Sepsis Flashcards
Sepsis
Severe infection leading to organ dysfunction: SIRS + infection (bacteremia or viremia)
SIRS
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
Peptidoglycan.
PAMPs
PAMPs - highly conserved parts of microbial molecules on organisms-Lps, peptidoglycan, flagellin
Tlrs
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
- Proinflammatory cytokines, tumor necrosis factor α and interleukin-1, stimulating inflammation
- Toxic oxygen byproducts
- 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
