Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 7 week 4 > Blood infections- sepsis - Hunter > Flashcards

Blood infections- sepsis - Hunter Flashcards

1
Q

Circulating microorganisms indicate what?

A
  1. it is part of the natural history of the infectious disease - i.e. Malaria
  2. is a reflection of a serious, uncontrolled infection - the spleen and liver were overwhelmed or the pt is immunocompromised
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some descriptive terms for intravascular infections?

A
  1. bacteremia
  2. viremia
  3. fungemia
  4. parasitemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Detection of viremia does not play a role in the diagnosis or management of most viral infections with the exception of what microbe?

A

Cytomegalovirus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Is fungemia common?

A

No it is rare but it can be serious - i.e. Candida mediated fungemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why might you see microbes in the blood?

A
  1. in most instances it represents a failure of the host defense system to localize an infection at its primary tissue site
  2. it can also reflect the failure of a physician to remove, drain or sterilize sites of infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How are microbes normally cleared from the blood?

A

The mononuclear phagocyte system consisting of splenic macrophages and liver Kupffer cells. If the numbers of microorganisms exceeds MPS clearance capacity then fungemia or bacteremia may result.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What type of microbe is poorly cleared from the circulation by fixed macrophages of the MPS?

A

Encapsulated bacteria and yeast are poorly cleared especially in the absence of opsonizing antibody.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What three types of clinical patterns are seen with bacteremia and fungemia?

A
  1. transient
  2. intermittent
  3. continuous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe some characteristics of transient blood infection.

A
  1. lasts minutes to hours
  2. is the most common
  3. reflects the release of organisms into circulation secondary to tissue trauma resulting from medical procedures
  4. examples are - manipulation of infected tissue, instrumentation of colonized mucosal surfaces such as a dental procedure, and surgery in contaminated areas such as a vaginal hysterectomy or debridement of burns
  5. can occur early in acute infections too such as pneumonia, meningitis and septic arthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe some characteristics of intermittent blood infection.

A
  1. occurs, clears, then recurs with the same organism and develops with undrained closed-space abcesses such as intra-abdominal, pelvic, perinephric and hepatic abcesses
  2. also seen in focal infections that fail to resolve such as pneumonia or osteomyelitis, reflecting irregular cycles of release into and clearance from the circulation of organisms infecting tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe some characteristics of continuous blood infection.

A
  1. is a cardinal feature of endocarditis and other types of endovascular infections such as supperative thrombophlebitis and infected aneurysms, reflecting continuous shedding of organisms from endovascular foci into the circulation
  2. also occurs early (first few weeks) in typhoid fever and brucellosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe some characteristics of blood collection and culture during blood infection.

A
  1. frequently see relatively few organisms in a given volume of blood - less than 1-10 colony forming units/mL of blood
  2. blood should not be obtained from an indwelling catheter unless a catheter related infection is suspected - use both a catheter and venous sample if catheter related infection suspected
  3. two culture sets - one anaerobic and one aerobic should be taken at different times and from different sites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How can blood infection be caused by intravenous devices such as catheters, cannulas and shunts?

A
  1. microbes form biofilms on the inner and outer surfaces of these devices
  2. from there the microbes continually seed the blood
  3. antibiotic Tx is often unsuccessful if device left in - it need to be removed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Most cases of clinically significant bacteremia or fungemia are the result of what?

A

They are the result of overflow from an extravascular infection - hematogenous spread.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How can microbes from a focus of infection reach the capillary and venous circulation?

A

Via lymphatic vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe some characteristics of extravascular sources of blood infection.

A
  1. process is dependent on the timing and interaction of multiple events and is thus much less predictable than intravascular infection
  2. if infection is extensive and uncontrolled such as with an overwhelming staph pneumonia - there may be hundreds or thousands of organisms per mL of blood and this is a poor prognostic sign
  3. an intra-abdominal abscess may seed only a few organisms intermittently until is is discovered and drained
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

The probability of blood infection is dependent on what?

A
  1. source of infection

2. type of microbe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the most common sources of bacteremia?

A
  1. urinary tract infections
  2. respiratory tract infections
  3. infections of skin or soft tissues such as wound infections or cellulitis
  4. any organism producing meningitis is likely to produce bacteremia at the same time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

The frequency with which any organism causes bacteremia is related to what?

A
  1. propensity of the bacteria to invade the blood stream
  2. how often that particular bacteria produces infections
  3. E. coli bacteremia is the most common type because E. coli is the most common cause of UTI - a common infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Blood cultures are often not helpful in finding the microbe causing the infection because…?

A

Some bacteria and fungi are very difficult to isolate from blood cultures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is supperative or septic thrombophlebitis?

A

An inflammation of a vein wall frequently associated with thrombosis and bacteremia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

The incidence of superficial thrombophlebitis has risen and represents a major complication in hospital patients. Why?

A

The use of intravenous catheters has increased.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What causes the thrombus formation in the vein wall during suppurative thrombophlebitis and what happens after?

A 
Factors that lead to thrombus formation
1. trauma to vein
2. extrinsic inflammation
3. hyper coagulable states
4. stasis of blood flow
5. combinations of the above factors
The thrombosed site is then seeded with organisms and a focus of infection is established
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What causes the suppurative thrombophlebitis to become complicated?

A
  1. extension of suppurative infection into adjacent structures
  2. further propagation of thrombi
  3. bacteremia and septic embolization follow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are some sites and common etiologic agents of suppurative thrombophlebitis?

A
  1. superficial veins (such as saphenous, femoral, antecubital) - Staph aureus, S. epidermidis, C. albicans, gram neg bacilli
  2. pelvic and portal veins - bacteroides spp, peptostreptococcus, E. coli, Group A and B strep
  3. Intracranial venous sinuses (such as cavernous, sagittal,lateral) - H. flu, Strep pneumoniae, Group A strep, Staph aureus, and peptostreptococcus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe superficial thrombophlebitis.

A
  1. often follows intravenous therapy in the hospital

2. nosocomial offenders predominate - ie. staph aureus, S. epidermidis, gram-neg aerobes and Candida albicans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe deep thrombophlebitis.

A
  1. more frequently caused by organisms that reside on or commonly infect adjacent mucous membranes
  2. includes Bacteroides spp in intestinal and vaginal sites, H.flu and Strep pneumonia in acute otitis media and sinusitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are some systemic responses to infection?

A
  1. acute phase response - protective

2. sepsis and septic shock - can be life-threatening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the progression of the systemic response to microbial infections.

A
  1. SIRS - part of progression to sepsis but has other etiologies also
  2. sepsis
  3. severe sepsis
  4. septic shock
  5. multiple organ dysfunction syndrome
    Each stage is defined by a combination of clinical and laboratory findings.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What type of microbe is the main cause of sepsis?

A

Bacteria

31
Q

Describe SIRS.

A
  1. systemic inflammatory response syndrome
  2. temperature above 38 C or less than 36 C
  3. heart rate of greater than 90 beats per minute
  4. tachypnea or hyperventilation - respiratory rate of greater than 20 breaths per minute or PaCO2 of less than 32 mmHg
  5. white blood cell count greater than 12,000 cells/uL or less than 4000 cells/uL or presence of greater than 10% bands
32
Q

Describe sepsis.

A

Defined as SIRS with a suspected or proven infectious source.

33
Q

Describe severe sepsis.

A
  1. sepsis in conjunction with at least one sing of organ failure or hypoperfusion
  2. signs of organ failure and hypoperfusion include - lactic acidosis (lactate greater than 4mmol/L), oliguria (urine output less than or equal to 0.5 mL/kg for 1 hour), abrupt change in mental status, mottled skin or delayed capillary refill, thrombocytopenia (platelets of less than or equal to 100,000 cells/uL), DIC, or acute lung injury/acute respiratory distress syndrome
34
Q

Describe septic shock.

A

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

35
Q

Describe MODS.

A
  1. multi organ dysfunction syndrome

2. defined as dysfunction of two or more organ systems such that homeostasis cannot be maintained without intervention

36
Q

Describe the epidemiology of sepsis.

A
  1. contributing factor in more than 200,000 US deaths per year and is increasing
  2. approx. 2/3 of cases occur in patients with significant underlying illness - incidence and mortality rates increase with age and preexisting comorbidity
  3. rising incidence attributable to aging of population, increasing longevity of pt’s with chronic disease and high frequency of association with AIDS
  4. widespread use of immunosuppressive drugs, indwelling catheters and mechanical devices also plays a role
37
Q

What microbe most often causes sepsis?

A
  1. bacteria most common - 45% gram pos and 45% gram neg

2. 10% are fungi related or are caused by a mixture of microorganisms - Candida albicans most common fungi

38
Q

If finding the infecting microbe in circulation is difficult then how is the etiologic agent identified?

A
  1. blood cultures yield bacteria or fungi in only 20-40% of cases of severe sepsis and only 40-70% of cases of septic shock
  2. if blood cultures are neg then microbe is identified by isolating the microbe from infected material from the local site/original site of infection- negative microbiologic findings are not unusual
39
Q

Name some sepsis causing microbes an their common sources.

A
  1. Lung infections - Strep pneumoniae, H. flu, Legionella spp, Chlamydia pneumoniae, aerobic gram neg rods
  2. wound/soft tissue infection - Strep pyogenes, staph aureus, clostridium spp, pseudomonas aeruginosa, anaerobes, coagulase-neg staph species, aerobic gram-neg rods
  3. UTI’s - E. coli, klebsiella species, enterobacter spp, proteus spp, enterococcus spp, aerobic gram neg rods
  4. CNS - Strep pneumoniae, Neisseria meningitidis, Listeria monocytogenes, E. coli, H. flu, Pseudomonas aeruginosa, Klebsiella spp, Staph spp
  5. Abdomen - E. coli, Bacteroides fragilis, areobic gram neg rods, anaerobes, Candida spp
40
Q

What is the most common etiologic agent for sepsis in neonates?

A

Usually caused by Group B strep (Streptococcus agalactiae) and less often by E. coli.

41
Q

How do neonates get infected by S. agalactiae or E. coli?

A

Approx. 2/1000 live-born infants are infected during labor and delivery - case fatality rate is 5-10%.

42
Q

How do neonates with sepsis originally present?

A

They often present first with pneumonia or meningitis.

43
Q

What is the most common cause of sepsis in older children?

A
  1. Strep pneumoniae
  2. Neisseria meningitidis
  3. Staph aureus
  4. older children may initially present with meningitis, skin infections, bacterial rhino sinusitis and otitis media
44
Q

Th biology of sepsis is associated with what?

A
  1. the direct toxic effects of the infecting organism and derangement of the normal inflammatory host response to infection
  2. in response to local infection there is concurrent activation of the immune system and of down-regulatory mechanisms to control the reaction
45
Q

The devastating effects of sepsis syndrome appear to be caused by some combination of what?

A
  1. expansion of the immune response to sites remote from that of infection
  2. derangement of the balance between pro inflammatory and anti-inflammatory cellular regulators
  3. dissemination of the infecting organism
46
Q

Describe the localized response to pathogens.

A
  1. localized infections produce inflammatory mediators such as TNF-a
  2. These inflammatory mediators produce protective responses such as increased release of plasma protein into tissue, increased phagocyte and lymphocyte migration to tissue, increased platelet adhesion to stop spread of microbe
  3. host response leads to elimination or sequestration of microbe - phagocytosis, local vessel occlusion OR engagement of adaptive immunity - antigens drain or are carried to local lymph node
47
Q

Describe the systemic response to pathogens.

A
  1. systemic infections produce the same mediators as local but in large quantities that cause significant pathophysiologic changes and possible death
  2. systemic vasodilation leads to hypotension and vascular collapse, systemic increase in vascular permeability leads to edema. other systemic effects of inflammation include hypoproteinemia, neutropenia followed by neutrophilia, hypercoagulation
  3. DIC can occur leading to wasting and multiple organ failure
48
Q

Describe the pathogenesis of sepsis.

A
  1. local infection leads to release of pro inflammatory cytokines due to microbial antigen triggering of macrophages and other local cells
  2. The cytokines attract leukocytes, trigger dilation of vessels, slow blood flow through venues and capillaries, increase ‘leakiness’ of vessel walls allowing leukocytes and fluid to move into the infected extravascular space
  3. the cytokines also induce the release and production of acute phase reactants which are antimicrobial but also serve as procoagulants
  4. when the two main effects of the inflammatory cascade - vasodilation and coagulation - spread beyond the site of local infection, the syndrome of sepsis may result in hypotension, hypo perfusion, coagulopathy and resultant organ failure
49
Q

What is the leading cause of acute renal failure?

A

Sepsis.

50
Q

How does sepsis cause endothelial injury?

A
  1. TNF-a and other stimuli induce vascular endothelial cells to produce and release a variety of cytokines, procoagulant molecules, platelet activating factor, NO and other mediators
  2. unregulated cell-adhesion molecules promote the adherence of neutrophils to endothelial cells and toxic mediators are released
  3. leukocyte derived mediators and platelet-leukocyte -fibrin thrombi may contribute to vascular injury
  4. endothelial cell activation can also promote increased vascular permeability, coagulopathy, microvascular thrombosis and hypotension
51
Q

What is DIC?

A
  1. disseminated intravascular coagulation

2. diffuse activation of the coagulation cascade - may be sepsis induced

52
Q

Describe sepsis induced DIC.

A
  1. diffuse activation of coagulation
  2. activation of the fibrinolytic system (breaks down clots)
  3. a feedback spiral ensues in which both systems are constantly and diffusely activated - new clots form and then are broken down
  4. clotting factors and platelets are consumed and patients are at risk for complications from both thrombosis and hemorrhage
  5. in this setting platelets and fresh-frozen plasma may be given to patients with signs of active bleeding
  6. coagulopathy in sepsis is a bad prognostic indicator
53
Q

Describe endotoxin tolerance.

A
  1. endotoxin tolerance is a down regulatory system that evolved to protect against the systemic effects of pro inflammatory cytokines induced by endotoxin
  2. on first exposure to endotoxin, macrophages produce large amounts of pro inflammatory mediators. Within a few hours, reexposure to even larger doses of endotoxin fails to induce a response
  3. an animal or human remains tolerant to endotoxin for 2-3 days
  4. exploiting the phenomenon of endotoxin tolerance may lead to a treatment for endotoxic shock
54
Q

Describe the clinical presentation of sepsis.

A
  1. begins with systemic inflammatory response - fever, tachycardia, tachypnea, leukocytosis
  2. progresses to hypotension and evidence of hypo perfusion
  3. may progress to MODS - altered mental status is often the first sign of organ dysfunction. Another sign is decreased urine output
55
Q

Do infants and the elderly always present the same way as adults?

A

No. They may lack some of the more salient features of sepsis. For example they may present with hypothermia instead of hyperthermia or with leukopenia rather than leukocytosis. In patients of extreme age any nonspecific systemic complaint should prompt concern for sepsis.

56
Q

What organ system is especially damaged in sepsis?

A
  1. inflammation induced sepsis is especially damaging to the lungs
  2. build-up of inflammatory fluid in the alveoli impairs gas exchange, favors lung collapse and decreases compliance - may result in respiratory distress and hypoxemia
  3. both ALI (acute lung injury) and ARDS (acute respiratory distress syndrome) can result
57
Q

How can you check to see how the lungs are being effected during sepsis?

A

If ALI or ARDS is a complication of sepsis then it will be apparent on chest X-ray - will see bilateral pulmonary opacities consistent with pulmonary edema.

58
Q

WHat is one of the early complications seen with septic shock?

A

Myocardial depression. The mechanism is thought to be direct binding of inflammatory molecules to cardiac myocytes leading to direct toxicity rather than a decreased perfusion.

59
Q

How is myocardial depression treated?

A
  1. sepsis places an unprecedented workload on a heart which can precipitate acute coronary syndrome or MI
  2. heart function is supported by careful attention to preload (hydration with close monitoring of CVP), after load (vasopressors), and contractility (dobutamine)
60
Q

What other organ systems are very susceptible to damage in sepsis?

A
  1. kidneys

2. liver

61
Q

What is indicative of liver failure?

A
  1. liver failure leads to an increase in bilirubin, aminotransferases and alkaline phosphatase. There may be cholestatic jaundice
  2. liver synthetic function is usually not affected (still make acute phase proteins) unless patients are hemodynamically unstable for long periods
62
Q

Describe kidney failure as a result of sepsis.

A
  1. sepsis causes hypoperfusion manifested by oliguria, azotemia, and inflammatory cells upon urinalysis. kidney cells can also be directly damaged by inflammatory agents
  2. hydration and vasopressors are used to support perfusion
  3. if renal failure is severe or the kidneys cannot be adequately perfused then hemodialysis is indicated
63
Q

Describe the laboratory findings of sepsis.

A
  1. CBC may show an increased or more ominously, a decreased WBC with evidence of a left shift
  2. thrombocytopenia should prompt evaluation for DIC - with evaluation of fibrinogen, fibrin degradation products, PT and PTT
  3. elevated BUN and creatinine may result from renal hypo perfusion and elevated liver function tests may result from hepatic hypo perfusion
  4. elevated lactate indicates poor overall perfusion
  5. blood glucose may be increased or decreased and electrolyte abnormalities are common
64
Q

Patient’s with severe sepsis should be transferred where?

A

To the ICU.

65
Q

Describe the treatment of sepsis.

A
  1. oxygenation and blood pressure should be continuously monitored
  2. supplemental oxygen given to maintain oxygen saturation of greater than 93%
  3. IV fluid bolus of 20-40 mL/kg of crystalloid should be administered for hypotension
  4. broad spectrum antibiotics covering most likely organisms for all possible sites of infection should be given within one hour of diagnosis
  5. targeted antibiotics can be given when microbe established
  6. urinalysis, urine culture and chest x-ray should be done to search for source of infection
  7. an ECG should be done to evaluate cardiac function
  8. removal of catheters or other devices should be removed if these are the source of infection
66
Q

What are the treatment goals for sepsis?

A
  1. resuscitate the patient from septic shock by using supportive measures to correct hypoxia, hypotension and hypo perfusion
  2. start adequate antibiotics as early as possible
  3. identify the source of infection and treat with antimicrobial or surgery or both as indicated
  4. maintain adequate organ system function
67
Q

Appropriate antibiotic therapy is critical to the early treatment of sepsis. Is anti fungal coverage routine also?

A

No. fungemia is rare and routine anti fungal coverage is not recommended unless the clinical picture dictates that it is.

68
Q

What is the only proven medical treatment in septic shock?

A

Early empiric antibiotic therapy. Use of broad-spectrum or multiple antibiotics provides the necessary wide coverage.

69
Q

What are some antibiotics given for Tx of sepsis?

A
  1. in immunocompetent adults - antipseudomonal penicillin such as ticarcillin-clavulanate or carbapenem are used as mono therapy
  2. combination therapy - third gen. cephalosporin such as cefepime plus anaerobic coverage with clindamycin or metronidazole or can give a fluoroquinolone plus clindamycin
  3. all antibiotics should be given IV
70
Q

What are some other Tx given in sepsis?

A
  1. crystalloid - for hypotension, improves cardiac output and organ perfusion
  2. norepinephrine - improves blood pressure and cardiac output. more effective than dopamine in refractory septic shock
  3. dobutamine - improves cardiac output, may be used in combo with a vasopressor
  4. Vasopressin - improves blood pressure
71
Q

What is early goal directed therapy?

A

A method of continual assessment and reassessment of clinical and lab markers, with interventions aimed at normalizing those markers.

72
Q

When is EGDT initiated?

A

If the patient continues to be hypotensive or has repeat lactate levels of greater than 4 mmol/L or has other signs of continued hypo perfusion.

73
Q

What are the goals of EGDT?

A
  1. Central venus pressure of 8-12 mm Hg - achieved by continued infusion of crystalloid
  2. Mean arterial pressure of greater than or equal to 65 mm Hg achieved by adding vasopressors such as norepinephrine or dopamine
  3. central venous oxygen saturation of greater than or equal to 70% achieved thru RBC transfusion, dobutamine to boost cardiac output or intubation and oxygenation

Block 7 week 4 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions