Airway Injury

It is essential to aggressively rule out upper airway injury in patients at risk (e.g., involving a fire that occurred in a closed space or the development of unconsciousness or stupor that prevented the patient from protecting his or her airway). Diagnosis is made by history, the circumstances surrounding the burn injury, and physical examination. Above the oropharynx, thermal injury can produce significant inflammation, occluding the airway. Heat rarely causes damage below the vocal cords because it is effectively dissipated. The other components of smoke such as particulate materials, systemic toxins, and respiratory irritants trigger a cascade of events, resulting in pulmonary edema and a ventilation/perfusion mismatch.²⁰ Airway examination is best accomplished by direct visualization of the airway with a laryngoscope or fiberoptic bronchoscopy.²¹ Fiberoptic bronchoscopy is the gold standard for the diagnosis of the severity of inhalation injury. Table 35-2 has a commonly used classification of fiberoptic injury findings and associated mortality.²² The chest radiograph is usually normal in the early phase of inhalation injury (unless aspiration of gastric or pharyngeal contents occurred during the accident), becoming abnormal once pulmonary edema or infiltration develops. Treatment of upper airway injury involves early endotracheal intubation, even if the burn patient is not yet demonstrating signs of airway decompensation. Even in the absence of an inhalation injury, the lungs are at risk for compromise if the burn area is large.

Thermal damage to soft tissues of the respiratory tract and trachea can make intubation an incredibly difficult task because of the malalignment of structures, swelling, and bleeding of the tissues involved. Intubation of the trachea is much easier to perform earlier rather than later, when there may be glottic or facial edema, which worsens after fluid resuscitation.18–25 In the pediatric population, intubation should be performed with an uncuffed endotracheal tube, usually one size smaller than expected according to age and weight. Fiberoptic-assisted or laryngeal airway mask (LMA) guided intubation techniques are useful. The use of a retrograde wire, light wand, or GlideScope video-assisted techniques have all been used successfully.²⁶ Nasotracheal intubation in children may be preferred because it is better tolerated, and tube displacement with movement is less likely. Cuffed endotracheal tubes are traditionally used for pediatric patients younger than 8 years old. They are commonly used in pediatric burns because of the added flexibility of not requiring replacement that can be necessitated by decreasing edema and air leaks, which is the case with uncuffed tubes.^3,26

In the absence of an airway abnormality, early tracheal intubation can usually be achieved using a rapid-sequence technique with an intravenous (IV) induction agent and a rapidly acting muscle relaxant. There is general agreement that succinylcholine administration to patients more than 24 hours after burn injury is unsafe,27,28 although some authors extend this safe period to slightly longer.²⁹ Receptor up-regulation occurs after a burn injury, with proliferation of acetylcholine receptors throughout the muscle membrane. Succinylcholine can cause potassium (K⁺) release from the entire muscle membrane rather than from discrete end-plate junctions, leading to hyperkalemia and possibly cardiac arrest.³⁰ The magnitude of K⁺ elevation appears to be related to the size of the burn. This process of receptor up-regulation takes days to develop, allowing an initial 24-hour window of safety. It is wise to avoid the use of succinylcholine in a burn patient more than 24 hours after injury.³¹

Intubation with a nondepolarizing relaxant or without a relaxant via the techniques mentioned above allow for safe airway control. Several factors converge to produce an increased dose requirement of nondepolarizing relaxants in burn patients. These include up-regulation of acetylcholine receptors, massive fluid shifts producing significant changes in volume of distribution, and a qualitative decrease in receptor sensitivity. Plasma protein-binding alterations do not effect relaxants clinically because they are not highly bound. Rocuronium, for example, is only 30% protein bound. Both the dose administered and the serum concentrations required in the burn patient may be increased three- to five-fold to achieve the desired paralysis with a nondepolarizer.32–34

With an abnormal airway or upper airway obstruction, the safest way to secure the airway is with the patient awake. Key actions include effective topical anesthesia, patient positioning, and supplemental oxygenation. Incremental doses of ketamine or dexmedetomidine infusion along with topical anesthesia and avoiding relaxants allow the patients to continue to breath spontaneously with airway reflexes relatively intact while the airway is secured. Administration of sedatives may worsen airway obstruction and should be given judiciously. However, IV opioid administration may be appropriate for the alert patient in pain. Methods to secure the airway include flexible fiberoptic bronchoscopy, direct laryngoscopy, LMA-assisted intubation, blind nasal intubation, retrograde wire, light wand, or GlideScope video-assisted techniques. When the upper airway is badly damaged and endotracheal intubation is not possible, a direct surgical approach such as tracheotomy is indicated.

For the most part, after airway management, the burn patient is taken to the intensive care unit and placed on ventilatory support.³⁵ Inspired gases should be humidified to aid clearing of tracheobronchial debris and prevent drying of secretions. The endotracheal tube must be kept in place until the surrounding laryngeal edema has subsided. A progressive air leak around the endotracheal tube, especially in uncuffed pediatric sizes, may be an indication that edematous tissue is returning to normal.^{14,18–20,36}

Administration of nebulized heparin and N-acetylcysteine with massive burn and smoke inhalation injury results in a decreased incidence of re-intubation for progressive pulmonary failure, decreased atelectasis, and reduced mortality. The Shriners Burns Hospital formula includes 5000 units of heparin and 3 mL of a 20% solution of N-acetylcysteine aerosolized every 4 hours for the first 7 days after the injury.²⁰

Carbon Monoxide Poisoning

Any burn victim rescued from an enclosed-space fire should be considered at high risk for carbon monoxide poisoning. It is estimated that 50% to 60% of all fire victims die from carbon monoxide poisoning.³⁷ Symptoms depend on the carboxyhemoglobin level, although it is actually the tissue carbon monoxide level that determines the toxicity of carbon monoxide (Table 35-3).

Carbon monoxide binds to the hemoglobin molecule with 200 times greater affinity than oxygen, leading to a fall in oxyhemoglobin saturation as tissues become unable to extract oxygen.¹⁴ The end result is a disruption in mitochondrial oxidative phosphorylation, which produces metabolic acidosis at the cellular level. Analysis of blood gases reveals a normal arterial oxygen tension but a decreased total oxygen content, indicating that the hemoglobin oxygen saturation is markedly reduced. Carbon monoxide increases the stability of the oxyhemoglobin molecule, decreasing the release of oxygen to the tissues and producing a leftward shift in the oxyhemoglobin curve (see Figure 17-6). Pulse oximeters do not detect carboxyhemoglobin (CoHgb) in blood and give falsely elevated readings for oxygen saturation in its presence. The diagnosis of carbon monoxide poisoning requires measurement of arterial CoHgb levels using a co-oximeter. The half-life of CoHgb is variable. In patients treated with 100% oxygen, it ranged from 26 to 148 minutes.³⁸ Treatment continues with 100% oxygen until the CoHgb level is less than 5% or for 6 hours.³⁹ A co-oximeter measures concentrations of all hemoglobin moieties (i.e., oxyhemoglobin, deoxyhemoglobin, carboxyhemoglobin, and methemoglobin).⁴⁰

Hyperbaric oxygen therapy (HBOT) is an alternative treatment and may be helpful if the CoHgb level exceeds 25% or if clinical signs of toxicity are evident. Hyperbaric oxygen accelerates the clearance of carbon monoxide beyond that achieved using 100% oxygen at 1 atmosphere. The main rationale for its use is prevention of delayed neurocognitive syndrome. It can be difficult to transport and care for patients in the chamber, and debate continues over its effectiveness.⁴¹

Cyanide Poisoning

Hydrogen cyanide (HCN) poisoning is another toxicity seen with fires. It is produced by the combustion of materials such as plastics, foam, paints, wool, and silk. Cyanide poisoning produces tissue hypoxia by blocking the intracellular use of oxygen. Cyanide binds to the terminal cytochrome on the electron transport chain, causing hypoxia, lactic acidosis, and elevated mixed venous oxygen saturation. The half-life of HCN is approximately 1 hour. Signs and symptoms of poisoning include loss of consciousness, dilated pupils, seizures, hypotension, tachypnea followed by apnea, and high lactate levels. Cyanide has several antidotes, with differing mechanisms of action and diverse profiles. Hydroxocobalamin (vitamin B₁₂a) actively binds cyanide by forming cyanocobalamin, which is directly excreted via the kidney.

Hydroxocobalamin has a rapid onset of action, neutralizes cyanide without interfering with cellular oxygen use, and has a good safety profile. It is safe for use with smoke-inhalation victims, easy to administer, and is the preferred antidote to this type of cyanide poisoning. A hydroxocobalamin dose of 50 mg/kg is recommended. In addition, aggressive stabilization of cardiopulmonary function augments the hepatic clearance of cyanide via rhodanase, and can resolve cyanide poisoning (blood levels, 5.6-9 mg/L), without the use of antidotes.14,20,42

Hypovolemic Shock Associated with Thermal Injury

After the airway has been secured and other life-threatening injuries have been managed, the burn patient must be resuscitated with large volumes of fluid. Aggressive fluid administration and restoration of blood volume are critical for improving chances of patient survival and preventing renal failure. Burns cause a form of hypovolemic shock. These changes are reflected in loss of circulating plasma volume, hemoconcentration, massive edema formation, decreased urine output, and depressed cardiovascular function.25,43 Fluid losses are greatest in the first 12 hours after burn injury and then begin to stabilize after 24 hours. Fluid losses occur secondary to direct transudation of plasma and plasma proteins from the wound and from diffuse capillary leakage that shift fluid from the intravascular space to the interstitium of unburned tissue. Capillary leak results from a loss of endothelial integrity and from reduction of intravascular oncotic pressure as plasma proteins are lost through the burn wound and incompetent capillary beds. The end result of changes in microvasculature caused by thermal injury is disruption of normal capillary barriers separating intravascular and interstitial compartments and rapid equilibration of these compartments. This causes severe depletion of plasma volume and a marked increase in extracellular fluid, clinically manifested as hypovolemia and burn-induced edema.^10,25,43

Inflammatory mediators are released from burned tissues after injury, causing localized inflammation and burn-wound edema. Localized mediators include oxygen radicals, arachidonic acid metabolites, histamine, prostaglandins, leukotrienes, products of platelet activation, and the complement cascade.23,37,44 Most edema occurs locally at the burn site and is maximal at 24 hours after injury. The edema itself results in tissue hypoxia and increased tissue pressure with circumferential injuries. Aggressive fluid therapy can correct the hypovolemia but will accentuate the edema process. In minor burns, the inflammatory process remains sequestered in the wound itself. However, in major burn insults, this local injury signals the release of systemic circulatory mediators resulting in a systemic response.

Fluid Resuscitation

Within seconds after an acute burn injury, massive fluid shifts begin to occur. Therefore, fluid resuscitation and airway management are the hallmarks of initial therapy and should be instituted by the first-response emergency medical providers. There are many formulas for calculating a burn patient’s initial fluid resuscitation requirements. Crystalloid resuscitation often provides substantial volumes of fluid, often in excess of that predicted by current formulas, resulting in numerous edema-related complications. This phenomenon is coined “fluid creep,” and fluid therapy after the initial 24 hours is constantly being refined. In most centers, two formulas are accepted as guidelines for the resuscitation of severely burned patients, the Parkland and modified Brooke formulas.45,46 The need for blood transfusion is usually not a major concern during the immediate resuscitation phase in acutely burned patients unless other coexisting trauma exists. Transfusion management is a prominent issue during subsequent surgical intervention.

The current ABA consensus formula for fluid resuscitation and urine output in burn patients is given in Box 35-1. Table 35-4

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