Sepsis

Question 1

Sepsis

Answer 1

Severe infection leading to organ dysfunction: SIRS + infection (bacteremia or viremia)

Question 2

SIRS

Answer 2

Systemic Inflammatory Response Syndrome (SIRS)- SIRS may be produced by entities other than infection and, in absence of viable organisms, microbial products are capable of producing this clinical picture. A reaction can be but does not have to be inection at least 2 of the following:
Temp > 38 or < 36, Heart rate > 90 bpm, Respiratory rate > 20 bpm, Resp alkalosis PaCO2 below 32, WBC > 12,000, < 4,000 or bands > 10%

Question 3

What are the governing factors of Sepsis?

Answer 3

underlying disease, age, infecting organism and appropriateness of therapy

Question 4

What are most cases of sepsis due to?

Answer 4

bacterial infection

Question 5

Septic shock

Answer 5

Sepsis with hypotension or perfusion abnormalities despite adequate volume replacement

Question 6

Characteristics of Septic Shock

Answer 6

Systolic BP below 90 or Mean BP is below 60 mmHg; Or a pressor is needed to exceed or maintain this BP: Epinephrine, Norepinephrine, Vasopresin, Dopamine

Question 7

Progression of sepsis

Answer 7

infection, SIRS, sepsis, severe sepsis, septic shock

Question 8

Pathophysiology of Sepsis: Cell wall factors

Answer 8

A wide variety of microorganisms cause sepsis: Interaction of specific cell wall factors: Pathogen Associated Molecular Patterns (PAMPs) with Toll-like receptors (Tlrs)
PAMPs can be: Lipopolysaccharide (LPS) or endotoxin
Peptidoglycan.

Question 9

PAMPs

Answer 9

PAMPs - highly conserved parts of microbial molecules on organisms-Lps, peptidoglycan, flagellin

Question 10

Tlrs

Answer 10

Tlrs -ancient receptors conserved on animal and plant cells

Question 11

Pathophysiology of Sepsis:

Answer 11

Surface antigens (PAMPs) bind to TLRs on WBC surface, Bacteria access blood stream, TNF and IL recruit macrophages, Cytokines lead to sepsis syndrome

Question 12

Secreted Bacterial Factors

Answer 12

Gram-positive bacteria also secrete exotoxins. S. aureus can secrete toxic shock syndrome toxin 1 (TSST-1). S. pyogenes secretes streptococcal pyrogenic exotoxin A (SPEA). Clinically identified in necrotizing fasciitis assoc w/ shock. Called “superantigens,” these exotoxins bypass macrophages and directly stimulate T cells

Question 13

Cytokine formation and the role of macrophages

Answer 13

Monocyte–macrophages or dendritic cells are the first cells to respond to endotoxin (LPS). Receptor binding stimulates monocyte–macrophages to release

1. Proinflammatory cytokines, tumor necrosis
factor α and interleukin-1, stimulating inflammation
2. Toxic oxygen byproducts
3. Products that activate the complement and coagulation cascades

Question 14

clinical manifestations of Sepsis

Answer 14

Fever (higher it is = more likely bacteremia) with hypothermia its a bad indicator, tachy is common, respiratory alkalosis, hyperventialtion

Question 15

Dx of Sepsis

Answer 15

difficult, blood tests for bacteremia, marked drop in peripheral WBCs and high shift toward immature granulocyte forms indicating a marked consumption of granulocytes.

Question 16

Laboratory Findings for Sepsis

Answer 16

Two blood tests, urine culture and sputum culture if CXR abnormalities. CBC with differential and platelets. ABG and metabolic panels, coagulation studies

Question 17

Use of IVF and corticosteroids for Sepsis

Answer 17

low doses of corticosteroids for 7 days are a/w improved survival (hyrdocrotisone). Volume expansion with normal saline must be 
initiated emergently

Question 18

What is the most important indicator of outcome?

Answer 18

HTN, failure to reverse early warm pre-shock leads to irreversible organ damage and death