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%.


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

Mediator Source Effect

Histamine Mast cells from burned skin Increases capillary permeability, arteriolar dilatation, and venular contraction
Prostaglandins Arachidonic acid released from burned tissue and inflammatory cells PGE2, PGI2: potent vasodilators; increase microvascular permeability
Thromboxanes Platelets in the burn wound Thromboxanes A2 and B2: vasoconstrictors; contribute to tissue ischemia
Kinins Inflammatory cells Increase venular permeability
Serotonin Inflammatory cells Vasoconstrictor; reduces blood flow to burn wounds
Catecholamines Adrenal medulla Vasoconstrictor; contributes to wound ischemia, increased systemic vascular resistance
Oxygen radicals Burned tissue Increase vascular permeability and burn edema
Platelet aggregation factor Burn wound platelets Increases capillary permeability
Angiotensin II and vasopressin Renal juxtaglomerular cells Vasoconstrictors; may be responsible for intestinal ischemia (angiotensin) and increased systemic vascular resistance (vasopressin)

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.



Inhalation Injury

Diagnosis and Management of the Burn Wound

Initial Treatment of a Child Who Has Extensive Burns

Initial Management

Early Excision and Grafting

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:

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


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

Gram-negative 8 to 12 h onset Temperature increased or normal, followed by hypothermia White blood cell count either low or high; blood cultures may be negative Wounds develop focal gangrene Burn wound biopsy with >105 organisms per gram of tissue Ileus, decreased blood pressure and urine output, obtundation
Gram-positive Gradual onset Temperature usually 104°F (40°C) or higher White blood cell count usually >20 x 103/mcL (20 x 109/L); blood cultures may be negative Wounds exudative, macerated Burn wound biopsy with >105 organisms per gram of tissue Ileus, decreased blood pressure and urine output, anorexia, irrationality


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{dagger}