CC Septis

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CC Septis
2014-07-06 17:12:02

sepsis exam II
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  1. we have learned that people dont die from the ifection, but actually from the body's immune response to the infection

    organ systems fail
  2. Sepsis
    infection with a systemic response to the infection
  3. bacteremia
    viable bacteria in the bldstream

    gram neg bacteria (e-coli) is bad b/c of endotoxin release
  4. 5 reccomended practices for placing cent venous line by CDC
    • handwashing
    • max barrier precautions during insertion (complete sterility)
    • use of chlorohexadine to prep
    • optimum site selection
    • remove if unecessary
  5. systemic inflamm response syndrome (SIRS)
    • inflamm process does not stay localized --> systemic
    • inflmm is unregulated and overwhelming to organ systems
    • uncontrolled coags
    • ineffective fibrinolysis (unable to brk clots)
  6. 3 categories of criteria for dx of sepeis
    • infection
    • SIRS
    • acute organ dysfunction
  7. needs one or more of these to claim infection
    • + culture
    • pt on antibiotics?
    • pnuemonia present?
    • inc WBC count
    • perforation in holow viscus like bowel
  8. need 2 or more of these to clain SIRS
    • body temp <36 OR >38
    • HR >90
    • tachypnea
    • WBC <4,000 OR >12,000
    •   OR >10% band cells
  9. also need to see changes in hemodynamics, or changes in organ functions to claim Acute Organ Dysfunciton in ONE OR MORE organs
  10. Sever sepsis
    infection + SIRS = organ dysfunction criteria meet
  11. risk fx of sepsis **
    • all critically ill pts
    • anyone on antibiotic
    • <1 yr or >65 yrs
    • invassive lines/devices
    • intra abd surgery
    • immunocompromised
    • resistant microorgs
    • cellulitits
  12. common sources of sepsis
    • lungs
    • abd
    • urinary tract -bladder, kidneys

    brain, bone, skin
  13. General Sx of sepsis
    • temp change
    • inc RR and HR
    • warm skin / rash
    • general weakness
  14. petechiae
    caused by dec platelet

    nl # 150-4500,00
  15. decreased Protein C is seen in sepsis and decreases fibrinolysis of clots

    3rd spacing is also seen, which dec circulating bld volume

    massive vasodilation

    excess coaguloation

    ischemia and ts death (SvO2 >80%)
  16. septic shock
    • distributive shock b/c of massive vasodilation
    • hypoTN and hypoperfusion despite fluid boluses and vasopressor

    two phases= early and late
  17. early/warm phase of sep shock
    • SNS activation
    • hyperdynamic (fever), skin warm and possibly flushed
    • occurs w/n 6-48 hours
  18. hemodynamic findings of early stage septic shock:
    • HR= inc, possible bounding pulse
    • Pre= dec b/c dilation
    • CO= inc
    • after= dec SVR
    • O2= nl to inc (ony shock with bad SvO2 d/t crappy tissue not extracting O2)
    • temp= INC
  19. Late/Cold pahse of sep shock
    • hypodynamic - cold
    • inc lactic acid, and K, acidodic
    • Similar to Cardio shock
    • Hydrogen hides in cell, K kicked out and hyperK bld developes
    • organs become ischemic
  20. hemodyn findings of late stage sep shock:
    • these are the same as cardio shock b/c the heart i starting to fail
    • HR inc
    • Pre inc
    • CO dec
    • After inc SVR
    • O2 high or low depending on tissue extraction
  21. monitor SvO2 and lactid acid levels to determine is tissues actually extracting O2
  22. Immediate care of sepsis
    • lactate levels
    • cultures w/n 1 hour of presumptive dx
    • antibios w/n 1 hr of culture
    • immediate fluid resuscitation
  23. initial resuscetation goals:
    • These goal are w/n first 6 hrs of Tx
    • The goal is improved perfusion and tissue oxygenation

    • CVP= 8-12mmHg
    • MAP > 65
    • OU > 0.5ml/hr
    • SvO2 > 70%
  24. Sepsis is a major cause of ARDS
    low tidal volumes are ideal
  25. Use the gut during sepsis if possible
    This prevents translocatiion of bacteria from gut to circ system
  26. multiple organ dysfunction syndrome
    • presence of altered organ function in an acutely ill patient such that homeostatis cant be maintained w/o intervention
    • 2 or more organs involved
    • mortatlity increases with # of organs
  27. MODS risk factors
    • >60 yrs
    • truama
    • ARDS
    • hypermetabolic states such as burns
    • multiple bld tranfusion
  28. primary


    secondary MODS
    • 1= result from direct insult cx'ing localized inflamm
    •  =less common

    • 2= from widesread SIRS resulting in dysfx of organs not involved in initial insult
    •  =more commone, occurs in bld
  29. typical order of organ failure
    • lungs
    • CV sys
    • liver
    • gut
    • kidneys
  30. Liver dysfx in MODS
    • decreases 75% before sx can be seen
    • inc in AST and ALT exzymes
    • inc clot times
    • jaundice
  31. Gastro dysfx in MODS
    • iliues
    • see inc TF residuals and dec bowel sounds
  32. Kidney dysfx in MODS
    • ARF from hypovolemia
    • olig/anuria
    • inc creatine and BUN
  33. Hematologic dysfx in MODS
    • decreased clotting
    • increase in petechia, PT, pTT, INR, and D-dymers
  34. MODS Tx
    • early recognition is key
    • support failing organs
    • monitor for progression to other organs
    • assess advanced directives