Sepsis and Septic Shock- Hunter Flashcards
1
Q
How can you describe intravascular infections?
A
bacteremia, viremia, fungemia, parasitemia
2
Q
With the exception of a few specific infections, the detection of (blank) does not play a role in the diagnosis or managment of most viral infections.
A
viremia
3
Q
Fungemia is (common/rare) but canbe serious
A
rare
4
Q
What is failing if you have a bacteremia or fungemia?
A
a failure of host defenses to localize an infection at its primary tissue site
5
Q
Bacteremia and fungemia can reflect the failure of a physician to do what?
A
remove, drain or sterilize sites of infection
6
Q
Bacteria and fungi are normally cleared from blood by the (Blank
A
MPS (mononuclear phagocyte system i.e splenic macrophages and liver kupffer cells)
7
Q
What 2 things comprise the MPS that clear bacteria and fungi?
A
splenic macrophages and liver kupffer cells
8
Q
Whats up with encapsulate bacteria and yeast and their ability to be cleared?
A
poorly cleared from circulation by fixed macrophages of the MPS especially in the absence of opsonizing antibody
9
Q
What is the most common bacteremia or fungemia?
A
Transient bacteremia or fungemia that lasts minutes to a few hours
10
Q
Why do you get transient bacteremia and fugemia?
A
due to release of organisms into circ secondary to tissue trauma resulting from medical procedures
11
Q
What are some ways you can get transient bacteremia and fugemia?
A
manipulation of infected tissue (abscesses, furuncles, cellulitis), instrumentation of colonized mucosal surfaces (dental procedures, cytoscopy, sigmoidoscopy)
12
Q
What can surgery in contaminated areas (prostate, resection, debridement of infected burns, vaginal hysterectomy) cause?
A
transient bacteremia, or transietn fungemia
13
Q
Transient bacteremia or fungemia also occurs early in (Blank) including pneumonia, meningitis, septic arthritis
A
acute infections
14
Q
Transient bactermias usually have no immediate clinical signif but they are important in the pathogenesis of (blank)
A
infective endocarditis
15
Q
(blank) occurs, clears, recurs with the same organism, and develops with undrained closed-space abscesses (intra-abdominal, pelvic, perinephric, hepatic)
A
Intermittent bacteremia or fungemia
16
Q
What can be seen in focal infections that fail to resolve (pneumonia, osteomyelitis), reflecting irregular cycles of release into and clearance from the circulation of organisms infecting tissue
A
intermittent bacteremia or fungemia
17
Q
What is a cardinal feature of endocarditis and other types of endovascular infections (suppurative thrombophlebitis, infected aneurysms)?
A
Continuous bacteremia or fungemia
18
Q
What does continuous bacteremia or fungemia reflect?
A
continous shedding of organisms from endovascular foci into the circulation
19
Q
Continuous bacteremia also occurs early (initial few weeks) in (Blank) and (Blank)
A
typhoid fever
brucellosis
20
Q
If you see a bacteremic spike (recur and quickly disappear) what kind of bacteremia is this and what causes this?
A
Transient:
Dental extraction
21
Q
If you see a bacteremia in small bell curve what kind of bacteremia is this and what causes it?
A
intermittent
-pneumococcal
22
Q
If you see a bacteremia that ebs and flows and lasts for a long time what kind of bactermia is this and what causes it?
A
intermittent-gram negative sepsis
23
Q
If you see a bacteremia that recurs and disappears continuosly what kind of bacteremia is this and what causes it?
A
intermittent
intra-abdominal abscess
24
Q
If you see a bacteremia that stays the same and does not change what kind of bacteremia is this and what causes it?
A
continuous
infective endocarditis
25
If you see a bacteremia that gradually increases steadily what kind of bacteremia is this and what causes it?
continuous
| catheter bacteremia
26
Bloodstream infections are frequently caused by relatively few organisms in a given volume of blood.
T or F
T
27
How many culture sets should you take when you are checking fo rbacteremia?
two culture sets
- aerobic
- anaerobic
28
Should you take two culture sets at the same time?
no at different times and at different sites
29
How much blood do you need per culture set?
20-30mL of blood per culture set
30
Blood should NOT be obtained from an (blank) or (blank) unless catheter-related infection is suspected
indwelling IV
| intra arterial catheter
31
For the eval of catheter-associated bloodstream infection what should you do?
concomitantly draw venipuncture specimen with a catheter specimen
32
Bacteremia or fungemia can occur secondary to spread from an (blank)
IV device
33
Bacteremia or fungemia may also result from microbial growth on the inner or outter sufaces of IV devices such as..?
Biofilms on catheters or cannulas, shunts
34
Antibiotic treatment is often (successful/unsuccessful) as an approach to a contaminates IV device.
unsuccessful
35
Contaminated IV devices need to be (blank)
removed
36
Most cases of clinically signif bacteremia or fungemia are the result of overflow from an (blank) infection
extravascular infection
37
Microorganisms from a focus of infection often reach the capillary and venous circ through (blank)
lymphatic vessels
38
Most cases of clinically signif bacteremia or fungemia are the result of overflow from an extravascular infection ,,,, called (blank) spread
hematogenous
39
Bacteremia and fungemia from extravascular infections is dependent on the timing and interaction of multiple events and is thus much (blank) predictable than intravascular infection
less
40
If the extravascular infection is extensive and uncontrolled, as with an overwhelming staph pneuomnia, there may be (blank) of organisms per milliliter of blood (a poor prognositc sign)
hundred to thousands
41
An (blank) abscess may give off only a few organisms intermittently until it is discovered and drained
intra-abdominal abscess
42
The (blank) of infection affects bacteremia and fungemia
source
43
The most common sources of bacteremia are...?
UTI
RTI
infections of skin and soft tissue (wound infection or cellulitis)
44
Any organism producing meningitis is likely to produce (blank) at the same time
bacteremia
45
The frequency with which any organism causes bacteremia is related to what?
propensity to invade the bloodstream and how often it produces infections
46
Cases of E. Coli bacteremia are (rare/common). Why?
comon, cuz E. coli is the most common cause of UTI
47
T or F
| some bacteria and fungi are very difficult to isolate from blood cultures
T
48
(blank) is an inflammation of a vein wall frequently associated with thrombosis and bacteremia
suppurative (or septic) thrombophlebitis
49
What is the pathogenesis of suppurative thrombophlebitis?
thrombus formation, which may result from trauma -> thrombosed site is then seeded with organisms and a focus of infection is established
50
What are some complications of suppurative thrombophlebitis?
complication include extension of suppurative infection into adjacent structures, further propagation of thrombi, bacteremia, and septic embolization
51
Staph aureus, S. epidermis, gram-negative bacilli, and candida albicans will result in suppurative thrombophlebitis in the (blank)
superficial veins (e.g saphenous, femoral, antecubital)
52
Bacteroides spp, peptostreptococcus, E. coli, group A or B strep will result in suppurative thrombophlebitis in the (blank)
pelvic veins, portal veins
53
H. influenza, strep pneumoniae, group A strep, peptostreptococcus, S. aureus will result in suppurative thrombophlebitis in (lank)
intracranial venous sinuses (cavernous, sagittal, lateral)
54
In superficial thrombophlebitis, which often follows IV therapy, organism that are common (Blank) offenders predoinate
nosocomial (found in hospital)
55
In superficial thrombophlebitis, which often follows IV therapy, organisms that are common nosocomial offenders predominate. What are these organisms?
Staph aureus, S. epidermis, gram-negative aerobes, candida albicans
56
Deeper infections of suppurative thrombophlebitis are more frequently causd by organisms that reside on (Blank) or (blank)
- adjacent mucous membranes
| - commonly infected adjacent sites
57
Deeper infections are more frequently caused by organisms that reside on adjacent mucous membranes, what are these organisms?
bacteroides species in intestinal and vaginal sites
| H influenza and strep pneumonia in acute otitis media and sinusitis
58
(blank) is suspected in patients with risk factors like surgery and presence of indwelling venous cannulas
suppurative thrombophlebitis
59
How can you find out what is causing your suppurative thrombophlebitis?
direct cultures of the infects site (bacteremia is usually present)
60
In some cases, (blank) is required, both for definitive treatment and to obtain specimens for cultures in suppurative thrombophlebitis
surgical exploration
61
How should you treat suppurative thrombophlebitis?
IV cather should be removed, vigorous antibiotic treatment of adjacent infections, and sometimes surgical excision and drainage
62
Humans mount both (blank) and (blnk) responses to microbes that transverse their epithelial barriers and enter underlying tissues
local and systemic
63
Some systemic responses are protective (blank), but others can be life threatening (Blank)
acute phase response
| sepsis and septic shock
64
For the non-protective responses, there is a progression of illness from systemic inflammatory response syndrome (SIRS) to (blank) that is defined by a combo of clinical and lab findings
multi-organ dysfunction syndrome (MODS)
65
In clinical parlance, any patient with sepsis, severe sepsis, septic shock, or MODS is said to be (blank)
septic
66
(blank) is used to describe pathogens in the blood that are causing sepsis
Septicemia
67
How do you go from systemic inflammatory response syndrome to multiple organ dysfunction syndrome?
systemic inflammatory response syndrome-> sepsis-> severe sepsis-> septic shock-> multiple organ dysfunction syndrome
68
What can cause SIRS?
trauma, burns, pancreatitis
69
What is the definition of SIRS?
having at least 2 of the following:
- Temperature >38°C or 90 beats per minute
- Tachypnea or hyperventilation (respiratory rate >20 breaths per minute or PaCO2 12,000 cells/mL or 10% bands
70
What is sepsis?
SIRS with a suspected or proven infectious source (not all SIRS has an infectious etiology)
71
what is severe sepsis?
Sepsis in conjunction with at least one sign of organ failure or hypoperfusion
72
What are these:
- lactic acidosis
- mental status change
- mottled skin
- delayed cap refill
- thrombocytopenia
- DIC
- acute lung injury
- acute respiratory distress syndrome
Signs of organ failure
73
What is septic shock?
severe sepsis with hypotension (or requirement of vasoactive agents e.g norepinephrine) despite adequate fluid resusctation in the form of 20-40ml/kg bolus
74
What is Multiorgan dysfunction syndrome (MODS)?
MODS is at the far end of the spectrum that begins with SIRS. It is defined as dysfunction of 2 or more organ systems such that homeostasis cannot be maintained w/out intervention
75
What is cystitis?
inflammation of the urinary bladder
76
A 34-year-old female patient presents with pelvic pain and burning on urination. A clean catch urine sample reveals >105 Escherichia coli per milliliter, confirming the diagnosis of acute cystitis. She now has tachypnea, a temperature of 39° C, and a heart rate of 100 bpm. Her serum lactate is normal, but her white blood cell count is 14,500/ml. How would you classify this septic patient?
sepsis
77
(blank) is a contributing factor in >200,000 US deaths per year
severe sepsis
78
The incidence of severe sepsis and septic shock has increased over the past 30 years and the annual number of cases is now (blank)
greater than 700,000
79
Who does 2/3rds of sepsis cases occur in?
patients with signif underlying illness
80
Sepsis related incidence and mortality rates increase with (blank) and (Blank)
age and preexisting comorbidity
81
The rising incidence of severe sepsis in the US is attributatble to the (blank) of the pop and the relatively high freq with which sepsis develops in patients with (blank)
aging
| AIDS
82
The widespread use of (blank), (blank), and (blank) play a role in sepsis development
immunosuppressive drugs, indwelling catheters, mechanical devices
83
Sepsis and septic shock can be a response to any class of microorganism, but (blank) are the most common
bacteria
84
(blank) accounts for 45% of sepsis cases
(blank) accounts for 45% of sepsis cases
(blank) accounts for 10% of sepsis cases
Gram-neg
Gram-pos
fungi, mix of microorganisms
85
T or F
| microbes that do not invade the bloodstream can elicit distant organ dysfunction and hypotension
T
86
Blood cultures yield bacteria or fungi in only (blank) of cases of severe sepsis and (blank) cases of septic shock
20-40%
| 40-70%
87
If you get a pnt with neg blood cultures how do you find the etiologic agent?
via culture or microscopic exam of infected material from local site
88
Is it weird to find neg microbiologic findings?
no :)
89
The sources for sepsis are infections elswehere in the body. T or F
T
90
What organisms are associated with lung infections?
strep pneumoniae, H influenzae, Legionella species, Chlamydia pneumonia, aerobic gram-neg rods
91
What organisms are associated with wound, soft-tissue infections?
strep pyogenes, staph aureus, clostridium species, pseudomonas aeruginosa, anaerobes, caogulase-neg stpah, aerobic gram-neg rods
92
What organisms are associated with UTI?
E coli, Klebsiella, Enterobact, Proteus species, Enterococcus, Aerobic gram-neg rods
93
What organisms are associated with CNS?
Strep pneumoniae, N meningitidis, Listeria monocytogenes, E coli, H. influenza, Pseudomas aeruginosa, Klebsiella, staph
94
What organisms are associated with abdomen?
E coli, bacteroides fragilis, aerobic gram-neg rods, candida species
95
Sepsis in neonates (less than 1 month old) is usually caused by (blan) and less often by (Blank)
strep agalactiae
| E. coli
96
App 2 of 1000 live-born infants are infected by S. agalactiae with a case fatalitiy rate of (blank)
5-10%
97
During labor and delivery the neonate can be infected with (blanK)
microorganisms
98
The most common cause of sepsis in older children inclued (Blank X 3)
strep pneumoniae, N meningitidis, Staph aureus
99
Children may initially present with (blank, blank, blank and blnk)
meningitis, skin infections, bacterial rhinosinusitis, otitis media
100
A 2-week-old baby girl hospitalized with fever and nuchal rigidity is now showing signs of neonatal sepsis. Blood cultures reveal a Streptococcus agalactiae bacteremia. What is the most likely way this infant was infected with the Group B streptococcus?
oral contamination during passage through the birth canal
101
Sepsis is a complex interaction between what 2 things?
1) direct toxic effects of infecting organism
| 2) derangement of the normal inflammatory host response to infection
102
In response to local infection there is concurrent activation of the immune system and of (blank) to control the reaction
down-regulatory mechanisms
103
What are the devastating effects of sepsis syndrome caused by?
combo of
1) expansion of the immune response to sites remote from that of infection
2) derangement of the balance b/w proinflammatory and anti-inflammatory cellular regulators
3) dissemination of infecting organism
104
Localized infections produce inflammatory mediators that induce (blank) responses and eliminate the pathogen or engage adaptive immunity
protective innate
105
(blank) produce the same mediators as localized infections but in larger quantities that cause signfic pathophysiologic changes and can lead to death.
Systemic infections
106
In (blank) infection, macophages activated to secrete TNF-alpha in the tissues-> increased release of plasma (blank) into tissue, increased phagocyte and lymphocyte migration into tissue, increased platelet adhesion to blood vessel wall-> phagocytosis of bacteria, local vessels occlusion. Containment of infection. Antigens drain or are carried to local lympho node-> survival and stimulation of adaptive immune response
local
| proteins
107
In systemic infection-> macrophages activated in liver and spleen secrete TNF alpha into bloodstream-> (blank) causes decreased blood volume, hypoproteinemia, and neutropenia, followed by neutrophilia. Decreased blood volume causes (blank). DIC leads to wasting and multiple organ failure: septic shock-> death
systemic edema
| collapse of vessels
108
During an immune response to infection, microbial antigens trigger local cells to release (blank)
proinflammatory cytokines
109
Proinflammatory cytokines attract (blank), trigger (blank) and slow (blank) through venules and capillaries, and increase (blank) of vessel walls allowing leukocytes and fluid to move into the infected extravasculr space.
```
leukocytes
dilation of vessels
blood flow
"leakiness"
(point is they make the vessels big and leaky and slow blood flow so stuff can get out)
```
110
The cytokines also induce the release and increase production of (blank), which are antimicrobial but also serve as procoagulants.
acute-phase reactants
111
When the 2 main effects of the inflammatory cascade (vasodilation and coagulation) spread beyond the site of loca infection, the syndrome of sepsis may result in (blank, blank, and blank)
hypoperfusion
coagulopathy
and resultant organ failure
112
If you have hemodynamic collapse, what will result?
hypoxic respiratory failure
shock
acute renal failure
113
With massive cytokine release, impaired (blank) can result due to impaired metabolite use
cardiac contractility
114
(blank) is a major mechanism for multiorgan dysfunction
Vascular endothelial injury
115
Stimuli such as TNF-alpha induce vascular endothelial cells to produce and release a variety of cytokines, (Blank), (blank) and (Blank)
procoagulant molecules, platelet-activating factor, nitric oxide
116
What promotes the adherence of neutrophils to endothelial cells?
upregulated cell-adhesion molecules
117
With sepsis and endothelial injury, (blank) mediators are released
toxic
118
(blank) mediators and (blank) thrombi may contribute to vascuar injury
Leukocyte-derived
| platelet leukocyte fibrin
119
Endothelial cell activation can also promote increased (blank), (Blank), (blank) and (blank)
- vascular permability
- coagulopathy
- microvascular thrombosis
- hypotension
120
In sepsis-induced DIC the (blank) is diffusely activated as part of the inflammatory reponse, at the same time the (blank) system is activated
coaguation cascade
| fibrinolytic system
121
SOOOO why does DIC happen?
cuz both the clotting system and the fibrinolytic system are being activated and deavtivated simultaneously, thus forming clots and breaking them down
122
Why is DIC so dangerous?
clotting factors and platelets are consumed in such clots, and patients are at risk for complications from both thrombosis and hemorrhage
123
How should you treat DIC?
platelets and fresh-frozen plasma
124
(blank) in sepsis is a bad prognostic facto
coagulopathy
125
A down-regulatory system has evolved to protect against the systemic effects of proinflammatory cytokines induced by (blank)
endotoxin (endotoxin tolerance)
126
On first exposure to endotoxin, macrophages produce a large amount of proinflammatory mediators; within a few hours, reexposure to even larger doses of endotoxin fails to induce a (blank) response
proinflammatory
127
An animal or human remains tolerant to endotoxin for (blank) days
2-3
128
Exploiting the phenomenon of (blank) may lead to a treatment for endotoxic shock
endotoxin tolerance
129
Sepsis begins with signs of a systemic inflammatory response. What are these signs?
fever, tachycardia, tachypnea, leukocytosis
130
What are the second signs of sepsis?
progression to hypotension and evidence of hypoperfusion
131
Altered (blank) is often the first sign of organ dysfunction, also decreased (blank) is another sign and both may be apparent prior to getting labs
```
mental status
urine output (less than .5 ml/kg/h)
```
132
In infants and the elderly, initial presentation may lack some of the more salient features, that is, they may present with (blank) rather than hyperthermia, leukopenia rather than leukocytosis.
hypothermia
133
In patients at the extremes of age, any nonspecific systemic complaint-vomiting, fatigue, behavioral changes should prompt concern for (blank)
sepsis
134
T or F
| a patient not intially meeting sepsis criteria can rapidly progress to full-blown septic shock
T
135
Inflammation induced in sepsis is especially damaging to the (blank), why?
lungs
-buildup of inflammatory fluid in the alveoli impairs gas exchange, favors lung collapse, and decreases compliance, with the end result of respiratory distress and hypoxemia
136
A septic patient who did not initially require mechanical ventilation may later require it if they develop (blank) after fluid resuscitation
ALI/ARDS
137
One of the early complication of septic shock is (blank)
myocardial depression
138
What is the mechanism behind cardiac failure induced by sepsis?
Direct toxicity caused by inflammatory molecues (not due to decreased profusion)
139
How do you keep the heart functioning in sepsis?
preload (hydration with close monitoring of CVP), afterload (vasopressors) and contractility (supported with dobutamine)
140
So how do you keep preload normal?
hydration
141
How do you keep afterload normal?
vasopressors
142
How do you keep contractility normal?
dobutamine
143
Sepsis places an unprecedented workload on a heart, which can precipitate (blank) or a (blank) especially in the elderly
acute coronary syndrome
| myocardial infarction
144
Inotropic agents and vasopressors can induce (blank) so you must be careful with them.
tachycardia
145
(blank) is indicative of liver failure, with increases in bilirubin, aminotransferases, and alkaline phosphatase
Cholestatic jaundice
146
In sepsis, Liver synthetic function is usually not affected (acute phase proteins are still produced), unless patients are hemodynamically (blank) for long periods.
unstable
147
Rena failure in sepsis is due to (blank).
hypoperfusion
148
How is renal failure in sepsis manifested?
oliguria, azotemia and inflammatory cells on urinalaysis
149
How do you support the hypoperfusion found in renal failure caused by sepsis?
hydration and vasopressors
150
If renal failure is severe or the kidneys cannot be adequatley perfused then (blank) is indicated
hemodialysis
151
Is there a specific diagnostic test for sepsis?
NO and the response can be quite variable among patients
152
What is suggestive of a diagnosis of sepsis?
a patient w/ susupected or proven infection, fever, hypothermia, tachypnea, tachycardia, leukocytosis, leukopenia, acutely altered mental status, thrombocytopenia, elevated lactate level, or hypotension
153
Definitive etiologic diagnosis requires (blank) from blood or a local site of infection. At least 2 blood samples should be obtained (from 2 different venipuncture sites) for culture.
isolation of microorganism
154
In many cases, blood cultures are neg in sepsis, this result can reflect prior (blank), the presence of (blank) or the absence of (blank) of the bloodstream. If this happens what should you do?
- antibiotic use
- slow growing or fastidious organisms
- microbial invasion
gram staining
155
Cultures of (blank X 3) if indicated should be collected from all patients with severe sepsis
blood, urine, sputum
156
What will a CBC show with sepsis?
may show increased, or decreased WBC with evidence of left shift
157
(blank) should prompt eval for DIC, w/ evaluation of fibrinogen and fibrin split products as well as partial thromboplastin (PT) and partial thromboplastin time (PTT)
Thrombocytopenia
158
Elevated blood urea nitrogen (BUN) and creatine may result from (blank).
renal hypoperfusion
159
Elevated liver function tests (LFTs) may result from (blank)
hepatic hypoperfusion
160
Elevated lactate (greater than 4 mmol/L) indicates (blank)
poor overall tissue perfusion
161
(blank) may be increased or decreased in sepsis, and (blank) abnormalities are common.
Blood glucose
| electrolyte
162
How should you treat sepsis?
if severe, put them in ICU
check oxygen and IV fluids w. crystalloid admin
-Broad-spectrum IV antibiotics, started w/in an hour (whether o not blood cultures have been drawn)
- MAKE SURE YOU COVER ALL CASES WITH ANTIBIOTICS
163
With sepsis, you need to find the source of infection, how do you do this?
UA, Chest X-ray, ECG
164
Why do you give a UA and chest-xray to find infection?
cuz majority of sepsis in the US is pneumonia, GI or UTI
165
Why do you give an ECG in sepsis?
to evaluate for cardiac ischemia secondary to hypoperfusion
166
Treatment of patients with septic shock has what goals?
- corrext hypoxia, hypotension and impaired tissue oxygenation (hypoperfusion)
- start antibiotis as early as poss
- identify source. kill it
- monitor CV. maintain organ function
167
In accordance with current guidelines, appropriate antibiotics should be given within the (blank) hour after sepsis is recognized
first
168
For antibiotic therapy, Blood, urine, and fluid cultures should be taken prior to (blank); but do not delay treatment for such purposes
initiation of therapy
169
When do you give empiric therapy in sepsis?
rapidly, if the source of infection is unknown swtich to correct antibotic when source is identified
170
T or F
| gram-positive organisms are now as common a source for sepsis as gram-negative organisms
T
171
Sepsis due to (blank), althoguh carrying a high mortality rate, is rare. What should you do about this
fungal organisms
| Only give antifungals if clinical picture dictates
172
How do you treat sepsis?
use broad spectrum or multiple antibiotics
173
In immunocompetent adults, an (blank) or a (Blank) is used as monotherapy
antispeudomonal penicillin (ticarcillin-clavulanate) or a carbapenem (impenem)
174
What is the combination therapy for sepsis?
third generation cephalosporin (e.g cefepime) plus anaerobic coverage (e.g clindamycin or metronidazole) or a fluoroquinolone plus clindamycin
175
How should you give antibiotics for sepsis?
IV
176
What are some other drugs used to treat sepsis?
crystalloid
norepinephrine
dobutamine
vasopressin
177
What is this:
Restores intravascular volume, which is depleted in patients with severe sepsis. Improves cardiac output, organ perfusion, and mortality in severe sepsis
Crystalloid
178
What is this:
| Improves blood pressure and cardiac output. More effective than dopamine in refractory septic shock
Norepinephrine
179
What is this:
| Improves cardiac output. May be used in combination with a vasopressor to increase cardiac output
Dobutamine
180
What is this:
| Improves blood pressure in patients with septic shock
vasopressin
181
If your patient is still hypotensive or greater than 4 mmol/L after the first fluid bolus than initiate (blank)
EGDT (early goal-directed therapy)
182
What is EGDT?
method of clinical assessment and reassessment of clinical and laboratory markers, with interventions aimed at normalizing those markers.
183
The overarching goal of EGDT is what?
eliminating mismatch between oxygen supply and oxygen demand
184
What are the 3 goals of EGDT?
1: Cental venous pressure (CVP) 8-12 mm Hg:
2: Mean arterial pressure (MAP) greater than 5 mm Hg
3: central venous oxygen saturation (greater than 70%)
185
How do get your CVP normal?
continous infusion of crystalloid
186
How do you get your MAP normal?
add vasopressors (norepinephrine or dopamine)
187
How do you get your central venous oxygen saturation normal?
RBC transfusion, dobutamine -> to boost cardiac output
| OR intubation and oxygenation
188
A 32-year-old woman is admitted to the hospital for acute pyelonephritis. The patient is treated with oral ciprofloxacin. After 4 days of therapy, she returns to the ED with persistent fever to 38.9°C (102°F), blood pressure of 90/55, and flank tenderness. The urine culture reveals Proteus mirabilis with greater than 100,000 colony-forming units per mL. When you arrive to examine her, you note that she is tachypnic, tachycardiac, and appears lethargic. Which of the following is the next step?
Obtain IV access and admin a fluid bolus
189
A 66-year-old female is noted to have acute pneumococcal pneumonia and is being treated with antibiotics, and with norepinephrine and dobutamine to maintain her blood pressure and urine output. Which of the following is a bad prognostic sign?
C. Lactic acid level of 6 mmol/L
| This is craziness because its above 4!
190
(blank) or drainage of a focal souce of infection is essential
surgical removal
191
(blank) should be removed and the tip rolled over a blood agar plate for quantitative culture; after antibiotic therapy has been initiated, a new catheter should be inserted at a different site
Indwelling IV or arterial catheters
192
What type of catheters should be replaced?
foley and drainage catheters
193
App (blank) percent of patients with severe sepsis and (blank) percent of patients with septic shock die within 30 days
20-35%
| 40-60%
194
T or F
| case-fatality rates are similiar for culture-positive and culture-negative severe sepsis
T
195
(blank) indicate that factoring in the patient's age, underlying condition, and various physiologic variables can yield estimates of the risk of dying of severe sepsis.
Acute phyisiology and Chronic Health Eval (APACHE III)
196
In patients with no known preexisting morbidity, the case-fatality rate remains below 10% until the (blank) decade of life; it gradually increased to exceed (blank) percent in the elderly
fourth decade of life
| 35%
197
Death is signif more likely in severely septic patients with (Blank), especially during the third to fifth decades
preexisting illness
198
(blank) offers the best opportunity to reduce morbidity and mortality from severe sepsis
prevention
199
In developed countries, most episodes of severe sepsis and septic shock are complications of (blank)
nosocomial infections
200
How can you prevent nosocomial infections?
- reducing number of invasive procedures
- limiting the use and duration of indwelling vascular and bladder catheters
- reducing incidence and duration of profound neutropenia
- aggressive treatment of localized nosocomial infections
201
What drugs should you not use so that you can prevent sepsis?
-indiscriminate use of antimicrobial agents
-glucocorticoids
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