Sepsis Flashcards
cytokines
- messenger molecules release after damage to cells/infection
- drive inflammatory process
- interleukons, TNF, interferons
localized inflammatory process
- vascular (localized vasodilation and increase capillary membrane permeability)
- immune (WBC enter site of injury)
- platelets aggregate, promote wound healing
- plasma proteins create compliment system to damage pathogens
sepsis
life-threatening organ dysfunction caused by dysregulated host response to infection
what can sepsis lead to?
circulatory, metabolic and cellular abnormalities; body’s normal immune system is overwhelmed resulting in a dysregulated response
arachadonic acid pathway
- activated by damage to cells, hypoxemia, ischemia
- results in increased capillary membrane permeability (loss of preload systemically)
- vasodilation and vasoconstriction occur to bring more blood to area and to allow WBC to cross into tissues
- systemically: maldistribution of blood
- platelet aggregation occurs
- release of prostaglandins also result in pain and fever increasing demand
drugs that can block inflammatory response
steroids, NSAIDs, bronchodilators
bradykinin pathway
- tissue damage activates Factor XIII (Hagemans Factor) = bradykinin released
- increase capillary membrane permeability
- Systemically: loss of preload
- potent vasodilator = systemic significant decrease in afterload, and increase in venous capacitance
- activates histamine causing systemic vasodilation and activation of AA pathway
what is major difference between arachadonic and bradykinin pathway?
arachadonic pathway you have platelet aggregation and in bradykinin you have histamine release
normal coagulation
- platelets form plug over injury/wound
- plug activates intrinsic pathway
- extrinsic pathway is activated by damaged endothelium
- meet at the common pathway = formation of thrombin which is converted into fibrin, which stabilizes the platelet plug
- when wound healing starts, plasmin breaks down fibrin mesh
coagulation cascade
- bacteria and cytokines cause damage to the endothelium = activates clotting cascade (microclots use up the clotting factors until there are no more left. Results in bleeding + micro clots)
- Inflammatory cytokines prevent conversion of plasminogen to plasmin. Clots can’t be broken down
- systemic maldistribution of blood
- AA and bradykinin pathways stimulated
complement system
- injury activates the complement proteins (synthesized by liver)
- undergo 1 of 3 pathways
- 4 actions: opsonization, chemotaxis, cell lysis (MAC complexes), agglutination
- systemically intensify inflmtn and other pathways; damage endothelium; cell adhesion and cell death occur
myocardial depressant factor
peptide released from pancreas ischemia that reduces contractility
effects of ABCCs on O2 S+D
- Systemic vasodilation (results in hypotension).
> Decreased afterload, increased venous capacitance - Increased capillary permeability
> Decreased preload - Inappropriate clotting in the microvasculature (activation of coagulation system and reduced synthesis of fibrinolytic system).
- Maldistribution of blood flow.
- Diminished myocardial contractility.
> Release of myocardial depressant factor from pancreas, cytokines reducing contractility, decreased preload
intrinsic sepsis risk factors
- Age: <1 year, >65 years
- Immunocompromising conditions and/or meds
- Multiple comorbidities
- Chronic diseases
- Obstructions
sepsis extrinsic risk factors
- Hospital acquired infection (e.g. VAP)
- breaks in skin (trauma, invasive medical devices, wounds)
- incomplete antibiotic regimes
- sx and diagnostic procedures
- ARO
multi organ dysfunction
- dysfunction CNS, CVS, Resp, GI, GU, hematologic
systems - Mortality up to 90%
- Can be triggered by non infectious causes
(pancreatitis)
sepsis and septic shock are considered
medical emergencies and require immediate treatment and resuscitation
qSOFA
scoring system used to ax severity of organ dysfunction in patients with a known infection.
GCS < 15
RR >= 22
SBP <=100
2/3 = positive for sepsis
treating sepsis
- treat cause
- manage O2 supply and CO
- manage demand (ventilation)
1 hr bundle
- measure lactate
- BCx2 prior to abx
- broad spectrum abx
- initiate 30mL/kg crystalloid for hypoTN or lactate >4mmol/L
- vasopressors if pt is hypotensive during or after fluid resus to maintain MAP >65
what is the goal of giving abx?
remove cause of sepsis
what is the goal of fluid resus?
restore preload
sepsis management - fluids
- use crystalloids, for hypotension or lactate >4
- 30ml/kg, may need more. don’t want to give too much. can use lactate or cap refill to assess need for more fluids (low SSC)
- POCUS/passive leg raise to assess need for more fluid too
vasoactive drugs in sepsis
- norepi is first line, vasopressin can be added if levophed insufficient to raise MAP
- corticosteroids can be used for adrenal insuff if present but is controversial
- goal = improve afterload
how do you know whether a pt is in sepsis vs septic shock?
when vasopressors are required, pt has transitioned into septic shock
inotropes in sepsis management
- if lactate not improving or MAP <65 despite fluid and pressors, next step is to add an inotrope
- usually dobutamine or epi
- goal = improve contractility
ventilation recommendations
- Protective lung strategies: lower tidal
volumes (6mL/kg) - use higher PEEP (to support gas exchange through thickened A/C membrane)
- Limit Plateau pressure to
30cm/H2O - using prone over supine position in adult patients with sepsis-induced ARDS and a PaO2/FIO2 ratio
<150
supportive management
manage demand: sedation, analgesia, RASS goal, ?temp management, nutrition, glycemic control, SCDs, stress ulcer prophylaxis
