Sepsis, SIRS, MODS Flashcards

1
Q

local inflammation reaction

A

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

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2
Q

cardinal signs of inflammation

A
  1. heat
  2. swelling
  3. redness
  4. pain
  5. loss of function

caused by vasodilation, increased vascular permeability, and inflammatory mediators stimulating sensory nerve endings

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3
Q

systemic inflammation reaction

A

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

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4
Q

systemic inflammatory response syndrome (SIRS)

A

systemic response to a non-infectious insult

caused by:
- heat stroke/burns
- trauma
- pancreatitis
- immune mediated disease
- neoplasia
- local infections spread systemically

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5
Q

when can SIRS criteria be applied

A

in systemically ill patients only

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6
Q

SIRS criteria

A
  1. temperature
  2. heart rate
  3. respiratory rate
  4. WBC count & %bands
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7
Q

dog SIRS criteria

A

must meet 2/4

  1. high or low temp
  2. high HR
  3. high RR
  4. high or low WBC count, high bands
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8
Q

cat SIRS criteria

A

must meet 3/4

  1. high or low temp
  2. high or low HR
  3. high RR
  4. high or low WBC count
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9
Q

sepsis

A

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

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10
Q

multi organ dysfunction syndrome (MODS)

A

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

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11
Q

severe sepsis

A

SIRS + infection + MODS

can progress to septic shock

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12
Q

septic shock

A

subset of sepsis that causes profound circulatory, cellular, and metabolic abnormalities

SIRS + infection + refractory hypotension

requires more therapy than just IV fluid bolus

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13
Q

why does sepsis, severe sepsis, and septic shock need to be differentitated

A

variable prognosis

sepsis > severe sepsis > septic shock

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14
Q

SIRS treatment steps

A
  1. CV stabilization - ER
  2. antimicrobials - ER, if suspected infection
  3. source control - procedure
  4. CV optimization - ICU
  5. manage secondary organ dysfunction - ICU
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15
Q

CV stabilization

A

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

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16
Q

antimicrobial therapy

A

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

  1. Unasyn
  2. Enrofloxacin
17
Q

source control

A

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

18
Q

cardiovascular optimization

A

improve CV parameters by increasing SVR and HR

19
Q

CV optimization steps

A

ALWAYS give O2 supplementation

  1. vasopressors
  2. inotropic therapy
  3. corticosteroids
  4. antiarrhythmics
20
Q

vasopressors

A

norepinephrine
- a1 agonist –> vasoconstriction –> inc SVR –> inc BP

indications: MAP < 65 after fluid therapy
goal: MAP > 65

21
Q

inotropic therapy

A

dobutamine
- increases contractility

indications: MAP < 65 after fluids and vasopressors
goal: MAP > 65

22
Q

corticosteroids

A

hydrocortisone
- increases tissue perfusion + reduces inflammation

indications: MAP < 65 after fluids, vasopressors, dobutamine
goal: MAP > 65

23
Q

antiarrhythmics

A

lidocaine bolus followed by CRI
- stabilizes CV function

indications: hemodynamically relevant ECG (tachyarrhythmia, multiform, clinical collapse)

24
Q

how does infection affect the tree of life

A

infection –> decreased preload, contractility, HR, O2 saturation, and SVR

proinflammatory cytokines:
- vasodilation
- increased permeability
- decreased myocardial function

leads to hypotension, hypovolemia, systolic dysfunction –> hypoperfusion