Sepsis Flashcards
Define SIRS
cytokine storm in response to a stimulus leading to multiple organ dysfunction
SRIS criteria
febrile (>38 or 100.4), or hypothermic (<36 or 96,8), tachycardia (>90), tachypnea (>20), leukocytosis or leukopenia (>12,000, <4,000)
Define sepsis
2 of the 4 SIRS criteria plus suspected or proven infection
Define severe sepsis
2 of the 4 SIRS criteria, suspected or proven infection, and end-organ dysfunction in one or more organ systems
Define septic shock
2 of the 4 SIRS criteria, suspected or proven infection, end-organ dysfunction in one or more systems, and severe hypotension (<90 or >40 decrease from baseline) despite fluid resuscitation, requires pressor therapy
Define refractory septic shock
septic shock that lasts for 1 hour despite fluid resuscitation and pressors, this is where patients often die
Define early sepsis (new)
infection based on clinical suspicion combined with RR >22, altered mentation, and/or systemic BP <100, sofa score >2
Define sepsis (new)
life-threatening organ dysfunction caused by an infection with a unregulated host response
Define septic shock (new)
vasodilation or distribution problem due to sepsis causing circulatory, cellular, and metabolic derangements, require vasopressors to maintain arterial BP of >65, lactate >2, 40% mortality vs 10% with sepsis alone,
Define shock
diminished cardiac output or reduced effective circulating blood volume, impairing tissue perfusion, leading to cellular hypoxia, reversible but can be fatal
Causes of shock
infection, anaphylaxis, cardiac abnormality, hypovolemia
Define multiple organ dysfunction syndrome
progressive illness caused either by a defined insult (primary) or as a result of the host response to an indirect insult, no universally accepted criteria, so use the SOFA score
28-day mortality of septic shock
40-70%
patient has a poor prognosis with sepsis if they are experiencing the following:
increased age, comorbidities, high APACHE II score, elevated lactate, insufficient response to vasopressors, delay in treatment
Infectious causes of sepsis
opportunistic infections, host factors such as comorbidities, indwelling devices, especially those leading to the obstruction of normal drainage, and microbial factors that allow infections to evade the immune system and produce toxins we can’t treat
cardiogenic shock
patient has MI, leads to loss of perfusion, reduced circulating volume, hypoxia, necrosis, and ultimately organ failure and death
hypovolemic shock
patient experiences trauma where they lose large volume of blood, leads to reduced circulating volume, hypoxia, necrosis, and ultimately organ failure and death
septic shock
patient has infection where overblown immune response leads to the shunting of blood away from peripheral vital organs leading to hypoxia, necrosis, and ultimately organ failure and death
anaphylactic shock
hypersensitivity leads to over exaggerated immune response against a benign invador leading to the shunting of blood, hypoxia, necrosis, organ failure, and death
toxic shock
bacteria associated with tampons lead to rapidly progressing infection leading to shunting, hypoxia, necrosis organ failure, and death within 48 hours in 65% of patients if left untreated
Catecholamine role in shock
peripheral vasoconstriction due to autonomic nervous system releasing adrenal catecholamines, shunt blood to heart and brain, lead to renal and liver failure, capillary acidosis, and hemodilution with hypovolemia
hemodilution with hypovolemia
when peripheral blood volume decreases, interstitial fluids move into the vasculature to replace this pressure, leading to dilute blood
DIC
disseminated intravascular coagulation, blood pools at site of infection, forms a clot, uses up all clotting factors in the body, leads to profuse bleeding everywhere else
Crepitus
crunching sound indicative of a friction rub between bone and cartilage
signs of inflammation
rubor, calor, tumor, dolor, functio laesa
differential diagnosis with leg pain
VINDICATE: vascular, infection, neoplasm, drugs/toxins, inflammation, congenital, autoimmune, trauma, endocrine
possible infections of the leg
cellulitis (skin), fasciitis (fascia), myositis (muscle), and osteomyelitis (bone)
labs collected with suspected sepsis
cultures, CBC, CMP, coagulation test
CBC
complete blood count, evaluates for leukocytosis or leukopenia, platelet count, and hemoglobin
blood culture test
2 separate sites, anaerobic and aerobic, total of 4 bottles, if patient as an implanted device, want one from there too
coagulation test
test for DIC, see if the clotting time is decreased
CMP
electrolytes, renal function, and liver function
What factors come into play when choosing an empiric drug treatment
site of infection, patient history
first things you do when septic patient is admitted
obtain labs, take x ray, administer IV fluids, start on broad spectrum antibiotics
slight lactate elevation on metabolic panel is a sign that
there is poor perfusion, patient needs a pressor, but if it is only slight, it is still reversible
minor elevation in liver enzymes is a sign that
liver is being poorly perfused, this is the beginning of an acute liver injury, still reversible, do something now
air in the subcutaneous tissue is indicative of
necrosis beyond the skin but before the muscle, that is fasciitis, so necrotizing fasciitis
debridement
surgical procedure to scoop out necrosed tissue
Bandemia
left shift in the bands, indicating excessive presence of immature white blood cells, infection is so acute and body is so desperate that WBCs are being released prematurely
lab sign of malnutrition
low albumin
low fibrinogen levels is indicative of
DIC
bacteremia
bacteria in the blood
sepsis therapies
treat underlying cause, increase BP, replace RBCs, platelets, and clotting factors if bleeding, ventilation, dialysis, corticosteroids, and nutritional support
IL10
calms the immune response, down regulating inflammation
IL7 and IL8
flags for help from neutrophils, attracting them to infection site
IL1B
causes fever, some patients have too much of this, have periodic fever syndrome
NLRP3
enhances production of IL1B, genetic defect would lead to periodic fever syndrome
TNFalpha
causes leukocytes and endothelial cells to produce and release cytokines, express cell-surface molecules to improve neutrophil adhesion, and increase prostaglandinin and leukotriene production
IL6
promotes clotting via tissue factor induction
cause of hemolytic anemia in septic patients
consumption coagulopathy, use up all complement mediators really fast, serious sign of end-stage sepsis
amniotic fluid embolism
pregnant patient experiences trauma i.e. car accident, fluid leaks from amniotic sac, travels to mother in the form of an embolism, causes DIC, obstetric emergency
how do patients develop DIC
tissue factor released in response to tissue damage, leads to intrinsic pathway coagulation, platelet aggregation, decreased antithrombin, protein C, protein S, ultimately unopposed clotting
what factor would worsen DIC
liver failure, patient can’t produce clotting factors, they’re already at a disadvantage, DIC will progress very quickly
quick laboratory test for DIC
D dimer test, D dimer produced from the breakdown of fibrin in peripheral tissues leading to bleeding
signs of organ failure
decreased urine output, altered mental status, decreased platelets, difficulty breathing, abnormal heart function, abdominal pain
why are biofilms dangerous
incurable by immune system, recalcitrant to antibiotic therapy, chronic
top pathogens that lead to sepsis
staph aureus, coagulase negative staph, e coli, and strep
features of staph
gram positive cocci in cluster, none motile, non spore forming, catalase positive and oxidase negative, facultative anaerobe, if coagulase positive, aureus, otherwise epidermis or saprophyticus, major component of normal flora
steps of septic shock
innate immune system recognizes microbes, immune factors activate endothelial cells and leukocytes, immune system over-responds, systemic endothelia damage, vasodilation, capillary leakage, multiple organ failure, death
microbial trigger on gram - bacteria
lipopolysaccharide, on E coli surface, exposed and easy to recognize
microbial trigger on gram + bacteria
lipoteichoic acid exposed on surface, peptidoglycan both inside and outside where it is sloughed off, and superantigens
microbial trigger on viruses
nucleic acid
PAMP
pathogen associated molecular patterns
PRR
pattern recognition receptors
Toll-like receptors
pattern recognition receptors that respond to PAMPs to release pro inflammatory cytokines
super antigens
exotoxins that cross link T cell receptors to class II MHC, amplifying the t cell stimulation from its normal 1 in 10,000 to 1 in 5, resulting in massive IFN gamma and IL2 production
IFN gamma
interferon gamma, proinflammatory cytokine, recruits leukocytes
IL2
interleukin 2, proinflammatory cytokine, recruits leukocytes
which bacteria produce super antigens
staph aureus and step pyogenes
super antigens are best known for causing
toxic shock syndrome
