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Infectious Diseases > Lecture 8: Sepsis > Flashcards

Lecture 8: Sepsis Flashcards

1
Q

How does bacteremia differ from sepsis

Which one can cause the other

A

Bacteremia = infxn in the bloodstream

Sepsis = over-response of the immune system

Bacteremia may lead to sepsis

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2
Q

A pt recently had dental procedure done, however their were complications and their mucosa was injured. What type of infxn is this pt now at risk for?

A

GI mucosa injury –> risk for Bacteremia

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3
Q
  1. Infxns (UTI, PNA)
  2. Surgery
  3. Catheters (CVCs, Urinary)
  4. Depressed immune sys (steroids, chemo, etc)
  5. Skin breakdown/wounds/bites
  6. Fluid collections (kidney stone, obstruction)
  7. GI mucosa injury
  8. Ischemic tissue

Are all RFs for _________

A

RFs for Bacteremia

  1. Infxns (UTI, PNA)
  2. Surgery
  3. Catheters (CVCs, Urinary)
  4. Depressed immune sys (steroids, chemo, etc)
  5. Skin breakdown/wounds/bites
  6. Fluid collections (kidney stone, obstruction)
  7. GI mucosa injury
  8. Ischemic tissue
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4
Q

Old Definition: Sepsis 2

  1. How many of the criteria need to be met to fufill SIRS?
  2. Sepsis = SIRS + _____
  3. Severe Sepsis = above + _____
  4. Septic Shock = above + _____
A

Old Definition: Sepsis 2

  1. 2+ criteria to fufill SIRS
  2. Sepsis = SIRS + infxn
  3. Severe Sepsis = above + organ damage
  4. Septic Shock = above + HoTN
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5
Q

What type of shock is septic shock?

A

Distributive shock

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6
Q

Life threatening organ dysfxn caused by exaggerated/dysregulated immune response

A

definition of Sepsis

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7
Q

What clinical criteria used for defining sepsis (newer)

A

SOFA

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8
Q

qSOFA at bedside: Clinical criteria for sepsis

  1. what are the 3 parameters (+ values) included?
  2. pt has 2+ what does that indicate?
A

qSOFA at bedside: Clinical criteria for sepsis

  1. RR > 22, AMS, SBP < 100
  2. pt has 2+ –> likely prolonged hospital stay or die
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9
Q

When vasopressor therapy needed to elevate MAP to 65+ and lactate > 2 after adequate fluid resuscitation what state in the continuum is this pt in?

A

Septic Shock

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10
Q

What is the only effective tx for sepsis

A

Tx for sepsis

  1. IV ABXs
  2. supportive care (IV fluids, etc)
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11
Q

Pathophys of sepsis:

once the bacteria invade the tissue what does cells become triggered and what do these cells then rel?

A

Pathophys of sepsis:

bacteria invade tissue –> macrophages triggered and rel pro inflammatory mediators (TNFs, ILs)

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12
Q

Pathophys of sepsis:

  1. How does Sepsis occur once the pro inflammatory mediators (TNFs, ILs) are released? (answer before looking below)
  2. Once the bacteria are in the bloodstream what do they do the blood vessels that ultimately cause organ hypoperfusion
A

Pathophys of sepsis:

  1. Sepsis occurs when pro-inflam > anti-inflam mediators –> infxn spread to bloodstream
  2. bacteria get in bloodstream –> leaky blood vessels –> impaired blood flow –> organ hypoperfusion
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13
Q

What are the 4 main bacterial causes of Sepsis

A

Bacterial Causes of Sepsis

  1. Gram (-)s w/ENDOTOXIN
  2. Staph aureus
  3. Pseudomonas exotoxin
  4. Strep (GAS M protein)
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14
Q

Bacterial Causes of Sepsis:

- How do endotoxins contribute to the progression of local infxn to sepsis (what do they activate)

A

Bacterial Causes of Sepsis:

Endotoxins activate the compliment, coag and fibrinolytic systems

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15
Q

Bacterial Causes of Sepsis:
- What are 2 toxins produced by Staph aureus that
contribute to sepsis

A

Bacterial Causes of Sepsis: Staph aureus toxins

  1. Staph enterotxin B
  2. TSS toxin-1
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16
Q

Sequelae of Sepsis: End Organ dysfunction seen w/:

  1. Circulation system
  2. lungs
  3. Brain
  4. Liver (3)
  5. Kidney (2)
  6. Heme
A

Sequelae of Sepsis: End Organ dysfunction seen w/:

  1. Circulation system vasodilation–> HoTN –> Hypoperfusion of all organs
  2. lungs –> ARDs
  3. Brain –> swelling –> Encephalopathy
  4. Liver –> liver dysfxn, incr Bili, clotting factors not made
  5. Kidney –> renal failure, decr/no UO
  6. Heme –> DIC
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17
Q

Manifestation of systemic inflammatory response

A

ARDS

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18
Q

What is the hypoxemic respiratory failure in ARDS caused by

A

pulm/alveolar edema

19
Q

How do pro-inflam cytokines (caused MC by sepsis) ultimately cause pulm/alveolar edema that is a/w ARDS

A

pro inflam cytokines –> diffuse alveolar damage –> incr permeability of alveolar-capillary barrier –> pulm/alveolar edema + influx of fluid into alveoli –> decr blood oxygenation

20
Q

ARDS

  1. Hallmark S/s of ARDS
  2. Classic sign on CXR
  3. what is the PCWP a/w ARDS (high or low, value)
A
  1. Hallmark = severe, hypoxemia that is refractory to 100% O@2
  2. CXR = WHITE OUT
  3. LOW PCWP ( < 18)
21
Q

Pt in sepsis presents sudden onset of dyspnea. You obtain labs and a CXR. Labs reveal severe hypoxemia. You put her on 100% O2 but no improvement is seen. Her CXR shows diffuse bilateral infiltrates sparing the costophrenic angles.

Dx?

A

ARDS

22
Q
  1. Main form of management for ARDs

2. what should be given for HoTN

A
  1. Ventilation

2. HoTN –> fluids

23
Q

Tx of ARDs: Ventilation

  1. what are 2 types (general)
  2. what are 2 specific methods of ventilating
A

Tx of ARDs: Ventilation

  1. non-invasive and mechanical ventilation
  2. PEEP or CPAP
24
Q

Septic Shock: infectious

  1. what is the MC infectious cause
  2. 3 other causes
A

Septic Shock: infectious

  1. MC infectious cause = PNA
  2. others = Intra-abd infxn, UTI, Bacteremia
25
Q

Septic shock: bacterial/fungal causes

  1. Which is more common cause: Gram - or +
  2. What are the 2 types of gram + likely to cause septic shock
  3. What fungus causes septic shock

Gram (-) Exs: E coli, Klebsiella, Enterobacter, Pseudomonas

A

Septic shock: bacterial/fungal causes

  1. MC = Gram (-)
  2. Gram (+) = s. aureus, strep pneumo
  3. Fungus = Candida
26
Q

ill appearing pt presents to ER w/ AMS and rigors. RR = 22, HR = 115, BP 95/50. Labs show incr WBC and lactate.

Dx?

A

Septic Shock

27
Q

Septic shock

- what should be obtained to identify the source of infxn (1 big thing)

A

Septic shock

- get cultures to identify source of infxn

28
Q

Septic Shock
- initial labs you should order (5)

+/- ABGs

A

Septic Shock: initial labs

  1. CBC
  2. CMP
  3. LFTs
  4. Coag studies (PT/PTT)
  5. Lactate
29
Q

What type of ABX Tx do pts need

and what should be covered

A

EARLY broad spectrum empiric ABXs, cover gram + and -

30
Q

Pt confirmed to be in septic shock. What is an example of good Tx combo that should be initiated ASAP?

A

Septic Shock Tx

Vanco + Carbepenem (maybe add fluroquinolone or aminoglycoside)

alt: Zosyn + (Ceftriaxone or Imipenem)

31
Q

What are 3 major signs of sepsis that need to be managed

A

Signs of Sepsis/Management

  1. Hypovolemia
  2. HoTN
  3. incr Lactate
32
Q

Signs of Sepsis/Management: #1 Hypovolemia

  1. how should you assess pts preload at bedside?
    - what result indicated hypovolemia
  2. What types of fluids should be given to hypovolemic pts (gen + spp)
  3. once a pt becomes euvolemic what can be added to assist w/txting their Hypovoemia
A

Signs of Sepsis/Management: #1 Hypovolemia

  1. asses preload w/bedside US
    - IVC collapse on inspiration = hypovolemia
  2. Fluids for hypovolemia = isotonic crytalloids
    - 1 L bolus of NS or LR
  3. euvolemic –> add pressors
33
Q

how do you know a pt is no longer hypovolemic

A

IVC not collapsing = euvolemic

note: BP NOT AN INDICATOR OF VOL STATUS

34
Q

What is the 1st line pressor for Septic pts

A

NE = 1st line pressor for septic pts

35
Q

Signs of Sepsis/Management: HoTN

what does prolonged HoTN lead to (2 steps)

A

Signs of Sepsis/Management: HoTN

prolonged HoTN –> tissue ischemia + anaerobic metab –> lactate production/lactic acidosis

36
Q

Signs of Sepsis/Management: HoTN

  1. what do you what at pts MAP to be above/equal to?
  2. if pts refractory to NE as pressor what can be added
A

Signs of Sepsis/Management: HoTN

  1. MAP 65+
  2. if pts refractory to NE–> stress dose steroids
37
Q

What is lactic acidosis a sign of (2 things)

A

Hypoperfusion/oxygenation

38
Q

5 y/o ill appearing kid presents w/rigors, AMS, tacypnea, tachycardia and HoTN to ER. Should you wait for labs, etc to begin treating him for suspected shock? why/why not?

A

dont wait, tx immed b/c HoTN - late sign of shock in kids

39
Q

Why is DIC called a consumptive coagulopathy

A

OVERactivate coag cascade –> widepsread microthrombi CONSUME coags factors/plts –> thrombocytopenia + diffuse bleeding

“clotting and bleeding at the same time”

40
Q

in DIC pts are “clotting and bleeding at the same time” so what are they at risk for

A

clotting and bleeding at the same time

- risk for thrombosis and hemorrhage simultaneously

41
Q

What stimulates/causes the overactivation of the clotting cascade that triggers DIC

A

procoagulant

- stimulates/causes the overactivation of the clotting cascade that triggers DIC

42
Q

Pt in ICU presents w/ new onset of bleeding of nose and blood in urinary catheter. On exam you notice various ecchymoses and petechiae. Her L leg is swollen and when you get a doppler US you Dx a DVT. Her labs reveal incr PT/PTT, INR, and D-dimer. Platelets, Hb, and fibrinogen are low. On blood smear Schistocytes are seen.

Dx?

A

DIC

43
Q

Tx of DIC

what does the tx depend on?
what should be given to replace blood loss

A

Tx of DIC

  • depends on Sxs (clotting vs bleeding)
  • PRBCS to replace blood loss
44
Q

Tx of DIC

  1. if pt is primarily bleeding what should you give
  2. if pt is primarily clotting what should you give
A

Tx of DIC

  1. if pt is primarily bleeding –> FFP/cryo
  2. if pt is primarily clotting –> heparin

Infectious Diseases (9 decks)

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