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77 Cards in this Set

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  • Back
What is the preferred vasopressor to correct hypotension in septic shock?
NE over dopamine, low dose dopamine doesn't maintain or improve renal function
What should goal blood glucose be?
What is used in pts with severe septic shock in pts with relative adrenal insufficiency?
low-dose hydrocortisone
Are total number of deaths per 100,000 from sepsis increasing or decreasing?
What is the most common site of infection leading to sepsis?
respiratory tract, intraabdominal space, urinary tract
What are the most common causes of sepsis?
gram positive, gram negative, and fungi
Wat is bacteremia (fungemia)?
presence of viable bacteria (fungi) in the bloodstream
What is infection?
inflammatory response to invasion of normally sterile host tissue by the microorganisms
What is SIRS?
systemic inflammatory response syndrome
systemic inflammatory response to a variety of clinical insults that can be infectious or noninfectious etiology.
2 or more of the following: T>38C (100.4F) or less than 36C(96.8F), HR>90bpm, RR>20breaths/min or PaCO2 less than 32 torr, WBC>12000 or less than 4000 or >10% immature (bands), positive fluid balance (>20mL/kg/day), hyperglycemia, plasma C-reactive protein/procalcitonin >2 SD above normal value, arterial hypotension, cardiac index >3.5L/min, arterial hypoxemia, acute oliguria, creatinine increase >0.5mg/dL, coagulation abnormalities, platelets less than 100000mcl, bilirubin>4 mg/dL, hyperlactatemia, decreased capillary refill
What is sepsis?
SIRS secondary to infection
What is severe sepsis?
sepsis with organ dysfunction, hypoperfusion or hypotension (ex. lactic acidosis, oliguria, acute alteration in mental status)
What is septic shock?
sepsis with persistent hypotension despite fluid resuscitation, along with perfusion abnormalities
What is MODS?
multiple organ dysfunction syndrome
presence of altered organ function requiring intervention to maintain homeostasis
What is the predominant sepsis organism since 1987?
gram positive, about half of cases
What are the common gram positive organisms in sepsis?
Staphylococcus aureus, Streptococcus pneumoniae, coagulase negative staphylococci, Enterococcus

Less common: Streptococcus pyogenes and viridans streptococci
What factors increas mortality?
shock, respiratory insufficiency, preexisting renal failure, rapidly fatal underlying disease
What is Staphylococcus epidermidis associated with?
infected intravascular devices (artificial heart valves and stents), IV and intraarterial catheters
Where are enterococci often found?
blood cultures after prolonged hospitalization and tx with broad spectrum ceph
How does gram negative compare to gram positive sepsis?
more pts develop clinical sepsis, more likely to produce septic shock, higher mortality rates
What is the major factor associated with outcome of gram negative sepsis?
severity of underlying condition: acute leukemia, aplastic anemia, more than 70% BSA burn have worse prognosis that nonfatal underlying conditions (DM or chronic renal insufficiency)
What are the most common gram negative in sepsis?
Escherichia coli and Pseudomonas aeruginosa most common
other common: Klebsiella, Serratia, Enterobacter, Proteus
What is the most frequent cause of sepsis fatality?
Pseudomonas aeruginosa
What is risk of sepsis from anaerobes?
low risk, if present it is a polymicrobial infection
mortality from polymicrobial infection similar to single organism
What other less common pathogens may cause sepsis?
meningococcus, gonococcus, rickettsia, chlamydia, spirochetes
What species cause fungal infection in sepsis?
Candida albicans is most common
other candida: Candida glabrata, Candida parapsilosis, Candida tropicalis, Candida krusei
others: Cryptococcus, Coccidioides, Fusarium, Aspergillus
What are risk factors for fungal infection?
abdominal surgery, poorly controlled DM, prolonged granulocytopenia, broad spectrum antibiotic tx, corticosteroid tx, prolonged hospitalization, central venous catheter, TPN, hematologic malignancy, foley catheter
What is the 4th most common bloodstream pathogen?
Which bloodstream pathogen has the highest mortality?
What is associated with poor outcome from fungal sepsis?
hematologic disease, neutropenia, high number of positive blood cultures
What is result of proinflammatory response?
contribute to eradication of invading microorganisms, inflammatroy response leads to damage to host tissue
What is result of antiinflammatory response?
control inflammation, causes leukocytes to activate
When dose systemic inflammatory response occur?
once the balance to control the local inflammatory process to eradicate invading pathogens is lost
What is unique to the outer membrane of the gram negative cell wall?
endotoxin, it is released with bacterial lysis
What is responsible for the most toxic effects from gram negative sepsis?
Lipid A, the innermost region of the lipopolysaccharide
What is lipid A predominant effect?
activate macrophages and trigger inflammatory cascades critical in progression to sepsis
What does endotoxin do?
forms a complex with lipopolysaccharide binding protein which engages the CD14 receptor and the surface of a macrophage
What exhibts proinflammatory activity in gram positive sepsis?
exotoxin peptidoglycan
What does peptidoglycan do?
competes with lipid A for similar binding sites on CD14, less potent than endotoxin
What are the key proinflammatory mediators in sepsis?
TNF-alpha, IL-1, IL-6
also IL-8
What is the primary mediator of sepsis?
What is the most consistent predictor of sepsis?
IL-6, because it remains elevated for a longer period of time
What are the antiinflammatory mediators?
IL-1 receptor antagonist (IL-1RA), IL-4, IL-10
What do antiinflammatory mediators do?
inhibit production of proinflammatory cytokines and down regulate some inflammatory cells
How does the balance of pro and antiinflammatory mediators work?
systemic spillover of excessive proinflammatory mediators causes SIRS and MODS (multiple organ dysfunction syndrome). Counterregulatory pathways activated and there is systemic spillover of excessive antiinflammatory mediators representing compensatory antiinflammatory response syndrome (CARS). The balance between the 2 determines the degree of inflammation.
What are pathophysiologic consequences of the activation of complement in sepsis?
generation of anaphylactic toxins and other substances that augment or exaggerate the inflammatory response
stimulation of leukocyte chemotaxis, phagocytosis with lysosomal enzyme release, increased aggregation and adhesion of platelets and neutrophils, production of toxic superoxide radicals
release of histamine from mast cells and resultant increase in capillary permeability and the "third spacing" of fluid in interstitial spaces
How is inflammatory process in sepsis related to coagulation system?
proinflammatory mechanisms that promote sepsis are procoagulant and antifibrinolytic
fibrinolytic mechanisms can be antiinflammatory
activated protein C enhances fibrinolysis and inhibits inflammation
protein C is reduced in sepsis
fig 123-3 pg 1946
What are the most frequent organ dysfunctions in sepsis?
respiratory, circulatory, renal
What is mortality rate of pts in septic shock?
What causes the severe hypotension in sepsis?
release of vasoactive peptides such as bradykinin and serotonin, and by endothelial cell damage leading to the extravasation of fluids into interstitial spaces
What is disseminated intravascular coagulation?
inappropriate activation of the clotting cascade that causes formation of microthrombi resulting in consumption of coagulation factors, organ dysfunction, and bleeding
What is most common cause of DIC?
sepsis, incidence of DIC increases as severity of sepsis increases
DIC occurs in 50% of gram negative sepsis
How is DIC formed?
proinflammatory cytokines are the principal mediators, along with endotoxin, activation of coagulation cascade and inhibition of fibrinolysis.
Combo of excessive fibrin formation, inhibited fibrin removal from depressed fibrinolytic system, and endothelial injury results in microvascular thrombosis and DIC
What complications from DIC?
depends on targec organ and severity
acute renal failurs, hemorrhagic necrosis of GI mucosa, pulmonary failure
often coexist with MODS
Which organ usually has dysfunction first?
What is ARDS?
activated neutrophils and platelets adhere to pulmonary capillary endothelium, initiating multiple inflammatory cascades with a release of a variety of toxic substances. There is diffuse pulmonary endothelial cell injury, increased capillary permeability, and alveolar epithelial cell injury. Consequently, interstitial pulmonary edema occurs that progresses to alveolar flooding and collapse. End result is loss of functional alveolar volume, impaired pulmonary compliance, and profound hypoxemia.
What activity does coagulation have in ARDS?
upregulated in injured lung
What activity does fibrinolytic activity have in ARDS?
What is tx for ARDS?
anticoagulant that block extrinsic coagulation pathway can protect against development of pulmonary fibrin deposition as well as lung dysfunction and acute inflammation
What are integral for the pathogenesis of ARDS?
fibrin deposition in lung and abnormalities of coagulation and fibrinolysis
What is hallmark hemodynamic effect of sepsis?
high cardiac output and low systemic vascular resistance
What cause depression of cardiovascular function?
TNF-alpha and endotoxin
What is concern with persistent hypotension?
balance of oxygen delevery to tissues and oxygen consumption by tissues
What happens if perfusion decrease?
oxygen extraction increases and arteriovenous oxygen gradient widens
oxygen delivery decreases, but oxygen consumption unaffected
What can cause ischemia in sepsis?
if perfusion decreases with high metabolic demands, reserve oxygen delivery is exceeded and tissue ischemia results
What is result of tissue ischemia?
organ dysfunction and failure
How do you optimize delivery of oxygen?
increasing oxygen delivery or decreasing oxygen consumption in a hypermetabolic patient
How often does renal dysfunction occur?
What is result of abnormal urine output?
fluid overload in extravascular space including lungs, leading to impairment of pulmonary gas exchange and severe hypoxemia
What is tx if oliguric or anuric with MODS?
adequate renal perfusion and trial of loop diuretics
renal replacement therapy such as continuous hemofiltration or intermittent hemodialysis to facilitate volume and electrolytes
What are s/s of early sepsis?
fever, chills, and change in mental status
if gram negative bacilli, hyperventilation can occur before fever and chills and lead to respiratory alkalosis as earliest sign
Which organisms are rapidly progressing cases?
meningococcemia, P. aeruginosa, Aeromonas infection
What causes metabolic acidosis in sepsis?
increased glycolysis with impaired clearance of lactate by liver and kidneys and tissure hypoxia from hypoperfusion result in elevated lactate levels
What causese hyper/hypoglycemia?
altered glucos metabolism (impaired gluconeogenesis and excessive insulin release)
table 123-2 pg 1947
Which pts have higher mortality rates?
advanced age, preexisting disease (COPD, neoplasm, HIV), ICU car, organ failure, positive blood cultures, Pseudomonas
How does lactate levels affect mortality?
level more than 4mmol/L with SIRS increases ICU admission and perisistent elevation for 24 hours associated with high mortality rate
if increased lactate clearance after 6hrs of emergency department intervention have improved outcome