Beyond IV Fluids: Plasma's Emerging Role in EMS Burn Treatment

Burns. Every EMS clinician can vividly recall the first time they cared for a patient who suffered a burn injury. Something from the call will stick out in their minds-eye, the scene, the sight of the injury, the smell. There are different types of burns, but thermal burns are the most common. Burn injuries result from exposure to excessive heat (e.g., flame, scalds, contact with hot surfaces, or steam) as defined by the American Burn Association (ABA).^1-2 The numbers are stunning, with 480,000 people in the United States suffering injuries from burns, with 45,000 being hospitalized and upwards of 3,200 dying, each year.¹ The overwhelming majority of the deaths that occur, 75%, happen at the scene or during transport, and most of these deaths are from smoke inhalation.^1,3 Most of these burn patients, 73%, suffered injuries in their homes, with 68% being male, with children under 15 comprising up to 30% of the burn population.¹

Advanced Burn Life Support (ABLS), a course designed by the ABA for clinicians who care for burn patients, is an 8-hour course that is excellent for EMTs and paramedics. It is being offered this year at EMS World EXPO as a pre-conference session at 8 a.m. to 5 p.m., Monday Oct. 20, at the Indianapolis Convention Center. It’s an excellent opportunity to improve your clinical skills, help you to develop some continuing education for your place of employment or write a new burn clinical protocol, and even speak with the best and brightest in burn resuscitation.

Anatomy and Physiology of the Skin

The skin is the largest organ of the human body, accounting for approximately 16% of the total body weight and covering an average surface area of 15 to 20 square feet in adults.^4-6

The skin is composed of three primary layers:

1. The epidermis, the outermost layer of the skin, is roughly 20 cell layers in depth, about the thickness of a sheet of paper. It provides a critical barrier function, preventing water loss and protecting against microbial invasion.
2. The dermis houses capillaries, lymphatic vessels, sudoforus (sweat) glands, sebaceous glands, hair follicles, and sensory receptors. It helps provide thermoregulation.
3. The hypodermis (the subcutaneous tissue) composed of adipose tissue and loose connective tissue. It functions as an energy reservoir, shock absorber, and insulator.^4-6

Working from the outside in, the first function of the skin is barrier protection. It prevents microbial invasion, chemical insult, and mechanical trauma. Next is thermoregulation which is mediated by vasodilation/vasoconstriction and sweat production. The skin is also a sense organ with mechano, thermos and noci-ceptors which detect touch, pressure, temperature, and pain.^5,7

Pathophysiology of Thermal Burns

Severe thermal injury initiates a complex and staggering systemic response that far exceeds the typical physiologic response to trauma. Although this response shares several core features with the systemic effects of blunt or penetrating trauma, it’s often more profound, sustained, and metabolically taxing in burn patients.

The pathophysiology of burns reflects both direct cellular injury from heat and secondary physiological responses, including inflammation, vascular permeability, and systemic shock. It’s this vascular permeability which is at the core of this cascade. This capillary leak syndrome, characterized by the movement of plasma from the intravascular to the interstitial space, is a process known as third spacing. This occurs secondary to widespread endothelial dysfunction, with a central role played by the endothelial glycocalyx.^2,8

There are three factors that influence the initial presentation.^2,8 First is the temperature of the heat source. Next is the duration of the exposure to the heat source. Finally, the thickness of the skin at the site of injury is the final factor.

Burn Depth Classification

1. Superficial (First-Degree), involves only the epidermis. Appears red, dry, and painful. If you have ever had a sunburn, you have had a superficial thickness burn. No blistering or scarring; heals within three to five days.
2. Partial-Thickness (Second-Degree), superficial partial-thickness involves the epidermis and upper dermis; blistering, moist, painful; capillary refill intact. If you have ever had a sunburn, that the next day developed blisters, you have had a superficial thickness burn that converted to a partial-thickness burn. Deep partial-thickness involves deeper dermis, including sweat glands and hair follicles; less pain due to nerve ending damage, slower healing.
3. Full-Thickness (Third-Degree) involves the entire epidermis and dermis. The skin is dry, leathery, and insensate due to nerve destruction. Requires grafting for wound closure.
4. Fourth-Degree extends beyond the skin to involve muscle, fascia, or bone. These are catastrophic injuries often requiring amputation and/or extensive reconstruction.²

It’s important to note that thermal burns can convert over a 24-hour period because of increased metabolic requirements and shock. Superficial burns can convert to partial thickness burns; partial thickness burns can convert to full thickness.²

Cellular and Molecular Pathophysiology

Burn wounds are anatomically and functionally classified into three concentric zones known as Jackson’s Zones of Injury.^5-8

• Coagulation Zone: The area of maximal damage where tissue is necrotic.
• Stasis Zone: Surrounds the coagulation zone; it is hypoperfused and at risk of progression to necrosis due to impaired microcirculation.
• Hyperemia Zone: Peripheral area with increased blood flow and inflammation; typically recovers with supportive care.

Our goal during the initial resuscitation of the burn patient is to prevent or reduce anything that will increase the metabolism of the patient, because as metabolism increases the Zone of Stasis will convert to the Zone of Coagulation. These are influenced by hypovolemia, hypoxia, hypothermia, and pain. Any one of these or in combination with one another will increase metabolism and prove disastrous for our burn patient.

Vascular Response and Capillary Leak

Thermal injury causes capillary endothelial damage, leading to increased vascular permeability within minutes of the burn.^2,6 Plasma proteins and fluid leak into the interstitial space, causing burn edema. The result is hypovolemia, hemoconcentration, and reduced cardiac output, the hallmark of burn shock in large Total Body Surface Area (TBSA) burns (>20%).^2,6

The burn injury will trigger a cytokine storm, further exacerbating shock. In this hypermetabolic state catecholamines, cortisol, and glucagon levels surge, increasing resting energy expenditure fueling the cytokine storm in a vicious cycle that if left unaddressed will result in the death of the patient.

Shock

Shock in a burn patient is unique.^2,6,7 There are two components to their shock: hypovolemic and distributive. Hypovolemic shock is due to massive third spacing and intravascular volume loss. Distributive shock is driven by inflammatory mediator-induced vasodilation, glycocalyx breakdown, and vascular dysregulation as we see fluid shift from the intravascular space into the interstitial space. This unique interplay places burn shock in a category of its own, requiring aggressive fluid resuscitation not only to replace volume but also to counteract the microvascular dysfunction that continues for hours to days after the injury.

Under normal physiological conditions, the glycocalyx functions as a selective barrier by playing a critical role in preserving vascular permeability and ensuring microcirculatory stability. In response to the thermal insult from a burn, a surge of inflammatory mediators rapidly degrade the glycocalyx. This breakdown leads to increased endothelial permeability and the uncontrolled movement of plasma, proteins, and solutes into the interstitial compartment causing third spacing.

Plasma oncotic pressure decreases as plasma proteins escape into the interstitial space, causing progressive intravascular hypovolemia, while interstitial compartments become pathologically fluid-laden, manifesting as burn edema. As third spacing continues unabated, preload to the heart diminishes, reducing stroke volume and cardiac output despite increased systemic vascular resistance (SVR).

Burn Patient Resuscitation

In short, first stop the burning process then complete the primary survey.^2,6 Hypothermia is deadly for the burn patient; once we have stopped the burning process get the burn patient warm. The rule of thumb for EMS clinicians is if it is comfortable for you in the back of the ambulance, it’s too cold for the burn patient. When covering the patients burn wounds you should use clean, dry sheets to reduce contamination and fluid loss. Once the burn wound is covered, wrap the patient in a blanket. Preserving body temperature will reduce metabolism.

EMS often encounters patients in confined or enclosed space fires who have suffered inhalation injuries. Early airway control is essential. If there is suspicion of inhalation injury (e.g., facial burns, carbonaceous sputum, soot around nose and mouth, audible stridor), the EMS clinician should be prepared for early endotracheal intubation. Aggressive airway management is key. This is not the time for a supraglottic airways.

Most burn deaths occur from smoke inhalation due to carbon monoxide and cyanide toxicity. Administer 100% oxygen via non-rebreather mask ASAP. If available, use CO-oximetry to evaluate carboxyhemoglobin levels. A reading of 10% indicates carbon monoxide (CO) poisoning. Respiratory decontamination is critical in these patients. Antidotes for potential cyanide poisoning as the result of being in a fire are critically important. Hydroxocobalamin binds directly to cyanide which forms cyanocobalamin is given IV, typically 5 g over 15 minutes. Sodium thiosulfate provides sulfur to support the conversion of cyanide to thiocyanate, which is then excreted. In cardiac arrest sodium thiosulfate works best after we regain pulses, while hydroxocobalamin may have benefit for patients in cardiac arrest and should be administered immediately. If neither of these are available, high flow oxygen is critical.

EMS is often responsible for initial IV access and fluid resuscitation. Under the current guidelines from the ABA in their ABLS course, initiation IV access with two large-bore IVs.

The Initial Fluid Rate and Adjusted Fluid Rate

In the pre-hospital and early hospital settings, prior to calculating the percent TBSA burned, the guidelines in the ABLS course are based on the patient’s age and are recommended as the initial fluid rate as a starting point in patients with burns >20% TBSA:

• ≤5 years old: 125 ml LR per hour
• 6–12 years old: 250 ml LR per hour
• ≥13 years and older: 500 ml LR per hour

The Parkland formula^2,8,9 is an excellent tool but may be cumbersome for use at the scene. If used in the field, once the patient’s weight (in kg) is determined, you need to calculate the TBSA (based on the percentage of second and third degree burns) in the secondary survey. If you are on a CCT team, use of the Parkland Formula will be useful to determine what we need to infuse based on the fluid infusions patients have already received and patient urine output.

If the TBSA is > 20% the Parkland formula is: 4 mL × patients weight in kg × %TBSA burn. Half is given in the first 8 hours post-injury.

For burn patients, IV access should be avoided when possible through the burn wound itself, unless there are no other viable sites. If you start an IV through a burn wound don’t use tape to secure the catheter, instead use gauze.

Lactated ringers is the fluid of choice for burn patients. It stays in the vascular space longer than normal saline, and it contains the electrolytes that burn patients require due to the massive fluid shifts they are undergoing. For pediatric burn patients D5 lactated ringers is best since children have much higher metabolic needs.

A better alternative to lactated ringers is plasma or freeze dried plasma.¹⁰ A protein-salt solution, plasma acts as a transportation system for all the red blood cells, white blood cells, and the platelets, which are suspended in this liquid. A straw-colored clear liquid that is 90% water, plasma helps in clotting and fighting infection, helping to maintain blood pressure and immunity.10 Most importantly it helps repair the glycocalyx in real time, thus preventing the third spacing and distributive shock that occurs with burns. For this reason, when you provide plasma to a patient you need to administer less plasma compared to lactated ringers to achieve the same response for improving blood pressure.

For regular plasma you still require all the storage logistics required for whole blood, but the cost of a unit of plasma is one tenth the cost of a unit of whole blood. If the ability to manage the logistics of a plasma is overwhelming, consider freeze dried plasma.¹⁰ It has the capability to be stored on the shelf for two years, no refrigeration required. Costs for freeze dried plasma have not been established yet, and while it is FDA approved, there is currently no freeze dried plasma offered in the U.S. marketplace.

One precept to keep in mind, if you are using crystalloids and you have particularly long transports to a burn center, remember to monitor for fluid overload and compartment syndromes, since over-resuscitation can exacerbate edema, especially after glycocalyx breakdown.

Conclusion

The skin is a complex, multifunctional organ with remarkable capacity for regeneration. The skin’s complex anatomy and multifaceted physiological roles underscore its vulnerability to and its critical role in the body’s response to thermal injury. Thermal injury disrupts this barrier, triggering profound local and systemic effects that can be life-threatening. The glycocalyx plays a crucial but often underappreciated role in maintaining microvascular integrity; its loss initiates a cascade of third spacing, hypovolemia, and distributive elements of shock. Effective burn management begins with securing an airway and ensuring oxygenation. Burn shock is not solely a matter of fluid loss, but a systemic disease of the vascular endothelium and its regulatory structures, demanding nuanced, timely, and pathophysiologically informed care from the outset. The use of plasma by EMS providers is the best choice for the initial treatment and fluid resuscitation of the burn patient, followed by ringers lactate.

References

1. American Burn Association 2016 National Burn Repository Report of Data From 2006–2015. Version 12.0. Chicago, IL
2. American Burn Association. (2023). Advanced Burn Life Support (ABLS) provider manual (Rev. ed.). American Burn Association.
3. Centers for Disease Control and Prevention. Injury Prevention and Control: Data and Statistics (WISQARS). 2016. Retrieved from: https://www.cdc.gov/injury/wisqars/fatal.html
4. Drake, R., Vogl, A. W., & Mitchell, A. W. (2009). Gray's anatomy for students E-book. Elsevier Health Sciences.
5. Cohen, B. J., & Hull, K. L. (2020). Memmler's the human body in health and disease. Jones & Bartlett Learning.
6. Chapleau W, Burba A, Pons, PM, Page D. (2011). The Paramedic Updated Edition (1st ed.). McGraw-Hill Education
7. Hall, J. E., & Hall, M. E. (2020). Guyton and Hall Textbook of Medical Physiology E-Book: Guyton and Hall Textbook of Medical Physiology E-Book. Elsevier Health Sciences.
8. PHTLS course manual National Association of Emergency Medical Technicians (US). 10th edition. Burlington, Massachusetts : Jones & Bartlett Learning, [2024] 
9. Mehta M, Tudor GJ. Parkland Formula. [Updated 2023 Jun 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537190/
10. Freeze-Dried Plasma in Emergency Medical Services EMSWorld June 2024 https://www.hmpgloballearningnetwork.com/site/emsworld/feature-story/freeze-dried-plasma-emergency-medical-services