This is unfinished, I will be updating it and writing more in increments.
Background:
Burns are some of the most devastating injuries that one can encounter. In burns, the line between medical and trauma is blurred, and there are a whole series of considerations that a provider needs to take into account, whether they are ALS, ILS, or BLS. Let’s for a moment stop thinking of things in the ALS, ILS, BLS sense, and instead look at burn management from a team approach. If you see something that is not within your scope of practice as an EMT-B, then you know that you can’t do that, you don’t need BLS/ALS lines to tell you that. By looking at this as a team effort, you will be better prepared to not only do your part in the initial management and transport, but will also get an idea why it is you are doing what you are doing, what is going to happen when the patient gets to us in the burn unit or ER (depending on severity), and will have a better understanding of burn management and shock states as a whole as well.
The Types of burns:
Whenever we think of burns fire enters our mind. However, this isn’t always the case. Burns can be Thermal, Mechanical, Chemical, Electrical, and from radiation (gamma, xray, uv). Examples of thermal burns can be house fires, explosions, and any process involving extreme heat or cold applied to the body. Mechanical burns can be from friction or abrasion, although you don’t usually hear about these in EMS all that much. Chemical burns are from acidic or alkali substances (examples: Sodium Hydroxide, Dry Lime, Hydrochloric Acid, Sulfuric Acid). Electrical burns are self-explanatory, and are the most fatal of burns. Radiation burns are particularly horrible in that one must not only worry about the burn, but a whole host of effects that can come later such as radiation poisoning, cancer, etc. (Examples can include: Sun burns (1st and 2nd degree) and gamma radiation.
Burn Classifications:
Burns can be classified based on severity and feature into 4 classifications known as degrees.
1st degree Partial thickness, painful, No Blisters, Pink and red and extend only to the epidermal strata.
2nd degree – Deep partial thickness, painful with blister, (+) blanching and refill, extends to both the epidermis and the dermis.
3rd degree - Full Thickness , pain will be discussed below, leathery, extends to fascia and muscle.
* (see note)
4th degree – Bones and visceral organs are affected.
*While many EMS providers will tell you that individuals with 3rd degree burns feel no pain because the nerve endings are burnt, this is largely a myth. Sure there are some patients that we come across who might have so much damage that they no longer can feel. However, this isn’t always the case, because there are factors such as inflammation, toxins in the blood stream, and a whole host of other issues that can cause pain. [1, 2]
Major Complications of Burn Patients:
Airway compromise, Fluid Loss (Shock, Electrolytic imbalance, etc), Hypothermia, and Infection.
Pathophysiology of Burn Shock:
Whenever the average person sees a burn, they are mainly focusing only on the damage they can observe. They do not think about the pathophysiology of the burn state and the subsequent alterations of physiology that occur in the molecular and cellular levels, resulting in a whole cascade of secondary injuries, just as we see happen in brain injury, where the secondary injury actually becomes more damaging than the initial insult in most cases.
Those of you here at EMTLife that have taken PHTLS remember the analogy of the trauma square where you imagine your patient standing within a square that represents the limits of their health at any particular time. Whenever that square is large, such as 100’ x 100’, it takes a lot more to knock us out of that square than it does if it were 10” x 10”. Imagine, if you will a burn injury causing that square to get smaller. Then on top of that, shock and cellular signaling causing that square to get even smaller until the point where the smallest thing can knock that person out of the square. This is most readily observed in ICU patients suffering from failure of multiple systems and multiple trauma etiologies, in which something as simple as about of flu can spell disaster, whereas before the trauma, they might’ve shaken it off in several days. Whenever a significant enough amount of damage has occurred from a burn, there is set into state, a whole cascade of events at the cellular level which lead to further disruption of an already detrimented homeostasis. The text, Total burn care goes into great detail with regard to burn shock, and the overall pathophysiology of burn edema, explaining the various forces that come into play in the acute burn patient. Most of these modicums can be applied to shock in general (Remember what I said in the first part about the lines of trauma and medical being blurred?).
The following is a direct excerpt from Total Burn Care about the overall pathophysiological mechanisms of burn shock and edema.
“Cutaneous thermal injury greater than one-third of the total body surface area (TBSA) invariably results in the severe and unique derangements of cardiovascular function called burn shock. Shock is an abnormal physiologic state in which tissue perfusion is insuffi cient to maintain adequate delivery ofoxygen and nutrients and removal of cellular waste products. Before the 19th century, investigators demonstrated that, after a burn, fl uid is lost from the blood and blood becomes thicker; and in 1897, saline infusions for severe burns were fi rst advocated. However, a more complete understanding of burn pathophysiology was not reached until the work of Frank Underhill. He demonstrated that unresuscitated burn shock correlates with increased hematocrit values in burned patients, which are secondary to fl uid and electrolyte loss after burn injury. Increased hematocrit values occurring shortly after severe burn were interpreted as a plasma volume defi cit. Cope and Moore showed that the hypovolemia of burn injury resulted from fl uid and protein translocation into both burned and non-burned tissues. Over the last 80 years an extensive record of both animal and clinical studies has established the importance of fluid resuscitation for burn shock. Investigations have focused on correcting the rapid and massive fl uid sequestration in the burn wound and the resultant hypovolemia. The peer-reviewed literature contains a large experimental and clinical database on the circulatory and microcirculatory alterations associated with burn shock and edema generation in both the burn wound and non-burned tissues. During the last 40 years, research hasfocused on identifying and defi ning the release mechanisms and effects of the many inflammatory mediators produced after burn injury. [What? Did you think that inflammatory mediators were only going to be present in IgE mediated type I hypersensitivities, aka Anaphylaxis? ] It is now recognized that burn shock is a complex process of cardiovascular dysfunction that is not easily or fully repaired by fluid resuscitation. Severe burn injury results in significant hypovolemic shock and substantial tissue trauma, both of which cause the formation and release of many local and systemic mediators. Burn shock results from the interplay of hypovolemia and multiple mediators of inflammation with effects on both the microcirculation as well as the function of the heart, large vessels, and lungs. Subsequently, burn shock continues as a signifi cant pathophysiologic state, even if hypovolemia is corrected. Increases in pulmonary and systemic vascular resistance (SVR) and myocardial depression occur despite adequate preload and volume support. Such cardiovascular dysfunctions can further exacerbate the whole body inflammatory response into a vicious cycle of accelerating organ dysfunction. Hemorrhagic hypovolemia with
severe mechanical trauma can provoke a similar form of shock.[3] ”
Mechanisms of Burn Edema:
Since I have probably already scared most of you with the above information on burn shock, I am going to spare you with regard to burn edema [and spare myself the typing], the landis starling equation, microcirculatory fluid exchange, and capillary filtration coefficients (If you want to read about this in great detail, see Total Burn Care[3]). Instead, I will move on to fluid rescuscitation and early management.
Fluid Resuscitation and early management of burns:
In my initial post on this thread, I said I was going to explain muir, parkland, and the other fluid rescuscitation formulas in this post. However, I have decided to only show Parkland, as I really don’t want to confuse some members any more than necessary and it is the most common formula for fluid rescuscitation in burns that I see used in the field.
Research conducted in the 1940s, cited hypovolemic or shock-induced renal failure as the leading cause of death after burn injury. Given the advances we have made in burn care, mortality due to volume loss in burns has decreased considerably, resulting in fewer deaths within the first 24-48 hours post-burn.
According to Total Burn Care, approximately 50% of all deaths in acute burns result in the first 10 days following burn injury from a multitude of various causes, and one of the most significant is INADEQUATE FLUID RESCUSCITATION THERAPY [3]. This is where you come in.
Crystalloids vs Colloids & other fluids
Crystalloid rescuscitation (particularly lactated Ringer’s solution with a sodium concentration of 130 mEq/L) is the most popular rescuscitation fluid being utilized in the field and in the literature, not to mention, the most feasible as it has not been shown to have any better outcomes in acute burns than the other solutions, specifically colloids, which are more expensive. However, there is a scientific basis for the choice of crystalloids over colloids as the most common reason for not using colloids is that even large proteins leak from the capillary following thermal injury, even though capillaries in nonburned tissues do continue to sieve proteins, maintaining relatively normal protein permeability characteristics [Now do you see the bigger picture of why we use TBSA?]
The Parkland Formula:
While there are many formulas for the estimation of fluid needs in the adult burn patient (Evans, Brooke, Slater, Parkland, modified Parkland, Brooke, Monafo, Warden, and Demling), we are only going to talk about Parkland. Again, if you want the others, Total Burn Care is the way to go. (TBSA is calculated by the Browd & Lunder, aka Rule of 9’s chart)
The Parkland formula calls for fluid replacement with Lactated Ringer’s at 4 cc/kg/% TBSA. Therefore,
in a patient weighing 100 lb (45 kg), with 30% full thickness burns, we would get out our calculator, and multiply
This is the volume of LR the patient needs over the next 24 hours. (5.4 L) HOLD, WE ARE NOT DONE.
The Parkland formula calls for us to give half of that in the first 8 hours, so we divide 5.4 L by 2, to get a total of 2.7 L that we have to give over the FIRST 8 HOURS. Now, obviously, we are not going to be with the patient for 8 hours, but it is critical that we start this process in the field, and keep up with our calculations, although for our purposes, we will just be running it wide open.
However, don’t just think, Oh I’ll run LR wide open to the hospital with no regard for what amounts were given or doing any calculations. YOU ARE THE EMS 2.0 Provider, YOU ARE BETER THAN THAT.
So, having used the Parkland formula to estimate the fluid requirements for this patient over the next 24 hours, I know that the patient needs:
5.4 Liters over the next 24 hours, with 2.7 of those liters administered over the first 8 hours.
All information below will be specifically focused on the acute full-thickness thermal burn patient with > 20% TBSA as per the Browd & Lunder calculations chart (Rule of 9s). (I might do a write up on electrical burns, myoglobinurea, output considerations, etc at some point, but I have too much on my plate right now.)
Emergency Management of the Acute Burn Patient:
The emergency management of burns (depending on who you ask) can be divided into 3 phases The first phase being the prehospital phase, the second phase being the in-hospital phase, and the third being rehabilitation (There can be more phases depending on if the patient is sent to an initial care facility first rather than a specialty center, but for our purposes, we will assume you are transporting the patient by whatever means, be it air or surface to a specialty center with a burn unit and trauma surgeons available).
Phase I: Pre-hospital Assessment, Interventions, & Transport for severe burns
• Remove patient from the source of the injury (i.e. stove, etc)
• ensure that you don’t get burnt by items on them such as clothing, jewelry especially, and other items.
• AIRWAY MANAGEMENT (Just because you have an airway now, doesn’t mean you will in 5 minutes, burn patients are notorious for difficult intubations due to swelling and inhalation from smoke injury, actual burn damage, edema, etc. )
• Pain Management (Fentanyl & Versed combination works well , refer to your protocols. As others have said, you don’t have enough narcotics on your unit to even begin to comfort this patient)
• Fluid Rescuscitation (See Parkland Above)
• Minimize heat loss (This is a BIG CONCERN)
• Protect against infection, the skin is your first line of defense against micro-organisms.
Phase II: In-hospital assessment, stabilization, and stepdown
COMING SHORTLY, I AM TIRED OF TYPING RIGHT NOW.
Note:
This is largely unfinished because I am about to have to move on to another project momentarily. However, I decided to post this anyways for the benefit of those reading. Not to mention, given all the content that there is to absorb, it is probably best that I deliver this in increments.
References
1. GJ., S., Mechanisms of pain following thermal injury [doctoral dissertation]. San Francisco: University of California, 2005.
2. Malenfant A, e.a., Tactile, thermal, and pain sensibility in burned patients with and without chronic pain and paresthesia problems. . Pain, 1998. 77(3): p. 241-51.
3. Herndon, D.N., Total Burn Care. 3rd ed. 2007.
G'night.