B3.002 Sepsis Flashcards
what is the less recent progression of sepsis?
SIRS
sepsis
severe sepsis
septic shock
what is SIRS
systemic inflammatory response syndrome
what occurs in SIRS
cytokine storm
- release large quantities of cytokines
- can cause multiple organ dysfunction bc these cytokines can be both harmful and toxic
what are the criteria for SIRS?
2 of the 4: fever or hypothermia (>100.4 or <96.8) tachycardia (>90) tachypnea (>24) leukocytosis (>12,000), leukopenia (<4000) or left shift (>10% immature band cells)
what are the criteria for sepsis?
SIRS
suspected or proven infection
what are the criteria for severe sepsis?
SIRS
suspected or proven infection
end organ dysfunction in one or more organ systems
what are the criteria for septic shock?
SIRS
suspected or proven infection
end organ dysfunction
hypotension despite adequate fluid resuscitation, requiring pressor therapy
what is a pressor?
increases BP by stimulating vasoconstriction
what are the criteria for refractory septic shock?
SIRS infection end organ dysfunction hypotension despite fluids hypotension lasts for more than 1 hour despite fluids and pressors
what is the sepsis continuum that is now more widely accepted?
early sepsis
sepsis
septic shock
what is a SOFA score?
sequential (sepsis related) organ failure assessment based on test variables from: respiratory (PaO2/FIO2) coagulation (platelets) liver (bilirubin) cardiovascular (hypotension) CNS (Glasgow coma score scale) renal (creatinine/urine output)
what is the APACHE II scale?
severity of disease classification system based on lab test results
what is the significance of a SOFA score of 2?
<2 has 3% risk of mortality
>2 is associated w poor outcomes and 18-24% mortality
what is septic shock?
vasodilation or distribution problem due to sepsis causing circulatory, cellular, and metabolic derangements
what is the process of shock?
diminished cardiac output or reduced effective circulating blood volume which impairs tissue perfusion and leads to cellular hypoxia
what are some causes of shock?
infection - due to inflammatory cytokines and a vasodilatory response
anaphylaxis
cardiac abnormality - heart cant pump properly
hypovolemia - losing blood volume from bleeding out
what is the difference between primary and secondary multiple organ dysfunction syndrome?
primary : result of a defined insult
secondary : result of an indirect insult due to the host’s response
why is the frequency of septic shock increasing?
more aggressive surgery
more resistant organisms
more immune compromise from disease and medications
increased elderly living w chronic diseases (AIDS)
widespread use of catheters/medical devices (implantable)
28 day mortality of septic shock
40-70%
what factors are associated with a poor prognosis in the event of sepsis?
increased age comorbid medical conditions high APACHE II score elevated lactate insufficient response to vasopressors delay in treatment
what are some infectious causes of sepsis?
opportunistic infections (don’t cause disease in immunocompetent hosts)
host factors (comorbid diseases)
indwelling lines/catheters/foreign bodies (obstruction of drainage)
microbial factors
-invading the immune system
-produce toxins (cant always be treated)
what are some common classes of shock?
cardiogenic
hypovolemic
septic
what are some rare classes of shock
anaphylactic
neurogenic
toxic
describe the mechanism of cardiogenic shock
failure of myocardial pump resulting from intrinsic myocardial damage, extrinsic compression, or obstruction to outflow
cardiac tamponade
heart leaks into space between muscle and pericardium, compressing heart and impairing pumping
describe the mechanism of hypovolemic shock
inadequate blood or plasma volume
describe the mechanism of systemic inflammatory shock
cytokine cascade activation peripheral vasodilation and pooling of blood endothelial activation/injury leukocyte induced damage disseminated intravascular coagulation
what are the 3 stages of shock
non-progressive (reversible)
progressive
irreversible
non-progressive shock
compensatory mechanisms allow for survival
progressive shock
failing compensatory mechanisms
increasing tissue hypoxia
beginning lactic acidosis due to anaerobic metabolism
irreversible shock
leads to death
physical signs of inflammation
rubor - redness calor - heat tumor - swelling dolor - pain functio laesa - loss of function
VINDICATE differential diagnosis
vascular infectious neoplasm drugs/toxins inflammatory congenital/genetic autoimmune trauma endocrine/metabolic
diagnostic evaluation of sepsis
blood cultures
CBC (white blood cell count, platelets, hemoglobin)
CMP (electrolytes, renal function, liver function)
coagulation tests
steps associated with empiric chemotherapy (what to do before lab results come back)
- establish evidence of infection and probable site
- obtain culture and susceptibility specimens
- propose microbiological diagnosis
- determine the need for empiric therapy
- initiate chemotherapy
range of pathogens affected by a given drug
narrow spectrum- effective against a few species/classes of pathogen
broad spectrum- effective against many species/classes of pathogens
when should narrow spectrum drugs be used
when the pathogen and its sensitivity to the drug are documented
when should broad spectrum drugs be used
mixed infections, or when pathogen identity and sensitivities are not known
maximize probability of toxicity to pathogens
combination chemotherapy
use of multiple drugs against the same pathogen
indications for combination chemotherapy
- for enhanced therapeutic effect
- to allow use of lower doses of individual drugs to minimize toxicity to patient
- to delay development of resistance
- for the treatment of mixed infections
- to initiate therapy in life threatening situations when the pathogen is not known
possible sources of air in subcutaneous tissue
gas produced by bacteria
tissue destruction
why is lactate elevated in septic shock?
tissue hypoxia from hypoperfusion
metabolic activity switches from oxidative metabolism to non oxidative or anaerobic metabolism
sepsis therapies
treat underlying cause
increased blood pressure (IV fluids, vasopressors, inotropes)
blood product (packed RBCs, platelets, clotting factors)
ventilator support w oxygen
dialysis for renal failure
corticosteroids for adrenal failure
nutritional support
bacteremia
bacteria in the bloodstream
source of redness
increased circulation to the area
source of swelling
increased vascular permeability
source of warmth
influx of inflammatory cells
local inflammation
innate mechanisms for eradication microbes
systemic disease
local defenses are enhances by increasing circulation to the area, increasing circulating neutrophils, and elevated microbial recognition molecules
cytokines
soluble proteins that interact with cells to produce changes in growth/activation of immune cells, inflammation, and the immune response
chemokines
soluble molecules which guide immune cells into a particular area
TNF alpha
causes leukocytes and vascular endothelial cells to:
- produce and release other cytokines
- express cell surface molecules to improve adhesion of neutrophils
- increase inflammatory production of prostaglandins and leukotrienes
IL-8 and IL-17
attract neutrophils
IL-1B
fever
intravascular thrombosis
key factor of local inflammation
wall off microbes, prevent spread of infection
intravascular fibrin deposition, thrombosis, and bleeding
dissemination intravascular coagulation
disseminated intravascular coagulation
consumption coagulopathy or microangiopathic hemolytic anemia
serious sign of end stages of sepsis
consumption of platelets and clotting factors due to tissue injury, endothelial damage, or both
what organ failure is particularly harmful in exacerbating DIC
liver failure
cant make clotting factors
what is a lab test to quickly assess for DIC
d-dimer
schistocytes
fibrin causes mechanical damage to the red blood cells
