Sepsis Flashcards
define SIRS
systemic inflammatory response syndrome
-clinical presentation associated with systemic response to infection, trauma
-SIRS criteria: not really specific
HR:
-dogs: >120
-cats: <140 or >225
-horse: tachycardia
RR:
-dogs: >40 or PaCO2 <30mmHg
-cats: >40
-tachypnea
temperature:
-dogs: <100.4 or >104.0
-cats: <100 or >104
-horses: pyrexia or hypothermia
leukogram:
-dogs: >18,000 or <5,000 WBC/uL
-cats: >19,000 or <5,000 WBC/uL
-horses: leukocytosis or leukopenia, >10% bands
describe multiple organ dysfunction syndrome (MODS)
abnormal organ function associated with SIRS
define sepsis
- life-threatening organ dysfunction caused by a dysregulated host response to infection
-organ dysfunction assessed as sequential (or sepsis-related) organ failure assessment (SOFA) score of at least 2 points or at least 2 SIRS criteria
define septic shock
a subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality
-pressor requirement (not responding to fluid therapy)
is sepsis the same as bacteremia? describe organisms of sepsis
NOOOOOOOO
organisms include: literally any type of organism that can cause enough inflam and deranged response to inflam = sepsis
describe conditions associated with sepsis
thoracic:
-pyothorax
-pneumonia/pleuropnuemonia
-endocarditis
-traumatic reticulopericarditis
-neoplasia
abdominal:
-perforated bowel (FB, ulcer)
-translocation
-hepatitis, cholangiohepatitis
-pyelonephritis
-pyometra
tissue injury: surgery, trauma, burns
cutaneous:
-bite wounds, pyoderma
hypotension/ischemia: especially GI
immunocompromise:
-chemo/immunosuppression
-DM, cushings
-immune system dysfunction
-failure of passive transfer
describe pathogenesis of sepsis
- some sort of stimulus from organism itself (PAMPs and DAMPs): LPS!!! fungal cell walls, flagellin, etc.
- cause release of cytokines: pro-inflam and anti-inflam
-release both types so inflamation can fight infection but also don’t go crazy and kill bodies - cytokines and chemokines recruit neutrophils and other inflammatory cells
-activate coag cascade, release enzymes and ROS to try to get infection under control - in some patients there is unchecked inflammations, in others there is immune paralysis where anti-inflam effects predominate
-either way there is an imbalance of the response and - disrupted homeostatic mechanisms
-vasomotor tone
-inflammatory and coagulation cascades
-microvascular changes: endothelial function, microvascular bloodflow, mitochondrial functions
describe vasomotor tone in sepsis
-normal tone is a balance between vasoconstriction and vasodilation
-vasodilation is a hallmark of sepsis!! due to nitric oxide under the influence of cytokines
describe inflammation and coagulation in sepsis
- proinflammatory cytokines released, many functions including release of tissue factor (activates extrinsic clotting cascade via factor VII) and leads to thrombin formation, which activates other platelets and stimulates inflam cells and cytokine release and cycle!!!
–inhibition of anticoagulation and fibrinolytic paths via decrease tissue plasminogen activator, antithrombin, and tissue factor pathway inhibitor
-also reduce protein C/S - end result is a pro-coagulant state, which leads to
-micro-thrombi formation
-decreased oxygen delivery to tissues: MODS and MOFS - progression to hypeocoagulable DIC can also occur
describe microvascular changes in sepsis
- loss of vascular muscle autoregulation
- microthrombosis
- leukocyte activation
- changes in RBC rheologic properties: RBCs get stiffer = harder to move through capillaries = stagnation = part of virchow’s triad of coag
- endothelial cell dysfunction
- disruption of endothelial glycocalyx
- changes in capillary permeability
describe cryptic shock
- decreased microcirculatory perfusion despite normal hemodynamic values
-completely normal vital signs but can still be in shock - mechanisms:
-decreased functional capillary density (clots in caps = fewer functional capillaries)
-increased diffusional distance to mitochondria due to:
a. edema from increased capillary permeability and
b. heterogenous microvascular bloodflow (arteriovenous shunting) due to loss of functional capillaries
describe cytopathic hypoxia
-mitochondria unable to utilize oxygen
-mitochondria also involved in apoptosis and cell death mechanisms so this doesn’t happen as efficiently
describe clinical signs of early sepsis (7)
- red mucous membranes due to vasodilation
- increased heart rate: in response to hypoxia and vasodilation
- brisk CRT due to increased cardiac output
- bounding pulses: due to decreased vascular resistance, lower diastolic pressure, and increased cardiac output
- depression
- fever
- hyper or hypoglycemia
-stress (early)
-decreased production, increased consumption
describe signs of sepsis in CATS
cats are not small dogs!
do not manifest a hyperdynamic phase: will not have red membranes in sepsis!!
-pale membranes: 100%
-bradycardia: 66%
-hypothermia: 60%
-abdominal pain: 95%
describe signs of late sepsis (7)
- thready pulses
- prolonged CRT
- pale/muddy MM
- hypothermia
- hypoglycemia-liver failure
- stupor/coma
- organ failure
