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Board Review 2020 > Sepsis > Flashcards

Sepsis Flashcards

1
Q

What is the veterinary definition of sepsis

A

Systemic inflammatory response to infection
SIRS+ Infection
Abnormal Temp, HR, tachypenia, or Abnormal WBCC
Dogs 2/4, Cats 3/4

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2
Q

What is the veterinary definition of severe sepsis

A

Sepsis with 1 or more organ dysfunction

No consensus statment

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3
Q

What is the veterinary definition of septic shock

A

Hypotension despite normal intravascular volume (pressor dependent)

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4
Q

What is the veterinary definition of MODS

A

2 or more organ dysfunction with SIRS or SEPSIS

Renal, CV, Resp, Hepatic (Tbili), coagulation, GI, Endothelial (Vasculatitis/edema), laminitis

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5
Q

What is the SEPSIS 3 Definition of Spesis

A

life threatening organ dysfunction caused by a dysregulated host response to infection
Acute increase of SOFA points and infection

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6
Q

What is the SEPSIS 3 definition of septic shock

A

underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality

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7
Q

What is not included in SEPSIS 3

A 
Severe sepsis (redundant)
SIRS (deemed not useful)
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8
Q

What are the 4 key components of innate immunity

A

Physical barriers
chemical barriers
Phagocytic cells
blood protiens (cytokines, chemokines)

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9
Q

What are the 5 key features of the innate immunity

A 
Constitutive ( always present)
rapid response
Limited diversity of receptors
No memory
Not specific for individual microbial antigens
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10
Q

What are pathogen associated molecular patterns

A

PAMPs small molecular motifs that recognize non-self

Highly conserved across bacteria/virus as have to be present for survival

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11
Q

What is the gram – and gram + PAMP

A

Lipopolysacchride – Gram -

Liptoechnoic acid and Peptidoglycan —Gram +

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12
Q

What are the phagocytic cells of the body and how does it work

A

Macrophages, Neutrophils, NK cells
PAMP binding to pattern recognition receptor causes reshaping of membrane around.
In the cell respiratory burst occurs to have ROS and NO attack organism

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13
Q

What does TLR 4 bind

A

Gram Neg LPS

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14
Q

What does TLR 2 bind

A

Gram +

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15
Q

What does TLR 5 bind

A

Flagelan

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16
Q

What is the major TLR 4 pathway that is important in cell signalling for the PAMP

A

MYD88 —-> i kappa B kinase —-> NFkappa B

Ultimately Increase in IL6, TNF alpha, and IL1

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17
Q

What are 4 key components of how cytokines function

A

Pleiotropism – one mediator had multiple functions
Redundancy - Multiple molecules have same outcome
Synergy – Two different on same cell increases effect
Antagonism — IL 10 most important anti-inflammatory

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18
Q

What are three common early pro-inflammatory cytokines

A

TNF alpha
IL1 Beta
IL-6
Recruit luekocytes to site of infection and activate them to kill

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19
Q

What are the fever inducing cytokines

A

IL-6 and TNF alpha stimulat hypothalmus to induce fever

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20
Q

What does HMGB-1 do in sepsis

A

Late pro-inflammatory to amplify inflammatory response

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21
Q

What is the major Anti-inflammatory cytokines

A

IL 10, TGF beta

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22
Q

How does the innate immunity contribute to sepsis coagulopathy

A

Increase procoagulatory pathways- trigger expression of TF on epithelial and wBCS
Decrease Reg of anticoagulant by decrease of Protien C and incrase of PAI 1
Activation of arachadonic cascade– phopholiase A2
Endothelial dysfunction- tight junctions become less tight

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23
Q

How does NO induce vasodilation in sepsis

A

inducible nitric oxide synthase by PAMPs and TNF alpha and IL-1
Leads to vasodilation

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24
Q

What are the most inflammatory compliment cascade

A

C5a and C3a

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25
Q

How does non infectious SIRS occur

A

Tissue damage results in damage associated molecular patterns
Heat shock protiens, ATP and DNA

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26
Q

What is the veterinary definition of SIRS

A

Inflammatory response to an insult that has systemic effects rather than localized at insult.

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27
Q

How does a positive fluid balance at day 3 affect outcome in Sepsis (CCM 2017, 2018)

A

Decreased survival

Does not mater why negative fluid balance it leads to increased survival

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28
Q

How does balanced fluids versus saline compare in pediatric patients with sepsis

A

improved survival, decreased AKI, shorter duration of vasoactive medications.
Suspect Cl load as a factor

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29
Q

What are the negative acute phase proteins

A

Alpha 1 proteinase inhibitor
Albumin
Transferin

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30
Q

CCM 2017 How did fever alter outcome in sepsis

A

Shorter hospitalization stay and decreased mortality in multivariate analsysis despite them getting better care

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31
Q

What are the benefits of fever

A

negative feed back on pyrogenic cytokiens, increase immune function, antibiotic activity during fever

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32
Q

CCM 2018, LOV-ED Data How did PaCO2 alter survival in mechanically ventilated septic patients

A

Increase of 1 mmHg was assocated with a 3% increase in survival
PaCO2 Survivors 44 mmHg
Non survivors 39 mmHg

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33
Q

JVECC 2017 How do platelet indices related to survival in dogs with sepsis

A

Larger= Increase MPV, more readily activiated

Increase in MPV 3 fold increase in non survivor

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34
Q

JVECC 2019 Which sepsis inflammatory biomarker was increased in dogs with sepsis compared to controls.

A

HGMB-1

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35
Q

JVECC 2019 Which sepsis inflammatory biomarker was a predictor of mortality

A

CCL2

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36
Q

JVECC 2018 in evaluating patients with sepsis was was found to increase survival if euthanized patients were excluded

A

Higher plasma cholesterol

Was not outside of reference range

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37
Q

JVECC 2019 In a review of cats with septic peritonitis what was the improvement with appropriate abx choice

A

4.4 x more likely to survive

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38
Q

JVECC 2019 In a review of cats with septic peritonitis what was found to decrease survivial

A

Hypocalcemia

Higher glucose in non survivors (stats not given)

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39
Q

Vet Journal 2017 What is the delta neutrophil index and how is it useful in sepsis

A

fraction of circulating immature granulocytes in peripheral blood. Machine calculates
Some overlap but was good for identifying sepsis

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40
Q

CCM 2018 How does SAP (glycoprotein) and TPA (serine protease) alter as a predictor of 14 day mortality

A

decrease SAP lead to death

Increased TPA led to death

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41
Q

CCM 2017 What is Procalcintonin useful for in sepsis

A

Discontinuation of antibiotic therapy as it it decrases

42
Q

CCM 2017 MOSES Study: How did a change in procalcitonin alter mortality in sepsis patients

A

Increased mortality rate if <80% decrease of PCT on day 4

43
Q

What were the initiation of EGDT in the Rivers study and what was the outcome difference?

A

SIRS 2/4; BP < 90 after fluid or Lactate > 4 mmlol/L

44
Q

What was EGDT In the Rivers study

A 
Central catheter
CVP 8-12 (500 ml q 30 minutes to reach)
MAP < 65 mmHg receives pressors
Vasodilators until MAP < 90 mmHg
CvO2 < 70% received RBC transfusion til HCT 30%. If still less then dobutamine
28 day mortality 49% standard, 33% EGDT
45
Q

What was the outcome of the ARISE 2014 trial (location)

A

Australia, New Zealand

EGDT did not reduce all cause mortality at 90 days

46
Q

What was the outcome of PROCESS 2014 trial (location)

A

US
Third group was protocolized standard care
No difference in mortality at 60 days
21% EGDT, 18% PSC, 18% usual

47
Q

What was the outcome in PROMIS 2015 trial (location)

A

England
No difference in 90 day mortality
EDGT 29.5%, Usual 29%

48
Q

What was PRISM and what was the outcome

A

Meta analysis of promise, arrise, and process
EGDT 24% and Usual 25%
No difference, did not include PSC group

49
Q

NEJM 2017 in time bundled care what changed the mortality outcome in septic pateints

A

Each hour to complete 3 hr bundle increased mortality (even in first three hours)
Same increase with antibiotics

50
Q

CCM 2017 How did time to second dose of antibiotics alter outcome in septic patients

A

association with the increase length of time for second dose of abx: Increased mortality, length of stay and MV days

51
Q

CCM 2018 In a time bundled care what was noted despite care being delivered within the time frame set by bundle

A

Delay of 50 mins for blood cultures led to stat significant mortality increased
3 hr ‘safe’ window not likely true

52
Q

CCM 2017 What was noted about antibiotic administration in the ED compared to pre ED

A

Delay in abx treatment in the ED but not pre ED increased in hospital mortality

53
Q

CCM 2017 In a comparision of previous cohorts of septic patients how many patients were no longer included in the septic shock 3 criteria (~%) and what was the change in mortality in the two groups.

A

57% of patients did not meet the Sepsis 3 criteria
Sepsis 3 mortalitiy 28.5%
Pts excluded from sepsis 3 14%

54
Q

CCM 2017 IN a study of time in German with training of staff what led to improved outcomes in septic patients

A

medical ICU, blood cultures before abx, adequate dose of abx, 1-2 L crystalloid bolus within 6 hrs, > 6 L in first 24 hrs, Less HES

55
Q

CCM 2017 In a Bayesian approach review of the River’s EGDT and the following larger trials what was noted to improve outcome and what was noted about EGDT effect for the most severe (apache score) patients

A

Faster ABX, survival reduced 10% for every 1 hr delay

EGDT may harm the most sick as mortality increased for incrased APACHE score

56
Q

What are 4 factors that synthetic glucocorticoids have versus endogenous

A

Less MC activity
Less tightly bound to cortisol binding protien in plasma
Undergoes less hepatic metabolism
Higher affinity for GC receptor

57
Q

JVECC 2017 List 5 effects GCs have on the body

A

Bronchodilation - increase B2 receptor expression
CNS- cerebral blood flow and lytes concentrations
Enhances vascular response to vascular substances
supppress production of vasodilators

58
Q

NEJM 2018 What was the outcome of hydrocortisone and fludrocortisone in septic shock administered for 7 days with no taper

A

Decrease mortality

Decrease vasopressor time, decreased MV, increased hyperglycemia

59
Q

Define CIRCI

A

Endocrinological dysfunction in critically ill patients resulting in inadequate cortisol activity for existing severity of illness leading to fluid and vasopressor refractory shock

60
Q

NEJM 2018 ADRENAL: How did hydrocortisone as a CRI alter outcome in septic patients

A

No difference in mortality

Faster resolution of shock, and no difference in ventilator days

61
Q

Which articles showed improvement with steroids, and which did not for septic shock patients

A

NEJM 2018 Hydrocortisone+ fludrocortisone and French 2002 showed benifit
Adrenal and Corticus no change in mortality

62
Q

CCM 2017 How did patients receiving oral prednisone prior to developing sepsis/ARDS have increased and decreased risks of

A

Decreased risk of ARDS

Possible increase in mortality

63
Q

CCM 2017 How did relative bradycardia alter outcome with septic shock

A

HR < 80; improved outcome

21% vs. 34 %

64
Q

NEJM 2017 ATHOS-3 How did the addition of angiotensin II to norepi in vasodilatory shock improvements

A

Increased BP with reduction of catecholamine dose

Best response in those with doses belwo 0.5 mcg/kg/min

65
Q

CCM 2017 Which patients should not receive Angiotensin II in a safety review

A

Worsens asthma and heart disease

66
Q

CCM 2017 In a review of VASST with the SEPSIS 3 outcomes what was the difference between norepi and vasopression

A

Vasopressin mortality was less than Norepi in patients with lactate of < 2 mmol/L
The less sick

67
Q

VASST- What was the out come between Norepi and vasopressin

A

Norepi and vasopression were equal

68
Q

Monett CCM 2011 How does Norepi alter the hearts ability to respond

A

increase right and left ventricular preload

Increase in cardiac index

69
Q

Lacelet 2007 What is the differences of Norepi + dobutamine versusus Epi

A

No difference in mortality or ICU stay

70
Q

VANISH How did Norepi or Vasopression + steroid alter AKI

A

Neither altered AKI

71
Q

CCM 2015 In pediatrics what was the outcome of dopamine versus epinephrine on mortality

A

Dopamine increased mortality and health associated infections
Dopamine was started about 1 hr later than EPI which may have altered outcomes

72
Q

JVECC 2019 How does the timing/route of nutrition in dogs with septic peritonitis alter outcome

A

parental nutrition decreased survival

If ate on own decreased LOH

73
Q

JVECC 2019 In 2 cases out did Esmolol used for

A

for tachycardia without hypovelmia

Human 2013 study that improved heart rate improved mortality significantly

74
Q

JVECC 2019 In a study of gastrotomy tubes in sepsis how did they alter outcome

A

~4 days to eat on own, 2/24 had major complications

~50% complication rate

75
Q

JVECC 2019 How did peritoneal lavage alter bacterial isolates

A

Pre 92.5 % positive
Post 87.5% positive
Isolation of MDR decreased by 1/3 post lavage

76
Q

JAVMA 2017 In cats with sepsis (all causes) what coagulation abnormalities were noted

A

increase PTT, D-dimers, decreased protien C and antithrombin

77
Q

JAVMA 2017 What was clinicopathological differences between dogs with sepsis and anaphylaxis

A

Anaphylaxis: younger, increse in eosinophils, Na Cl, ALT, decrease pH fibrinogen
Sepsis: Increased band neutrophils, glob, alp and decrease gluc

78
Q

VET Journal 2018 How does calcitril in vitro work for WBC inflammation

A

shift from pro-inflammatory leukocyte to anti-inflammatory leukocyte

79
Q

CCM 2018 What is the mortatilty difference when culture – versus culture + septic shock is compared

A

Survival the same

80
Q

CCM 2018 How may thiamine administration alter lactate clearance in sepsis

A

May improve lactate clearance

Alcoholics and females likely to respond

81
Q

CCM 2018 in pediatric kids in India how did probiotics alter cytokine levels

A

Decrease in IL-6 and TNF alpha; increase in IL10 and TGF beta
No mortality change

82
Q

CCM 2017 How does calcium channel blockers alter mortality in Sepsis

A

decreases if receiving before

NO change for ACe inhibitors, ARBS, or beta blockers

83
Q

JVECC 2019 Evaluation of host cytokine response what differences were present between Sepsis and SIRS

A

Not able to discern

84
Q

JVIM 2019 How are angiopoietin-2 and Vascular endothelial growth factor (VEGF) altered in SIRS or Sepsis

A

ANG-2 increase in sepsis/SIRS and non survivors

VEGF- higher in sepsis only

85
Q

JVECC 2017: What leads to an increase in CF DNA in dogs

A

sepsis and trauma with an ATT> 5

Not sarcomas

86
Q

JVIM 2011 Is NT-pCNP an indicator of Septic peritonitis and where is it expressed from

A

No

expressed by vascular endotheilum and macrophages

87
Q

CCM 2011 How does intestinal decontamination alter gram – bacteria

A

Oropharynx past of colistin, tobramycin, amphotericin B/NG tube
Decreased Gram - bacteria in gut

88
Q

NEJM 2011 How did plasminogen activator and DNAse in plerural infections change outcomes

A

Together reduced surgical needs and had increased drainage,

DNAse as monotherpy had 3x surgical referal

89
Q

CCM 2009 What is the PIRO models for staging severe sepsis

A

P- predisposition
I- Insult/infection
R- response
O- organ disfuction

90
Q

How does lactate increase due to sepsis

A

Sepsis impares local tissue O2 extraction

91
Q

How does prolonged decreased BP alter response

A

may lead to depletion of vasopressor stores, V1 receptors in smooth muscle inhibits NO production

92
Q

CCM 2011 How does source and infection type location alter mortaltity and how does matter in PIRO

A

Does not change hospital mortality it is more important to receive the right antibiotics
The I in PIRO is irrelevant

93
Q

What receptors and effects does dobutamine have

A

B1 ++; B2 +; Alpha +
Increases contractility, HR, CO
Decreases vasomotor tone
Variable BP

94
Q

What receptors and effects does Dopamine have

A

B1 ++; B2 +; Alpha ++
Increase contractility, HR, Vasomotor tone, and BP
Variable effect of CO

95
Q

What receptors and effect does epinephrine have

A

B1 +++; B2 +++; Alpha +++

Increases contractility, HR, CO, vasomotor tone, and BP

96
Q

What receptors and effect does Norepi have

A

B1 +; B2 - ; Alpha +++
Increases contractility, vasomotor tone, and BP
Variable effects on HR and CO

97
Q

What is the MOA of phylephrine

A

Sympathomemtic

98
Q

What receptors and effect does Phylephrine have

A

B1 - ; B2 - ; Alpha +++
Increase in vasomotor tone and BP
Decrease in CO and HR
No effect on contractility

99
Q

What is the MOA of vasopressin in BP

A

V1 receptors on vascular smooth muscle to cause vasoconstriction through the IP3 signal transduction pathway

100
Q

What receptors and effect does vasopressin have

A

B1 – ; B2 - ; Alpha -
Increase vasomotor tone and BP
Decrease in HR and CO
No effect on contractility

101
Q

What does IL-8 do

A

Rolling of WBC before diapodesis

102
Q

What do Alpha adergnic agonists alter BP/Heart

A

Increase vasculomotor tone, but may decrease regional blood flow (splanchnic, renal)

Board Review 2020 (37 decks)

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