Burns and Frostbite

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Chapter 66 Burns and Frostbite

Shawn P. Fagan, MD , Jeremy Goverman, MD, FACS

1 What determines the degree of tissue destruction after a thermal injury?

The degree of tissue injury is directly related to the temperature and duration of contact with the heat source. Children are particularly susceptible to thermal injury because of the thinner dermal layer. At 156° F (68.9° C), it requires less than 1 second to have a full-thickness thermal injury. As temperature of the heat source decreases, the time necessary for a clinical significant thermal injury is prolonged. This is evident by the 10 seconds required to produce a full-thickness thermal injury at 130° F (54.4° C). For this reason, the American Burn Association recommends setting the thermostat of a household water heater to 120° F (48.9° C) to prevent clinically significant thermal injuries in the household.

2 What determines the physiologic impact of a thermal injury on the human body?

The physiologic impact of the thermal injury is directly related to the extent of second- and third-degree thermal injury. This is why most burn fluid resuscitative formulas are based on the extent of second- and third-degree thermal injury. Of interest, the depth of thermal injury does not affect the physiologic consequences but may affect the wound management techniques required for effective wound healing. Most second-degree thermal injuries can be managed until healing with topical antimicrobials, whereas third-degree thermal injuries, dependent on size, generally require excision of nonviable tissue and closure with skin grafts.

3 How are thermal injuries classified?

Thermal injuries are classified by the depth of injury to the underlying skin’s structure. The skin is composed of an outer epidermis and inner dermis. The regenerative capacity of the skin, the stem cells, reside in the dermis and hair follicles. Thus the ability to heal a thermal injury is directly related to the degree of damage of the dermis and the presence of hair follicles at the site of thermal injury. Burn wounds are classified from first through fourth degree:

First degree: Thermal injury only affects the epidermis—sunburn.

Second degree: Thermal injury affects the epidermis and superficial dermis. The injury results in blistering and mild to moderate edema to the affected area. The wound is painful because of damaged nerves but should heal with simple topical antimicrobials in approximately 14 to 21 days.

Third degree: The thermal injury affects both the epidermis and dermis. A true third-degree thermal injury should be without pain because of the complete destruction of the sensory nerves. However, few thermal injuries are composed of only one class of injury. The majority of deep thermal injuries are a mixture of depths, thus making lack of sensation a poor marker to classify depth of injury. A more specific marker of a third-degree thermal injury is the white and leathery appearance. Healing of a third-degree thermal injury will require excision and grafting.

Fourth degree: Thermal injuries that affect structure deep to the skin–fat, fascia, muscle, and/or bone. Treatment and presentation are similar to those of third-degree thermal injuries.

4 What are the initial steps in the management of an individual who had a thermal injury?

The management of a thermally injured patient should proceed in a similar manner as the clinician would evaluate any trauma patient with the understanding of a few burn-specific nuances. The first step is to stop the burning process. This may be as simple as removing smoldering clothing or copious irrigation of chemical or radiation injuries. As the burning process is being addressed, the patient should undergo a primary survey consisting of airway, breathing, circulation, disability, and exposure.

Airways can be challenging in a burn patient. Therefore clinicians must be aware of potential inhalation injuries that may affect the supraglottic airway (airway obstruction) and/or infraglottic airway (chemical pneumonitis). Children are particularly susceptible to supraglottic obstruction because of progressive edema and relatively narrow upper airways. Individuals demonstrating airway compromise or having large thermal injuries should have an endotracheal tube placed to avoid airway issues. The important point to remember is that maximal edema occurs approximately 24 hours after thermal injury.

Appropriate and rapid resuscitation is critically important to avoid future morbidity and mortality after a thermal injury. Studies have demonstrated that the timing of initial resuscitation is directly related to mortality. Delay in resuscitation must be avoided, but the rate of fluids administered must be appropriate. Recently, studies have demonstrated increased morbidity and mortality associated with overresuscitation. Thus calculating the estimated fluid requirement for a thermally injured patient should be performed early in the evaluation process and titrated on the basis of urine output and normalization of resuscitative laboratory results.

It is critically important not to be distracted by the extent or depth of thermal injury during the initial evaluation. All thermally injured patients should have a comprehensive trauma evaluation to avoid missed injuries. It is not uncommon for thermal injuries to be associated with significant trauma.

5 What is burn shock?

Classically, burn shock was simply defined by a state of hypovolemia. However, it is now realized that burn shock is a complex process not only affecting preload but also influencing cardiac output and systemic vascular resistance. During the first 8 hours after thermal injury a substantial increase in capillary permeability occurs resulting in a state of intravascular volume depletion. This relative intravascular volume depletion is coupled with a decrease in cardiac output and increased systemic vascular resistance. The degree of impaired cardiac output and increased vascular tone cannot be completely attributed to the state of post–burn injury hypovolemia. Therefore a goal-directed approach to the resuscitation of a thermally injured patient is warranted. The specific impairment (preload, cardiac output, systemic vascular resistance) should be identified and appropriate therapeutic measures initiated to improve the specific problem. Simply stated, burn shock is not simply a state of hypovolemia.

6 How do you determine the initial fluid requirements of a thermally injured patient?

Although burn shock can influence preload, cardiac output, and systemic vascular resistance, burn patients do differ from other intensive care unit populations with the substantial intravascular fluid depletion that occurs over the first 24 hours. This is directly related to increased capillary permeability. Therefore thermally injured patients require a considerable amount of volume administration in the first 24 hours.

The Parkland Burn Center published the most widely used burn resuscitation formula. The formula states that the total amount of lactated Ringer’s solution necessary during the first 24 hours is directly related to the size of thermal injury (second and third degree) and the preburn weight (kilograms) of the patient. The Parkland formula is 2 to 4 mL/kg body weight/Total body surface area (TBSA) thermal injury. Half of the volume is administered during the first 8 hours from time of injury with the remaining amount administered over the following 16 hours. The formula is an estimate of the fluids necessary during the initial 24 hours; therefore the rate of fluid administration must be adjusted on the basis of the monitoring of resuscitative parameters with the primary goal of avoiding overresuscitation.

Some centers modify the resuscitative formula for children because of the larger surface area per kilogram body weight compared with an adult. The Galveston resuscitation formula is based on TBSA affected by thermal injury but also includes a maintenance infusion rate. The Galveston formula is 5000 mL lactated Ringer’s/TBSA thermal injury +1200 mL/TBSA. In addition, infants and young children should have a continuous source of glucose administered via the maintenance fluids. Similar to that for adults, the resuscitative formula is an estimate of the fluids necessary during the first 24 hours; adjustment must be made on the basis of response to the initial resuscitation.

7 Should a primary survey be repeated during the first 24 hours after thermal injury?

The primary survey must be repeated frequently during the first 24 hours to avoid complications associated with progressive edema after thermal injury. Airway and breathing may be initially stabilized with early endotracheal intubation but can progressively deteriorate during the first 24 hours because of edema. This is particularly true for individuals who have circumferential thermal injuries to the chest. Progressive edema of the underlying soft tissues with restriction of chest expansion by eschar can limit tidal volumes and thus influence minute ventilation. Constant monitoring of airway pressures and tidal volumes are necessary to identify and treat this potential airway emergency. Should constriction of the chest cavity become physiologically significant, bilateral anterior axillary line escharotomies coupled with an escharotomy across the costal margin to join the axillary line escharotomies should be performed. The goal is to allow expansion of the chest cavity and to separate the chest cavity from the abdominal cavity.

Similar to the chest, extremities must also be monitored for compromise due to progressive edema limited by circumferential eschar. Initially, all thermally injured extremities should be elevated to 45 degrees and monitored on an hourly basis. All constricting jewelry should be removed immediately. If possible, patients should be encouraged to move the affected extremities. Should vascular compromise be identified, by increasing pain on passive movement or diminished pulses, lateral escharotomies should be performed with documentation of return of perfusion. If perfusion is not reestablished with a lateral escharotomy, medial escharotomies should be performed initially followed by fasciotomies if necessary to establish effective perfusion.

8 How do you determine the fluid needs of a thermally injured patient after the first 24 hours?

Although everyone is exposed to the Parkland Burn Resuscitation Formula at sometime during his or her career, the fluid needs after the initial 24 hours are not as well known or published. The exact fluid requirement is individualized on the basis of the TBSA affected by thermal injury, the body’s physiologic response to the thermal injury, and ambient environment surrounding the patient.

The goal is always to administer the appropriate amount of fluid and to avoid a hypervolemic state and/or a generalized edematous state. Proper fluid administration can be achieved by adjusting the infusion rate frequently on the basis of the urine output. If the urine output is greater than 0.5 mL/kg per hour, the infusion rate can be decreased by one third and resuscitative laboratories and urine output monitored. After 3 hours of monitoring, fluid rates should again be adjusted on the basis of the urine output and trends of resuscitative parameters. To aid in estimating this fluid requirement, the Galveston burn group developed a formula to calculate this fluid requirement. The formula is 3750 mL/TBSA affected by thermal injury +1200 mL/TBSA.

9 Who should be referred to a verified burn center?

The American Burn Association recommends that individuals with the following conditions be referred to a verified burn center for evaluation and treatment:

10 How should potential ocular involvement be evaluated after thermal injury?

Potential ocular involvement requires immediate attention during the first 24 hours after thermal injury. Appropriate referral to an ophthalmologist is critical not only for initial assessment of direct ocular injury but to monitor ocular pressures during the time of resuscitation. Most direct ocular injuries can be treated conservatively with ocular ointments or the application of amniotic membranes. Increases in ocular pressures due directly to the thermal injury or resulting from a generalized edematous state require aggressive monitoring and treatment. Initially, conservative therapy should be initiated with head-of-bed elevation to 30 degrees. However, high initial or progressively increasing ocular pressures should be aggressively treated with a lateral canthotomy. The goal is to prevent ocular compartment syndrome.

11 What is burn-induced hypermetabolism?

After a major thermal injury (TBSA >30%), several metabolic derangements have been identified and include the following:

A relative decrease in insulin secretory capacity

Peripheral insulin resistance

Exaggerated protein catabolism

A significantly elevated resting energy expenditure

The catecholamine surge after thermal injury results in a reset of the hypothalamus thermostat by 2° C and alterations in the neuroendocrine axis. Combined, this results in an elevated resting energy expenditure that can be approximately 60% to 80% greater than the normal basal metabolic rate. Therefore appropriate nutrition must be instituted immediately supplying approximately 30 to 35 kcal/kg body weights with 20% to 25% of the total caloric requirement being composed of protein. In addition, several techniques are routinely used to reduce the impact of the postburn generalized hypermetabolic state:

Maintenance of appropriate ambient temperature surrounding the burn patient

Early excision and grafting of all third-degree thermal injuries

Administration of anabolic agents, isolated or in combination (oxandrolone, propranolol, insulin)

Early range of motion and exercise

12 What are the four main advances in burn care that have dramatically reduced mortality over the last 50 years?

Appropriate resuscitation: Restoration of end-organ perfusion while avoiding overresuscitation.

Control of infection: Application of topical antimicrobial agents to prevent wound infections and using systemic antimicrobials only after documentation of invasive wound infection (cellulitis), not colonization, and presence of systemic infection (bacteremia).

Modulation of hypermetabolism: Early and appropriate nutrition, anabolic agents, early occupational and physical therapy.

Early excision and grafting: Protein catabolism progressively worsens with the presence of third-degree thermal injury. The goal is to remove all nonviable tissue within 96 hours to lessen the degree of catabolism.

13 What is the treatment of hydrofluoric acid exposure?

The treatment begins the same for any potential chemical burn. First stop the burning process, remove all saturated items, irrigate the wound bed, and arrange for burn center transfer. Next determine the exact agent involved, concentration of agent, duration of contact, and mechanism of action of the specific agent. Never attempt to neutralize any chemical injury.

For hydrofluoric acid exposure it is critically important to determine the concentration of the agent. Hydrofluoric acid is a weak acid, but the fluoride can prove to be very toxic. Fluoride has a high affinity for free calcium and can potentially create a life-threatening hypocalcemia. Dilute hydrofluoric acid exposure (<10%) can be managed conservatively. The patient typically has a delayed presentation of severe pain to the affected region. It can be safely treated with topical calcium gluconate gel. Unknown or high-concentration exposure to hydrofluoric acid requires aggressive and specialized wound management coupled with serial serum calcium measurements to avoid severe hypocalcemia. Burn center transfer should not be delayed.

14 How are electrical injuries treated?

Electrical injuries can range from a minor “shock” without any consequences to significant morbidity due to complete conduction of the electrical current. The key concept to remember when evaluating an electrical injury is that the superficial cutaneous injuries may underestimate the total extent of injury specifically to the deeper tissues. The tissue damage caused by an electrical source is directly dependent on the strength of the current and duration of contact. This is summarized by the Joule effect, which states that the heat generated (tissue damage) is directly dependent on the current (I) squared times the resistance (tissue type) (R) times the duration of contact (T) (J = I² × R × T). Surprisingly, the epidermis has one of the highest resistances in the human body and thus, when overcome, the affected body part acts as a volume conductor. When this occurs, the current can pass along the very dense and highly resistant skeletal bone resulting in significant muscular damage.

All electrical burn patients should undergo a standard trauma and burn primary and secondary evaluation with particular attention to a few specific items:

First, all patients must be evaluated for potential cardiac dysrhythmias; however, if absent, the most recent data would suggest no clinical need for continued cardiac monitoring.

Second, all patients should be suspected of having deep tissue damage, particularly when voltages are greater than 600 V.

Finally, all patients should have a baseline eye examination to rule out cataracts because of the potential for cataract formation after any significant electrical injury.

15 How are frostbite injuries treated?

Until recently, frostbite injuries were treated with rapid, moist rewarming followed by conservative management. This included allowing damaged digits and extremities to autoamputate to preserve as much length as possible after the cold injury.

Within the last few years, the concept of frostbite injuries has significantly changed from one of local tissue damage to one of local tissue damage combined with vascular occlusion. Several groups have demonstrated significant reduction in the need for amputation when rapid tissue rewarming is coupled with urgent angiography and catheter-directed fibrinolysis. Currently, all patients presenting within 24 hours from time of injury with second- and third-degree frostbite injuries should have the affected body part rapidly rewarmed and, if an extremity, urgent angiography for evaluation of potential fibrinolytic therapy.

16 What are the known and common complications of topical antimicrobials?

Topical antimicrobial therapy is the mainstay of the treatment for small and large thermal injuries. Although most antimicrobials have a broad range of activity against gram-positive and gram-negative organisms (silver sulfadiazine [Silvadene], silver nitrate, mafenide [Sulfamylon]), some have a narrow spectrum of activity but work well on minor thermal injuries (bacitracin, mupirocin [Bactroban]). As with any pharmacologic agent, a physician must know the indications and potential complications of the agent being prescribed. Although most topical antimicrobials are well tolerated, several have known complications associated with them. See Table 66-1.

Table 66-1 Topical antimicrobial therapy

Key Points Burns and frostbite

1. Thermal injuries are classified by the extent of damage to the skin’s underlying structure; the physiologic impact is dependent on the extent of second- and third-degree injury.

2. All patients who have a thermal injury should have a complete primary and secondary survey performed with particular attention to airway (potential obstruction) and circulation (potential compartment syndrome).

3. Burn shock is not simply a state of hypovolemia; appropriate resuscitation is mandatory to avoid morbidity and mortality.

4. Burn-induced hypermetabolism is a significant metabolic disturbance following a major thermal injury. Proper nutrition coupled with early excision, grafting, and exercise is the best treatment.

5. Hypocalcemia can develop after exposure to concentrated hydrofluoric acid.

6. Frostbite injuries should be treated with rapid rewarming and potential catheter-directed thrombolysis.

1 American Burn Association. Advanced burn life support providers manual. Chicago: American Burn Association; 2005.

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3 Bruen K.J., Ballard J.R., Morris S.E., et al. Reduction of the incidence of amputation in frostbite injury with thrombolytic therapy. Arch Surg. 2007;142:546–551.

4 Greenhalgh D.G. Topical antimicrobial agents for burn wounds. Clin Plast Surg. 2009;36:597–606.

5 Hart D.W., Wolf S.E., Chinkes D.L., et al. Effects of early excision and aggressive enteral feeding on hypermetabolism, catabolism, and sepsis after severe burn. J Trauma. 2003;54:755–761.

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8 Kirkpatrick J.J., Enion D.S., Burd D.A. Hydrofluoric acid burns: a review. Burns. 1995;21:483–493.

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10 Krammer G.C., Lund T., Beckum O.L. Pathophysiology of burn shock and burn edema. In: Herndon D.N., ed. Total Burn Care. 3rd ed. Philadelphia: Saunders; 2007:93–106.

11 Pham T.N., Gibran N.S., Heimbach D.M. Evaluation of the burn wound: management decisions. In: Herndon D.N., ed. Total Burn Care. 3rd ed. Philadelphia: Saunders; 2007:119–126.

12 Rosen C.L., Adler J.N., Rabban J.T., et al. Early predictors of myoglobinuria and acute renal failure following electrical injury. J Emerg Med. 1999;17:783–789.

13 Sheridan R.L. Comprehensive treatment of burns. Curr Probl Surg. 2001;38:657–756.

14 Sheridan R.L., Ryan C.M., Quinby W.C.Jr. et al: Emergency management of major hydrofluoric acid exposures. Burns. 1995;21:62–64.

15 Sullivan S.R., Ahmadi A.J., Singh C.N., et al. Elevated orbital pressure: another untoward effect of massive resuscitation after burn injury. J Trauma. 2006;60:72–76.

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