Sepsis and Bacteremia Flashcards

1
Q

Why have incidences of sepsis and septic shock continued to increase

A

Increased use of invasive devices, cytotxic and immunosuppressive drugs for cancer and transplants, increased lifespan of cancer and diabetes patients, and increased infections with antibiotic resistant bacteria

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2
Q

Systemic Inflammatory Response Syndrome or SIRS

A

Temperature above 38 or below 36, HR above 90bpm, respiratory rate above 20, WBC count above 12000 or below 4000 OR 10% immature forms, requires 2 or more of those symptoms

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3
Q

Sepsis

A

SIRS plus blood infection with any microorganism, it is often assumed and treated as such if patient shows symptoms with no other clear or likely diagnosis

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4
Q

Septic shock

A

Sepsis plus organ dysfuntion, hypotension, or hypoperfusion

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5
Q

What is the mortality rate once septic shock progresses to multiple organ dysfunction syndrome (MODS)

A

90%

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6
Q

Is microbial blood stream invasion required to produce sepsis

A

No, microbe invasion is usually involved but systemic spread of signal molecules and toxins can elicit the same response

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7
Q

What are the most common microbes involved in sepsis and septic shock

A

Fungi and bacteria, mostly gram negatives

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8
Q

What factors predispose people to bacteremia, especially with gram negative rods

A

Diabetes, lymphoproliferative diseases, cirrosis, burns, invasive procedures or devices, renal insufficiency, alcoholism, and drugs that cause neutropenia

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9
Q

What types of infections are more likely to lead to sepsis

A

Any infection can progress to sepsis BUT pylelonephritis, pneumonia, peritonitis, cholangitis, cellulitis, meningitis, or abscesses are more likely causes (many nosocomial)

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10
Q

Are you more likely to find the original site of infection in an immunocometant or immunocomprmised patient

A

Competent, immunocompromised patients, esp neutropenic, often have clinically unapparent infections in skin or bowel

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11
Q

What is the most potent gram negative bacterial antigen

A

Lipopolysaccharide

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12
Q

What is correlated with detectable plasma levels of bacterial endotoxin

A

Positive blood cultures, decreased systemic resistance, depressed ventricular ejection fraction, and lactic academia

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13
Q

What do endotoxins activate/release

A

They activate complement and release anaphylotoxins C5a and C3a that cause vasodilation/platelet aggregation and they activate factor XII which releases bradykinin that causes vasodilation and coagulation and can lead to consumption of coagulation factors and DIC

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14
Q

Examples of bacterial antigens that illicit inflammatory response

A

Polysaccharides, extracellular enzymes, peptidoglycan, lipoteichoic acid, and other toxins

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15
Q

Components of the innate immune system

A

Neutrophils, macrophages, complement, and cytokines

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16
Q

Anti-inflammatory cytokines to modulate inflammatory response

A

IL-4, IL-10, IL-11, and transforming growth factor

17
Q

What can cause imbalance in inflammatory response

A

Overproduction of pro-inflammatory mediators, underproduction of anti-inflammaroty mediators, or genetic absence of any component, resulting aberrant response leads to diverse clinical signs of sepsis

18
Q

Describe cardiac function in sepsis

A

Low vascular resistance, high CO, decreased ventricular ejection fraction and a dilated ventricle

19
Q

Describe cardiac function in sepsis

A

Low vascular resistance, high CO, decreased ventricular ejection fraction and a dilated ventricle

20
Q

Progressive hypotension or complete failure od one or more organ systems (ARDS, DIC, renal failure, or hepatic failure)

A

What infections are not cleared from the blood by the reticuloendothelial system

21
Q

What infections are not cleared from the blood by the reticuloendothelial system

A

Endocarditis and severe intravascular infections

22
Q

3 categories of sepsis/septic shock clinical manifestations

A
  1. signs related to the primary focus of infection found through history, labs, imaging and exam 2. Signs of systemic infection such as fever, hyperventilation, and disorientaiton 3 rapid end organ responses showing cytokine effects
23
Q

What causes tachycardia and hyperventilation in septic shock

A

Initial increase in sympathetic tone

24
Q

What causes edema in septic shock

A

Low vasomotor tone causing leaky capillaries

25
Q

What causes mental status changes like agitation in septic shock

A

Increased catecholamines

26
Q

What cause is stupor or coma in septic shock

A

CNS hypoperfusion

27
Q

What causes lactic acidosis in septic shock

A

Hypoperfusion of the liver and periphery

28
Q

What happens to liver metabolism in septic shock

A

A switch from anabolism to catabolism which causes the release of acute phase proteins

29
Q

Lab abnormalities seen in sepsis

A

Leukocytosis from bone marrow stimulation or lekopenia from consumtion, thrombocytosis or thrombocytopenia (DIC), RBC production decrease to sequester iron stores, and other abnormal chemistries related to affected organ

30
Q

Antibiotic treatment of sepsis

A

Take sterile fluid samples for culture before regimen and determine the most likely pathogen based on history and treat with emperic broad spectrum drugs

31
Q

Antibiotic treatment of sepsis

A

Take sterile fluid samples for culture before regimen and determine the most likely pathogen based on history and treat with emperic broad spectrum drugs

32
Q

What have studies shown about broad spectrum antibiotics used alone and in combination for sepsis

A

A single broad spectrum is as efficacious as a combination, combining penicillins and aminoglycosides show synergistic killing, refinement to the most specific drug lowers antibiotic pressure toward resistance

33
Q

Non-antibiotic treatment for sepsis

A

Evaluation and possible resection and drainage of primary site of infection, removal of indwelling devices, and support of failing organ systems

34
Q

Treatment for septic shock

A

Initially predetermined and titrated blous fluids to treat hypotension and hyperperfusion and vasopressors (dopamine, norepinephrine, epinephrine, phenylephrine, and dobutamine) if that fails

35
Q

What does dopamine do at low, medium, and high doses

A

Low doses stimulate dopaminergic receptors that dilate renal mesenteric and coronary capillaries, medium stimulates beta-1 receptors to increase HR and contractility and high stimulates alpha receptors that constrict arteries

36
Q

What do norepinephrine and epinephrine do

A

Increase MAP