Burns

1. A first-degree burn is superficial, dry, painful to touch, and heals in less than 1 week. A first-degree burn is exemplified by prolonged exposure to sunlight
2. A second-degree burn is partial thickness and pink or possibly mottled red. It exhibits bullae or frank weeping on the surface. It usually is painful unless classified as deep and heals in 1 to 3 weeks. Second- and third-degree burns can result from contact with hot fluids (scald) or hot objects, such as an iron (contact burn), flames (flame burn), high-voltage electricity (electrical burn); various chemical agents, including acid and alkali (chemical burn); or very cold objects or environments (frostbite).
3. A third-degree burn is the most serious. It appears pearly white, charred, hard, or parchmentlike. The dead skin (eschar) is white, tan, brown, black, and occasionally red. Superficial vascular thrombosis can be observed; there also can be focal tissue loss with prolonged exposure and a soapy-looking lesion that is found in alkali burns.

Figure. The "rule of nines" altered for the anthropomorphic differences of infancy and childhood. Reprinted with permission from Herndon DN, ed. Total Burn Care. 2nd ed. London, England: Saunders: 2002.

Also, palm = 1%.

Pathogenesis

Once sustained, the burn injury, especially full-thickness burns that occupy 40% or more TBSA, give rise to many complications. The most immediate are burn shock and burn edema, as well as inhalation injury, if sustained. Within a few days of the burn injury, other responses are detected, including hypermetabolism, systemic inflammatory response syndrome (SIRS), and sepsis.

Acute Changes: Burn Shock and Burn Edema

Burn injury results in loss of fluid from the intravascular space and excessive fluid accumulation in the interstitial space, resulting in hypovolemia and swelling of the burned skin. When burns exceed 25% TBSA, noninjured tissues also swell. The cause of the fluid shift is believed to be the presence of various mediators stimulated by the burn injury. These mediators also impair cardiac contractility and increase vascular resistance, creating a scenario for hypovolemia, hypoperfusion, tissue ischemia, renal failure, cardiovascular collapse, and death, if aggressive resuscitation therapy is not initiated early.

Mediators of Burn Shock and Edema

Electrical Burns

Electrical burns cause additional complications. Cardiac arrhythmia, including ventricular fibrillation, can occur at the time and site of the injury, as can myocardial damage. Tissues that are most resistant to electric current, such as bone, sustain the greatest heat injury, and soft tissue next to the bone frequently is damaged. Myoglobinuria, renal failure, and neurologic damage, including Guillain-Barré syndrome, transverse myelitis, amyotrophic lateral sclerosis, paresis, and paralysis, can develop up to 2 years following an electrical burn. Eye injuries complicate 5% to 20% of electrical burns; cataracts are the most common complications.

Hypermetabolism

• Children who have large burns experience an increase in energy expenditure and protein metabolism of approximately 50% after the first few days following injury.
• Results in negative nitrogen balance and depletion of body protein stores, which can last for 9 months following the burn. Leads to:
  • weight loss of up to 20%
  • impaired growth velocity
  • muscle wasting
  • impaired immunity
  • delayed wound healing
  • markedly reduced bone formation, with acute skeletal bone loss and increased risk of fracture.
  • Epinephrine, cortisol, and glucagon are produced in excess and mediate the increased gluconeogenesis, glycogenolysis, muscle breakdown, and bone loss. They also antagonize the anabolic effects of insulin and growth hormone. The body is less able to use fat for fuel, and muscle becomes an energy source.

SIRS

• incr HR, RR, WBC, fever, decr BP, shock, and multisystem organ failure.
• hyperactive immune response causes a generalized inflammation that damages healthy tissue as well as infected burn wounds.
• Microvascular permeability leads to decreased tissue oxygenation, and blood flow is reduced due to microthrombi. During this reaction, the intestinal and, possibly, the respiratory barriers to infection are damaged, allowing the entry of additional bacteria into the circulation, known as bacterial translocation.
• Coexisting with SIRS is another reaction termed the counter anti-inflammatory response syndrome (CARS), which attempts to limit the damage created by inflammatory cells. However, the CARS reaction also promotes immunosuppression. These reactions are generated by chemokines, which are located in the macrophages and endothelial cells, and attract inflammatory cells to the site of damage. The inflammatory cells produce cytokines, which also stimulate the inflammatory response and tissue destruction. Differentiating SIRS and CARS from sepsis, which is the leading cause of death in burns, is extremely challenging.

Inhalation Injury

• Inhalation of the toxins associated with flame smoke accounts for 80% of burn-related deaths.
• carbon monoxide and hydrogen cyanide, which can potentiate tissue hypoxia and acidosis.
• It is important to know both the source of the fire and the nature of the gases it produces to treat the injury adequately.
• inhaled hot gases cause oropharyngeal edema in the same way that they affect other tissues, as discussed previously.
• aldehydes, can cause contact damage to the trachea and bronchi, resulting in inflammation and formation of fibrin casts that can obstruct the lower airway completely and lead to decreased oxygenation due to pulmonary vascular vasoconstriction

Diagnosis and Management of the Burn Wound

• obtain a complete history of the burn injury because certain sources, such as alkali, may require additional treatment to stop the penetration of skin layers.
• If less than 10% TBSA: usually can be treated on an outpatient basis unless abuse is suspected.
  • apply a cotton gauze occlusive dressing to protect the damaged skin from bacterial contamination, eliminate air movement over the wound (thus reducing pain), and decrease water loss. (Telfa pads)
  • change dressings daily
  • topical antimicrobial agent should be applied to the wound prior to the dressing for prophylaxis. The agent used most commonly is silver sulfadiazine, which has activity against Staphylococcus aureus, Escherichia coli, Klebsiella sp, Pseudomonas aeruginosa, Proteus sp, and Candida albicans. The primary adverse effect of silver sulfadiazine is leukopenia, which occurs in 5% to 15% of treated patients. However, there is no increase in the incidence of infection.
  • Daily clinical inspection and wound culture, if necessary, should determine when the wound is healed, but such wounds generally heal in fewer than 2 weeks.
  • Also, the application of Biobrane® by experienced practitioners can be of value in partial-thickness burns. The product consists of a coat of cellophane topped by a protein that adheres to the wound and protects it while healing.

Initial Treatment of a Child Who Has Extensive Burns

• fluid resuscitation to prevent shock
• early excision and grafting of the burn wound
• early nutrition support
• identification of airway involvement due to inhalation injury
• treat sepsis.
• more specific measures can be taken to diagnose acute complications, such as cardiac arrhythmias, or to use antidotes for toxic inhalants.

Initial Management

• any jewelry removed (sources of heat)
• in the case of a chemical burn, any saturated clothing removed and skin thoroughly irrigated with water, taking care not to spread any chemical to unburned skin.
• chest should be exposed to assess respiratory effort, and pulse should be obtained.
• Any accompanying injuries, such as fractures, also should be assessed.
• two large-bore intravenous catheters
• past medical history, allergies, and current medications at the scene is advisable if time permits.
• Once the nature and extent of injury are assessed, fluid resuscitation is begun. The Galveston formula:
  • Ringer’s lactate 5,000 mL/m² burned surface area per day, with an additional 2,000 mL/m² TBSA per day of Ringer’s lactate and 5% dextrose for maintenance.
  • The first half of the fluid load is infused over the first 8 hours postburn; the remainder is infused over the ensuing 16 hours.
  • adjust to maintain a urine flow of 1 mL/kg per hour.
  • During the second 24 hours, fluid administration is reduced to 3,750 mL/m² surface area burn, with 1,500 mL/m² TBSA per day as maintenance, which almost always can be administered in the form of enteral feeding through a feeding tube.

Early Excision and Grafting

• Early excision and grafting of the burn wound should be performed at a burn center.
• The rationale for rapid closure of all unequivocal deep burns is to reduce wound infection, fluid loss, and concomitant complications.
• Most burn surgeons close deep wounds within 1 to 2 weeks of the injury.

Early and Aggressive Nutrition Support

With early and aggressive nutrition support, burn centers have been able to reduce the resting energy expenditure from 1.6 to 2 times normal to less than 1.5 times normal. Because other processes beyond hypermetabolism, such as fluid loss, sepsis, and inflammation, contribute to energy expenditure, intensive nutrition support can help minimize protein catabolism and weight loss. A high-carbohydrate diet is needed because of the relative inability of the burn victim to use fat, as discussed previously. If indirect calorimetry is not available, use of the Galveston formula is recommended:

• Infants: 0 to 1 y: 2,100 kcal/m² plus 1,000 kcal/m² burn
• 1 to 11 y: 1,800 kcal/m² plus 1,300 kcal/m² burn
• 12 years and older: 1,500 kcal/m² plus 1,500 kcal/m² burn

Vitamins, minerals, and trace elements are provided according to the recommended daily intakes. However, severe burn injury may produce additional requirements, which have not been investigated completely, including calcium, magnesium, and vitamin D as well as zinc and, possibly, other micronutrients. Following burn injury, patients experience hypocalcemia and magnesium depletion, despite receiving large quantities of enteral and parenteral calcium and magnesium. This is believed to be due to an upregulation of the parathyroid gland calcium-sensing receptor (the body senses more calcium than it has - JS), but treatment is limited to providing the minerals in quantities to cause serum levels to return to normal.

Recognition of Airway Involvement

• A history of closed-space exposure to smoke should raise suspicion of inhalation injury.
• Physical signs
  • hoarseness and stridor, which indicate partial obstruction of the airway and a risk for total obstruction.
  • Patients who exhibit these signs require immediate endotracheal intubation.
• Patients who are obtunded or comatose may have been exposed to carbon monoxide,
  • diagnosed by measurement of blood carboxyhemoglobin concentrations.
• However, the correlation between inhalation injury and symptoms and signs often is poor, which necessitates bronchoscopic examination during evaluation at the burn center.
• Intravenous radionuclide scans using xenon133 can identify small airways that are affected by inhalation injury. Areas retaining xenon for more than 90 seconds are assumed to be obstructed.
• Treatment of inhalation injury is supportive. With combined burn and inhalation injury, fluid requirements are increased by 40% to 75% in the first 24 hours postinjury.
• For carbon monoxide exposure, patients should receive 100% oxygen until the blood carboxyhemoglobin levels are less than 10%.
• Patients who have hypoxia require supplemental oxygen.
• Chest physiotherapy and spirometry generally are used to treat airway secretions.
• Wheezing is an indication for diagnostic bronchoscopy to determine whether there is plugging of the airway or bronchospasm and edema.
• If there is plugging, therapeutic bronchoscopy and aerosolized heparin and humidification are administered.
• For bronchospasm, treatment initially is with nebulized beta₂ agonists and, if needed, intravenous aminophylline.
• If respiratory failure ensues, the treatments of choice are intubation, mechanical ventilation, and tracheostomy.
• If ventilation remains inadequate, permissive hypercapnia may stimulate respiratory effort.

Sepsis

Burn wound sepsis is defined as the site showing proliferating microorganisms that exceed 10⁵/g tissue and invasion of underlying unburned tissue. Bacteremia is indicated by the transient presence of microorganisms in the blood; sepsis is defined as invasion of the blood by pathogenic bacteria from local foci of infection, such as the burn wound. Sepsis frequently is accompanied by hyperthermia, hypothermia, and prostration.

Some of the more common infections seen with severe burn injury include pneumonia, subacute bacterial endocarditis, catheter infections, thrombophlebitis, suppurative chondritis and sinusitis, urinary tract infections, cholecystitis, and intestinal infections. Antibiotic therapy should be based on sensitivity of the organism(s) involved.

Table 2. Features of Bacterial Sepsis Following Large Burns

Prognosis

Despite the seriousness of large burn injury in children, the prognosis for survival is good and improving steadily. Recent data analyzed at the United States Army Institute for Surgical Research showed that adults older than 50 years of age who had burns of less than 50% TBSA accounted for 19% of the admissions to burn units, but greater than 50% of the deaths. In contrast, children younger than 4 years of age who were similarly burned accounted for 19% of admissions but only 12.5% of the deaths. Other challenges remain, including physical and emotional rehabilitation, reconstructive surgery, treatment of the hypermetabolic state with anabolic agents such as growth hormone, and reintegration of children into their communities. Work is ongoing in these and other areas.

Pediatrics in Review. 2004;25:411-417.  Burns. Gordon L. Klein, MD, MPH^*. David N. Herndon, MD