Algorithm 12-1. Protocol for frostbite injury.

PHYSIOLOGY OF BURNS

Burn Shock

Most patients with large burn or inhalation injuries will meet criteria for systemic inflammatory

response syndrome (SIRS) (body temperature less than 36°C [96.8°F] or greater than 38°C [100.4°F],

heart rate greater than 90 beats per minute, tachypnea greater than 20 breaths per minute, arterial

partial pressure of carbon dioxide less than 4.3 kPa [32 mm Hg], blood leukocyte count less than 4,000

cells/mm3, or greater than 12,000 cells/mm3); or the presence of greater than 10% immature

neutrophils (band forms). SIRS with infection is defined as sepsis and sepsis in addition to hypoperfusion

is defined as “septic shock.” Burn shock does not equate to septic shock in the acute setting as true

sepsis from a burn injury with subsequent infection usually does not occur until after the first 48 to 72

hours.

Burn shock is unique in the degree of vascular permeability coupled with increased hydrostatic

pressure.26 This increased permeability is thought to result from the release of histamine from mast cells

in burned skin following burn injury.27 Histamine interferes with the venous tight junctions and thereby

allows efflux of fluid and proteins causing intravascular hypovolemia despite total volume

hypervolemia.

Platelet activation products such as eicosanoids and serotonin also act to increase pulmonary vascular

resistance and amplification of the vasoconstrictive effects of norepinephrine and angiotensin II.28 In

addition to the increased vascular leak, platelet-activating factor and clotting factor dysregulation

creates a hypercoagulable state with bleeding that resembles disseminated intravascular coagulation.

This coagulation disorder is further amplified if patients become hypothermic during their

resuscitation.29 Thus, patient temperature monitoring and maintenance is crucial during resuscitation.

Arachidonic acid metabolism products such as eicosanoids also play a role in burn edema. Eicosanoids

increase prostaglandins such as PGE2 and prostacyclin which cause arterial dilation and increased blood

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flow and hydrostatic pressure in regions of injury resulting in increased edema.

Changes in cardiac output are also seen acutely in burn patients as these patients often have an

increase in heart rate, and systemic vascular resistance but hypovolemia. Though not defined as

“cardiogenic shock,” cardiac function is altered due to inflammatory mediators.30–33 With appropriate

burn resuscitation, cardiac output should return to normal levels within 24 to 72 hours.

Metabolic Response to Burn Injury

Hypermetabolism is a physiologic response unique to burn injury. Hypermetabolism is characterized by

increased body temperature, glycolysis, gluconeogenesis, proteolysis, lipolysis, and prolonged substrate

cycling.34,35 The degree of the hypermetabolic response is proportional to the size of burn injury and

appears to plateau at 70% TBSA. Overall the basal level of glucose is elevated despite a high insulin

state which can complicate outcomes and exacerbate muscle catabolism.

Lipolysis also occurs at a rate that is higher than normal due to abnormal substrate cycling. This

results in hepatic accumulation of triglycerides causing steatosis. Recent work to combat peripheral

lipolysis has had some success using propranolol.36

Proteolysis is also increased in burn patients compared to nonburn patients. This is due to a

combination of increased muscle breakdown and increased plasma protein production by the liver.

Wound healing requires an increase in protein synthesis leading to the recommendation of enteral

nutrition with elevated protein levels.

There are three ways to influence hypermetabolism: nutrition, medication, and surgery. Current

protocols preferentially recommend continuous enteral nutrition with a high-carbohydrate diet

consisting of 82% carbohydrate, 3% fat, and 15% protein. This diet is thought to stimulate protein

synthesis, increase endogenous insulin production, and improve overall lean body mass when compared

to standard formulas.35

Catecholamines are significantly elevated following a burn injury and are thought to play a role in the

hypermetabolic response. This elevation is one reason why propranolol administration is thought to be

helpful. Interestingly, growth hormone levels have been shown to be decreased in burn shock leading

clinicians to supplement patients with the anabolic steroid oxandrolone in large burn injuries. Positive

results to avoid or reduce the loss of muscle mass with oxandrolone have made its use standard in most

burn units for large TBSA burn patients.37–44 With regard to thyroid hormone, total thyronine and

thyroxin (T3 and T4) are reduced whereas reverse T3 is elevated. Burn injuries also cause alterations in

diurnal glucocorticoid levels leading to persistent hypercortisolemia.

Surgery represents the last way to combat hypermetabolism as early debridement and grafting is the

mainstay to mitigate the hypermetabolic syndrome.

Immunologic Response to Burn Injury

The immune system in burn patients demonstrates significant dysregulation that may explain increased

risk of infection. Serum levels of IgA, IgG, and IgM are decreased indicating decreased B-cell function.

T-cell function or cell-mediated immunity is also impaired which is why prolonged homograft and

xenograft take is seen. Interleukin 2 (IL-2) production is also decreased whereas IL-10 is increased.

Similar to other types of nonthermal trauma, burn patients also have elevated tumor necrosis factor

alpha and IL-6. Polymorphonuclear neutrophils have impaired chemotaxis as well as decreased oxygen

consumption and impaired bactericidal capabilities.

EMERGENCY CARE

Initial care in the field and emergency room is similar to that of any trauma patient. The airway should

be stabilized, IV access should be obtained, concomitant life-threatening injuries should be excluded,

and escharotomies should be performed if there are any circumferential areas of full-thickness injury.

Escharotomies should be placed on the lateral aspects of the extremities avoiding the sites of potential

nerve and large vessel injury (Fig. 12-1). Escharotomies should be extended across the chest if there is

full-thickness injuries and if difficult ventilation arises. Abdominal escharotomies can also help with

ventilation.

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Figure 12-1. Incision lines for escharotomies. In general incisions should be kept on the lateral aspect of extremities to avoid

damage to neurovascular structures. (From Holzman RS, Mancuso TJ, Polaner DM, eds. A Practical Approach to Pediatric Anesthesia,

2e. Philadelphia, PA: Wolters Kluwer; 2016.)

Table 12-1 Burn Center Referral Criteria45

Guidelines from the American College of Surgeons Advanced Trauma Life Support and the ABA

Advanced Burn Life Support programs have standardized the care of trauma patients and have improved

overall patient outcomes. A complete history and physical should be performed with specific focus

placed on the cause and timing of the injury, risk of smoke inhalation injury, concomitant injuries, and

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treatments including IV fluids received prior to patient arrival. The primary goal is to stabilize the

patient, ensure standard injury assessment, and transfer to a burn center as necessary. The ABA has

published criteria to follow regarding when to transfer a patient to a verified burn center (Table 12-1).

Airway Assessment

Primary survey assessment should begin with evaluation of the airway. Inhalation injuries occur in

approximately 10% of all burn patients, but are present in 70% of those who eventually die of their

burn injury.46 Thus, it is important to specifically note such findings as soon as the patient presents. Risk

for inhalation injury can be first assessed by the history. In general, patients burned outside (not in an

enclosed space) very rarely suffer inhalational injuries. If, however, the patient was in a burning home

or a burning building, one’s suspicions should be raised. Close physical examination should note facial

burns, changes in voice, shortness of breath, singed nasal vibrissae, carbonaceous sputum, and intraoral

swelling. If these findings are present and the patient appears to be in distress, oral intubation should be

performed immediately by an experienced airway physician. In addition to a laryngoscope, the trauma

team should have a video laryngoscope available and a surgeon present in case a surgical airway is

required. If the patient is not in extremis and the level of inhalation injury is unknown, nasoendoscopy

or bronchoscopy should be performed to directly visualize the airway and vocal cords. If significant

swelling exists and the patient is expected to receive large volume IV fluid resuscitation, the airway

should be immediately secured. If a patient is transferred with an endotracheal tube that the accepting

physician feels is no longer needed, a spontaneous breathing trial should be performed followed by

direct laryngoscopy to assess for cord swelling and assessment for a cuff leak should be performed

before removing the endotracheal tube.

Oxygenation in a burned patient may be altered by carbon monoxide (CO) poisoning. Physical

examination findings include red lips and altered mental status. Formal diagnosis should be based on

history and evidence of CO levels in the blood. CO binding is assessed by measuring the level of

carboxyhemoglobin in a peripheral arterial blood gas sample. Symptoms of CO poisoning typically

begin with headaches at levels around 10%, while CO in the blood becomes lethal at around 50% to

70%. The half-life of CO is normally 4 hours when breathing room air, however, half-life is shortened

considerably with administration of supplemental oxygen. Treatment with 100% oxygen (FiO2 100%)

reduces the half-life of CO to 30 to 90 minutes. Hyperbaric oxygen treatment can reduce the half-life of

CO to 15 to 23 minutes. However, if the patient has additional burn injuries or is unstable, the patient

should not be placed in a hyperbaric chamber. Also, the time needed to transfer patients to hyperbaric

facilities and the subsequent difficulty of resuscitating a critically ill patient in a closed chamber make

hyperbaric oxygen an impractical option. Prompt and aggressive evaluation and maintenance of the

airway is the most important initial step in management of a burn patient.

Fluid Resuscitation

It is important to have large bore IV access with 16- or 18G peripheral IVs. IV access catheters should

preferentially be placed in nonburned areas of skin although this is not always possible. If the patient

will require invasive hemodynamic monitoring, a central line should be placed under sterile conditions.

Peripherally inserted central catheter (PICC) lines can be used in burn patients, however, their infection

rate remains high. If a central line is used, this does not need to be changed out at a certain timepoint

but rather should be monitored daily for signs of infection. Ideally, burn and critical care surgeons

would have access to a minimally invasive monitor of cardiac output. Though several technologies exist

including esophageal Dopplers, arterial waveform monitors, and thermodilution modalities, the trend of

these values is more useful than the absolute values. If a PiCCO device (Pulsion Medical Systems AG,

Munich, Germany) is used to monitor the patient, it is best to have the central venous line located in the

internal jugular vein and the arterial line in the femoral artery. This technology uses thermodilution to

determine cardiac performance. Studies have demonstrated efficacy of this technology when compared

to use of a pulmonary artery catheter.47 Burn injury and soft tissue edema make noninvasive blood

pressure measurement difficult and inaccurate, hence arterial line placement is frequently necessary.

The Parkland or Consensus formula is most commonly used to estimate fluid requirements for the

first 24 hours and should be used to guide initial fluid infusion rates. This is a start point and should not

be construed as a dogmatic prescription of the total fluid volume to be given during the first day after

injury.48 It is extremely important to note that the original time of the injury is used in the calculation,

not the time of initial presentation to care providers. Partial- and full-thickness burns are totaled to

calculate burned TBSA.

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Consensus formula: First 24-hour requirement= 2–4 cc × %TBSA × weight (kg)

Half of this fluid volume is planned to be administered in the first 8 hours after burn injury and the

second half is administered over the next 16 hours. For example, if a 70-kg patient with 20% TBSA burn

sustained at 10 AM presents 2 hours later, the crystalloid fluid to be administered in the first 8 hours is

calculated using the following formula: ([4 cc × 20% × 70 kg]/2)/6 hours. Lactated Ringers crystalloid

solution is recommended as the first choice fluid to avoid complications associated with metabolic

acidosis.48 Currently data do not support hypertonic saline, dextran, or albumin during the first 24 hours

of resuscitation in standard clinical situations.49,50 Studies have suggested that limited albumin usage

may play a role in reducing the rate of abdominal compartment syndrome when the patient requires

substantially more fluid administration than estimated by the Parkland formula (>1.5 times).51

Additionally, D5/LR is commonly used for maintenance of fluid in children under 1 year of age to avoid

hypoglycemia. Once the Parkland formula is begun, the patient’s vital signs and urine output should be

closely monitored and laboratory studies should be drawn frequently. Although such formulas exist, it is

important to note that proper fluid resuscitation should be guided by overall clinical response and the

trend of vital signs and laboratory values. IV fluid infusion rate should be increased or decreased based

on the response of the patient on an hourly basis with fluid administration titrated to maintain urine

output goals of 0.5 to 1 mL/kg/hr in adults and 1 to 1.5 mL/kg/hr in children. Blood pressure and heart

rate should be monitored; burn patients are often tachycardic regardless of the degree of resuscitation.

Though urine output is considered a “gold standard,” it often lags the fluid status and thus clinicians

must be cautious not to reflexively increase fluids with low urine output but rather consider the entire

clinical picture. In addition, close monitoring of the patient’s laboratories is necessary to determine the

trend in organ perfusion. Laboratory values that help assess organ perfusion include lactate, base deficit,

central venous O2

, and/or pH. Although any one of these values alone does not provide a sensitive

marker of the patient status, trending these values during resuscitation can help direct resuscitation

adjustments if the current fluid rate is causing a positive trend. If the end organs are adequately

perfused, decrease in lactate and base deficit as well as increase in central venous O2 and normalization

of pH should be observed.

In the second 24 hours, all patients should receive crystalloid sufficient to maintain urine output and

to maintain parameters of perfusion including lactate, pulse volume variation, and cardiac output.

Infusion rate will often be at a maintenance rate plus adjustment for losses of fluid into the burn wound.

Nutritional support should be started enterally within 24 hours. After 24 to 36 hours, providers can cut

fluids by 1/3 if the patient continues to make adequate urine. One may decrease fluids again by 1/3 for

hours 36 to 48 (assuming urine output does not drop off). Colloid can be given after initial crystalloid

resuscitation (5% albumin at 0.3 to 0.5 mL/kg per %TBSA over 24 hours).

After 48 hours, fluid infusion rate should maintain urine output at 0.5 to 1 mL/kg body weight per

hour. Insensible losses and hyperthermia are associated with hyperdynamic states and increase fluid

requirements. Daily patient weights can be helpful to determine insensible fluid loss or retention.

Pediatric fluid resuscitation does have some differences with regard to fluid management. Due to the

limited reserve in children under 20 kg, a glucose-based maintenance fluid is recommended.

Additionally, fluid requirements may be as high as 6 mL/kg per TBSA and their urine output should be

1.0 to 1.5 mL/kg/hr.52 Since burn resuscitation should be considered in the setting of a 10% TBSA in

children, transfer to a burn center is recommended.

Pulmonary status is also an indicator of fluid status but in a delayed fashion. Complications such as

pulmonary edema result from fluid overload and necessitate daily evaluation of oxygen requirements

and ventilator settings.

Difficult to Resuscitate Patients

If the fluid resuscitation required during the first 24 hours is 1.5 times greater than initially estimated,

the physician should reassess the clinical picture. Giving excessive crystalloid fluids and failure to use

appropriate early resuscitation adjuncts are associated with significantly worse outcomes. Physicians

often will give additional fluid due to low urine output not realizing that the kidney, like other organs

during burn shock, often lags behind the clinical picture. Specific complications associated with

excessive resuscitation include compartment syndrome of both the extremities and the abdomen. Signs

of abdominal compartment syndrome include abdominal distention, decreased urine output, elevated

ventilator pressures, and desaturation. Surgeons should have a low threshold to assess for this

devastating complication in any patient requiring resuscitation above the Parkland formula. Diagnosis

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