Hunter: Sepsis and Septic Shock Flashcards Preview

Block 7 Week 4 > Hunter: Sepsis and Septic Shock > Flashcards

Flashcards in Hunter: Sepsis and Septic Shock Deck (89):
1

(blank) is rare, but can be serious

Fungemia (fungus in the blood)

2

How are bacteria and fungi normally cleared from the blood?

via the mononuclear phagocyte system (splenic macrophages and liver Kupffer cells)

3

Bacteremia or fungemia results when the numbers of microorganisms exceeds (blank)

the MPS clearance capacity

4

These two things are poorly cleared from the circulation by fixed macrophages of the MPS especially in the absence of opsonizing antibody

encapsulated bacteria and yeast

5

This type of bacteremia/fungemia occurs, lasting minutes to a few hours, and resolves; usually due to tissue trauma during medical procedures, can be due to manipulation of infected tissue, surgery in contaminated areas, or in early acute infections

transient bacteremia/fungemia

6

This type of bacteremia/fungemia occurs, clears, then recurs with the same organism, and develops with undrained closed-space abscesses (intra-abdominal, pelvic, perinephric, hepatic)

intermittent bacteremia/fungemia

7

Intermittent bacteremia can be seen in (blank) that fail to resolve, reflecting irregulat cycles of release into and clearance from the circulation of organisms infecting tissue

focal infections

**pneumonia, osteomyelitis

8

This form of bacteremia or fungemia is a cardinal feature of endocarditis and other types of endovascular infections (suppurative thrombophlebitis, infected aneurysms), reflecting constant shedding of organisms from endovascular foci into the circulation

continuous bacteremia/fungemia

9

What is the main example in which you would see continuous bacteremia or fungemia?

endocarditis

**continuous shedding of organisms from endovascular foci into the circulation

10

Continuous bacteremia also occurs early in these two cases

typhoid fever
brucellosis

11

Compare transient, intermittent, and continuous bacteremia on a scale

transient: bacteria level spikes and then it falls
intermittent: cycles of spikes and falls
continuous: always present or ever increasing

12

T/F: Bloodstream infections are usually caused by a massive amount of organisms in a given volume of blood

false; Bloodstream infections are frequently caused by relatively few organisms in a given volume of blood (<1- 10 colony forming units/mL of blood)

13

How should you draw blood if you expect a bloodstream infection?

draw 20-30mL of blood twice from two different sites and culture them in both aerobic and anaerobic conditions

**do not take blood from an indwelling IV or intra-arterial catheter unless you suspect a catheter-related infection

14

Bacteremia or Fungemia Can Occur Secondary to Spread from an (blank)

intravenous device
ex: biofilms on catheters or cannulas

**treat by removing the device, antibiotics won't work

15

Most cases of clinically significant bacteremia or fungemia are the result of overflow from (blank)

an extravascular infection via hematogenous spread

16

In extravascular infection leading to bacteremia, microorganisms from a focus of infection often reach the capillary and venous circulation through (blank)
The process is dependent on the timing and interaction of multiple events and is thus much less predictable than intravascular infection

lymphatic vessels

17

The probability of bacteremia or fungemia is dependent on what two factors?

1. source of infection
2. the microorganism

18

Most common sources of bacteremia?

UTI (E. Coli)
resp tract infections
infections of skin and soft tissues (ex: wound infection or cellulitis)

19

Any organism producing (blank) is likely to produce bacteremia at the same time

meningitis

20

The frequency with which any organism causes bacteremia is related to both (blank) and how often it produces infections

its likelihood to invade the bloodstream

21

T/F: Some bacteria and fungi are very difficult to isolate from blood cultures, so although the bacteria may be invading the bloodstream, it may be hard to find the bacteria in the blood

True

22

an inflammation of a vein wall frequently associated with thrombosis and bacteremia

suppurative (septic) thrombophlebitis

23

Why has the rate of superficial thrombophlebitis increased?

increasing use of IV catheters

24

What happens in septic thrombophlebitis?

there is formation of a thrombus resulting from trauma to the vessel, stasis of blood flow, or hypercoagulable state
the thrombus is then seeded with organisms and an infection is established
the infection can then spread to adjacent structures, leading to septic embolization

25

What is the difference between organisms that cause infection in superficial thrombophlebitis and deep thrombophlebitis?

superficial: usu nosocomial bacteria (S. aureus, S. epidermidis, gram-negative anaerobes)

deep infections: caused by organisms that reside on adjacent mucous membranes or commonly infected sites (Bacteroides, E. Coli, H. influenzae, S. pneumo)

26

This is suspected in pts with risk factors like surgery and indwelling venous cannulas; bacteremia is usually present; surgical exploration might be required; removal of IV catheter is necessary

suppurative (septic) thrombophlebitis

27

used to describe pathogens in the blood that are causing sepsis

septicemia

28

Some systemic responses to infection can be protective. But for non-protective responses, there is a progression of illness from (blank) to (blank)

systemic inflammatory response syndrome; multi-organ dysfunction syndrome

29

List the order of severity from systemic inflammatory response syndrome to multiple organ dysfunction syndrome

1. systemic inflammatory response syndrome
2. sepsis
3. severe sepsis
4. septic shock
5. multiple organ dysfunction syndrome

30

What are the SIRS criteria (systemic inflammatory response syndrome)

Pt must have at least 2 of the following:

1. temp > 38C or 36C
2. HR > 90bpm
3. resp rate >20
4. white blood cells > 12,000 or <4,000

31

Sepsis in conjunction with at least one sign of organ failure or hypoperfusion, such as lactic acidosis (lactate >4 mmol/L), oliguria (urine output ≤ 0.5 mL/kg for 1 hour), abrupt change in mental status, mottled skin or delayed capillary refill, thrombocytopenia (platelets ≤ 100,000 cells/mL) or disseminated intravascular coagulation, or acute lung injury/acute respiratory distress syndrome

severe sepsis

32

Severe sepsis with hypotension (or requirement of vasoactive agents, (e.g., norepinephrine) despite adequate fluid resuscitation in the form of a 20-40-ml/kg bolus

septic shock

33

Dysfunction of two or more organ systems such that homeostasis cannot be maintained without intervention

multiorgan dysfunction syndrome

34

Approximately two-thirds of the cases of severe sepsis occur in patients with significant underlying illness. Sepsis-related incidence and mortality rates increase with (blank) and preexisting (blank)

age; comorbidity

35

Why is the incidence of cases of severe sepsis on the rise?

aging population
increasing longevity of patients w chronic diseases
high frequency in AIDS pts
widespread use of immunosuppressive drugs, indwelling catheters and mechanical devices

36

What is the most common microorganism that causes sepsis and septic shock?

gram-negative and gram-positive bacteria (45% of cases)

37

Do you always yield bacteria and fungi on a blood culture in cases of severe sepsis and septic shock?

no! negative findings are not unusual; in 20-40% of cases of severe sepsis, no bacteria shows up on the culture!

38

Sepsis in neonates is usually caused by (blank) and less often by (blank)

Streptococcus agalactiae;
E. coli

39

How do neonates infected w Strep. agalactiae or E. coli usually present?

pneumonia
meningitis

40

What are the organisms most likely to cause sepsis in older children?

Strep pneumo
Neisseria meningitidis
Staph. aureus

41

What is the most likely way an infant would be infected with Strep agalactiae?

oral contamination during passage through the birth canal

42

Sepsis is a complex interaction between what two components?

the direct toxic effects of the infecting organism
the derangement of the normal inflammatory response to infection

43

In response to local infection there is concurrent activation of the immune system and of (blank) mechanisms to control the reaction

down-regulatory

44

The devastating effects of sepsis syndrome are caused by a combination of what 3 factors

1. expansion of the immune response to other sites besides site of infection
2. derangement of the balance b/w proinflammatory and anti-inflammatory cell regulators
3. dissemination (spreading) of the infecting organism

45

What is the difference between a localized and systemic infection?

a localized infection does produce inflammatory mediators that induce protective innate responses and eliminate the pathogen; systemic infections produce these same mediators but in large quantities that cause significant pathophysiologic changes and can lead to death

46

During an immune response to infection, microbial antigens trigger local cells to release (blank)
These molecules attract leukocytes, trigger dilation of vessels, slow blood flow through venules and capillaries, and increase (blank) of vessel walls allowing leukocytes and fluid to move into the infected extravascular space
The cytokines also induce the release and production of (blank), which are antimicrobial but are also serve as procoagulants

proinflammatory cytokines; leakiness; acute phase reactants

47

When vasodilation and coagulation spread beyond the site of infection, sepsis can result in...

hypotension
hypoperfusion
coagulopathy
resultant organ failure

48

Vascular endothelial injury is a major mechanism for multiorgan dysfunction
Stimuli such as (blank) induce vascular endothelial cells to produce and release a variety of cytokines, procoagulant molecules, platelet-activating factor, nitric oxide, and other mediators

TNF-alpha

49

Upregulated cell-adhesion molecules promote the adherence of (blank) to endothelial cells; toxic mediators released
Leukocyte-derived mediators and (blank) may contribute to vascular injury
Endothelial cell activation can also promote increased (blank), coagulopathy, microvascular thrombosis, and hypotension

leukocytes; platelet-leukocyte-fibrin thrombi; vascular permeability

50

In sepsis-induced DIC the (blank) is diffusely activated as part of the inflammatory response
At the same time, the (blank), which normally acts to keep the clotting cascade in check, is activated

coag cascade; fibrinolytic system

51

In DIC, describe the feedback spiral that is occurring.

both the coag system and fibrinolysis are activated, so new clots are always being formed, then broken down

52

In DIC, clotting factors and platelets are consumed in forming clots, and patients are at risk for complications from what two things

thrombosis (from the clots)
hemorrhage (from low platelets)

53

What can be given to patients with DIC?

platelets
fresh-frozen plasma

54

This is a bad prognostic indicator in sepsis

coagulopathy

55

What are the initial symptoms of sepsis?

signs of a systemic inflammatory response (fever, tachycardia, tachypnea, leukocytosis)

56

Sepsis can then progress to (blank)

hypotension

**this would be considered septic shock

57

Two signs of organ dysfunction in sepsis

altered mental status
decreased urine output

58

T/F: A patient not initially meeting sepsis criteria can rapidly progress to full blown septic shock

True

59

In infants and the elderly, how can sepsis present differently?

may present w hypothermia instead of hyperthermia
leukopenia instead of leukocytosis

60

These are two lung pathologies that are present in most cases of severe sepsis

acute lung injury
acute respiratory distress syndrome

**end result of respiratory distress and hypoxia

61

One of the early complications of septic shock is (blank)

myocardial depression

**thought to be caused by direct toxicity caused by inflammatory molecules

62

How is preload monitored in sepsis?
Afterload?
Contractility?

hydration; vasopressors; dobutamine

63

Sepsis places an unprecedented workload on the heart, which can precipitate these two conditions, especially in the elderly

acute coronary syndrome
MI

64

This is an indicator of liver failure in sepsis

cholestatic jaundice

**also increased bilirubin, aminotransferases, and alkaline phosphatase

65

Is liver synthetic function usually affected by sepsis?

no, acute phase proteins are still produced unless the pt has been hemodynamically unstable for a really long time

66

Renal failure in sepsis is due to (blank), and is manifested by oliguria, azotemia, and inflammatory cells on urinalysis
Hydration and vasopressors are used to support perfusion
If renal failure is severe or the kidneys cannot be adequately perfused, then (blank) is indicated

hypoperfusion;
hemodialysis

67

T/F: There is no specific diagnostic test for sepsis, and the septic response can be quite variable among patients

True

68

Definitive etiologic diagnosis of sepsis requires (blank) of the microorganism from blood or a local site of infection. At least (blank) blood samples should be obtained (from two different venipuncture sites) for culture
In many cases, blood cultures are (blank); this result can reflect prior antibiotic administration, the presence of slow-growing or fastidious organisms, or the absence of microbial invasion of the bloodstream
In these cases, (blank) and culture of material from the primary site of infection or from infected cutaneous lesions may help establish the microbial etiology

isolation; two; negative; gram staining

69

Thrombocytopenia should prompt evaluation for (blank), with evaluation of fibrinogen and fibrin split products as well as partial thromboplastin (PT) and partial thromboplastin time (PTT)

DIC

70

Elevated blood urea nitrogen (BUN) and creatinine may result from renal (blank), and elevated liver function tests (LFTs) may result from hepatic (blank).

hypoperfusion; hypoperfusion

71

If this is elevated, it indicates poor overall tissue perfusion

lactate (>4mmol/L)

72

How to initially treat a patient with sepsis?

give O2
give IV fluid bolus
give broad-spectrum IV antibiotics w/i 1 hour (whether or not blood cultures have been drawn)

73

Things that should be ordered in the work up of sepsis

urinalysis
chest X-ray (to look for source of infection)
ECG (to look for ischemia secondary to hypoperfusion)

74

What are the 4 treatment goals for patients with sepsis?

1. resuscitate the patient from septic shock by using measures to correct hypoxia, hypotension, and impaired tissue O2
2. start antibiotics as early as possible
3. identify the source of infection
4. maintain adequate organ system function

75

When to give antibiotics in cases of sepsis?

within the first hour after sepsis is recognized

76

T/F: Antibiotics should be initiated rapidly, even if the source of the infection is unknown. When you figure it out, you can switch the antibiotic.

True.

77

Which bacteria, gram-positive or gram-negative causes most cases of sepsis?

gram positives are now just about as common as gram negatives

78

Sepsis due to (blank) organisms is rare, although the mortality rate is high

fungal organisms

79

Only therapy proven to treat septic shock

early IV antibiotic therapy

80

What combination of antibiotics should be used in adults w sepsis?

third-generation cephalosporin
+ clindamycin or metronidazole for anaerobes

or

fluoroquinolone + clindamycin

81

Restores intravascular volume, which is depleted in patients with severe sepsis. Improves cardiac output, organ perfusion, and mortality in severe sepsis

crystalloid (fluid bolus)

82

Improves blood pressure and cardiac output. More effective than dopamine in refractory septic shock

norepi

83

Improves cardiac output. May be used in combination with a vasopressor to increase cardiac output

dobutamine

84

Improves blood pressure in patients with septic shock

vasopressin

85

A method of continual assessment and reassessment of clinical and laboratory markers, with interventions aimed at normalizing those markers
The overarching goal is to eliminate mismatch between oxygen demand and oxygen supply (the hallmark of sepsis) by increasing supply and—where possible—by decreasing demand

early goal-directed therapy

86

This is one major part of treatment for sepsis

remove the source of infection!!

**surgical removal or drainage of infection site
remove indwelling IV or arterial catheters
replace foley and drainage catheters

87

T/F: Approximately 20-35% of patients with severe sepsis and 40-60% of patients with septic shock die within 30 days
Case-fatality rates are similar for culture-positive and culture-negative severe sepsis

True

88

T/F: Acute Physiology and Chronic Health Evaluation III (APACHE III) 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
In patients with no known preexisting morbidity, the case-fatality rate remains below 10% until the fourth decade of life; it gradually increases to exceed 35% in the very elderly

True

89

How can you prevent sepsis?

1. reduce the number of invasive procedures
2. limit use of indwelling vascular or bladder catheters
3. treat nosocomial infections more aggressively
4. don't use antibiotics or glucocorticoids when not absolutely necessary