Burns pt 2 Flashcards
What are the hallmarks of initial burn therapy?
Within seconds after an acute burn injury, massive fluid shifts begin to occur. Therefore, airway management and volume resuscitation are the hallmarks of initial therapy.
Why is aggressive fluid administration important?
To prevent renal failure.
-Loss of circulating plasma volume, hemoconcentration, massive edema formation, decreased urine output, and depressed cardiovascular (CV) function
Fluid losses are the greatest at what point? When do they stabilize?
Fluid losses greatest in the first 12 hours, stabilize after 24 hours.
How do fluid losses occur?
-Capillary leak results from loss of endothelial integrity and plasma proteins
-Release of inflammatory mediators from burned tissues
What is optimal UOP in adults?
0.5 mL/kg/hr
When is invasive monitoring indicated?
Invasive hemodynamic monitoring indicated (ABP/CVP/PACs)!!! Espec in patients who do not respond to fluid, have preexisting cardiopulmonary disease, or are at risk of intra abdominal HTN and Abdominal Compartment Syndrome (IAH and ACS significant M&M).
-Catheters removed ASAP due risk of infection
What is the Acute Phase of CV response?
Hypovolemia, Hypotension, and Circulatory compromise:
-Loss of intravascular fluid volume
-Loss of vascular/endothelial integrity
-Loss of plasma proteins
-Release of inflammatory mediators
Decreased CO: Hallmark of burn related shock
-Initially preserved via catecholamine response with tachycardia and vasoconstriction
Coronary blood flow can be reduced
SVR increased
What is the Hypermetabolic/Dynamic Phase of the CV response?
Increased metabolic rates, multiorgan dysfunction, muscle protein degradation, blunted growth, insulin resistance, and increased risk for infection.
What are the primary mediators of the hypermetabolic response after severe burns?
Catecholamines and corticosteroids
What are the S/Sx of systemic inflammatory response that occurs with severe burns?
Increased CO
Tachycardia
Decreased SVR
Increased O2 consumption and CO2 production
Inc myocardial oxygen consumption
What is the treatment of the hypermetabolic/dynamic phase of severe burns?
-Beta blockers, anti hyperglycemic agents, prevention of sepsis, thermal neutrality, nutritional intervention
-Require aggressive fluid resuscitation in the first 24-36 hours
-Restore intravascular volume and cardiac function
What are the immune system effects related to burns?
Within hours, altered immunologic response:
-Depressed leukocyte activity, humoral and cellular responses
-Burn eschar is a prime medium for bacterial growth
-Colonization of Gram (-) bacteria increases mortality
-Sepsis and pneumonia especially with prolonged endotracheal intubation
-Strict aseptic technique is required!!!
-Infection is the leading cause of death in up to 100% children and 75% of adults
How common is AKI after burn injuries?
-Acute Kidney Injury (AKI) ~ 40% after major burn injuries
-Myoglobinuria most common after electrical injury
-Hemoglobinuria common after cutaneous burn > 40% TBSA
What is the mechanism of AKI developing in burn patients?
Decreased renal blood flow alters GFR, stimulates renin-angiotensin-aldosterone system and the release of ADH to conserve Na+ and water
-Intravascular depletion / hypovolemia
-Decreased CO
-Increased plasma catecholamines
Hourly urine output remains the gold standard!!!
-Minimum 0.5mL/kg/hr
What are the GI & Hepatic effects from burns?
-Aggressive nutrition support
-Whole-body catabolism, muscle wasting, cachexia
-Hyperalimentation and lipid infusions
-Tight glucose control secondary to insulin resistance (Monitor perioperatively)
-Overall decrease in GI function with increased risk of ileus
-Increased risk acute GI ulcerations (Acid suppressive therapy: H2 blockers, PPIs, antacids)
-Hepatic effects are variable