Burns


Etiology

  1. Scald Burns
    • most common cause of burns
    • usually from hot water
    • depth of injury is proportionate to the temperature applied, duration of contact, and the thickness of the skin
    • commonest form of reported child abuse

  2. Flame Burns
    • 2nd most common cause of burns

  3. Flash Burns
    • explosions of natural gas, propane, gasoline, and other flammable liquids cause intense heat for a very short period of time
    • clothing is protective, unless it ignites
    • have a distribution over all exposed skin
    • may be associated with significant thermal damage to the upper airway

  4. Contact Burns
    • result from contact with hot or cold objects
    • usually limited in extent, but are very deep

  5. Electrical Burns
    • frequently more serious than they appear on the surface
    • extremities and digits are especially prone to injury, with extensive muscle necrosis
    • early exploration and debridement of affected muscle beds is necessary
    • fasciotomies are often necessary
    • rhabdomyolysis can cause acute renal failure
    • cardiac arrhythmias and ventricular fibrillation may occur

  6. Chemical Burns
    • result from exposure to alkalis, acids, and petroleum products
    • exposure times may be long
    • alkali burns penetrate more deeply than acid burns
    • hydrocarbons cause cell membrane dissolution and skin necrosis
    • must flush away the chemical with large amounts of water
    • neutralizing agents should be avoided as they can cause further damage by releasing heat

Pathophysiology of Burn Injuries

  1. Local Changes
    • thermal injury causes coagulation necrosis of the epidermis and underlying tissues

    Burn Wound Zones of Injury
    1. Zone of Coagulation (Necrosis)
      • tissue irreversibly damaged at the time of injury

    2. Zone of Ischemia (Stasis)
      • associated with vascular damage and capillary leakage from release of wound cytokines
      • injured tissue in this zone tends to progress to a deeper wound in 24 – 48 hours
      • in animal models, treatment aimed at reducing local inflammation may prevent the wound from progressing

    3. Zone of Hyperemia (Inflammation)
      • characterized by vasodilation from inflammation
      • tissue in this zone is expected to make a complete recovery

  2. Burn Depth
    • primary determinant of long-term appearance and function, as well as survival
    • clinical observation by an experienced physician is the usual method for determining burn depth
    • the burn wound is a dynamic process and it may take 72 hours before a definitive decision about burn depth can be made
    • laser Doppler flowmeter holds promise for measuring burn depth quantitatively

    1. First-Degree Burns
      • involve only the epidermis
      • result from sunburn or a mild scald
      • do not blister
      • become erythematous because of dermal vasodilation and blanch to the touch
      • painful
      • heal without scarring
      • treatment is aimed at comfort with topical ointments

    2. Second-Degree Burns
      1. Superficial Dermal Burns
        • involve the papillary dermis, sparing most of the skin appendages
        • form blisters
        • hypersensitive, erythematous, blanch with pressure
        • usually heal spontaneously in less than 3 weeks with no functional deficits
        • rarely causes hypertrophic scarring

        Superficial Second-Degree Burn
        Superficial 2nd-Degree burn

      2. Deep Dermal Burns
        • extend into the reticular dermis, where most of the skin appendages (hair follicles, sweat glands, sebaceous glands) exist
        • also form blisters
        • wound surface usually is a mottled pink and white color
        • do not blanch to touch
        • patient complains of discomfort rather than pain
        • capillary refill occurs slowly or not at all
        • usually heal within 2 to 5 weeks, but impaired joint function and hypertrophic scarring are common

        Deep Second-Degree Burn
        Deep 2nd-Degree Burn

    3. Third-Degree Burns
      • full-thickness lesions
      • insensitive
      • may appear white, cherry red, or black
      • usually are leathery and firm
      • do not blanch with pressure
      • develop a classic burn eschar
      • heal only by contracture and epithelization, or skin grafting

      Third-Degree Burn
      3rd-Degree Burn

    4. Fourth-Degree Burns
      • involve the subcutaneous fat and deeper tissues such as muscle or bone
      • almost always have a charred appearance

  3. Burn Size
    • burn size is quantified as a percentage of total body surface areas (TBSA) and is estimated using the rule of nines
    • children < 4 years old have proportionately larger heads than adults and smaller lower extremities
    • for smaller burns, size can be estimated using the patient’s palm (1% TBSA)
    • most important factor in predicting mortality

    Rule of Nines for calculating Burn Size

Physiological Response to Burns

  1. Burn Shock (Ebb Phase)
    • hypodynamic phase lasting 48 – 72 hours
    • hypovolemic in nature, characterized by ↓ cardiac output, ↓ plasma volume, oliguria, ↓ O2 consumption, ↓ metabolic rate
    • insulin levels are high, but plasma glucose levels are also high, reflecting a state of insulin resistance
    • major component of burn shock is the increase in total body capillary permeability, presumably from the massive release of wound cytokines
    • most of the changes occur locally at the burn site, with maximal edema formation occurring 12 – 24 hours post injury
    • early phase of burn edema is attributed to mediators such as histamine, cytokines, bradykinin, prostaglandins, thromboxane A2 and components of the complement cascade
    • support of this phase requires massive fluid resuscitation

  2. Hyperdynamic Response (Flow Phase)
    • develops after patients have been successfully resuscitated and may last for months
    • characterized by fever, increased metabolic rate, tachycardia
    • results from sustained increases in catecholamines, cortisol, glucagon, and inflammatory mediators
    • cardiac output is 1.5 times that of healthy volunteers; metabolic rate is 1.4 times that of healthy volunteers
    • myocardial oxygen consumption surpasses marathon runners

  3. Metabolic Changes
    • liver undergoes profound hepatomegaly

    1. Protein Catabolism
      • uncomplicated severely burned patients can lose up to 25% of lean body mass; septic burn patients have even greater protein losses
      • unchecked, a lethal cachexia can develop in less than one month
      • negative nitrogen balance can persist for almost a year post burn

    2. Glucose and Fat Metabolism
      • gluconeogenesis, primarily from alanine, and glycogenolysis are increased by 250% post severe burn
      • lipolysis is also greatly accelerated
      • hyperglycemia and insulin resistance characterize the post burn period for up to 3 years
      • much of the glucose oversupply goes to support fibroblasts and other inflammatory cells in the wound, which utilize anaerobic metabolism

  4. Immune System Changes
    • burns cause a global depression of immune function
    • degree of immune impairment is proportional to burn size
    • macrophage, neutrophil, T cell, and B cell function are all impaired following thermal injury

  5. GI Tract Changes
    • severe burns cause mucosal atrophy, changes in digestive absorption, and increased gut permeability
    • GI tract blood flow is also decreased

Initial Evaluation and Resuscitation

  1. ABCs
    • ‘forget about the burn’
    • must search for and treat other life-threatening injuries
    • if the mechanism of injury suggests a possible cervical spine injury, the neck must be immobilized

    1. Respiratory Injury
      • clinical indications of respiratory injury are subtle and may not manifest themselves in the first 24 hours
      • endotracheal intubation and mechanical ventilation should be instituted early when respiratory injury is suspected
      • as airway edema progresses, intubation may be impossible and a surgical airway may be necessary

      1. Direct Thermal Injury
        • larynx protects the subglottic airway from direct thermal injury
        • supraglottic airway is extremely susceptible to obstruction from heat exposure
        • should be suspected in any flame or flash burn
        • clinical indications of thermal airway injury include:
          • facial burns; singeing of the eyebrows and nasal vibrissae
          • erythema, edema, and ulceration of the oropharynx
          • copious mucus production and carbonaceous sputum
          • explosion with burns to the head and torso
          • carboxyhemoglobin levels > 10% if patient involved in a fire
        • bronchoscopy should be considered in every burn patient

      2. Carbon Monoxide Poisoning
        • should be assumed in patients burned in enclosed areas
        • responsible for 60% to 70% of deaths from house fires
        • diagnosis is made primarily by a history of exposure
        • cherry red skin color is usually only seen in moribund patients
        • patients with carboxyhemoglobin levels < 20% usually have no symptoms
        • higher levels of carboxyhemoglobin may result in headache and nausea (20% - 30%), confusion (30% - 40%), coma (40% - 60%), and death (>60%)
        • CO has a high affinity for hemoglobin (240 times that of oxygen) and displaces oxygen from hemoglobin
        • CO also dissociates very slowly from hemoglobin and its half-life is 250 minutes on room air and 40 minutes when the patient is breathing 100% oxygen
        • patients suspected of CO exposure should receive high-flow oxygen via a non-rebreathing mask

      3. Smoke Inhalation
        • doubles the mortality when compared to burn patients without inhalation injury
        • inhalation of toxic fumes and smoke particles may lead to chemical tracheobronchitis, edema, and pneumonia
        • wheezing and air hunger are common early symptoms
        • blood gas analysis typically shows a falling P/F ratio (ratio of arterial PO2 to the percentage of FIO2
        • treatment is supportive

    2. IV Access and Initial Fluid Resuscitation
      • will be required in patients with burns over 20% TBSA
      • at least two large-bore IV should be started
      • upper extremities are the preferred sites for IVs because of the high incidence of septic thrombophlebitis in the lower extremities
      • OK to place IVs through burned skin
      • begin lactated Ringer’s @ 1000 cc/hr until resuscitation formula can be calculated
      • Foley catheter should be placed to monitor urine output

  2. Initial Wound Management
    • tetanus prophylaxis should be administered if the patient’s immune status is not known
    • prophylactic antibiotics are not indicated in the early postburn period
    • wounds should be thoroughly cleaned and debrided
    • deep 2nd and 3rd degree burns should be covered with an antimicrobial dressing such as Silvadene

    1. Escharotomy
      1. Chest Escharotomy
        • deep circumferential burn wound of the chest may compromise ventilatory function
        • performed in the anterior axillary line bilaterally
        • if the burn extends onto the abdominal wall, the escharotomy incisions should be connected by a transverse incision along the costal margin
        • can be performed in the ER

      2. Escharotomy of the Extremities
        • edema formation underneath the tight unyielding eschar of a circumferential extremity burn may lead to vascular compromise
        • increasing pain or decreased motor or sensory function indicates the need for escharotomy or fasciotomy
        • in equivocal cases, compartment pressures can be monitored directly
        • procedure may be done at the bedside
        • since 3rd-degree burns are insensate, local anesthesia is not necessary
        • incisions should be placed along the medial and lateral aspects of the extremity and carried across involved joints
        • depth of the incision should be full thickness through the eschar into the subcutaneous fat

        Escharotomy Incisions
        Escharotomy Incisions

Fluid Management

  1. Resuscitation
    • goal is to replace the sequestered edema fluid
    • in burn shock, massive fluid shifts occur even though total body water remains unchanged
    • the intracellular and interstitial compartments gain volume at the expense of the intravascular volume
    • successful resuscitation requires replacing the salt, as well as the water, that is lost into the intracellular and interstitial compartments

    1. Crystalloid Resuscitation
      • LR is the most common resuscitation fluid
      • urinary output is used to guide the adequacy of resuscitation
      • the Parkland formula (4ml/kg/%burn over 24 hours, with one-half the volume given in the first 8 hours) was designed to produce a urinary output of 1ml/kg/hr
      • infusion rates need to be adjusted hourly based on physiologic endpoints
      • crystalloid resuscitation exacerbates edema formation
      • severe hypoproteinemia also develops, which may also worsen edema

    2. Hypertonic Saline Resuscitation
      • may result in less edema formation because of the smaller total fluid requirements
      • intracellular water is decreased
      • serum sodium concentrations must be monitored and should not exceed 160 mEq/dl
      • no study has shown a superiority of hypertonic saline over crystalloid in burn resuscitation

    3. Colloid Resuscitation
      • goal of colloid is to generate an inward oncotic force and keep fluid in the intravascular space
      • however, in the first 8 – 10 hours following injury, capillary permeability allows even large protein molecules to leak into the interstitial space, and so colloid resuscitation is no more effective than crystalloid in preventing edema
      • some burn centers add colloid (as FFP) to the resuscitation fluids beginning 8 – 10 hours post burn
      • again, the goal is to minimize the amount of fluid (and edema formation) required for resuscitation
      • colloid resuscitation may be of value in older patients, patients with concomitant inhalation injury, and patients with burns > 50% TBSA

  2. Postresuscitation
    • burn edema is maximal at 24 hours postburn, and then rate of fluid loss slows considerably over the next several days
    • burn patients can lose 4000 mL/m2 burned/day of water through evaporative loss through the wound
    • because of the loss of intracellular potassium during burn shock, the potassium requirements are high (120meq/day)
    • magnesium and phosphate must also be repleted
    • because of intravascular protein loss, protein repletion (albumin) is usually needed

Nutritional Support

  1. Caloric Requirements
    • the hypermetabolic state may last for months and is maintained by elevated levels of cortisol, epinephrine, and glucagon
    • resting energy expenditure (REE) is most accurately determined with a metabolic cart measuring oxygen uptake and carbon dioxide production
    • patient’s caloric goal is 150% of the REE

  2. Routes of Administration
    1. Enteral Nutrition
      • should be started immediately
      • initially the N-G tube can be used, but a Dobhoff tube should be placed at the first opportunity
      • every effort should be made to use an intact GI tract

    2. Parenteral Nutrition
      • should only be used if the GI tract is unavailable (prolonged ileus) or as a bridge to enteral nutrition
      • complications of parenteral nutrition include line sepsis, gut mucosal atrophy, and elevated insulin levels

  3. Dietary Composition
    • protein goal is 1 - 2 g/kg/day
    • most calories should be supplied as glucose
    • zinc (220 mg/day), Vitamin A (10,000 – 25,000 IU/day), and Vitamin C (1000 mg/day) are often administered to augment wound healing

Wound Management

  1. Conservative Management
    • consists of once or twice daily dressing changes, topical therapy, and wound debridement
    • appropriate for superficial 2nd-degree burns
    • another indication is a question about the wound depth (superficial 2nd-degree vs deep dermal burns)
    • any patient who is too unstable to be transported to the operating room will also have to be treated in this manner
    • silver sulfadiazine (Silvadene) is the most common form of topical therapy and is active against most bacterial pathogens

  2. Excision
    • early excision and closure reduces morbidity and mortality from otherwise inevitable burn wound sepsis
    • excision should be performed as soon as possible after the patient is stabilized, usually within the first few days of injury

    1. Tangential Excision
      • involves shaving thin layers of burn eschar sequentially with a dermatome until viable tissue is reached
      • bleeding can be massive and is controlled with epinephrine-soaked sponges, cautery, fibrin or thrombin spray
      • areas on the extremities can be excised using a tourniquet

      Tangential Excision
    2. Fascial Excision
      • reserved for patients with very deep burns
      • fascia is more vascular than fat and accepts grafts better
      • cosmetic deformity can be severe
      • severe lymphedema of the extremities can result

  3. Burn Wound Closure
    1. Autograft
      • split-thickness skin graft is the preferred method of closure
      • donor skin can be expanded with mesh, but this gives a poorer cosmetic result
      • in cases of large burns, there may be insufficient autograft to close the entire wound
      • donor sites may be reused once they have healed

    2. Skin Substitutes
      1. Allograft
        • temporary cover because of rejection
        • will need to be replaced with autograft
        • promotes the vascular bed

      2. Xenograft
        • temporary cover because of rejection
        • inexpensive, long shelf life

      3. Cultured Epidermal Autograft
        • requires 3 weeks to grow cultured keratinocytes
        • take is fair to poor
        • poorly adherent and extremely fragile
        • extremely expensive
        • can be life-saving in patients with massive burns and no available donor sites

      4. Dermal Substitutes
        • goal is to find a dermal matrix onto which thin epidermal grafts or cultured epidermal autografts can be placed
        • Integra is a bilaminar dermal regeneration template for use in patients with limited donor sites

  4. Wound Infection
    1. Pathogenesis
      • all burn wounds become contaminated soon after injury
      • bacteria and fungi may penetrate the avascular eschar, without clinical significance
      • burn wound sepsis occurs when pathogens invade the underlying viable tissue
      • before antibiotics, streptococci and staphylococci were the major infecting organisms; now Pseudomonas species predominate

    2. Clinical Manifestations
      • foul smelling discharge from the wound with a darkening appearance
      • surrounding cellulitis
      • areas of lysis of the eschar, or a very rapid separation of the entire eschar
      • may be corresponding systemic signs of sepsis as well

      Infected Burn Wound
      Infected Burn Wound

    3. Diagnosis
      • small piece of eschar and underlying viable tissue should be excised and sent for quantitative biopsy
      • part of the specimen should be sent to pathology to look for histologic evidence of invasion and the rest should be sent for culture
      • sensitivities should be performed against systemic and topical antibiotics

    4. Treatment
      • topical therapy with a sensitive agent
      • systemic antibiotics may be used as well
      • wound should be excised and closed as soon as possible

  5. Multiorgan Failure (MOF)
    • has replaced burn shock as the leading cause of death in burn patients
    • sepsis is not required to develop MOF, only an inflammatory focus

    1. Pathophysiology
      • infectious sources are most commonly from the wound or lung; failure of the gut barrier is another possibility
      • inflammation from necrotic tissue and open wounds can stimulate the same cytokine cascade as infectious organisms

    2. Prevention
      • early excision of deep burn wounds removes devitalized tissue and reduces wound infection and wound inflammation
      • prompt initiation of resuscitation fluids reduces reperfusion injury after low-flow states
      • topical antibiotics reduces burn wound sepsis
      • systemic perioperative antibiotics
      • scheduled intravascular catheter changes to reduce line sepsis
      • early weaning and protocols to reduce ventilator associated pneumonias
      • early enteral feedings protect the gut mucosal barrier and reduce mortality

Attenuation of the Hypermetabolic Response

  1. Environmental Control
    • since patients have heat loss associated with evaporative losses, the body attempts to raise core temperature to cover this heat loss
    • raising the room temperature to 33 C lowers the resting energy expenditure associated with this obligatory heat loss

  2. Drugs
    • human growth hormone and insulin-like growth factor have not shown to be effective in clinical trials
    • oxandrolone reduces protein catabolism, reduces weight loss, improves donor site healing, reduces hospital stay

    1. Propranolol
      • propranolol is the most efficacious anticatabolic therapy
      • reduces cardiac work, reduces fatty infiltration of the liver, increases protein synthesis, and reduces the amount of insulin necessary to decrease postburn insulin levels

    2. Insulin
      • anabolic effects include increased muscle protein synthesis, improved donor site healing times, lessened LBM losses
      • has significant anti-inflammatory effects
      • reduces sepsis and MOF associated with hyperglycemia
      • ideal glucose level has not been determined - current recommendation from the Surviving Sepsis campaign is to keep glucose levels < 150 mg/dL







References

  1. Sabiston, 20th ed., pgs 505 - 529
  2. Cameron, 11th ed., pgs 1128 - 1131, 1131 - 1138
  3. ATLS Manual, 10th ed., pgs 169 - 185