## Pathophysiology of Burn Shock **Key Point:** Burn shock in the acute phase (0–48 hours) is primarily **hypovolemic** in nature, not cardiogenic or septic. ### Mechanism of Fluid Loss 1. **Increased capillary permeability** — thermal injury damages the endothelial lining of capillaries, allowing fluid and proteins to leak into the interstitial space (third spacing). 2. **Protein extravasation** — albumin and other plasma proteins escape into the interstitium, creating an osmotic gradient that draws additional fluid out of the vasculature. 3. **Massive intravascular volume depletion** — can result in loss of 30–50% of plasma volume within the first few hours, leading to shock if fluids are not aggressively replaced. ### Clinical Correlate **High-Yield:** The **Parkland formula** (4 mL × body weight in kg × %TBSA burned) is used to calculate fluid replacement in the first 24 hours precisely because of this hypovolemic mechanism. Half the calculated volume is given in the first 8 hours, and the remainder over the next 16 hours. ### Why Not Cardiogenic, Septic, or Anaphylactic? - **Cardiogenic shock** may occur later (after 24–48 hours) due to myocardial depression from inflammatory mediators (TNF-α, IL-1), but is not the primary mechanism in the acute phase. - **Septic shock** develops days later when the burn wound becomes infected; bacteria do not translocate significantly in the first 24–48 hours. - **Anaphylactic shock** is not a feature of thermal injury; histamine release contributes to local inflammation but does not cause systemic anaphylaxis. [cite:Parikh Textbook of Forensic Medicine Ch 10]
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