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burn-shock-pathogenesis-complications-and-clinical-findings

Burn Shock: Pathogenesis, Complications, and Clinical Findings Thermal burn injury > 20% Total Body Surface Area Authors: Shayan Hemmati Reviewers: Christy Chong Ben Campbell Donald McPhalen* * MD at time of publication ↑ Production of local inflammatory markers (ex. histamine, bradykinin, and prostaglandins) Endothelial cell lining in blood vessel walls is compromised ↑ Local vessel permeability Shift of plasma + proteins from vessel into interstitial space Direct vascular thermal injury (within burn wound) ↑ Production of circulating inflammatory mediators (ex. IL-1, IL-6, TNF-!) ↑ Systemic vessel permeability ↑ Circulating reactive oxygen species Damage to DNA, proteins, and lipids throughout body, including myocardium (muscle cells of the heart) ↑ Myocardial stress Myocardial dysfunction ↓ Cardiac contractility ↓ Stroke volume ↓ Cardiac output Cardiogenic Shock Refer to Cardiogenic Shock: Pathogenesis, Complications and Clinical Findings ↓ Protein concentration in vessels causes ↓ intravascular oncotic pressure Further shift of plasma from vessel into interstitial space (↑ interstitial proteins pull plasma into interstitium) ↓ Intravascular plasma ↑ RBCs per unit volume of plasma ↑ Systemic vasoconstriction to maintain blood pressure (↑ Afterload) ↓ Circulating blood volume leads to less venous return (↓ Preload) ↑ Hematocrit Pitting edema (burned & unburned tissue) ↓ Circulating blood volume Hypovolemic Shock Refer to Hypovolemic Shock: Pathogenesis, Complications and Clinical Findings Burn Shock: A complication of large burns causing end-organ hypoperfusion with resultant organ dysfunction Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published August 15, 2022 on www.thecalgaryguide.com