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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
What severe disorder can occur as a result of sepsis?
DIC** = Disseminated Intravascular Coagulation
26
DIC= widespread imbalance b/w inflammation, ________ and ______
coagulation and fibrinolysis
27
Laboratory findings in DIC: | -Elevated _____
PT PTT Fibrin monomers D-dimer
28
Laboratory findings in DIC: | Decreased ________
Protein C Fibrinogen Platelet count
29
Lab/Clinical findings in severe sepsis: | Elevated _______
Creatinine ALT,AST, T bili **Lactate (>4 mmol/L) (if it's above 5--> RLLY WORRY) Procalcitonin (>2.0 ng/ml (worry
30
Lab/Clinical findings in severe sepsis: | decreased _______
Urine output Mental status Blood pressure
31
What is procalcitonin a protein biomarker for?
* *bacterial infection (elevated in bacterial infxns) | - Can be utilized to deescalate antibiotics
32
Normal procalcitonin level=
≤ 0.15 ng/ml
33
Procalcitonin levels > ____ ng/mL highly suggestive of sepsis
>2
34
______ is the earliest marker for bacterial infcetion
procalcitonin
35
Pts at risk of developing sepsis=
- 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
Pts who are at GREATER risk of developing sepsis=
- Older age- 65+ - Underlying comorbidity - Higher body weight
37
``` S- E- P- S- I- S- ```
``` S- shivering/fever/cold E- Extreme pain P- pale S- sleepy/confused I- I feel like I might die S- SOB ```
38
What is the number 1 cause of sepsis?
community acquired PNA**
39
Recognizing Sepsis: | Is SIRS required?
yes and no, new criteria each year
40
List the SIRS criteria (some places still use this in addition to qSOFA score)
Temp >100.4 or <96.8 Heart rate >90 bpm Tachypnea-resp rate >20 or PaCO<32 mm hg >12,000 WBC
41
What are examples of potential mimics of SIRS?
``` Pancreatitis GI bleed SLE flare DKA Anaphylaxis Adrenal insufficiency PE/DVT ```
42
Sepsis with acute organ dysfunction: - areas of ______ skin - Cap refill time > or equal to ___ seconds - Urine output ___ hour or RRT - Lactate > ____ mmol/L
Areas of mottled skin Capillary refill time ≥ 3 seconds Urine output <0.5 mL/kg > 1 hr or RRT Lactate >2 mmol/L
43
Sepsis with acute organ dysfunction: - Abrupt change in _____ status - Platelets: < ________ OR DIC present - Acute _____ injury or ______ - Cardiac _______
Abrupt change in mental status Platelets <100,000 or DIC Acute lung injury, ARDS Cardiac dysfunction
44
The MCC of severe sepsis=
Pneumonia most common cause (~50% of cases)
45
In severe sepsis: | -blood cultures are only positive in ____ of cases
* *1/3 - **Gram negative bacteria in 62% - Gram positive bacteria in 47% -Fungi in 19%
46
Group B strep=
** 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
How do we treat beta hemolytic strep in general?
PCN-- which is safe in pregnancy
48
Beta hemolytic vs alpha hemolytics strep
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
Neonatal: | -2 MC sepsis organisms?
E coli, Group B strep (aka Streptococcus agalactiae)=MC for neonates
50
Issues with IV drug users and Sepsis tx?
- 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
MC organisms associated with sepsis in IV drug users?
staph aureus!!! | MRSA
52
Screening Pts for Severe Sepsis: A= B= C=
A- infection B- SIRS C- organ dysfunction/failure yes or no Positive screen suggestive of severe sepsis
53
Sepsis Tx: | list the 3 phases
- Resuscitation Phase (1st 6 hours/ sooner the better –strive for within first 3 hours) - Initial Management Phase (24 hours) - Maintenance Phase (>24 hours)
54
Resuscitation Phase: - access and _______ airway - ____ culture - initiate appropriate abx therapy**=
- maintain - pan-culture - generally vanco + piptaz
55
Resuscitation Phase: -IV fluids (If MAP ___) initial volume 30ml/kg - Tight glycemic control (continuous ________) - Vasopressors: list exs?
- <65 or lactate >4 - insulin drip - Vasopressors: dobutamine, **norepinephrine=1st line, dopamine= 2nd or 3rd line, phenylephrine, epinephrine, vasopressin
56
Resuscitation Phase: | -other measures?
- sedation (PT will be sedated if ventilation is an issue) | - +/- steroids (adrenal insufficiency?) sometimes prednisone will be given
57
Septic shock abx tx:
no source: piptaz + vanco
58
Sepsis w/ unknown source empiric tx (Pg 66 Sanford)=
-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
which fluid type for resuscitation is better in sepsis?
30ml/kg/hr of crystalloid!!** know this for boards. (either normal saline or lactated ringers) better for rehydration
60
``` Sepsis Resuscitation: Goals for the first 6 hours -CVP= ? -MAP= ? -urine output= ? Central venous or mixed venous O2 sat= ```
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
Goals of first 6 hours of sepsis resucitation help reduce _____
*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
Hour 1 Bundle: Initial Resucscitation (list 5 steps) KNOW!
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
What are Vasopressors? which one is preferred 1st line?
* *Norepinephrine-preferred first line - Vasopressin - Epinephrine - Dopamine-use discouraged - Phenylephrine- commonly used as add on but data limited
64
Initial Management Phase (includes?) (**this is within the first 24 hours)
- Continue resuscitation phase - Monitor cultures for targeting antibiotic therapy - Constant monitoring of vasopressors--> Maintenance of MAP ≥ 65mmHg
65
Respiratory support: | -ARDS is common and needs _____
- special attention to pressures and volumes - Elevate head of bed - Use weaning protocols
66
"bilateral diffuse fluffy infiltrates, normal cardiac size" =
ARDS
67
CNS Support includes? -NM blockers in Pts with or without ARDS?
- Sedation protocols - Avoid neuromuscular blockers if possible (in pts WITHOUT ARDS) - Short course of neuromuscular blocker for patient with early, severe ARDS
68
Maintenance Phase: | -IF Pt survives > 24 hours, attention to preventing _______
**nosocomial infections - Restore premorbid condition - Tailor antibiotic therapy as culture info available
69
General Supportive Care (describe): - blood glucose management? - ______ for renal failure - Prophylaxis for ______ ?
- 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
What causes Sepsis? What bacteria MCC sepsis?
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
How can you make a difference as a provider in the future with a septic Pt?
Early recognition is key! First signs may be subtle -->First hours are crucial **Volume resuscitation is first step
72
What are some concerns with PPIs given to critically ill Pts?
- C diff - hypomagnesia - some places have replaced PPIs w/ H2 blockers (famotidine) for stress ulcer prophylaxis
73
Covid update with sepsis: | ICU Patients w/ severe or critical COVID-19 Recommendations?
- **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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