Sepsis and Septic Shock - Hunter Flashcards
(164 cards)
1
Q
T/F: the presence of viremia does not play a role in the treatment of viruses
A
true
2
Q
T/F: when fugemia is present you’re really fucked
A
true dat
3
Q
bacteremia or fungemia represents a failure of host defenses to to neutralize an infx at (blank)
A
site of local infection
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
5
Q
Bacteremia results when the number exceeds the (blank) capacity
A
MPS clearance
6
Q
(encapsulated/neked) bacteria and yeast are poorly cleared from the circ. by the MPS system if they are not opsonized
A
encapsulated
7
Q
How long does transient bacteremia last?
A
a few hours
8
Q
What normally causes transient bacteremia?
A
tissue trauma from medical procedures (flossing)
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)
10
Q
T/F: transient bacteremia or fungemia also occurs early in acute infections
A
true
11
Q
Describe intermittent bacteremia?
A
occurs, clears, then recurs with the same organism and develops with undrained closed-space abscesses.
12
Q
Osteomyelitis that has failed to resolve can cause what type of bacteremia?
A
intermittent
13
Q
Continuous bacteremia or fungemia is a CARDINAL feature of what disease?
A
endocarditis and other endovascular infections (suppurative thrombophlebitis, infected aneurysms)
14
Q
(blank) bacteremia occurs early in typhoid fever and brucellosis
A
continuous
15
Q
What type of bacteremia reaches the highest blood bacteria concn
A
transient!
16
Q
What type of bacteremia has a single, broad, tall peak?
A
intermittent bacteremia in pneumonia
17
Q
What is the bacteremia like in sepsis?
A
undulant, with each wave worse than the last
18
Q
T/F: infective endocarditis reaches an equally high blood bacteria concn as a transient bacteremia
A
false; low level and constant
19
Q
what type of bacteremia starts with a high shed and just goes off the fuckin chart?
A
catheter bacteremia
20
Q
How many CFU/mL are needed to cause a bloodstream infection?
A
only 1-10
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
22
Q
what is the optimal sample volume for blood culture?
A
20-30 mL
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
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
25
Bacteremia can result from bacterial (blanks) on the catheters, cannulas, and shunts
biofilms
26
T/F: Abx is an effective Tx against contaminated IVs
false
27
How do you treat a contaminated IV?
take that shit out
28
What is the primary cause of most clinically sig. cases of bacteremia?
hematogenous spread from overflow from extravascular infection
29
How do bugs get into the blood stream from a local infx?
via the lymphatics
30
T/F: the higher the bacteria concn in the blood, the worse the prognosis
true
31
Describe the bacteria concn in the blood coming from an intra-abdominal abscess
that thing may only pump out a few organsims every now and then, so it can be hard to see on blood work
32
The probability of going into bacteremia is dependent on what two things?
location of initial infx and the bug itself
33
What are the most common sources of bacteremia?
UTI
respiratory tract infx
soft tissue/skin infx
34
T/F: if you got meningitis, you've got bacteremia
yup
35
Why is E. coli bacteremia common?
Becuase it commonly causes UTI, its just a numbers thing
36
What six bugs have a greater than 90% chance of causing bacteremia?
1. H. flu b
2. N. meningitidis
3. Strep pneumoniae (meningitis)
4. Brucella spp.
5. Salmonella serovar typhi
6. Listeria spp.
37
(blank) is an inflammation of a vein wall frequently associated with thrombosis and bacteremia
Suppurative (or septic) thrombophlebitis
38
Increasing use of (blank) is thought to be the cause of increases cases of Suppurative (or septic) thrombophlebitis
IV catheters
39
Describe the progression of suppurative thrombophlebitis
1. thrombus formation
2. thrombus is seeded with bugs, infx established
3. extension of suppurative infx into adjacent structures, propagation of thrmobi, SEPTIC EMBOLIZATION
40
What bug causes suppurative thrombophlebitis in superficial veins?
Staph aureus, Staph epidermidis, gram neg. bacilli, Candida
41
What bug causes suppurative thrombophlebitis in pelvic and portal veins?
Bacteroides spp., Peptostreptococcus, E. coli, Group A and B strep (pyogenes and agalactiae)
42
What bug causes suppurative thrombophlebitis in the intracranial venous sinuses?
H. flu, Strep pneumo, GAS, peptostreptococcus, S. aureus
43
Bugs that cuase common nosocomial infections cause suppurative thrombophlebitis where?
superficial veins
44
Bugs that reside on the mucous membranes cause supp. thrombophlebitis where?
deeper sites
45
What are the risk factors for suppurative thrombophlebitis?
surgery and presence of indwelling venous cannulas
46
T/F: direct cultures of sites of supp. thrmbophelbitis yield the offending organism
true
47
T/F: blood cultures of supp. thrombophlebitis are positive for bacteremia
true
48
T/F: surgery is not necessary in supp. thrombophlebitis
sometimes it is
49
What determines the abx used in supp. thrombophlebitis?
based on the culture and susceptibility testing
50
T/F: Bugs that traverse the epithelial barriers are attacked by local and systemic responses.
true
51
T/F: some host responses to infx can be life threatening
true, aka sepsis
52
What is the definition of septicemia?
pathogens in the blood that are causing sepsis
53
Describe the progression from SIRS to multiple organ dysfunction
1. SIRS
2. sepsis
3. severe sepsis
4. septic shock
5. MODS
54
Trauma, burns, and pancreatitis can lead to what type of systemic response?
SIRS BUT NOT A BLOOD BORNE INECTION
55
What are the criteria for SIRS?
At least two of the following:
1. Temperature >38°C or 90 beats per minute
3. Tachypnea or hyperventilation (respiratory rate >20 breaths per minute or PaCO2 12,000 cells/mL or 10% bands
56
What are the temp guidelines for SIRS?
Temperature >38°C or <36°C
57
What is the heart rate cutoff for SIRS?
Heart rate >90 beats per minute
58
What is the breathing cutoff for SIRS?
Tachypnea or hyperventilation (respiratory rate >20 breaths per minute or PaCO2 <32 mm Hg)
59
What is the WBC count needed for SIRS?
White blood cell count >12,000 cells/mL or 10% bands
60
What is the difference between SIRS and sepsis?
Sepsis is SIRS with a SUSPECTED or proven infectious source
61
What is severe sepsis?
Sepsis with at least one sign of organ failure or hypoperfusion
62
What are the signs of organ failure or hypoperfusion?
1. lactic acidosis (lactate >4mmol/L)
2. oliguria (urine <100k
6. DIC
7. acute lung injury/ARDS
63
What is septic shock?
severe sepsis with hypotension DESPITE fluid resuscitation
64
What is MODS?
dysfunction of 2 OR MORE organ systems such that homeostasis cannot be maintained without intervention
65
Why has sepsis been increasing in the US?
it increaes with age and comorbidity, and we have an old and sick population
66
What particular disease has a high risk of developing sepsis?
AIDS
67
Gram neg and gram pos bacteria account for what percent of sepsis?
45% each, so 90% between the two
68
T/F: organisms that DO NOT invade the bloodstream can still cause organ dysfunction and hypotension
true
69
T/F: blood cultures are often negative in severe sepsis
fucking true! only pos 20-40% of the time and 40-70% in septic shock
70
T/F: negative microbiological findings of infected material in pts with sepsis is not uncommon
true
71
What organ do these infect?
| Streptococcus pneumoniae, Haemophilus influenzae, Legionella species, Chlamydia pneumoniae, aerobic gram-negative rods
the lung
72
What organ do these infect?
Streptococcus pyogenes, Staphylococcus aureus, Clostridium species, Pseudomonas aeruginosa, anaerobes, coagulase-negative Staphylococcus species, aerobic gram-negative rods
wounds and soft tissue
73
What organ do these infect? Escherichia coli, Klebsiella species, Enterobacter species, Proteus species, Enterococcus species; aerobic gram-negative rods
urinary tract
74
What organ do these infect?
Streptococcus pneumoniae, Neisseria meningitidis, Listeria monocytogenes, Escherichia coli, Haemophilus influenzae, Pseudomonas aeruginosa, Klebsiella species, Staphylococcus species
CNS
75
What organ do these infect?
| Escherichia coli and Bacteroides fragilis, aerobic gram-negative rods, anaerobes, Candida species
abdomen
76
What causes sepsis in neonates?
strep agalactiae (group B) and less often by E. coli
77
When is the neonate infected with strep agalactiae?
during labor and delivery
78
How does a neonate present with sepsis?
meningitis or pneumonia
79
What are the most common causes of sepsis in older kids?
strep pneumo, N. meningitidis, staph aureus
80
How to children initially present with staph?
meningitis, skin infections, bacterial rhinosinusitis, and otitis media
81
what are the three physiologic properties that make sepsis particularly deadly?
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
T/F: the same proinflammatory signals that will save your life on a local level will kill you on a systemic level
true
83
large scale release of TNF-a into the blood stream has what effects?
```
decreased blood volume
hypoproteinemia
neutropenia followed by neutrophilia
vessel collapse (low volume)
DIC`
```
84
Release of proinflammatory cytokines from microbial antigens attracts (blank) cells
leukocytes
85
Release of proinflammatory cytokines dilates blood vessels, increases vascular permeability, and (increases/decreases) speed of blood flow
decreases flow speed
86
T/F: acute phase reactants have antimicrobial properties
true
87
T/F: proinflammatory cytokines cause the release of acute phase reactants
true
88
What are the two main effects of the inflammatory cascade?
vasodilation and coagulation
89
When vasodilation and coagulation spread byeond the local infection, sepsis may result in what four bad physiologic responses?
1. hypotension
2. hypoperfusion
3. coagulopathy
4. organ failure
90
T/F: the kidneys are DIRECTLY effected by cytokine release
true; renal function decreases
91
How is the heart impacted by cytokine release?
impaired contractility due to impaired metabolite use
92
How do you suffer an acute lung injury as a result of cytokine release?
vasodilation and increased capillary permeability leading to pulmonary edema
93
What three things constitute hemodynamic collapse in sepsis?
hypoxic respiratory failure
Shock
acute renal failure
94
(blank) injury is a major mechanism for multiorgan dysfunction
vascular endothelium injury
95
When upregulated cell adhesion molecules promote the adherence of neutrophils to the endothelium (blank) mediators are released that cause vascular injury
toxic mediators
96
What leukoctye derived mediator may cause vascular injury?
PLT-leukocyte-fibrin thrombi
97
What type of thrombus is seen in sepsis?
fibrin thrombus
98
Explain the downward spiral of the coagulation cascade and fibrinolytic system activation in sepsis induced DIC
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
What can you give to a patient with sepsis induced DIC to stabilize them?
PLTs and fresh frozen plasma
100
(blank) in sepsis is a bad prognostic indicator
coagulopathy
101
Explain the down regulatory system against endotoxin exposure?
first exposure to endotoxin causes a huge release of TNF-a, reexposure after a few hours doesn't cause a proinflammatory response
102
How long do you remain tolerant to endotoxin after primary exposure?
2-3 days
103
First, sepsis presents with what four general symptoms?
1. fever
2. tachycardia
3. tachypnea
4. leukocytosis
104
As sepsis progresses, the pt may become (blank) and show evidence of hypoperfusion
hypotensive
105
What is the first sign of organ dysfunction?
altered mental status and decreased urine output
106
T/F: elderly and kids may have hypothermia instead of fever
true, and leukopenia instead of leukocytosis
107
Buildup of inflammatory fluid in the lung impairs (blank) exchange, favors lung collapse, decreases (blank) and results in respiratory distress and hypoxemia
impairs gas exchange
| decreases compliance
108
A pt with bilateral pulmonary opacities consistent with pulmonary edema who is also septic meets criteria for (blank)
acute lung injury
109
A septic pt may require mechanical ventilation if they develop ALI/ARDS after (blank)
fluid resuscitation
110
What effects the direct myocardial toxicity in sepsis?
ROS and NO inflammatory molecules
111
How do you support heart preload?
hydration
112
How do you support heart afterload?
vasopressors
113
How do you support heart contractility?
dobutamine
114
What two bad things can happen to the heart of old people who are septic?
acute coronary syndrome or MI
115
what is the danger of using inotropic agents or vasopressors?
they can over elevate the HR
116
Increased bili, aminotransferases, and alk phos and CHOLESTATIC JAUNDICE indicates what?
liver failure
117
T/F: liver synthesis of actue phase proteins is not changed unless pts are unstable for a long time
true
118
What is the cause of renal failure in sepsis?
hypoperfusion
119
What symptoms do you see with renal failure in sepsis?
oliguria, azotemia (nitrogen in blood), inflamm cells in UA
120
What two treatments are used to support perfusion?
hydration and vasopressors
121
T/F: hemodialysis is not indicated in sepsis induced renal failure
false
122
What are some of the reasons that a blood culture may be negative in a septic patient?
1. prior abx use
2. slow growing/fastidious organisms
3. absence of microbial invasion into blood stream
123
Taking cultures from multiple different locations and sample types may help you identify what?
the source of the infection
124
What is worse? An increased WBC or a decreased WBC with left shift?
decreased WBC with left shift
125
If you see thrombocytopenia in someone with sepsis, what labs should you order right away?
PTT and PT
| D-dimer
126
Elevated creatinine and BUN signals what?
renal failure
127
T/F: blood glucose may be increased or decreased in sepsis
true
128
T/F: electrolyte abnormalities are not common in sepsis
false
129
How soon after septic presentation should abx therapy be started?
within 1 hour
130
T/F: abx therapy should be started regardless of whether blood cultures have been drawn
true
131
T/F: bad abx selection doubles mortality in sepsis
true
132
Besides blood cultures, what other labs should be done in the "aggressive" search for the source of infx?
UA
CXR
ECG; ischemia secondary to hypoperfusion
133
What are the majority of cases of sepsis caused by
pneumonia, GI, or urinary tract infections
134
If the sepsis is coming from an infected catheter, should you always remove the line?
as long as the pt is stable enough to undergo the procedure
135
What are the four major treatment goals when dealing with sepsis?
1. Resuscitate and correct hypoxia, hypotension, and hypoperfusion
2. Start abx
3. ID source of infx
4. Maintain organ system function
136
Should you delay abx Tx to get blood and urine cultures?
no
137
T/F: gram pos are just as common in producing sepsis as gram neg
true
138
T/F: antifungal coverage is not recommended unless the clinical pictures specifically indicates a fungal sepsis
true
139
What is the only proven treatment of septic shock?
empiric abx therapy
140
How do you obtain the necessarily wide spectrum coverage in empiric abx therapy?
broad spectrum or MULTIPLE abx usage
141
Through what route of administration should all abx be given in sepsis>?
IV, YOU WANT THAT SHIT FAST
142
In immunocompetent adults, what abx can you give in monotherapy for sepsis?
antipseudomonal penicillin (ticarcillin-clavulanate) or carbapenem
143
What is given to immunocompetnent adults for combo abx therapy for sepsis?
1.third gen cephalosporin (cefepime) plus anaerobic coverage (clindamycin or metronidazole)
OR
2. fluoroquinolone plus clindamycin
144
T/F: crystalloid improves blood pressure without altering cardiac output
false; improves both
145
T/F: NorEpi is more effective than dopamine in refractory septic shock
true
146
T/F: NorEpi increases cardiac output but lowers blood pressure
false; increases both
147
T/F: dobutamine increases cardiac output and blood pressure
false; only increases cardiac output, need to use a vasopressor to increase BP
148
How soon after the first fluid bolus should the patient be reassessed?
immediately
149
Goal 1 of early goal directed therapy (EGDT) is the maintain central venous pressure in what range?
CVP: 8-12 mmHg
150
How is the CVP maintained?
infusion of crystalloid
151
Goal 2 of EGDT is the maintain the Mean Arterial Pressure in what range?
>65 mmHg
152
How is the MAP maintained in EDGT?
use of vasopressors such as NorEpi or dobutamine
153
Goal 3 of the EDGT is the maintain central venous O2 sat (SvcO2 in what range?
>70%
154
how is the SvcO2 maintained?
RBC transfusion, dobutamine to boost cardiac output, or intubation and oxygenation
155
T/F: surgical removal of a focal infection is necessary to end a sepsis
true
156
What are the common locations of occult infections?
lung, abd, and urinary tract
157
(blank) % of patients with severe sepsis and (blank)% of patients with septic shock die within 30 days
20-35 % severe sepsis
| 60% septic shock
158
T/f: case fatality rates are similar for culture pos and culture neg severe sepsis
true
159
Septic case fatality remains below 10% until what decade?
4th
160
What is the case fatality in the elderly?
>35%
161
What is the best way to reduce morbidity and mortality from sepsis?
prevention
162
T/f; most cases of severe sepsis in developing countries are from nosocomial infections
true :(
163
How do we reduce nosocomial infection induced sepsis?
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
T/F: indiscriminate use of antimicrobials and glucocorticoids should be avoided
true
