Capstone - Burns and Sepsis Flashcards
1st degree - description, layer, clinical, associated, healing
Superficial epidermis Epidermis Red and dry Tenderness Sveral Days
2nd degree superficial partial thickness - layer, clinical, association, healing
Papillary dermis
Red, fluid filled blisters
Tenderness
2-3 weeks
2nd degree deep partial thickness - layer, clinical, associated, healing
Reticular dermis
Blanched white and pink fluid-filled blisters
Decreased sensation and no capillary refill
3-6 weeks with hypertrophic scar
3rd degree burn - description, layer, clinical, associated, healing
Full thickness Subq fat White, leathery, black and charred No sensation or capillary refill No spont healing
4th degree burn
bone and fascia exposed
Zone of coagulation
Surface coagulation necrosis - irreversible cell death
No cap blood flow
ZOne of stasis
Injured, but viable cells
Sluggish cap flow
Susceptible to hypoperfusion injury, infection
Zone of hyperemia
Inflammatory response
Vasodiliation and increased cap permeability
Pathophys of large burns
Loss of fluid and protein (heat injured capillaries and vasoactive amine increasing permeability)
Systemic inflamm response (cytokines)
Hypermetabolic response
Dysregulated immune response (suppression)_
Inflammatory phase of wound healing
Hemostasis…macrophage nad neutrophil migratrion and release of grwoth factors, collagenases, and elastases
Fibroblasts migrate into wound
Blood coagulates
Proliferative phase of wound healing
Epitheliazation - basal epidermal cells migrate laterally
Fibroplasia - fibroblast proliferation (secrete procollagen, elastin, fibronectin…form new ECM)
Angiogenesis
Create granulation tissue
Maturation phase of wound healing
Collagen remodeling through cycle of synthesis and removal
Parallel and collagne fibers
SIRS criteria
Temperature more than 38 or less than 36 HR> 90 RR> 20 PaCO2 < 32 mmHg Inflammatory response WBC greater than 12000 or less than 4000 greater than 10% band form neutrophils
Sepsis criteria
Evidence of infection
SIRS
Organ dysfunction which is
RR>22
Altered mentation
SBP<100 mmHG
Septic shock criteria
Evidence of infection
SIRS
Sepsis
Despite adequate fluid restoration attempts,
Vasopressor therapy necessary to maintain MAP>65 mm Hg
Lactate>2
What can cause SIRS without systemic infection
Trauma, aspiration, pancreatitis, Burns
Management of Sepsis (in order)
Reverse hypoxia by adding volume to increase perfusion and added oxygen to increase blood O2
Control the septic source (think urinary, blood, pneumonia) and administer antibiotics
Manage hypotension with vasopressors
Best drug to use against sepsis
Norepinephrine (alpha and B1 agonists)
Recombinant human act protein C
Promotes fibrinolysis and initiates thrombosis
Modulates procoagulant response that contributes to Organ dysfuncti
Antithrombin
Inactivates factor 2 and 10
Modulates procoagulant response
TLR 4 antagonists
Supress cytokine production
G-CSF
Enhances neutrophil production and functiomn
Anti-TNF monoclonal antibody and TNF receptor antagonists
Supress cytokine production leading to shock and clotting cascade activation
IL-1 receptor antagonist
Suppress acute phase reactant production contributing to shock
Glucocorticoids
No benefit in patients with SIRS or sepsis but maybe septic shock
Increase anti-inflam cytokines and decrease inflam cytokines
SIRS stage 1
Activate innate immune system
PAMPs activate dendritic cells and macophages
Heat shock proteins produce in response to stress
Macrophage releases (IL-1, IL-6, TNF-alpha along with prostaglandins, leukotrienes and PGF)
Dendritic release (IL-12) then move to help activate T cells
IL -1
Neutrophil and macrophage migration
Upregulates adhesion molecules
Fever
Acute phase reactant formation
IL-6
Induces B and T cell differentiation
Fever
Acute phase reactant formation
TNF-alpha
Enhances NK cell and CD8 cell cytotoxicity Increase vascular permeability Fever Shock Pro-inflam cytokine production
IL-12
Activates NK cells
Induces T differentiation
Supress IL-17 formation
Increase IFN-gamma
SIRS stage 2
Pro-inflamm cytokines released into systemic circulation (leuko and lymph cytes)…stimulate acute phase reactant formation
Balanced by endogenous anti-inflamm mediators (IL-10, PGE2, IL-1 receptor antagonist)
IL-10
Inhibits activityof Th1 cells, NK cells, and macrophages
PGE2
Suppresses T-cell rceptor signlaing
IL-1 receptor antagonist
Inhibits IL-1 activity
SIR stage 3
Uncontrolled
Hypotnesion - decreased perfusion and shock…cytokines cause vasodilators
TIssue edema - permeability of endothelium
Maldistribution of microvascular blood flow - seuqestration of lymphocytes and platelets…activation of coag cascade
Impaired cellular oxygen utilization leads to cell death
