Unit 2 - Blood Stream Infections Flashcards
what are factors contributing to increasing incidence of sepsis?
- increasingly aggressive oncological chemotherapy and radiation therapy
- widespread use of corticosteroid and immunosuppressive therapies for organ transplantation and/or inflammatory diseases
- increasing survival of patients predisposed to sepsis (neonates, elderly, diabetics, cancer, major organ failure, granulocytopenia)
- increased use of invasive devices (surgical prostheses, inhalation equipment, IV and urinary catheters)
- indiscriminate use of antimicrobial drugs that create conditions for overgrowth, colonization, and subsequent infection by aggressive, antimicrobial-resistant pathogens
mortality of sepsis?
varies according to degree of pathologic derangement and presence of documented infection
- SIRS up to 7%
- sepsis 16-28%
- septic shock 45-65%
what are complications from sepsis?
19% CNS dysfunction 2-8% ARDS 12% liver failure 9-23% acute renal failure 8-18% DIC
what are complications from septic shock?
18% ARDS
38% DIC
50% ARF
what is the definition of infection?
presence of microorganisms in a normally sterile site
-not the same as colonization
what is the definition of colonization?
presence of microorganisms on an epithelial surface
-not the same as infection
what is the definition of bacteremia?
cultivatable bacteria in the bloodstream
- may be transient or associated with sepsis and organ failure
- may be primary (w/o identifiable source) or secondary (with intravascular or extravascular focus of infection)
what is the definition of septicemia?
same as bacteremia, but implies presentation of clinical manifestations associated with the bacteria in bloodstream
what is the definition of sepsis?
confirmed or clinical evidence of infection plus evidence of systemic response
- SIRS is called sepsis in American consensus
- with the exceptions of leukopenia and hypothermia, these changes are among the body’s normal systemic responses and don’t imply poor prognosis
what is the definition of SIRS?
systemic inflammatory response syndrome (whole body, without proven source of infection)
- systemic response to a wide range of stresses; need 2+ of the following:
- -temp > 38 C or < 36 C
- -HR > 90bpm
- -RR > 20, or PaCO2 < 32 mmHg
- -WBC > 12K, 10% bands
what is severe sepsis?
sepsis associated with dysfunction of organ(s) distant from the site of infection, plus 1+ of the following:
- hypotension (reversible by administering fluids)
- confusion
- oliguria
- hypoxia (not explained by primary respiratory disease)
- metabolic (lactic) acidosis)
- DIC
- hepatic dysfunction (not explained by primary liver disease)
also known as sepsis syndrome
what is the definition of septic shock?
sepsis-associated hypotension associated with lactic acidosis or organ hypoperfusion
- cannot be reversed by IV fluids
- if lasts for > 1 hr and doesn’t respond to vasopressor administration, use the term “refractory septic shock”
what happens if you have SIRS with proof of bloodstream infection?
it’s called sepsis
what are complications of SIRS?
results in multiple organ dysfunction syndrome
what are causes of SIRS other than BSI?
- severe trauma
- surgical complication
- burns
- acute pancreatitis
- immunodeficiency (like AIDS)
how is SIRS related to cytokine storm?
subset of cytokine storm/dysregulation
describe the role of TLRs in mediating SIRS?
- TLR4 - plays the most critical role in mediating severity, recognizing and transmitting LPS signal to cell interior
- -engagement of TLR4 leads to release of proinflammatory mediators (TNF-alpha, IL-1, IL-6) in cytokine storm
- TLR2 - peptidoglycan and lipoteichoic acid
explain what occurs in endotoxic (G-) shock
excessive release of cytokines, often triggered by LPS of G- bacteria
-diffuse intravascular coagulation with consequent defective clotting, changes in vascular permeability, loss of fluid into tissues, fall in BP, circulatory collapse, hemorrhagic necrosis
what do TNF and IL-1 specifically do to endothelial cells?
cause them to express cell adhesion molecules and tissue thromboplastin
- promote adhesion of circulating cells and deposition of fibrin
- PAF enhances these effects
why do you not want to give antibiotics if a patient has G- septicemia?
if antibiotics lyse the bacteria, then there’s massive release of TLDR4, which causes more endotoxic (cytokine) shock
what is the role of activated protein C?
APC is a naturally occuring modulator of coagulation and inflammation, as well as antithrombin
- blocks the inflammation/coagulation cascade at several points
- formulation of recombinant human APC has been approved for treating sepsis
what are transient types of bacteremia?
- chewing
- teeth brushing
- manipulation of infected tissue (popping zits)
- surgery involving non-sterile sites
in people with working reticuloendothelial system (liver/spleen), bacteremia is of little problem
what are types of intermittent bacteremia?
due to same microorganism that is detected intermittently in the same patient due to cycle of clearance and recurrence
-most often due to extravascular infection that provides portal of entry for bacteria (undrained infections, abscesses, osteomyelitis, meningitis)
what are the types of continuous bacteremia?
persistent
- found in bacterial endocarditis and other endovascular infections
- during early stages of specific infections
- -typhoid fever
- -brucellosis
- -leptospirosis
what are the two types of vascular infections and their definitions?
intravascular (primary) - within cardiovascular system
extravascular (secondary) - bacteria enter bloodstream through lymphatic system from another site of infection
what are examples of intravascular infections?
- infective endocarditis
- mycotic aneurysm
- thrombophlebitis
- IV catheter-associated bacteremia
what is infective endocarditis?
infection of endocardial surface of heart
-implies physical presence of microorganisms in the lesion
what are the classifications of infective endocarditis?
acute - follows fulminant course, with high fever, systemic toxicity, and leukocytosis; death occurs in several days to less than 6 weeks
subacute - death occurs in 6 weeks to 3 months
chronic - death occurs later than 3 months
explain the pathogenesis of infective endocarditis?
- damage to cardiac endothelium
- deposition of platelets and fibrin
- organisms gain access to bloodstream and stick to damaged area, leading to colonization
- protective layer of fibrin and platelets matrix
- bacterial multiplication
- vegetation formation
what must first occur to the valve before infective endocarditis can occur?
valve surface must first be altered to produce a suitable site for bacterial attachment and colonization
what are organisms associated with infective carditis?
- Staphylococcus aureus
- Streptococci viridans
- Staphylococci (coagulase ngetavie)
- HACEK group are less frequently seen
what is a mycotic aneurysm?
intravascular infection
- results from damage to endothelial cells lining the arteries, leading to seeding of the organism in wall of aorta
- infection causes inflammatory damage and weakening of arterial wall
- usually from staphylococci, streptococci, or Salmonella
what is suppurative thrombophlebitis?
intravascular infection
- results from damage to endothelial cells lining a vein
- results in clot formation and seeding of clot by organisms
- most frequently seen in PICC lines
what are catheter-associated bloodstream infections?
dwelling catheter (central) is colonized with bacteria -more accessible, long-term venous access for both good and bad
what are risk factors associated with CRBSI’s (cather-related)?
- prolonged catheterization
- frequent manipulations
- occlusive plastic dressings
- contaminated skin solutions
- poor aseptic technique
- catheter material
- location of catheter
what are the 5 potential sources for catheter colonization and catheter-related sepsis
- insertion site
- catheter hub
- hematogenous seeding of the cather
- contamination of the infusate
- hands of health care personnel
what are secondary (extravascular) BSI’s defined as?
dcoumented portal of bacterial entry and/or known associated site of infection
- most cases of clinically significant bacteremia
- from skin infection, pneumonia, UTI, hospital-associated infection
explain the pathogenesis of secondary BSI?
local site of infection –> lymphatics spread –> bloodstream
what are organisms associated with neoplasms?
- Clostridium septicum
- -Other relatively uncommon Clostria species
- Streptococcus bovis
- Aeromonas hydrophilia
- Plesiomonas shigelloides
- Campylobacter species
how does one diagnose BSI?
blood culture (esp. if febrile)
- establishes presence of infection (excluding non-infectious causes)
- reassures clinician about emperical therapy
- streamlines antibiotic treatment after assessment of antibiotic sensitivity of isolate
what is the best number of blood culture sets to get?
3 sets (of anaerobic and aerobic) in 24 hours
- sets drawn from different sites to ensure the site itself is sterile
- each bottle has 10 mL total
how do you choose volume of blood?
blood culture yield is highly dependent on volume of blood cultured
-adult usually <1 CFU/mL blood
0
preparation of the site for culture drawing
- After the vessel site is selected, a 5 cm area of skin should be disinfected by swabbing concentrically with 70% alcohol, from the venipuncture site outward.
- The site should be cleansed once again, with 10% povidone-iodine or 2% tincture of iodine again in a circular motion.
- Allow the iodine to dry completely before performing venipuncture (1
- 2 minutes)
what is procalcitonin?
PCT is marker of inflammatory response stimulated by bacterial products and cytokines
- used as biomarker for bacterial pneumonia and sepsis
- levels increase within 3-6 hours of stimulus (higher = poorer prognosis)
- levels can be used to indicate appropriate therapy and suggest infection is not controlled if it doesn’t decline
what to PCT concentrations and sepsis risk mean if:
-2 ng/mL
-2 ng/mL - high risk of progression
