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Medicine II: Infectious Disease > Sepsis > Flashcards

Flashcards in Sepsis Deck (18):


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



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%


What are the governing factors of Sepsis?

underlying disease, age, infecting organism and appropriateness of therapy


What are most cases of sepsis due to?

bacterial infection


Septic shock

Sepsis with hypotension or perfusion abnormalities despite adequate volume replacement


Characteristics of Septic Shock

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


Progression of sepsis

infection, SIRS, sepsis, severe sepsis, septic shock


Pathophysiology of Sepsis: Cell wall factors

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



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



Tlrs -ancient receptors conserved on animal and plant cells


Pathophysiology of Sepsis:

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


Secreted Bacterial Factors

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


Cytokine formation and the role of macrophages

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


clinical manifestations of Sepsis

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


Dx of Sepsis

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


Laboratory Findings for Sepsis

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


Use of IVF and corticosteroids for Sepsis

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


What is the most important indicator of outcome?

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