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SEPSIS Flashcards

1
Q

What is Sepsis?

A

Life-threatening organ dysfunction caused by dysregulated host response to infection

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2
Q

What is Bacteremia?

A

Bacteria in the bloodstream

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3
Q

T/F: Bacteremia can be transient or overwhelming?

A

True.

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4
Q

Is a UTI a transient or overwhelming bacteremia?

A

Transient

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5
Q

Signs of Overhwhelming Bacteremia

A

(+) BCx, Sx

Fever, chills

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6
Q

SEPSIS SxS

A 
Shivering/Fever
Extreme Pain
Pale skin
Sleepy/confused
"I feel like I might die"
SOB
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7
Q

Sepsis v Septic Shock.

A 
Septic shock can progress quickly
Inability of body to compensate.
- Lactic acid >2
-HYPOTENSION
(MAP <65)
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8
Q

Severe Sepsis definition

A

Infection + SIRS+Organ dysfunction

“SIRS” in the setting of infection, assoc w/acute organ dysfunction

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9
Q

How do we quantify organ dysfunction?

A

Acute change in SOFA score

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10
Q

Septic Shock Definition. Key finding?

A

Subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound

HYPOTENSION

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11
Q

What is the Sofa Score?

What does a high score mean?

A

Sequential Organ Failure Assessment

High SOFA score means worse sepsis

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12
Q

Baseline SOFA score?

A

Baseline Sofa score is 0

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13
Q

How high does mortality risk increase with a SOFA score >2?

A

10% mortality risk in admitted pts

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14
Q

What lab value is not found in a sofa score?

A

lactic acid

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15
Q

is qSOFA sensitive enough to meet Sepsis Dx?

A

No

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16
Q

What are the disruptions to homeostasis in Severe Sepsis?

A

Inflammation activated
Coagulation Activated
Fibrinolysis Suppressed

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17
Q

What is the driving force in acute organ dysfunction and death?

A

Coagulopahty

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18
Q

What (Bacterial) cause of inflammation is activated in sepsis?

A 
Lipopolysaccharide wall
from gram (-) bacteria
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19
Q

What factors/mediators are released in response to sepsis?

A

Proinflammatory mediators, TNF, Interleukins, platelet activating factors

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20
Q

4 classic signs of Inflammation

A

Rubor-redness
Calor-Heat
Tumor- swelling
Dolor- Pain

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21
Q

Which mediators are responsible for cytokine storm?

A

Excess TNF, IL1 IL6

cause tissue & diffuse capillary injury

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22
Q

What are the 3 ways coagulation is activated in Sepsis?

A
  • Inflammatory mediators released to fight infect also activate coagulation
  • Infectious agent itself can cause endothelial damage=promotes coagulation
  • Factors activated upon blood contacting damaged tissue= more clotting
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23
Q

T/F: D-dimer is a screening tool for Sepsis

A

False

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24
Q

What is PAI-1?

A
  • Plasminogen activator inhibitor

- Key inhibitor of fibrinolysis in Sepsis

25
What 2 factors increase PAI-1 activity in sepsis?
- Endothelial cells | - Endotoxins released by gram (-) rods
26
What are 2 reasons for increased anaerobic metabolism in sepsis?
- Decreased O2 delivery because of capillary damage | - Decreased cardiac output
27
What metabolite is increased in anaerobic metabolism
Lactic aid
28
What disease state can result from Sepsis?
DIC
29
What is SIRS in regard to sepsis?
systemic inflammatory response syndrome, an overwhelming response to infection SIRS criteria: (2+ to meet criteria) 1. temp >100.4 or <96.8 2. HR > 90bpm 3. tachypnea-resp rate > 20 or PaCO < 32mmhg 4. >12,000 WBC, or <4,000, or > 10% immature neutrophils ie a left shift
30
What do you need to confirm Dx of Sepsis?
SIRS + a suspected source of infection=confirm diagnosis of sepsis.
31
SIRS clinical utility
SIRS is used as early recognition to make a diagnosis and early intervention to impact survivability
32
What is DIC? What are the labs of DIC (high/low)?
- Disseminated Intravascular Coagulation - Widespread imbalance between inflammation, coagulation and fibrinolysis ↑PT, PTT, Fibrin monomers, D-dimer ↓Protein C, Fibrinogen, Platelet count
33
What are the labs/findings of Severe Sepsis (high/low)?
↑ Creatinine, ALT,AST, Total bilirubin, Lactate (>2 mmol/L),- Procalcitonin (>2.0 ng/ml) ↓ Urine output, Mental status, BP
34
What is procalcitonin? | What level is indicative of Sepsis?
Protein biomarker→ bacterial infect Utilized to deescalate ABX > 2.0 ng/ml → highly suggestive Sepsis
35
Severe Sepsis pts are lively to have (5)?
``` ↑ mortality rates Long lengths of stay ↑ ventilator usage ↑ costs ↑ probability of outlier status ↓ payment-to-cost ratios (Low SES) ```
36
Pts at risk for sepsis?
- All critically ill - Severe CAP - Intra abdominal surgery - MENINGITIS - Chronic Disease (DM, HF, CRF and COPD) - ↓ immune function –HIV, transplants (Solid organ & blood), chemo - Cellulitis - UTI
37
Decrease in what 2 findings can negate cessation of fluid rescuscitation?
↓ Cap refill time & ↓ Lactate
38
What is the MCC of Severe Sepsis?
PNA
39
Phases of Sepsis Management?
``` 1. Resuscitation Phase (6hrs-sooner=better –strive for 3hrs) 2. Initial Management Phase (24 hours) 3. Maintenance Phase (>24 hours) ```
40
Resuscitation Phase algorithm
1. Access & maintain airway 2. BCx & Blood work 3. Initiate ABX therapy 4. IV fluids **30ml/kg** (If MAP <65 or lactate >2) 5. Tight glycemic control Insulin continuous IV drip 6. Vasopressors-**NOREPINEPHRINE, 7. Sedation? 8. Steroids? use for pts in septic shock
41
ABX therapy?
Broad Spectrum: Vanco=gram (+), & resistant gram (+) Pip/tazo (Zosyn) =(-), anaerobes, Pseudomonas can also use carbapenems (not ertapenem)
42
Vasopressor therapy?
**Norepinephrine-use first dobutamine, phenylephrine, epinephrine, vasopressin, dopamine- use LAST pts often need combo of pressors
43
Goals of 1st 6hrs
* *MAP <65 - urine output 0.5mL/hr - Central venous O2 sat >70%
44
Hour 1 bundle
- Measure lactate level - Obtain BCx before admin of ABX - Admin broad spectrum ABX - Begin rapid admin of 30ml/kg crystalloid for hypotension or lactate>2 - Maintain MAP ≥ 65 mmHg via Vasopressors
45
Goals of Initial management phase?
- Continue Rescusitation - Monitor ↓Cap refill time &↓Lactic acid to reduce fluids - Monitor Cx for ABX therapy - Constant monitor Vasopressors - Maintain MAP >65
46
Types of Support in Management phase?
Respiratory support: - Watch for ARDS - ↑ HOB - Use weaning protocols CNS Support (sedation protocols) - Avoid NM blockers if possible (in pts w/o ARDS) - Short course NM blocker for pt w/ early, severe ARDS
47
Maintenance Phase goals?
- Preventing nosocomial infections - Restore premorbid condition - Tailor antibiotic therapy as culture info available
48
General supportive care in Maintenance phase sepsis
- BGL <180 mg/dl - Dialysis for renal failure or fluid overload - DVT prophylaxis - Stress ulcer prophylaxis =Stress on GI system- sitting in pool of stomach acid (Tx: PPI's) - Enteral feeding if possible tube feeds
49
What bacteria are most common in Sepsis? | What sources for infection MC?
``` Gram (-) rods, Strep PNA (gram (+)) ``` Lungs Urinary tract GI Skin/Soft tissue
50
T/F: COVID sepsis will have (+) BCx?
False
51
How do we manage ICU pts w/severe COVID-19?
Recommend use of: - Corticosteroids (**dexamethasone) - VTE prophylaxis Recommend Use in non ventilated pts: - Remdisivir -Recommend prone ventilation: when ventilation is necessary Recommend AGAINST use of: - Hydroxychloroquine
52
Severe sepsis is ____, ______, and ______.
Common Deadly Costly
53
______ is key in sepsis tx
Early recognition
54
1st signs of sepsis are _____ 1st hours of sepsis are ______ _____ resuscitation is 1st step
Subtle Crucial Fluid
55
MAP calculation?
(SBP+2DBP)/3
56
Procalcitonin uses:
``` Can detect severity of Bacterial infect - higher number-more severe Dz Role in ABX stuartship: - When to start ABX - to reduce or r/o ABX use Also: - Arthritis (infectious or not) - Acute Endocarditis - Meningitis (bacterial or not) ```
57
MC bacteria for sepsis in neonates?
Ecoli, GBS = colonizations | Listeria = mom exposure
58
How can mom be exposed to listeria? | What can Listeria cause?
``` Soft cheeses (unpasteurized) Deli Meat ``` Meningitis-->sepsis
59
MC bacteria for sepsis in IVDU?
Staph/Strep & MRSA

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