Sepsis, SIRS, MODS Flashcards
local inflammation reaction
tissue damage –> release of pro-inflammatory cytokines (TNF-a, IL-1, IL-6)
beneficial/protective mechanism for tissue healing as long as cytokines remain LOCAL
cardinal signs of inflammation
- heat
- swelling
- redness
- pain
- loss of function
caused by vasodilation, increased vascular permeability, and inflammatory mediators stimulating sensory nerve endings
systemic inflammation reaction
severe/widespread tissue damage OR local inflammation spread systemically –> systemic release of TNF-a, IL-1, IL-6
NOT a beneficial/protective mechanism for tissue healing
results in SIRS
systemic inflammatory response syndrome (SIRS)
systemic response to a non-infectious insult
caused by:
- heat stroke/burns
- trauma
- pancreatitis
- immune mediated disease
- neoplasia
- local infections spread systemically
when can SIRS criteria be applied
in systemically ill patients only
SIRS criteria
- temperature
- heart rate
- respiratory rate
- WBC count & %bands
dog SIRS criteria
must meet 2/4
- high or low temp
- high HR
- high RR
- high or low WBC count, high bands
cat SIRS criteria
must meet 3/4
- high or low temp
- high or low HR
- high RR
- high or low WBC count
sepsis
SIRS that is caused by an infectious insult
must have infection AND systemic signs of inflammation
causes:
- septic peritonitis
- pneumonia
- pyothorax
- prostatitis
- pyelonephritis
- systemic mycoses
- viral/parasitic/protozoal infections
multi organ dysfunction syndrome (MODS)
classified as two or more organs that become dysfunctional in a systemically ill patient to the point where they can no longer sustain the patient
subjective evaluation by clinician
severe sepsis
SIRS + infection + MODS
can progress to septic shock
septic shock
subset of sepsis that causes profound circulatory, cellular, and metabolic abnormalities
SIRS + infection + refractory hypotension
requires more therapy than just IV fluid bolus
why does sepsis, severe sepsis, and septic shock need to be differentitated
variable prognosis
sepsis > severe sepsis > septic shock
SIRS treatment steps
- CV stabilization - ER
- antimicrobials - ER, if suspected infection
- source control - procedure
- CV optimization - ICU
- manage secondary organ dysfunction - ICU
CV stabilization
fluid resuscitation
- isotonic crystalloid bolus at shock dose (start at 1/4 to 1/2)
- do NOT used synthetic colloids
want to reach endpoint (normalized perfusion parameters) within 6 HOURS of admission
- lactate < 2
- MAP > 65
- UOP: > 0.5 mL/kg/hr
antimicrobial therapy
IV antibiotics in all patients that have SUSPECTED infection
want to administer within 1 HOUR of admission
- start with empiric than adjust once culture and susceptibility performed
- Unasyn
- Enrofloxacin
source control
identify the anatomic site of infection and initiate source control (usually surgical)
want to remove the source of infection within 12 HOURS of stabilization
- always resuscitate patient first
cardiovascular optimization
improve CV parameters by increasing SVR and HR
CV optimization steps
ALWAYS give O2 supplementation
- vasopressors
- inotropic therapy
- corticosteroids
- antiarrhythmics
vasopressors
norepinephrine
- a1 agonist –> vasoconstriction –> inc SVR –> inc BP
indications: MAP < 65 after fluid therapy
goal: MAP > 65
inotropic therapy
dobutamine
- increases contractility
indications: MAP < 65 after fluids and vasopressors
goal: MAP > 65
corticosteroids
hydrocortisone
- increases tissue perfusion + reduces inflammation
indications: MAP < 65 after fluids, vasopressors, dobutamine
goal: MAP > 65
antiarrhythmics
lidocaine bolus followed by CRI
- stabilizes CV function
indications: hemodynamically relevant ECG (tachyarrhythmia, multiform, clinical collapse)
how does infection affect the tree of life
infection –> decreased preload, contractility, HR, O2 saturation, and SVR
proinflammatory cytokines:
- vasodilation
- increased permeability
- decreased myocardial function
leads to hypotension, hypovolemia, systolic dysfunction –> hypoperfusion
