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Clinical Decision making- Summer final > Sepsis: slides 12-55 schoeny > Flashcards

Sepsis: slides 12-55 schoeny Flashcards

1
Q

Severe sepsis results from the body’s _____ to infection

A

over response

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2
Q

Severe Sepsis disrupts homeostasis:
_____ are activated
_____ are suppressed

A

Coagulation & Inflammation are activated

Fibrinolysis is suppressed

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3
Q

________ is the driving force in acute organ dysfunction and death

A

**Coagulopathy

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4
Q

_____= a normal response to infection

A

inflammation

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5
Q

Gram ______ lipopolysacharide wall activates in sepsis

A

negative

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6
Q

What is activated in Sepsis as part of the inflammatory response?

A

Proinflammatory mediators TNF, interleukins and platelet activating factor are released

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7
Q

Inflmation in latin= “to set on fire”

-list 4 classic signs of inflammation

A

Redness: Rubor
Heat: Calor
Swelling: Tumor
Pain: Dolor

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8
Q

Proinflammatory mediators repair existing damage and _______

A

limit new damage

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9
Q

Body has a check system in interleukin system : ____& _____ to down regulate initial proinflammatory response

A

**IL4 and IL10

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10
Q

In sepsis, regulation of ____ ______ to infection is lost

& a Massive systemic reaction occurs

A

early response

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11
Q

In sepsis:

Excess TNF and ___, & ___ are released causing excess tissue injury and diffuse capillary injury (=“cytokine storm”)

A

**IL1 & IL6

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12
Q

What does the inflammatory effect of a cytokine storm lead to?

A

tissue damage and organ dysfunction

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13
Q

_______ is activated in sepsis

A

coagulation

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14
Q

______ _______ released to fight infection also activate coagulation

Infectious agent itself can cause ______ damage-promotes coagulation

A

Inflammatory mediators–> Factors activated upon blood contacting damaged tissue

endothelial

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15
Q

Presence of ______ indicates activation of clotting

A

D-dimer

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16
Q

Fibrinolysis=

A

Normal process to remove clots

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17
Q

T/F: fibrinolysis is suppressed in sepsis

A

true

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18
Q

______ is a key inhibitor of fibrinolysis

A

Plasminogen activator inhibitor-1 (PAI-1)

–PAI-1 produced by endothelial cells

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19
Q

Endotoxins released by gram negative rods _____ activity of PAI-1

A

increase

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20
Q

Microcirculation=

A

vast systme responsible for transport of O2 to tissue in the body
–microcirc fx is essential for adequate tissue oxygenation delivery and organ fx

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21
Q

Injury to microvascular system=

-(what is increased?)

A
  • INCREASED neutrophil migration and adhesion, coagulation, inflammation, endothelial injury and loss of barrier integrity
  • DECREASED fibrinolysis,
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22
Q

Microvascular injury results in _____

A

altered microcirculatory function

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23
Q

Results of Sepsis:

______ and _____ are decreased

A

Decreased O2 delivery because of capillary damage

Decreased cardiac output

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24
Q

Result of Sepsis:

What anaerobic metabolite is increased during sepsis?

A

INCREASED anaerobic metabolism–> so increased lactate levels**

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25
Q

What severe disorder can occur as a result of sepsis?

A

DIC** = Disseminated Intravascular Coagulation

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26
Q

DIC= widespread imbalance b/w inflammation, ________ and ______

A

coagulation and fibrinolysis

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27
Q

Laboratory findings in DIC:

-Elevated _____

A

PT
PTT
Fibrin monomers
D-dimer

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28
Q

Laboratory findings in DIC:

Decreased ________

A

Protein C
Fibrinogen
Platelet count

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29
Q

Lab/Clinical findings in severe sepsis:

Elevated _______

A

Creatinine
ALT,AST, T bili

**Lactate (>4 mmol/L) (if it’s above 5–> RLLY WORRY)

Procalcitonin (>2.0 ng/ml
(worry

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30
Q

Lab/Clinical findings in severe sepsis:

decreased _______

A

Urine output
Mental status
Blood pressure

31
Q

What is procalcitonin a protein biomarker for?

A
  • *bacterial infection (elevated in bacterial infxns)

- Can be utilized to deescalate antibiotics

32
Q

Normal procalcitonin level=

A

≤ 0.15 ng/ml

33
Q

Procalcitonin levels > ____ ng/mL highly suggestive of sepsis

A

> 2

34
Q

______ is the earliest marker for bacterial infcetion

A

procalcitonin

35
Q

Pts at risk of developing sepsis=

A
  • All critically ill
  • Severe CAP (comm. acquired PNA)
  • Intra abdominal surgery
  • Meningitis
  • Chronic Disease (diabetes, heart failure, CRF and COPD)
  • Decreased immune function –HIV, transplants, chemo
  • Cellulitis
  • UTI
36
Q

Pts who are at GREATER risk of developing sepsis=

A
  • Older age- 65+
  • Underlying comorbidity
  • Higher body weight
37
Q 
S-
E-
P-
S-
I-
S-
A 
S- shivering/fever/cold
E- Extreme pain 
P- pale 
S- sleepy/confused
I- I feel like I might die
S- SOB
38
Q

What is the number 1 cause of sepsis?

A

community acquired PNA**

39
Q

Recognizing Sepsis:

Is SIRS required?

A

yes and no, new criteria each year

40
Q

List the SIRS criteria (some places still use this in addition to qSOFA score)

A

Temp >100.4 or <96.8

Heart rate >90 bpm

Tachypnea-resp rate >20 or
PaCO<32 mm hg

> 12,000 WBC

41
Q

What are examples of potential mimics of SIRS?

A 
Pancreatitis
GI bleed
SLE flare
DKA
Anaphylaxis
Adrenal insufficiency
PE/DVT
42
Q

Sepsis with acute organ dysfunction:

  • areas of ______ skin
  • Cap refill time > or equal to ___ seconds
  • Urine output ___ hour or RRT
  • Lactate > ____ mmol/L
A

Areas of mottled skin

Capillary refill time ≥ 3 seconds

Urine output <0.5 mL/kg > 1 hr or RRT

Lactate >2 mmol/L

43
Q

Sepsis with acute organ dysfunction:

  • Abrupt change in _____ status
  • Platelets: < ________ OR DIC present
  • Acute _____ injury or ______
  • Cardiac _______
A

Abrupt change in mental status

Platelets <100,000 or DIC

Acute lung injury, ARDS

Cardiac dysfunction

44
Q

The MCC of severe sepsis=

A

Pneumonia most common cause (~50% of cases)

45
Q

In severe sepsis:

-blood cultures are only positive in ____ of cases

A
  • *1/3
  • **Gram negative bacteria in 62%
  • Gram positive bacteria in 47%

-Fungi in 19%

46
Q

Group B strep=

A

** also known as Streptococcus agalactiae, is recognized as a leading cause of postpartum infection and neonatal sepsis. Infection in healthy, nonpregnant adults is becoming more common, especially among young to middle-aged women with diabetes.

47
Q

How do we treat beta hemolytic strep in general?

A

PCN– which is safe in pregnancy

48
Q

Beta hemolytic vs alpha hemolytics strep

A

Alpha-hemolytic species cause oxidization of iron in hemoglobin molecules within red blood cells, giving it a greenish color on blood agar. Beta-hemolytic species cause complete rupture of red blood cells. On blood agar, this appears as wide areas clear of blood cells surrounding bacterial colonies

49
Q

Neonatal:

-2 MC sepsis organisms?

A

E coli, Group B strep (aka Streptococcus agalactiae)=MC for neonates

50
Q

Issues with IV drug users and Sepsis tx?

A
  • compliance
  • delay in seeking care (fear of judgement)
  • difficulty finding IV access** (venous access for tx)
  • AMS
  • MUST be cognizant of central line access (if you discharge Pt with access and you know they are IV dug users)
51
Q

MC organisms associated with sepsis in IV drug users?

A

staph aureus!!!

MRSA

52
Q

Screening Pts for Severe Sepsis:
A=
B=
C=

A

A- infection
B- SIRS
C- organ dysfunction/failure yes or no

Positive screen suggestive of severe sepsis

53
Q

Sepsis Tx:

list the 3 phases

A
  • Resuscitation Phase (1st 6 hours/ sooner the better –strive for within first 3 hours)
  • Initial Management Phase (24 hours)
  • Maintenance Phase (>24 hours)
54
Q

Resuscitation Phase:

  • access and _______ airway
  • ____ culture
  • initiate appropriate abx therapy**=
A
  • maintain
  • pan-culture
  • generally vanco + piptaz
55
Q

Resuscitation Phase:
-IV fluids (If MAP ___) initial volume 30ml/kg

  • Tight glycemic control (continuous ________)
  • Vasopressors: list exs?
A
  • <65 or lactate >4
  • insulin drip
  • Vasopressors: dobutamine, **norepinephrine=1st line, dopamine= 2nd or 3rd line, phenylephrine, epinephrine, vasopressin
56
Q

Resuscitation Phase:

-other measures?

A
  • sedation (PT will be sedated if ventilation is an issue)

- +/- steroids (adrenal insufficiency?) sometimes prednisone will be given

57
Q

Septic shock abx tx:

A

no source: piptaz + vanco

58
Q

Sepsis w/ unknown source empiric tx (Pg 66 Sanford)=

A

-vancomycin (covers MRSA and gram +s)
JUST KNOW: best empiric tx= vanco + pip taz

  • pip taz (covers pseudomonas (gram -) and other gram -‘s, BUT does not cover MRSA)
  • levofloxacin/amoxocillin
  • carbapenems (also cover pseudo and gram -‘s) BUT ertapenem does not have pseudo coverage)

**pip taz has tazobactam which protects against beta lactamase which is produced by bacteria)

59
Q

which fluid type for resuscitation is better in sepsis?

A

30ml/kg/hr of crystalloid!!** know this for boards. (either normal saline or lactated ringers) better for rehydration

60
Q 
Sepsis Resuscitation: Goals for the first 6 hours
-CVP= ?
-MAP= ?
-urine output= ?
Central venous or mixed venous O2 sat=
A

CVP 8-12 mm Hg

MAP 65 mm Hg

Urine output 0.5 ml/kg/hr

Central venous or mixed venous O2 sat 70% or 65% respectively

61
Q

Goals of first 6 hours of sepsis resucitation help reduce _____

A

*28-day mortality rate

**MAP calculation: (2 x diastolic pressure) + (systolic BP) all divided by 3, swanz catheter is inserted into an artery to determine MAP

-MUST maintain MAP above 65, if it falls below 65– keep going with fluid resuscitation

62
Q

Hour 1 Bundle: Initial Resucscitation (list 5 steps) KNOW!

A
  1. Measure lactate level
  2. Obtain blood cultures before admin of antibiotics
  3. Administer broad spectrum antibiotics
  4. Begin rapid admin of 30ml/kg crystalloid for hypotension or lactate >4
  5. Maintain MAP ≥ 65 mm Hg-via Vasopressors
63
Q

What are Vasopressors? which one is preferred 1st line?

A
  • *Norepinephrine-preferred first line
  • Vasopressin
  • Epinephrine
  • Dopamine-use discouraged
  • Phenylephrine- commonly used as add on but data limited
64
Q

Initial Management Phase (includes?) (**this is within the first 24 hours)

A
  • Continue resuscitation phase
  • Monitor cultures for targeting antibiotic therapy
  • Constant monitoring of vasopressors–> Maintenance of MAP ≥ 65mmHg
65
Q

Respiratory support:

-ARDS is common and needs _____

A
  • special attention to pressures and volumes
  • Elevate head of bed
  • Use weaning protocols
66
Q

“bilateral diffuse fluffy infiltrates, normal cardiac size” =

A

ARDS

67
Q

CNS Support includes?

-NM blockers in Pts with or without ARDS?

A
  • Sedation protocols
  • Avoid neuromuscular blockers if possible (in pts WITHOUT ARDS)
  • Short course of neuromuscular blocker for patient with early, severe ARDS
68
Q

Maintenance Phase:

-IF Pt survives > 24 hours, attention to preventing _______

A

**nosocomial infections

  • Restore premorbid condition
  • Tailor antibiotic therapy as culture info available
69
Q

General Supportive Care (describe):

  • blood glucose management?
  • ______ for renal failure
  • Prophylaxis for ______ ?
A
  • Blood glucose management: <180 mg/dl
  • Dialysis for renal failure or fluid overload
  • DVT prophylaxis= compression stockings, lovenox=LMWH**
  • Stress-ulcer prophylaxis= gastric ulcers are very concerning, generally give a Pt PPI short-term
  • Enteral feeding if possible
70
Q

What causes Sepsis?

What bacteria MCC sepsis?

A

Lungs, UTI–urosepsis, GI: colitis, diverticulitis, GI surgeries, skin and ST infxns: ie cellulitis, deep wounds,

MC bacteria OVERALL= strep pneumo**, staphs (staph aureus) and gram negative side which is E coli= these are the top 3

71
Q

How can you make a difference as a provider in the future with a septic Pt?

A

Early recognition is key!
First signs may be subtle
–>First hours are crucial
**Volume resuscitation is first step

72
Q

What are some concerns with PPIs given to critically ill Pts?

A
  • C diff
  • hypomagnesia
  • some places have replaced PPIs w/ H2 blockers (famotidine) for stress ulcer prophylaxis
73
Q

Covid update with sepsis:

ICU Patients w/ severe or critical COVID-19 Recommendations?

A
  • **recommend use of corticosteroids (1st line= dexamethasone) and VTE prophylaxis
  • **Recommend AGAINST use of hydroxychloroquine
  • **Recommend Remdisivir in non-ventilated Pts

Clinical Decision making- Summer final (8 decks)

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