SIRS And MODS Flashcards

1
Q

What is SIRS?

A

Systemic inflammatory response syndrome

Widespread systemic inflammation

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2
Q

What are the hallmarks of SIRS?

A

Perfusion abnormalities
Disruption of microcirculation
Organ damage

** untreated, leads to MODS

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3
Q

T/F: SIRS is always a secondary condition to an underlying disease process

A

True

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4
Q

What are the diagnostic criteria for SIRS in the Canine??

A

Two or more of any of the following:

Temp either LOW(<100.6) or HIGH(102.6)
Heart rate HIGH (>120bpm)
Resp rate HIGH (>20bpm)
WBC either LOW (<6000) or HIGH (>16,000)

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5
Q

What are the diagnostic criteria for SIRS in cats>

A

Three or more of the following..

Temp LOW (<100) or HIGH (104)
Heart rate LOW (<140) or HIGH (>225)
Resp rate HIGH (>40bpm)
WBC either LOW (<5000) or HIGH (>19000)

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6
Q

You have identified SIRS in your patient.. what steps will you take in this patient??

A

Identify underlying dz or pathology

Rule out sepsis

Provide hemodynamic support

Identify, track,and support organ dysfunction

Treatment targeted to underlying dz

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7
Q

Common sources of Infectious SIRS?

A
Septic peritonitis 
Pyothorax
Endocarditis 
Bacterial fasciitis 
Parvoviral enteritis
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8
Q

Common sources of non-infectious SIRS?

A
Pancreatitis 
Immune mediated dz 
Heat stroke 
Trauma 
Burns
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9
Q

If the patient fits SIRS criteria but you cannot find an underlying disease … what should you do?

A

KEEP LOOKING if patient is sick

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10
Q

What is the definition of sepsis?

A

Systemic inflammatory response (SIRS) due to INFECTION

—can be caused by bacteria, fungus, virus, or protozoa

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11
Q

What is the most common type of sepsis?

A

Gram negative — usually ecoli in the GI system

LPS is bound by LPS binding protein
Activated Toll like receptors and other pro inflammatory things in Tcells => leads to cytokine storm

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12
Q

What is the neurohormonal response induced by SIRS?

A

Pro-inflammatory molecules induce …

Baroreceptor-mediated catecholamine release

Counterregulatory hormones

  • glucagon
  • ACTH
  • cortisol
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13
Q

T/F: septic patients also have SIRS

A

True

Sepsis is defined as SIRS + infection

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14
Q

Signs of septic shock in dog?

A

Hyperdynamic
Hypermetabolic

Tachycardia 
Tachypnea 
Hyperemia 
Decreased CRT 
Pyrexia
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15
Q

Signs of septic shock in cats?

A

Lethargic

Bradycardia
Hypothermic
Pale or icterus

Weak pulses

— never seen hyperdynamic phase, go straight to deocompensated state

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16
Q

What clinical signs do you see in early decompensated sepsis?

A

Failure of compensatory responses

Hypotension and hypoperfusion
Collapse
Decreased mentation

17
Q

What are the goals of treatment for SIRS>

A

Hemodynamic optimization

IV fluids (hypovolemia)

Vasopressor therapy (refractory hypotension; distributive shock -> septic shock)

Resuscitation end points

18
Q

What type of early antibiotic therapy will you do for suspected sepsis patients?

A

4 quadrant therapy!

Gram pos
Gram neg
Aerobes
Anaerobes

19
Q

Should you ever delay early antibiotic treatment in sepsis to get a culture?

A

NO!

Better survival if antibiotics are started right away

20
Q

What is MODS?

A

Altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention

21
Q

In what systems can organ dysfunction be seen in?

A

Endothelial

Cardiopulmonary

Renal

Hepatic

Nervous

Endocrine

GI

— all associated with progression of uncontrolled systemic inflammation and DIC

22
Q

T/F: there is an increase in mortality with the number or organ systems affected

A

True

23
Q

What is the pathophysiology leading to MODS?

A

SIRS (infectous or non-infectous) —> microvascular dysfunction causing altered blood flow, hypoxia, ischemia, DIC, and reperfusion injury —> MODS —> mortality

24
Q

When does SIRS become MODS?

A

When there is activation and dysregulation of the inflammatory cascade

Endothelial damage exposes tissue factor leading to coagulation derangement

25
Q

What are the three models of MODS?

A

1 hit model — result of a massive initial insult (eg trauma or septic peritonitis )

2-hit model — multiple insults: a priming insult followed by second hit —> exaggerated inflammatory response (eg aspiration pneumonia following trauma)

Sustained hit model— continuous insult (eg drug resistant bacterial infection)

26
Q

What are the mechanisms of organ dysfuntion>

A

Ischemia and reperfusion injury

Compartment syndrome

Bacterial translocation and endotoxemia

Endothelial cell activation and chemotaxis

Idiosyncratic drug reactions/toxicities

27
Q

What are risk factors for bacterial translocation across the GI mucosa?

A
Drugs - ulceration 
Metabolic disease 
Hypotension/ischemia 
Inflammatory disease 
Infectous disease 
Toxins
Neoplasia 
Paraneoplasic 

—> inflammation in occurring in response.. when you have ischemic gut that is reperfused, the inflammatory mediators are elaborated and distributed through the lymphatic to distant organs