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