NBME 23 Answers ↦
This is directly from Goljan
I) Hypovolemic shock may occur due to loss of plasma from the burn surface (refer to
• Loss of protein from the plasma loss may result in generalized pitting edema.
II) Infection of the wound site and sepsis may occur.
(a) Sepsis due to Pseudomonas aeruginosa is the most common cause of infection in burn patients.
(b) Other pathogens include methicillin-resistant S. aureus and Candida species.
(3) Curling ulcers may occur in the proximal duodenum (refer to Chapter 18).
(4) Hypermetabolic syndrome may occur if >40% of the body surface is burned.
Can someone explain why is it not increased ECF?
i picked same. Increased ECF but cant remember why. Can you explain WHY it is increased ECF? what was ur reasoning
Burns would lead to a decrease in ECF because the protection from fluid loss is absent; it can lead to shock. :)
My reasoning behind picking ↑ ECV was that your losing fluid but not electrolytes with the burn ⇒ the ecv would have increased osmolarity, so the fluid from the ICV would be pushed the the ECV. It made sense to me at the time. I guess technically its wrong because the loss of fluids and the gain of fluids would amount to pretty much the same thing. But the insulation and heat loss thing makes sense I guess.
Increased ECF, bc I was thinking about the edema formation.... :-/
I picked increased ECF because burns increase the capillary permeability coefficient, but now that I am going over it I realized that increasing the permeability would only transfer plasma volume to the interstitial volume, which are both a part of the ECF so therefore ECF would not change. SMH
Burns (and Diarrhea) cause ISOsmotic volume contraction; Costanzo BRS Physio
in severe burned patient, also has increased fluid in third spacing or interstitial (leading EDEMA). Different extracellular space is interstitial and vascular
"The post-burn hypermetabolic response increases the metabolic rate to compensate for the profound water and heat loss severe burn patients suffer. Water loss approaches 4000 milliliters per meter squared burn area per day [38-41]. The body’s natural response to this insult, partially mediated by increased ATP consumption and substrate oxidation, is to raise core and skin temperatures 2°C above normal compared to unburned patients . This response is similar to the response seen during cold acclimatization. In fact, patients that do not mount this response are likely septic and or have exhausted physiologic capabilities to maintain needed body temperature ."
I thought so too but did a little digging and turns out this happens in nephrotic syndrome bc low oncotic pressure directly stimulates apolipoprotein B synthesis. They still don't know why lol. But in burn victims there's actually increased lipid metabolism, so nothing to do with hypercholesterolemia.