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ECC SIRS Sepsis

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sihirlifil's version from 2018-05-02 00:10

SIRS= systemic inflammatory response syndrome!!

Question Answer
what does SIRS happen? The body’s systemic response to an insult that is *infectious OR *non-infectious in origin
what is bacteremia?presence of live bacterial organisms in the blood stream
what is Sepsis?the clinical syndrome caused by infection and the hosts inflammatory response to it; can be bacterial, viral, protozoal, fungal
what makes it "Severe" sepsissepsis complicated by dysfunction of one or more organs
what is Septic shock?acute circulatory failure and persistent arterial hypotension (despite fluid resuscitation) with sepsis
what is Multiple Organ Dysfunction Syndrome? physiologic derangements of organ systems associated with progressive uncontrolled systemic inflammation and disseminated intravascular coagulation (sequelae of SIRS/sepsis)
**SIRS is a clinical state rather than a disease process. there has to be at least 2 (or 3 if youre a cat) abnormal parameters in the 4 things here...temp, HR, RR, WBC count
what triggers the clinical state of SIRS?Any disease state known to cause widespread release of pro-inflammatory endogenous mediators & subsequent inflammation (sepsis, trauma, burn wounds, major sx, pancreatitis)
what are the major consequences of SIRS?Homeostatic disruption, Multiple organ failure (MODS), shock, death. ** The magnitude of the inflammatory response alone can trigger any of these!
Systemic inflammation: helpful?Actication of leukocytes --> fight infection
Activation of platelets --> stop bleeds
Proinflammatory cytokines --> vessels “leaky” so neuts can get out
Vasodilation --> bring blood flow & leukocytes to area needed
Systemic inflammation: not helpful?If inflammation snowballs unchecked:
Activation of leukocytes --> if no infxn to fight…
Activation of platelets --> excessive clotting --> using up clotting factors --> bleeding (DIC)
Proinflammatory cytokines --> leaky vessels --> edemaVasodilation --> hypotension
Why does inflammation go from helpful to not helpful?Dz factors: overwhelming infxn (pyometra), progressive inflam dz (pancreatitis)
Patient factors: decreased immune fxn (immunosuppressive meds), fighting multiple diseases
Cytokines: NF-kb, TNF-a, IL-6, NO, leukotrienes
Infectious causes of SIRS (septic SIRS) can includeinfections with Gram positive & gram negative (LPS i.e. E. coli) bacteria (etiology = GIT, respiratory, urinary tract), fungi, protozoa, Viruses (parvo).
Noninfectious things that can cause SIRS in animals include..Any inflammatory dz or trigger, Heat stroke, Pancreatitis, Immune disease, Neoplasia, Severe polytrauma, Burns
how do SIRS and sepsis relate?SIRS is an important part of sepsis, but SIRS can happen without sepsis (Can be inflammatory not just infectious)
how do you differentiate septic SIRS vs non-septic SIRS?Culture is one option (takes a while, wont detect viral or protozoal, media makes a diff)... You can also look at BIOLOGICAL MARKERS though, which May help to identify the presence or lack of bacterial infection in patients with clinical signs of SIRS.
(+/-) **2 biological markers which can help you differentiate between infectious and non-infectious SIRS? C-reactive protein (CRP), Procalcitonin
(+/-) what is C-reactive protein? what does it tell you?it is a Acute-phase protein made in hepatocytes In response to inflammatory cytokine release.HOWEVER, May be elevated secondary to other inflammatory causes (Trauma, surgery, pancreatitis) and has a long half life. Therefore not the ideal marker
(+/-) what is Procalcitonin? What does it tell you? Precursor molecule to calcitonin, Produced by thyroid gland, In sepsis comes from leukocytes that have been stimulated by cytokines & endotoxins and Peak levels for up to 24 hours. May be useful in identifying “bacterial” sepsis (not so much for viral)...might be able to used as a guide to starting abx
Clinical signs of SIRS +/- sepsis?Signs may be non-specific (Vary depending on underlying disease process) but can see Loss of appetite, Depression, “Injected” hyperemic mucus membranes, Bounding peripheral pulses, Compensated hyper dynamic state, Vomiting, diarrhea
May be related to SIRS progression --> DIC, ARDS, MODS (petechiae, harsh lung sounds & crackles, icterus)
Patients w/ SIRS: CS of vasodilationTemp too low or high
HR bradycardia or tachy
Resp rate elevated
Hyperemic mm
Brisk CRT
Hypotension
SIRS: TPR of dog?2/4 required
T: <100.6 OR >102.6*
P: >120
R: >20
WBC count <6 or >16; >3%
SIRS: TPR of cat?3/4 required
T: <100 OR >104*
H: <140 or >225 (usu low)
R: >40
WBC count >19 or <5
(Skip some compensatory phases)
what are common lab parameters to see with SIRS? Neutrophilia w/ LS, low platelets (DIC), Hyper/hypoglycemia, hypoalbuminemia, elevated ALT, AST, Tbili (Potentially many other changes /abnormalities such as Acid-base, electrolytes, renal values……..) globulins high (inflam)
Why is glucose high or low with SIRS?due to Altered carbohydrate metabolism! There is increased gluconeogenesis in early phases (hyperglycemia), and then Hypoglycemia occurs later as Excessive utilization exceeds production (cant match increased demant)
why is there hypoalbuminemia in SIRS?Reduced 2’ to acute-phase protein production. Loss due to vascular permeability
why are there inc liver enzymes/Tbili with SIRS?Changes in perfusion and oxygen delivery (in the DOG, LIVER IS THE SHOCK ORGAN) and cholestasis can lead to elevated Tbili (MODS)
why are renal values high with SIRS?Pre-renal dehydration, decreased perfusion, MODS, or 1’ cayse of SIRS/sepsis
Why is it important to ID cause of SIRS (i.e. septic or not)Temp, HR, RR, WBC count help ID SIRS, but don’t tell us if the patient is septic (aka has an infxn somewhere and needs antibx STAT)
Only way to tell if patient is septic?Go look for it!
SIRS diagnosticsCBC/Chem/UA
Radiographs
A-FAST/T-FAST +/- full abd US
Abd/thoracocentesis --> cytology & culture
Abdominal exploratory
If you do abdominocentesis & see this on cytology, what do?
EMERGENCY CELIOTOMY! neutrophils w/ bunch of intracellular bact
Criteria for exploratory celiotomyAbd rads: pneumoperitoneum, loss of serosal detail
Abd US: pneumoperitoneum, underlying etiology
Abd effusion cytology: Toxic a/o degenerate neuts w/ foreign debris, intracellular bact
Biochem: Blood:abdomen fluid glc difference >20 mg/dL, lactate >2.0 mmol/L; fluid [lactate] >2.5 mmol/L
Treatment of SIRSTreat underlying dz!
If SEPSIS suspected: antibx ASAP, get sample for culture, start broad spec IV antibx (= g(+), g(-), AND aerobe + anaerobe)
No sepsis: no antibx
IF NOT SURE: start antibx, then discontinue once you know
Supportive care for SIRSFLUID THERAPY! colloidal support (plasma, albumin) if leaky vessels
Vasopressors (BP support)
Anti-emetics (GI support) PPI
Nutrition
O2
What is fluid therapy like?Shock dose
MDO
Colloids if inflammation (leaky vessels), hypoalb (low oncotic pressure)
+/- dextrose
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