Transcript - for easy reading! So let's learn a bit more about the pathophysiology and the mechanism of disease. When a burn occurs on the skin, it causes changes within the skin, that could be divided into sort of three regions or three zones. These zones of a burn were described by Jackson in 1947, and so it is also called the Jackson model. The first zone is the zone of coagulation. Then it's the zone of stasis on the outside, and then the furthest part is the zone of hyperaemia. So, zone of coagulation is essentially the point of maximum damage. In this zone, there is irreversible tissue loss due to coagulation of proteins. Thus you get coagulative necrosis. Surrounding the coagulation zone of necrosis, is the zone of stasis. Now in this zone, it's essentially characterized by decreased perfusion. This ischemic zone may progress to full necrosis, unless the ischemia is reversed. At the very outside, is the zone of hyperaemia. In this outermost zone, tissue perfusion is increased. The tissue here is invariably recovered unless there is severe sepsis or prolonged hypoperfusion. Again, the stasis zone is characterized by ischemia and may progress to full necrosis unless the ischemia is reversed. Therefore, the main aim of burns resuscitation is to increase tissue perfusion here and prevent any further damage, any damage becoming irreversible. So that is a general pathophysiology or mechanism of disease. Concept of burns. When you assess a burn, it is important to know the cause of the burn as we have learned, such as if it's a thermal or radiation burn. The other important aspect of a burn assessment is to know the depth of the burn. To make it super easy, just think of burns as initially being superficial burns or deep burns. So let's zoom into the skin here to look at what happens in a superficial burn and what happens in a deep burn. Let's take a look at a superficial burn first. If it's a superficial burn, it will cause damage to the epidermis and the upper dermis only. So, like the capillary layer of the dermis. Again, you have blood vessels here, capillaries. Superficial burns will damage the keratinocytes, which are your cells in the epidermis and will also activate an immune response, so it will activate immune cells around the area such as mast cells and macrophages. The damaged keratinocytes, the mast cells and the macrophages will secrete proinflammatory cytokines, triggering an immune response. The cytokines will stimulate nerve endings around the dermis. The sensory nerve endings here can be the ones that detect pain, for example, and pain is an important feature of superficial burns. Some cytokines will cause increase in vascular permeability. The increase in vascular permeability will cause fluid to leak out and may lead to interstitial oedema. As the fluid leaks out, it can result in hypotension. Remember that the increase in vascular permeability causes fluid to leak out. The fluid can actually accumulate in one area, causing a blister on the skin surface. The sensitive blister can rupture and release fluid on to the damaged skin surface. Thus superficial burns have a moist appearance. The cytokines secreted by the cells above will also cause concurrent vasodilation, causing further hypotension, in severe cases. The vasodilation contributes to the warmth in the area as well as causing blanching of the skin and erythema. Blanching means that when you press on the burnt skins surface, blood will quickly fill it up because of the increase in blood flow to the area. The blanching skin is a feature of superficial burns. In deep burns, you have more than just damage to the epidermis and the upper part of the dermis. You have damage all the way down, extends all the way to the hypodermis, so it's a pretty deep burn. Deep burns can thus damage blood vessels in the skin. Because you have damaged blood vessels everything will leak out. You have no blood supply to the area, so you eventually get this dry, non-blanching surface. It is dry and inelastic. The non-blanching dryness is an important feature of deep burns. Further, deep burns extending to the reticular layer of the dermis can destroy nociceptors and other sensory nerve fibers. Initially, pain can be detected, but as the sensory nerve fibers are damaged, you get hypoesthesia, so you get reduction in sensation. Loss of sensation is an important feature of deep burns. Obviously not all your blood supply is damaged or your blood vessels are damaged. The functional blood vessels will react to the cytokines produced around the area. The vessels will increase vascular permeability, which will cause fluid to shift out, causing interstitial oedema. So fluid shifts out from the intravascular space or the blood vessel, into the interstitium, and this huge amount of fluid coming out of the vessels will result in hypotension, so circulatory shock even. Hypotension as a result of the shift of fluid occurs more in deep burns rather than superficial burns. NAssink Transcriptions nassink.transcribe@gmail.com
Please help me i burn from 9 months After that I do 4 session fractional co2 to reduce a scar but the redness don't get rid of still now What i can do plz
This is great. Especially for us coming from a 3rd world country with an INSANELY high number of severe burns presenting to our healthcare centres each year! Thank you for doing this!
Please help me i burn from 9 months And i do 4session co2 to get rid of scar But the redness don't get rid of still now And the dr say its taleangiectaia or erythema
He said that in the stasis zone, there is decreased perfusion (lower fluid flow). Presumably, that means that blood is blocked off from flowing to the wound site.
I dont know if you're aware but your opening logo drawing is unreadable unless you know in advance what it says or pause the video a good 20 seconds to read
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Transcript - for easy reading!
So let's learn a bit more about the pathophysiology and the mechanism of disease. When a burn occurs on the skin, it causes changes within the skin, that could be divided into sort of three regions or three zones. These zones of a burn were described by Jackson in 1947, and so it is also called the Jackson model. The first zone is the zone of coagulation. Then it's the zone of stasis on the outside, and then the furthest part is the zone of hyperaemia. So, zone of coagulation is essentially the point of maximum damage. In this zone, there is irreversible tissue loss due to coagulation of proteins. Thus you get coagulative necrosis. Surrounding the coagulation zone of necrosis, is the zone of stasis. Now in this zone, it's essentially characterized by decreased perfusion. This ischemic zone may progress to full necrosis, unless the ischemia is reversed. At the very outside, is the zone of hyperaemia.
In this outermost zone, tissue perfusion is increased. The tissue here is invariably recovered unless there is severe sepsis or prolonged hypoperfusion. Again, the stasis zone is characterized by ischemia and may progress to full necrosis unless the ischemia is reversed. Therefore, the main aim of burns resuscitation is to increase tissue perfusion here and prevent any further damage, any damage becoming irreversible. So that is a general pathophysiology or mechanism of disease. Concept of burns. When you assess a burn, it is important to know the cause of the burn as we have learned, such as if it's a thermal or radiation burn. The other important aspect of a burn assessment is to know the depth of the burn. To make it super easy, just think of burns as initially being superficial burns or deep burns. So let's zoom into the skin here to look at what happens in a superficial burn and what happens in a deep burn.
Let's take a look at a superficial burn first. If it's a superficial burn, it will cause damage to the epidermis and the upper dermis only. So, like the capillary layer of the dermis. Again, you have blood vessels here, capillaries. Superficial burns will damage the keratinocytes, which are your cells in the epidermis and will also activate an immune response, so it will activate immune cells around the area such as mast cells and macrophages. The damaged keratinocytes, the mast cells and the macrophages will secrete proinflammatory cytokines, triggering an immune response. The cytokines will stimulate nerve endings around the dermis. The sensory nerve endings here can be the ones that detect pain, for example, and pain is an important feature of superficial burns. Some cytokines will cause increase in vascular permeability. The increase in vascular permeability will cause fluid to leak out and may lead to interstitial oedema. As the fluid leaks out, it can result in hypotension. Remember that the increase in vascular permeability causes fluid to leak out. The fluid can actually accumulate in one area, causing a blister on the skin surface. The sensitive blister can rupture and release fluid on to the damaged skin surface. Thus superficial burns have a moist appearance.
The cytokines secreted by the cells above will also cause concurrent vasodilation, causing further hypotension, in severe cases. The vasodilation contributes to the warmth in the area as well as causing blanching of the skin and erythema. Blanching means that when you press on the burnt skins surface, blood will quickly fill it up because of the increase in blood flow to the area. The blanching skin is a feature of superficial burns.
In deep burns, you have more than just damage to the epidermis and the upper part of the dermis. You have damage all the way down, extends all the way to the hypodermis, so it's a pretty deep burn. Deep burns can thus damage blood vessels in the skin. Because you have damaged blood vessels everything will leak out. You have no blood supply to the area, so you eventually get this dry, non-blanching surface. It is dry and inelastic. The non-blanching dryness is an important feature of deep burns. Further, deep burns extending to the reticular layer of the dermis can destroy nociceptors and other sensory nerve fibers. Initially, pain can be detected, but as the sensory nerve fibers are damaged, you get hypoesthesia, so you get reduction in sensation. Loss of sensation is an important feature of deep burns. Obviously not all your blood supply is damaged or your blood vessels are damaged. The functional blood vessels will react to the cytokines produced around the area. The vessels will increase vascular permeability, which will cause fluid to shift out, causing interstitial oedema. So fluid shifts out from the intravascular space or the blood vessel, into the interstitium, and this huge amount of fluid coming out of the vessels will result in hypotension, so circulatory shock even. Hypotension as a result of the shift of fluid occurs more in deep burns rather than superficial burns.
NAssink Transcriptions
nassink.transcribe@gmail.com
Thanks for the great work!
Please help me i burn from 9 months
After that
I do 4 session fractional co2 to reduce a scar but the redness don't get rid of still now
What i can do plz
This is great. Especially for us coming from a 3rd world country with an INSANELY high number of severe burns presenting to our healthcare centres each year!
Thank you for doing this!
You deserve more fans for your amazing art. I support you.
Waiting for for million subscribers!
You too❤️
Dr Smurf
You’re so good at drawing and explaining. I wish you were my A&P lecturer.
Your teaching method and your drawing diagram is really amazing sir🔥
Love that you just did this 20hours ago and I really need a good video for my tut tomorrow, thanks!
Thank you for this video! I would love to learn about fluid protocols s/p burns too!
I love your videos, they are easy to understand.
May I have video about breast anatomy and Cancer....
Please help me i burn from 9 months
And i do 4session co2 to get rid of scar
But the redness don't get rid of still now
And the dr say its taleangiectaia or erythema
Can you make a video on the cut sections of brain at different levels mentioning all the relevant structures present at each level?
Amazing videos, so helpful! Thanks :D
Like if you’re hear because of Patti Mac
You are amazing!!!!
Why there is no bleeding with burns🤔
He said that in the stasis zone, there is decreased perfusion (lower fluid flow). Presumably, that means that blood is blocked off from flowing to the wound site.
Thank you so much, you make it easier
Awesome video
it's great. thank u so much
I dont know if you're aware but your opening logo drawing is unreadable unless you know in advance what it says or pause the video a good 20 seconds to read
Thanks!
Awesome