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Block 7 Week 4 Colt > Sepsis and Septic Shock - Hunter > Flashcards

Sepsis and Septic Shock - Hunter Flashcards

1
Q

T/F: the presence of viremia does not play a role in the treatment of viruses

A

true

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2
Q

T/F: when fugemia is present you’re really fucked

A

true dat

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3
Q

bacteremia or fungemia represents a failure of host defenses to to neutralize an infx at (blank)

A

site of local infection

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4
Q

Bacteria and fungi are cleared from the body via the (blank) system

A

mononuclear macrophage system, aka splenic macs and liver Kupffer cells

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5
Q

Bacteremia results when the number exceeds the (blank) capacity

A

MPS clearance

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6
Q

(encapsulated/neked) bacteria and yeast are poorly cleared from the circ. by the MPS system if they are not opsonized

A

encapsulated

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7
Q

How long does transient bacteremia last?

A

a few hours

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8
Q

What normally causes transient bacteremia?

A

tissue trauma from medical procedures (flossing)

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9
Q

What are some common medical procedures that result in bacteremia?

A

Manipulation of infected tissue (abscesses, furuncles, cellulitis), instrumentation of colonized mucosal surfaces (dental procedures, cystoscopy, sigmoidoscopy)

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10
Q

T/F: transient bacteremia or fungemia also occurs early in acute infections

A

true

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11
Q

Describe intermittent bacteremia?

A

occurs, clears, then recurs with the same organism and develops with undrained closed-space abscesses.

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12
Q

Osteomyelitis that has failed to resolve can cause what type of bacteremia?

A

intermittent

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13
Q

Continuous bacteremia or fungemia is a CARDINAL feature of what disease?

A

endocarditis and other endovascular infections (suppurative thrombophlebitis, infected aneurysms)

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14
Q

(blank) bacteremia occurs early in typhoid fever and brucellosis

A

continuous

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15
Q

What type of bacteremia reaches the highest blood bacteria concn

A

transient!

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16
Q

What type of bacteremia has a single, broad, tall peak?

A

intermittent bacteremia in pneumonia

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17
Q

What is the bacteremia like in sepsis?

A

undulant, with each wave worse than the last

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18
Q

T/F: infective endocarditis reaches an equally high blood bacteria concn as a transient bacteremia

A

false; low level and constant

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19
Q

what type of bacteremia starts with a high shed and just goes off the fuckin chart?

A

catheter bacteremia

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20
Q

How many CFU/mL are needed to cause a bloodstream infection?

A

only 1-10

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21
Q

Two culture sets, (blank and blank) should be taken at different times and at different locations when growing bugs from blood

A

anaerobic and aerobic

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22
Q

what is the optimal sample volume for blood culture?

A

20-30 mL

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23
Q

T/F: you may draw blood for culture from an indwelling IV or intra-arterial catheter

A

false; only when you suspect the line to be contaminated

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24
Q

What special thing do you need to do when you’re checking to see if the IV is infected?

A

on the other arm draw a straight venipuncture simultaneously to see if shit grows from that too

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25
Q

Bacteremia can result from bacterial (blanks) on the catheters, cannulas, and shunts

A

biofilms

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26
Q

T/F: Abx is an effective Tx against contaminated IVs

A

false

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27
Q

How do you treat a contaminated IV?

A

take that shit out

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28
Q

What is the primary cause of most clinically sig. cases of bacteremia?

A

hematogenous spread from overflow from extravascular infection

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29
Q

How do bugs get into the blood stream from a local infx?

A

via the lymphatics

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30
Q

T/F: the higher the bacteria concn in the blood, the worse the prognosis

A

true

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31
Q

Describe the bacteria concn in the blood coming from an intra-abdominal abscess

A

that thing may only pump out a few organsims every now and then, so it can be hard to see on blood work

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32
Q

The probability of going into bacteremia is dependent on what two things?

A

location of initial infx and the bug itself

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33
Q

What are the most common sources of bacteremia?

A

UTI
respiratory tract infx
soft tissue/skin infx

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34
Q

T/F: if you got meningitis, you’ve got bacteremia

A

yup

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35
Q

Why is E. coli bacteremia common?

A

Becuase it commonly causes UTI, its just a numbers thing

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36
Q

What six bugs have a greater than 90% chance of causing bacteremia?

A
  1. H. flu b
  2. N. meningitidis
  3. Strep pneumoniae (meningitis)
  4. Brucella spp.
  5. Salmonella serovar typhi
  6. Listeria spp.
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37
Q

(blank) is an inflammation of a vein wall frequently associated with thrombosis and bacteremia

A

Suppurative (or septic) thrombophlebitis

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38
Q

Increasing use of (blank) is thought to be the cause of increases cases of Suppurative (or septic) thrombophlebitis

A

IV catheters

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39
Q

Describe the progression of suppurative thrombophlebitis

A
  1. thrombus formation
  2. thrombus is seeded with bugs, infx established
  3. extension of suppurative infx into adjacent structures, propagation of thrmobi, SEPTIC EMBOLIZATION
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40
Q

What bug causes suppurative thrombophlebitis in superficial veins?

A

Staph aureus, Staph epidermidis, gram neg. bacilli, Candida

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41
Q

What bug causes suppurative thrombophlebitis in pelvic and portal veins?

A

Bacteroides spp., Peptostreptococcus, E. coli, Group A and B strep (pyogenes and agalactiae)

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42
Q

What bug causes suppurative thrombophlebitis in the intracranial venous sinuses?

A

H. flu, Strep pneumo, GAS, peptostreptococcus, S. aureus

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43
Q

Bugs that cuase common nosocomial infections cause suppurative thrombophlebitis where?

A

superficial veins

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44
Q

Bugs that reside on the mucous membranes cause supp. thrombophlebitis where?

A

deeper sites

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45
Q

What are the risk factors for suppurative thrombophlebitis?

A

surgery and presence of indwelling venous cannulas

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46
Q

T/F: direct cultures of sites of supp. thrmbophelbitis yield the offending organism

A

true

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47
Q

T/F: blood cultures of supp. thrombophlebitis are positive for bacteremia

A

true

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48
Q

T/F: surgery is not necessary in supp. thrombophlebitis

A

sometimes it is

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49
Q

What determines the abx used in supp. thrombophlebitis?

A

based on the culture and susceptibility testing

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50
Q

T/F: Bugs that traverse the epithelial barriers are attacked by local and systemic responses.

A

true

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51
Q

T/F: some host responses to infx can be life threatening

A

true, aka sepsis

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52
Q

What is the definition of septicemia?

A

pathogens in the blood that are causing sepsis

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53
Q

Describe the progression from SIRS to multiple organ dysfunction

A
  1. SIRS
  2. sepsis
  3. severe sepsis
  4. septic shock
  5. MODS
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54
Q

Trauma, burns, and pancreatitis can lead to what type of systemic response?

A

SIRS BUT NOT A BLOOD BORNE INECTION

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55
Q

What are the criteria for SIRS?

A

At least two of the following:

  1. Temperature >38°C or 90 beats per minute
  2. Tachypnea or hyperventilation (respiratory rate >20 breaths per minute or PaCO2 12,000 cells/mL or 10% bands
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56
Q

What are the temp guidelines for SIRS?

A

Temperature >38°C or <36°C

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57
Q

What is the heart rate cutoff for SIRS?

A

Heart rate >90 beats per minute

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58
Q

What is the breathing cutoff for SIRS?

A

Tachypnea or hyperventilation (respiratory rate >20 breaths per minute or PaCO2 <32 mm Hg)

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59
Q

What is the WBC count needed for SIRS?

A

White blood cell count >12,000 cells/mL or 10% bands

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60
Q

What is the difference between SIRS and sepsis?

A

Sepsis is SIRS with a SUSPECTED or proven infectious source

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61
Q

What is severe sepsis?

A

Sepsis with at least one sign of organ failure or hypoperfusion

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62
Q

What are the signs of organ failure or hypoperfusion?

A
  1. lactic acidosis (lactate >4mmol/L)
  2. oliguria (urine <100k
  3. DIC
  4. acute lung injury/ARDS
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63
Q

What is septic shock?

A

severe sepsis with hypotension DESPITE fluid resuscitation

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64
Q

What is MODS?

A

dysfunction of 2 OR MORE organ systems such that homeostasis cannot be maintained without intervention

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65
Q

Why has sepsis been increasing in the US?

A

it increaes with age and comorbidity, and we have an old and sick population

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66
Q

What particular disease has a high risk of developing sepsis?

A

AIDS

67
Q

Gram neg and gram pos bacteria account for what percent of sepsis?

A

45% each, so 90% between the two

68
Q

T/F: organisms that DO NOT invade the bloodstream can still cause organ dysfunction and hypotension

A

true

69
Q

T/F: blood cultures are often negative in severe sepsis

A

fucking true! only pos 20-40% of the time and 40-70% in septic shock

70
Q

T/F: negative microbiological findings of infected material in pts with sepsis is not uncommon

A

true

71
Q

What organ do these infect?

Streptococcus pneumoniae, Haemophilus influenzae, Legionella species, Chlamydia pneumoniae, aerobic gram-negative rods

A

the lung

72
Q

What organ do these infect?
Streptococcus pyogenes, Staphylococcus aureus, Clostridium species, Pseudomonas aeruginosa, anaerobes, coagulase-negative Staphylococcus species, aerobic gram-negative rods

A

wounds and soft tissue

73
Q

What organ do these infect? Escherichia coli, Klebsiella species, Enterobacter species, Proteus species, Enterococcus species; aerobic gram-negative rods

A

urinary tract

74
Q

What organ do these infect?
Streptococcus pneumoniae, Neisseria meningitidis, Listeria monocytogenes, Escherichia coli, Haemophilus influenzae, Pseudomonas aeruginosa, Klebsiella species, Staphylococcus species

A

CNS

75
Q

What organ do these infect?

Escherichia coli and Bacteroides fragilis, aerobic gram-negative rods, anaerobes, Candida species

A

abdomen

76
Q

What causes sepsis in neonates?

A

strep agalactiae (group B) and less often by E. coli

77
Q

When is the neonate infected with strep agalactiae?

A

during labor and delivery

78
Q

How does a neonate present with sepsis?

A

meningitis or pneumonia

79
Q

What are the most common causes of sepsis in older kids?

A

strep pneumo, N. meningitidis, staph aureus

80
Q

How to children initially present with staph?

A

meningitis, skin infections, bacterial rhinosinusitis, and otitis media

81
Q

what are the three physiologic properties that make sepsis particularly deadly?

A
  1. expansion of the immune response outside of the local infection
  2. derangement of the balance between proinflamm and anti-inflamm regulators
  3. dissemination of the infection organism
82
Q

T/F: the same proinflammatory signals that will save your life on a local level will kill you on a systemic level

A

true

83
Q

large scale release of TNF-a into the blood stream has what effects?

A 
decreased blood volume
hypoproteinemia
neutropenia followed by neutrophilia
vessel collapse (low volume)
DIC`
84
Q

Release of proinflammatory cytokines from microbial antigens attracts (blank) cells

A

leukocytes

85
Q

Release of proinflammatory cytokines dilates blood vessels, increases vascular permeability, and (increases/decreases) speed of blood flow

A

decreases flow speed

86
Q

T/F: acute phase reactants have antimicrobial properties

A

true

87
Q

T/F: proinflammatory cytokines cause the release of acute phase reactants

A

true

88
Q

What are the two main effects of the inflammatory cascade?

A

vasodilation and coagulation

89
Q

When vasodilation and coagulation spread byeond the local infection, sepsis may result in what four bad physiologic responses?

A
  1. hypotension
  2. hypoperfusion
  3. coagulopathy
  4. organ failure
90
Q

T/F: the kidneys are DIRECTLY effected by cytokine release

A

true; renal function decreases

91
Q

How is the heart impacted by cytokine release?

A

impaired contractility due to impaired metabolite use

92
Q

How do you suffer an acute lung injury as a result of cytokine release?

A

vasodilation and increased capillary permeability leading to pulmonary edema

93
Q

What three things constitute hemodynamic collapse in sepsis?

A

hypoxic respiratory failure
Shock
acute renal failure

94
Q

(blank) injury is a major mechanism for multiorgan dysfunction

A

vascular endothelium injury

95
Q

When upregulated cell adhesion molecules promote the adherence of neutrophils to the endothelium (blank) mediators are released that cause vascular injury

A

toxic mediators

96
Q

What leukoctye derived mediator may cause vascular injury?

A

PLT-leukocyte-fibrin thrombi

97
Q

What type of thrombus is seen in sepsis?

A

fibrin thrombus

98
Q

Explain the downward spiral of the coagulation cascade and fibrinolytic system activation in sepsis induced DIC

A

first the coag cascade is diffusely activated. then, the fibrinolytic system is activated to counter all the clots you’re making. BUT, round and round we go, and we keep making and breaking down clots and now you’ve got DIC because you’ve consumed ALL of your coag factors

99
Q

What can you give to a patient with sepsis induced DIC to stabilize them?

A

PLTs and fresh frozen plasma

100
Q

(blank) in sepsis is a bad prognostic indicator

A

coagulopathy

101
Q

Explain the down regulatory system against endotoxin exposure?

A

first exposure to endotoxin causes a huge release of TNF-a, reexposure after a few hours doesn’t cause a proinflammatory response

102
Q

How long do you remain tolerant to endotoxin after primary exposure?

A

2-3 days

103
Q

First, sepsis presents with what four general symptoms?

A
  1. fever
  2. tachycardia
  3. tachypnea
  4. leukocytosis
104
Q

As sepsis progresses, the pt may become (blank) and show evidence of hypoperfusion

A

hypotensive

105
Q

What is the first sign of organ dysfunction?

A

altered mental status and decreased urine output

106
Q

T/F: elderly and kids may have hypothermia instead of fever

A

true, and leukopenia instead of leukocytosis

107
Q

Buildup of inflammatory fluid in the lung impairs (blank) exchange, favors lung collapse, decreases (blank) and results in respiratory distress and hypoxemia

A

impairs gas exchange

decreases compliance

108
Q

A pt with bilateral pulmonary opacities consistent with pulmonary edema who is also septic meets criteria for (blank)

A

acute lung injury

109
Q

A septic pt may require mechanical ventilation if they develop ALI/ARDS after (blank)

A

fluid resuscitation

110
Q

What effects the direct myocardial toxicity in sepsis?

A

ROS and NO inflammatory molecules

111
Q

How do you support heart preload?

A

hydration

112
Q

How do you support heart afterload?

A

vasopressors

113
Q

How do you support heart contractility?

A

dobutamine

114
Q

What two bad things can happen to the heart of old people who are septic?

A

acute coronary syndrome or MI

115
Q

what is the danger of using inotropic agents or vasopressors?

A

they can over elevate the HR

116
Q

Increased bili, aminotransferases, and alk phos and CHOLESTATIC JAUNDICE indicates what?

A

liver failure

117
Q

T/F: liver synthesis of actue phase proteins is not changed unless pts are unstable for a long time

A

true

118
Q

What is the cause of renal failure in sepsis?

A

hypoperfusion

119
Q

What symptoms do you see with renal failure in sepsis?

A

oliguria, azotemia (nitrogen in blood), inflamm cells in UA

120
Q

What two treatments are used to support perfusion?

A

hydration and vasopressors

121
Q

T/F: hemodialysis is not indicated in sepsis induced renal failure

A

false

122
Q

What are some of the reasons that a blood culture may be negative in a septic patient?

A
  1. prior abx use
  2. slow growing/fastidious organisms
  3. absence of microbial invasion into blood stream
123
Q

Taking cultures from multiple different locations and sample types may help you identify what?

A

the source of the infection

124
Q

What is worse? An increased WBC or a decreased WBC with left shift?

A

decreased WBC with left shift

125
Q

If you see thrombocytopenia in someone with sepsis, what labs should you order right away?

A

PTT and PT

D-dimer

126
Q

Elevated creatinine and BUN signals what?

A

renal failure

127
Q

T/F: blood glucose may be increased or decreased in sepsis

A

true

128
Q

T/F: electrolyte abnormalities are not common in sepsis

A

false

129
Q

How soon after septic presentation should abx therapy be started?

A

within 1 hour

130
Q

T/F: abx therapy should be started regardless of whether blood cultures have been drawn

A

true

131
Q

T/F: bad abx selection doubles mortality in sepsis

A

true

132
Q

Besides blood cultures, what other labs should be done in the “aggressive” search for the source of infx?

A

UA
CXR
ECG; ischemia secondary to hypoperfusion

133
Q

What are the majority of cases of sepsis caused by

A

pneumonia, GI, or urinary tract infections

134
Q

If the sepsis is coming from an infected catheter, should you always remove the line?

A

as long as the pt is stable enough to undergo the procedure

135
Q

What are the four major treatment goals when dealing with sepsis?

A
  1. Resuscitate and correct hypoxia, hypotension, and hypoperfusion
  2. Start abx
  3. ID source of infx
  4. Maintain organ system function
136
Q

Should you delay abx Tx to get blood and urine cultures?

A

no

137
Q

T/F: gram pos are just as common in producing sepsis as gram neg

A

true

138
Q

T/F: antifungal coverage is not recommended unless the clinical pictures specifically indicates a fungal sepsis

A

true

139
Q

What is the only proven treatment of septic shock?

A

empiric abx therapy

140
Q

How do you obtain the necessarily wide spectrum coverage in empiric abx therapy?

A

broad spectrum or MULTIPLE abx usage

141
Q

Through what route of administration should all abx be given in sepsis>?

A

IV, YOU WANT THAT SHIT FAST

142
Q

In immunocompetent adults, what abx can you give in monotherapy for sepsis?

A

antipseudomonal penicillin (ticarcillin-clavulanate) or carbapenem

143
Q

What is given to immunocompetnent adults for combo abx therapy for sepsis?

A

1.third gen cephalosporin (cefepime) plus anaerobic coverage (clindamycin or metronidazole)
OR
2. fluoroquinolone plus clindamycin

144
Q

T/F: crystalloid improves blood pressure without altering cardiac output

A

false; improves both

145
Q

T/F: NorEpi is more effective than dopamine in refractory septic shock

A

true

146
Q

T/F: NorEpi increases cardiac output but lowers blood pressure

A

false; increases both

147
Q

T/F: dobutamine increases cardiac output and blood pressure

A

false; only increases cardiac output, need to use a vasopressor to increase BP

148
Q

How soon after the first fluid bolus should the patient be reassessed?

A

immediately

149
Q

Goal 1 of early goal directed therapy (EGDT) is the maintain central venous pressure in what range?

A

CVP: 8-12 mmHg

150
Q

How is the CVP maintained?

A

infusion of crystalloid

151
Q

Goal 2 of EGDT is the maintain the Mean Arterial Pressure in what range?

A

> 65 mmHg

152
Q

How is the MAP maintained in EDGT?

A

use of vasopressors such as NorEpi or dobutamine

153
Q

Goal 3 of the EDGT is the maintain central venous O2 sat (SvcO2 in what range?

A

> 70%

154
Q

how is the SvcO2 maintained?

A

RBC transfusion, dobutamine to boost cardiac output, or intubation and oxygenation

155
Q

T/F: surgical removal of a focal infection is necessary to end a sepsis

A

true

156
Q

What are the common locations of occult infections?

A

lung, abd, and urinary tract

157
Q

(blank) % of patients with severe sepsis and (blank)% of patients with septic shock die within 30 days

A

20-35 % severe sepsis

60% septic shock

158
Q

T/f: case fatality rates are similar for culture pos and culture neg severe sepsis

A

true

159
Q

Septic case fatality remains below 10% until what decade?

A

4th

160
Q

What is the case fatality in the elderly?

A

> 35%

161
Q

What is the best way to reduce morbidity and mortality from sepsis?

A

prevention

162
Q

T/f; most cases of severe sepsis in developing countries are from nosocomial infections

A

true :(

163
Q

How do we reduce nosocomial infection induced sepsis?

A
  1. reduce number of invasive procedures
  2. limit the duration of indwelling IV and bladder catheters
  3. reduce duration of neutropenia
  4. use more aggressive treatment of local nosocomial infections
164
Q

T/F: indiscriminate use of antimicrobials and glucocorticoids should be avoided

A

true

Block 7 Week 4 Colt (9 decks)

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