sepsis
Severe Sepsis
Septic Shock

A
  • an appropriate response to infection/ inflammation
  • SIRS + infection
  • sepsis + organ damage
  • severe sepsis + hypotension
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4
Q

SOFA criteria

A
  • sepsis is associated with an increase in SOFA score by 2 or more
  • respiratory rate equal to or over 22
  • SBP equal to or under 100
  • GCS equal to or under 13
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5
Q

Septic Shock

A
  • need vasopressors to maintain mAP of 65
  • serum lactate over 2mmol/L
  • absence of hypovolemia
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6
Q

Investigations for Shock
- Hour 1
- Within 3 hours
- Within 6 hours

A
  • always do concurrently with management!
    *WBC, platelets, coags, lytes, renal, liver, glucose, ABG, LACTATE
  • blood/ urine/ sputum/ abscess cultures, CXR, CT/US, biopsy
    *if low likelihood of sepsis, defer ABX and monitor

Hour 1
- measure lactate, remeasure if over 2
- obtain blood cultures then administer broad spectrum ABX (1 hour is high likelihood, 3 if possible)
- rapid administration of 30ml/kg crystalloid for hypotension or lactate over 4
- give vasopressors if hypotensive during or after fluid resuscitation to maintain mAP of 65

3 Hours
- measure lactate, remeasure if over 2
- obtain blood cultures then administer broad spectrum ABX
- rapid administration of 30ml/kg crystalloid for hypotension or lactate over 4

6 Hours
- give vasopressors if hypotensive during or after fluid resuscitation to maintain mAP of 65
- re-measure lactate if initial was elevated
- if persistent hypotension after initial fluids or if lactate is still over 4, re-asses volume status and tissue perfusion

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7
Q

Albumin with Crystalloids

A
  • recommended when patients need a large amount of crystalloids infused
  • helps draw fluid into the vessels
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8
Q

Primary vs Secondary Blood Stream Infection

A

Primary –> unknown organism source
Secondary –> identified organism source (UTI, pneumonia)

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9
Q

Most Common Culture Positive Sepsis Source
Most Common Community Blood Stream Infxn
Most Common Hospital Blood Stream Infxn

A
  • the lungs
  • E.coli (90+ is most common age group)
  • coagulase negative staphylococci
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10
Q

Staph Aureus
- investigations
- treatment

A
  • gram (+) cocci in CLUSTERS (identical to coagulase (-) staphylococci)
  • soft tissue, catheter associated BSI, bone/joint, surgical and prosthetics, HAP, increased risk for endocarditis
  • repeat 2 sets of blood cultures every 48h until clear, ID consult
  • echo for endocarditis
  • drain abscesses
  • replace central venous catheters
  • MSSA –> cloxacillin and cefazolin
  • MRSA (resistant to cloxacillin) –> vancomycin
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11
Q

Strep Pneumo
- investigations
- treatment

A
  • gram (+) cocci in PAIRS
  • otitis media most common, CAP and bacterial meningitis are most serious
  • repeat blood cultures are usually unnecessary unless peristent sepsis and fever after 48h of treatment
  • endocarditis is rare but check if cultures remain (+)
  • penicillin, ampicillin, ceftriaxone
  • occasionally will have penicillin resistance
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12
Q

Common causes of (+) blood cultures due to skin flora contamination. What is NEVER a contaminant?

A
  • coagulase (-) staphylococci (though may be real if catheter/prosthetics), cutibacterium acnes, corynebacterium, bacillus
  • don’t treat, repeat culture to confirm
  • staph aureus, gram (-) bacilli, and yeast are never considered contaminants
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13
Q

Strep Pyogenes (Group A Strep)
- investigations
- treatment

A
  • gram (+) cocci in CHAINS
  • strep pharyngitis and cellulitis most common, can also cause pneumonia/empyema/nec. fasciitis/ toxic shock/ rheumatic fever
  • repeat blood cultures are usually unnecessary unless persistent sepsis and fever after 48h of treatment
  • endocarditis is rare but check if cultures remain (+)
  • PENICILLIN, ampicillin, cephalosporins
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14
Q

Viridans Group Strep
- investigations
- treatment

A
  • gram (+) cocci in CHAINS (large group that all behave similarly)
  • abscesses in brain/lungs/liver/abdomen, normal part of oral flora but can cause aspiration pneumonia, can cause endocarditis
  • repeat cultures after 48h to ensure clearance
  • look for endocarditis if cultures remain (+)
  • ceftriaxone, drain abscesses
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15
Q

Enterococcus
- investigations
- treatment

A
  • gram (+) cocci in CHAINS
  • faecalis more community, faecium more hospital
  • UTIs, hepatobiliary infections, endocarditis
  • assess urine and biliary function
  • repeat blood cultures after 48h to ensure clearance
  • faecalis –> ampicillin, pip-tazo, imipenem
  • faecium –> linezolid (likely amp and vanco resistant)
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16
Q

Enterobacterales (coliforms)
- investigations
- treatment

A
  • gram (-) bacilli (i.e. E.coli, proteus, enterobacter, klebsellia, citrobacter)
  • UTIs, hepatobiliary and intra-abdominal infections, infections from catheters and HAP
  • salmonella, shigella, yersinia cause enteritis
  • repeat blood cultures are usually unnecessary unless persistent sepsis and fever after 48h of treatment
  • endocarditis is VERY rare but check if cultures remain (+)
  • major ABX resistance, refer to local antibiogram
  • community and not septic –> ceftriaxone
  • hospital or septic –> pip-tazo or meropenem
  • drain abscesses
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17
Q

Pseudomonas
- investigations
- treatment

A
  • gram (-) bacilli
  • lower resp. tract infections in patients with chronic lung disease, HAP
  • repeat cultures after 48h to ensure clearance
  • look for endocarditis if cultures stay (+)
  • refer to local antibiogram
  • empiric –> pip-tazo, meropenem, imipenem, ceftazidime
  • if critically ill, double coverage with an aminoglycoside (gentamicin) or ciprofloxacin
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18
Q

Candida
- investigations
- treatment

A
  • gram (+) staining yeast, large oval, budding
  • C.albicans is #1
  • part of normal flora but can be opportunistic (HIV, neutropenia), oral/ cutaneous/ vaginal infections, often serious if nosocomial, can form biofilms, can cause endocarditis/ peritonitis/ meningitis and seed to the eyes
  • repeat 2 sets of cultures every 48h until cleared, ID consult
  • echo if persistent candidemia or valvular disease
  • ophthalmology to look for endopthalmitis
  • micafungin empirically, can eventually switch to fluconazole
  • replace catheters
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19
Q

Most common cause of non-purulent vs. purulent cellulitis? Treatment?

A
  • non-purulent –> strep pyogenes
  • penicillin
  • purulent –> staph aureus
  • cloxacillin
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20
Q

Most common cause of bacterial sinusitis? Treatment?

A
  • strep pneumo and H. flu
  • amoxicillin
  • sometimes H.flu will have amoxicillin resistance, so amox-clav is used
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21
Q

Common causes of CAP and HAP? Treatment?

A

CAP –> step pneumo
- penicillin or amoxicillin

HAP –> pseudomonas
- pip-tazo

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22
Q

Common causes of intra-abdominal infections?

A
  • E.coli is most common (also for UTIs)
  • NEVER treat with penicillin, sometimes amoxicillin but more commonly amox-clav or pip-tazo
  • Viridans group strep
  • penicillin or amoxicillin
  • E. faecalis
  • penicillin or amoxicillin (NOT if faecium)
  • Anaerobes
  • amox-clav or pip-tazo
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23
Q

Cephalosporins
- 1st gen
- 2nd gen
- 3rd gen

  • what do they not generally treat?
A
  • 1st gen –> soft tissue and skin infections
  • oral cephalexin or IV cefazolin to treat cellulitis (unless MRSA)
  • 2nd gen –> respiratory tract infections
  • cefuroxime for sinusitis, otitis media, CAP
  • 3rd gen –> respiratory tract infections
  • ceftriaxone for CAP, best against E.coli (unless ESBL) and viridans-group abscesses
    *if HAP from pseudomonas, ceftazidime (3rd) and cefipime (4th)
  • cannot use alone to treat E.faecalis and often anaerobes
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24
Q

Carbapenems
- which one can treat enterococcus?
- which one cannot treat pseudomonas?

A
  • back-up when nothing else works
  • drug of choice to treat ESBL and AmpC (meropenem, imipenem, ertrapenem)
  • only IMIpenem can treat enterococcus
  • ERTRApenem is not useful for pseudomonas
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25
Q

Fluroquinolones
- which one can treat anaerobes?

A
  • mostly used from belly up (except ciprofloxacin which can help with gram (-) GI/GU bugs like E.coli/ESBL/AmpC)
  • all effective against atypical bacteria that cause CAP
  • only moxi and levo are good against strep pneumo (CAP)
  • cipro and levo can treat HAP for pseudomonas
  • moxifloxacin can treat anaerobes
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26
Q

Macrolides

A
  • good in the respiratory tract
  • azithromycin effective against s. pneumo (CAP) and atypical bacteria
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27
Q

Tetracyclines

A
  • all over the place
  • doxycycline for purulent MRSA cellulitis, s.pneumo (CAP), and atypical bacteria
  • doxycycline also good prophylaxis for malaria (plasmodium) and to treat Borrelia Burgdorferi (lyme disease)
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28
Q

Clindamycin

A
  • works similarly to penicillin, but also treats purulent cellulitis caused by MRSA
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29
Q

Drugs that can cover MRSA

A
  • doxycycline, clindamycin, cotrimoxazole (TMP-SMX)
  • vancomycin, linezolid, daptomycin (gram + specialists, NO gram - activity)

*linezolid and daptomycin are reliable against VRE (vancomycin resistant enterococcus)

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30
Q

Common Resistance Mechanisms against:
- B-lactams (penicillins, cephalosprins, carbapenems)
- Glycopeptides (vancomycin)
- Aminoglycosides (gentamicin)
- Sulfonamides (TMP-SMX)
- Quinolones (floxacins)
- Macrolides (azithro/clarithro/erythro)

A
  • B-lactams –> B-lactamases (ESBL, AmpC, penicillinase in S.aureus, carbapenemases), mutations in PBPs (MRSA), decreased uptake
  • Glycopeptides –> altered target (cell wall mutation in VRSA, VRE)
  • Aminoglycosides –> enzymatic modification, altered target, decreased uptake
  • Sulfonamides –> altered target (DHPS/DHFR enzyme mutations)
  • Quinolones –> decreased uptake, altered target (DNA gyrase mutation)
  • Macrolides –> efflux pumps (staph and strep), altered target (ribosomal alteration)
31
Q

MIC
Breakpoint

A
  • minimum inhibitory concentration
  • the concentration of ABX where growth is fully halted
  • the MIC at which an organism is interpreted to be resistant or susceptible
32
Q

Which ABX:
- inhibit folate
- inhibit NA
- inhibit protein
- disrupt cell membrane
- inhibit cell wall

A

folate –> sulfonamides, trimethorpin
NA –> quinolones, metronidazole
protein –> aminoglycosides, tertracyclines, erythromicin, clindamycin, linezolid
membrane –> daptomycin
wall –> B-lactams (penicillins, cephalosporins, carbapenems), vancomycin

33
Q

Pseudomonas Aeruginosa Resistance Mechanisms

A
  • lower OprD (carbapenem channel) leads to low permeability and periplasm concentration –> resistance to imipenem
  • multidrug efflux pumps (Mex-OPR) and single drug efflux pumps for tetracyclines (tet)/ macrolides (mef)/ quinolones (norA)
34
Q

PBP Mutations
Ribosomal Mutations
DNA Gyrase Mutations

A
  • confers B-lactam resistance (MRSA, penicillin resistant strep)
  • confers tetracycline, aminoglycoside, and macrolide resistance
  • confers quinolone resistance
35
Q

How does ______ resistance occur?
- vancomycin
- sulfonamide (TMP-SMX)

A
  • vanco –> vanA in VRE encodes for altered peptidoglycan precursor (prevents binding)
  • SMP-TMX –> mutations on DHPS/DHFR prevent binding
    –> enterococcus can scavenge for pre-formed folic acid in vivo
36
Q

What drugs is Klebsellia resistant to?

A
  • carbapenems and other B-lactams due to ESBL and carbapenemases
37
Q

Differences between animal and fungal cell walls.

A
  • both eukaryotic
  • fungi have cell walls and the cell walls have glucan
  • human cells have cholesterol while fungi have ergosterol
38
Q

Drugs used for fungi and their MOAs

A
  • flucytosine –> antimetabolite that competes with uracil
  • azoles (fluconazole) –>interrupt ergosterol synthesis
  • polyenes (amphotericin, nystatin) –> bind ergosterol and form ion channels that cause cell leakage
  • ehcinocandins (micafungin)–> inhibit B-glucan synthesis = lysis
39
Q

Molds

A
  • composed of filamentous cells called hyphae, can fuse into mycelia
    -dermatiaceous hyphae are pigmented, hyaline are clear

Septate –> dermatophytes (infections of skin/hair) and opportunists (aspergillus)
Aseptate –> zygomycetes

40
Q

Dimorphic Fungi

A
  • can be both a yeast or a mold depending on temperature
  • 25-30 mold
  • 37 yeast
  • crytptococcus, blastomycosis
41
Q

Yeast

A
  • single cell fungi, round oval, reproduce by budding (increased volume and then mitosis) or fission (divides in 1/2, cytoplasm split equally)
  • may have pseudo (constrictions) or true hyphae (candida has both)
42
Q

Methods to Dx Fungal Infections

A
  • culture is gold standard for candida, can identify species and susceptibility (but fungi growth is SLOW)
  • do a fungal blood culture if suspected blastomyces, coccidiodes, histoplasma, malasezzia, aspergillus, etc. or many (-) blood cultures with no improvement especially if immunocompromised
  • direct microscopy (20% KOH, light microscope, fluorescent staining)
  • GMS and PAS stains (H+E will not identify fungi)
  • galactomannan, cryptococcal, and B-D-glucan Ag tests (enzyme-linked immunoassays)
  • PCR for P.jirovecii only and sometimes aspergillus
43
Q

Risk Factors for Candidemia
- how to dx?
- tx

A
  • immune supression (HIV as T cells are most important for control, neutropenia, corticosteroids)
  • broad spectrum ABX
  • prolonged hospital stay
  • central venous catheters, total parenteral nutrition, recent abdominal surgery
  • blood cultures
  • start with micafungin and then switch to fluconazole (if albicans/tropicalis/parapsilosis) or amphotericin B (if other)
44
Q

Aspergillus
- risks
- complications
- dx
- tx

A
  • A. fumigatis #1
  • alveolar macrophages recruit neutrophils –> most important defence against aspergillus
  • prolonged neutropenia, corticosteroids
  • ABPA (allergic bronchopulmonary asp)–> hypersensitivity reaction in ppl with asthma/CF (nodules/cavities/aspergilloma)
  • IPA (invasive pulmonary asp) –> can be angioinvasive, hyphae in tissue, aspergilloma
  • dx–> body and fluid tissue samples for histopath/ culture > serum and BAL fluid galactomannan > serum 1,3-B-D glucan > serum and BAL PCR
  • tx –> voriconazole or amphotericin B, immune supression, surgical debridement for sinusitis/ endocarditis/ aspergilloma
45
Q

Cryptococcus
- neoformans vs. gatii
- dx
- tx

A
  • C. neoformans and C.gatii (PNW and australia) are #1
  • soil, trees, bird droppings –> aerosolized spores that transform into yeast at body temperature
  • neoformans –> often asymptomatic, controlled with alveolar macrophages/ granulomas, ring enhancing lesion with central hypo-intensity on MRI, can disseminate to CNS if immunosupressed, top cause of meningitis in HIV endemic areas (CD4 under 100)
  • gatii –> more common in immunocompetenet, more commonly pulmonary disease, less often meningitis
  • common in people over 50 with lung conditions
  • dx –> serum and CSF cryptococcal Ag, CSF/ sputum/ BAL microscopy and culture, lung tissue histopathology
  • tx –> LONG, mostly done with fluconazole over months/years (lifetime if transplant patient)
  • if disseminated, start with induction of amphotericin and flucytosine and switch to fluconazole once culture is clear
46
Q

Fluconazole
- what does it not cover?
- considerations

A
  • does not cover molds, and C. kreusi/ C.glabrata
  • 90% renal excretion so need to adjust if renal failure
  • p450 inhibitor so check drug-drug interactions
  • very water-soluble –> good for meningitis/ UTIs
47
Q

Voriconazole
- what can it not treat?
- considerations/ side effects

A
  • fairly broad-spectrum, covers Candida/molds and drug of choice for aspergillus
  • cannot treat UTIs (no active form in urine)
  • 96% bioavailable and variant half-life so must monitor
  • many drug interactions
  • S/E –> photosensitivity, transient visual disturbances, periostitis, can build up in renal failure
48
Q

Random considerations

A
  • the most common cause of fever in neutropenic patients is gram (-) bacteremia, so do not start empiric fungal therapy at 1st presentation even if (-) blood cultures
  • cavitary mass in a neutropenic patient is aspergillus until proven otherwise (esp. if ground glass/ halo sign)
    –> bronchoscopy with tissue biopsy
49
Q

Purulent Infections
- likely cause
- tx

A
  • folliculitis, furuncles, carbuncles, cutaneous abscesses, purulent cellulitis
  • Majority are staph aureus (60% are MRSA)
  • tx –> incision and drainage, send pus for gram stain and culture
  • ABX if large, multiple, immunosuppressed, drainage not possible, systemic toxicity, poor response to drainage
  • no signs of systemic toxicity/ immunocompetent —> TMP/SMX or Doxy or Clinda
  • signs of systemic toxicity/ immunocompromised –> Vancomycin or Daptomycin or Linezolid (and switch to cloxacillin or cefazolin if MSSA)
50
Q

Non-bullous vs bullous impetigo
- dx
- tx
- consequences

A

Non-bullous –> highly infectious, school aged children
- staph aureus > group A strep
- clinical dx
- can cause glomerulonephritis
- tx –> topical ABX (muciporin) or oral cephalexin

Bullous –> most common in neonates
- toxin producing S.aureus (exfoliative toxin A and B)
- clinical dx + blood cultures
- can cause dehydration, sepsis
- tx –> oral cephalexin, IV cefazolin, vancomycin if risk of MRSA

51
Q

Erysipleas
- likely cause
- tx

A
  • limited to upper dermis and superficial lymphatics
  • sharp/raised well-demarcated erythema, facial involvement common
  • rapid onset, fever, systemic toxicity
  • almost always Group A Strep
  • tx –> oral penicillin/amoxicillin/cephalexin or IV penicillin/ cefazolin
52
Q

Cellulitis
- simple vs severe
- likely cause
- dx
- tx

A
  • commonly a break in the skin leads to normal flora invading the dermis and SC tissue
  • lower extremities most common
  • simple + localized –> no systemic symptoms, normal WBC, lymphadenopathy and lymphangitis are common
  • severe –> systemic symptoms, bullae, hemorrhage, severe swelling
  • 75% are Strep A (Pyogenes), staph aureus less commonly but consider if IV drug use/ wounds
  • blood cultures are rarely positive, only do if signs of systemic toxicity

simple –> Cephalexin or Amoxicillin or Pen V
severe/ immunocomp/ failed oral ABX –> cefazolin IV
signs of sepsis/ nec fasc –> pip-tazo and vancomycin, +/- surgery

53
Q

Septic Arthritis
- likely cause
- dx
- tx

A
  • surrounding soft tissue infection, hematogenous spread is common
  • clinical triad of fever, pain, and decreased ROM
  • S.aureus > strep > gram (-) > mycobacterium and fungi
  • dx –> synovial fluid (WBCs, gram stain, no crystals)
  • tx –> vancomycin (gram (+) cocci), ceftriaxone (gram (-) bacilli), vancomycin and ceftriaxone if mixed
  • source control with needle aspiration or open drainage
54
Q

Special Considerations for infections of a prosthetic joint?

A
  • S. aureus is great at forming biofilms –> rifampin
  • can retain with debridement only if prosthesis is well fixed, susceptible to oral antibiotics, no sinus tract, and symptoms have lasted less than 3 weeks
  • also (if retained) –> IV ABX for 6 weeks followed by oral ABX for 4 months, rifampin throughout
  • otherwise need to surgically remove prosthesis
55
Q

Animal Bites
- drug of choice for all?

A
  • polymicrobial (animal mouth flora and human skin flora)
  • 80% of cat bites become infected (pasturella multocida, empiric treatment every time)
  • 5% of dog bites become infected (pasturella canis, only treat if severe or immunocompromised)
  • human (clenched fist injury) –> very infectious, risk of septic joint and osteomyelitis, IV ABX and imaging
  • drug of choice for all is amox-clav
56
Q

Tetanus and Rabies

A
  • only give tetanus Ig if major wound and has not had at least 3 vaccine doses
  • rabies is very unlikely in vaccinated domestic pets, but assess anyway
57
Q

Diabetes Related Infection
- mechanism
- dx
- tx
- common complication

A
  • hyperglycemia impairs neutrophil chemotaxis and adherence to vascular endothelium as well as bactericidal activity of leukocytes, peripheral neurovascular disease impairs flow to the foot, microvascular disease lead to local tissue ischemia
  • peripheral neuropathy leads to pressure ulcers
  • autonomic neuropathy leads to dry/cracked feet (susceptible to infection)
  • only culture moderate to severely infected wounds –> clean with saline and remove necrosis, swab viable tissue at the base –> send for gram stain and culture
  • mild –> strep and staph –> cephalexin +/- TMP-SMX
  • mod –> strep/staph/gram (-) anaerobes –> amox-clav +/- TMP-SMX
  • severe –> strep/staph/gram (-) anaerobes/ pseudomonas –> pip-tazo and vancomycin
    *if patient has received ABX in the last month, cover gram (-)
  • debridement and sometimes amputation, wound care, glycemic control
  • common complication –> osteomyelitis, dx clinically and with bone/tissue culture and ideally MRI, sometimes XR, wound swabs wont always predict cause
58
Q

Chain of Transmission
- aerosols vs droplets

A
  • susceptible host
  • infectious agent
  • reservoirs
  • portals of exit
  • modes of transmission
  • portals of entry
  • aerosol <100um
  • droplet >100um

*point of care risk assessment is made every interaction
*alcohol based hand rub is less drying, rapid killing
*remove any catheters or IVs as soon as possible

59
Q

Indications for a urinary catheter?

A
  • monitoring output in a critically ill patient
  • acute urinary retention
  • surgeries
  • grade 3/4 pressure ulcers
  • palliation
60
Q

Main drivers of ABX resistance?

A
  • selection pressure and transmission
  • NOT new mutations
61
Q

Toxic Shock Syndrome
- cause
- pathogenesis

A
  • s. aureus and strep pyogenes are the culprits
  • acute toxin-mediated illness resulting in shock and multi-organ failure
  • s. aureus –> TSS toxin-1, staphylococcal enterotoxins (SEB and SEC)
  • strep –> strep pyrogenic exotoxin A
  • these toxins are super Ag, and thus bind as unprocessed proteins to MHCII and TCR which leads to massive immune activation –> cytokine storm leading to damage
62
Q

Staphylococcal TSS
-tx

A

Staph –> classified as menstrual vs. non-menstrual
- fever, myalgias, GI upset, macular rash –> progresses to hypotension, organ dysfunction, skin desquamation
- rarely can lead to bacteremia (5%)

  • Tx –> source control (tampon, surgical debridement)
  • IV vancomycin and clindamycin for the first 72 hours (IV cloxacillin or cefazolin if MSSA)
63
Q

Streptococcal TSS

A
  • group A strep usually in the context of invasive disease
  • hypotension, organ dysfunction
  • M-protein –> virulence protein, adheres to epithelium, assists in evading phagocytosis/ Ab binding, additional cytokine release
64
Q

Necrotizing Fasciitis
- what is it, sx
- two different types
- risks

A
  • severe and rapid infection of the muscle fascia and subcutaneous fat (can involve epidermis or muscle)
  • lower limbs more common but can involve any body part
  • severe pain, progressive edema, fever –> can mimic cellulitis early on
  • late signs –> bullae, gas in soft tissues (crepitus), cutaneous anesthesia (if strep A, general sx of TSS)

Type 1 –> polymicrobial (gram (-) and anaerobes)
Type 2 –> monomicrobial (group A strep)

  • preceding skin breach, diabetes, obesity
65
Q

Diagnosis and Treatment of Necrotizing Fasciitis

A
  • CBC and differential, blood cultures, liver/renal, CK/AST for muscle damage, CRP
  • risk calculators (lab indicators of NF –> Na under 135, Cr over 141, glucose over 10, CRP over 150)
  • imaging findings are often late (gas on plain film/CT/MRI), often unhelpful
  • diagnosis is surgical! debridement and send for gram stain
  • Tx –> source control (debridement), septic support
  • Vanco/Pip-tazo/Clindamycin if suspected
  • proven group A strep –> penicillin/ clindamycin, minimum of 14 days, clindamycin remains active in large inoculum and may lower M-protein production
  • IV Ig –> pooled Ab from many donors, neutralize super Ags, decrease chemokine receptors and cytokines
66
Q

Lupus Cerebritis
- tx

A
  • neuropsych manifestations of SLE
  • headache, confusion, lethargy, seizures, depression, psychosis, coma
  • treat with prednisone and cyclophosphamide
67
Q

When should you do a CT before an LP?

A
  • decreased LOC
  • papilledema
  • focal neurological deficit
  • immunocompromised
  • history of CNS disease (stroke, infection)
  • seizure within the last week
  • perform LP only if no signs of increased ICP
68
Q

Signs of Meningitis
What should you cover if meningitis is suspected?
What to give if confirmed N. meningitidis?

A
  • stiff neck, positive jolt accentuation
  • purpuric skin rash is suggestive of N. meningitidis (pink, kissing kidney beans)
  • should cover N. meningitidis, S. pneumo, and H. flu
  • ceftriaxone, vancomycin, and dexamethasone (which decreases mortality from S. pneumo and hearing loss from H. flu in kids, decreases inflammation)

N. meningitidis –> Penicillin G for 7 days (most narrow)

69
Q

How do you take a urine culture in someone with a catheter?
Empiric ABX for suspected catheter-associated UTI?

A
  • replace the urine catheter before collecting the urine culture
  • pip-tazo (if shown to be gram (-) bacilli, switch to meropenem for empiric)
70
Q

Charcot’s Triad
Reynold’s Pentad

A
  • signs of acute cholangitis
  • RUQ or epigastric pain, fevers/chills, and jaundice
  • if all of the above + hypotension + decreased LOC, suspect sepsis (Reynold’s pentad)
  • assess with an abdominal U/S
71
Q

Most common pathogen causing acute cholangitis?
How to manage?

A
  • e.coli –> start on ceftriaxone empirically (unless Reynold’s pentad, then Pip-tazo or a penem)
  • switch to oral cotrimoxazole to finish for 7 days
  • want source control ASAP –> biliary drainage with ECRP
72
Q

Empiric Tx for someone with a urinary catheter, IJ CVC, and fever?
Comes back as candida?

A
  • pip-tazo and vancomycin
  • start empiric micafungin, get echo, consult ophthalmologist, repeat 2 sets of cultures every 48h until cleared, remove central line
  • can eventually switch to fluconazole for 14 days when blood cultures clear
73
Q

Mixed Bag

A
  • no tophi does NOT mean no gout
  • a DVT will not likely have significant erythema - consider a diabetic infection (cellulitis)
  • Cefazolin IV is best for MSSA/ GAS polymicrobial osteomyelitis related to diabetic infection

Med School (21 decks)

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