Inhalation Injury Treatment & Management

Decision to admit

Evaluate patients who present with inhalation injury for the extent of disease and degree of hypoxemia. A child who is at low risk for injury with no clinical symptoms can usually be observed for 4-12 hours and discharged with close follow-up and instructions to return if symptomatic.

Observe the high-risk child with only minimal symptoms for 4-12 hours and, if any symptoms or concerns arise, admit to the hospital for further observation and oxygenation monitoring.

The symptomatic child with any signs of airway obstruction, bronchospasm, respiratory distress, or concurrent burns is admitted to the hospital for appropriate monitoring because edema and obstruction typically worsen over the next 24-48 hours.

Airways

Ensure patency and stability. Check for exposure to heat and thermal injury to the nose, mouth, face, and singed hair. Consider smoke involvement if soot is on the face and in sputum, although smoke inhalation is possible without evidence of soot.

Direct laryngoscopy and fiberoptic endoscopy are useful to evaluate the extent of airway edema and burns, although vasoconstriction from hypovolemia may result in underappreciation of the severity of injury. When upper airway injury is suspected, elective intubation should be considered because progression of edema over the next 24-48 hours may make later intubation difficult if not impossible.

Breathing

Check for upper airway compromise, difficulty breathing, stridor, cough, retractions, and bilateral breath sounds. Administer 100% oxygen because of the likelihood of CO inhalation in fires.

The direct effects of inhalation injury are usually evident within 24 hours, although late pulmonary dysfunction may result from complex hemodynamic and infectious complications associated with surface burns.

Circulation

Patients whose injury involves cutaneous burns have ongoing circulatory derangements. Fluid loss through burned areas from intense inflammation with vasodilatation and capillary leak or from the subsequent infectious complications necessitates large fluid volume resuscitation. Even minor errors in estimation of body surface area; burned surface area; and fluid, electrolyte, and protein requirements can produce profound hemodynamic and respiratory embarrassment.

Large-bore intravenous catheter access may be needed to facilitate fluid resuscitation. Frequent evaluation of heart rate, perfusion, and blood pressure are needed to determine stability and guide therapy.

Neurology

Patient responsiveness helps determine the ability to protect the airway and is also an excellent indicator of adequacy of resuscitation success.

The neurologic examination is frequently clouded by hypoxic and toxic neurologic injury and the necessary use of potent analgesics.

Burns

Check all body areas for additional injury and burns. Wash unburned skin to remove any remaining toxic residues.

Medications

Corticosteroids are attractive for suppressing inflammation and reducing edema. Controlled studies assessing their effects on various forms of chemical pneumonitis are disappointing, and no direct data support their use in smoke inhalation. Because of the increased risk of infection and delayed wound healing, prolonged use of steroids is discouraged. Studies report increased incidence of pulmonary infection and mortality in patients receiving steroids. However, consider a brief course of steroids in those patients with otherwise unresponsive severe lower airway obstruction. In addition, patients receiving steroids prior to injury who may experience adrenal insufficiency should receive stress doses of steroids.

Patients with pulmonary damage from inhalation injury are at increased risk for secondary bacterial infection. The most common organisms are Staphylococcus aureus and Pseudomonas aeruginosa. Direct parenteral coverage with antibiotics to cover these bacteria if infection is suspected.

Antimicrobial therapy should be reserved for patients with definitive microbiologic evidence of infection that is not responding to aggressive support therapy or when clinical deterioration occurs in the first 72 hours, when infection is most likely to occur. Prophylactic antibiotics are not only nonprophylactic, but increase the risk of emergence of resistant organisms. Discerning secondary infection from the effects of inhalation injury can be very difficult because both may produce fever, elevated WBC counts, and abnormal radiography findings.

Although pulmonary damage includes inactivation of surfactant, the effectiveness of artificial surfactant administration has not been proven.

Cyanide is detoxified to thiocyanate (SCN-), predominately by rhodanese in the liver. Thiocyanate is excreted by the kidneys in the presence of normal renal function. Rhodanese is located around the mitochondria within the cells, placing it in close proximity to the major site of cyanide toxicity, the cytochrome oxidases. Sulfur is required for this enzymatic process to occur.

Oxygen and sodium thiosulfate are the most widely accepted cyanide antidotes. Less accepted cyanide antidotes include hydroxocobalamin and dicobalt ethylenediaminetetraacetic acid (EDTA). The mechanism of action of oxygen as a cyanide antidote is unclear but it potentiates the effect of other antidotes. When used in the setting of smoke inhalation, it is also therapeutic for CO poisoning. Thus, high concentrations of oxygen should be promptly delivered.

Sodium thiosulfate increases the sulfur pool and dramatically favors conversion of cyanide to thiocyanate. In the presence of renal failure, thiocyanate is not eliminated and hemodialysis should be offered.

Nitrites convert hemoglobin to methemoglobin. Cyanide becomes bound to methemoglobin because of its very high affinity for the ferric iron of methemoglobin. The induction of methemoglobinemia in the setting of smoke inhalation should be undertaken with caution because coexisting carboxyhemoglobinemia can seriously decrease oxygen carrying capacity and is potentially dangerous.

Antidote kits (eg, Lily Cyanide Antidote Kit) that include amyl nitrite, sodium nitrite, and sodium thiosulfate are commercially available.

Bronchodilators are used in those patients with bronchoconstriction. Intravenous bronchodilators may be needed in severe cases. See Medication for specific instructions.

Heparin has been administered topically, subcutaneously, intravenously, or via aerosol in several studies.^[6] Currently, no strong evidence suggests that heparin can improve clinical outcomes in the treatment of burn injuries.

Oxygen

Oxygen is used in cases with significant inhalation injury. See Medication for specific instructions.

A team experienced in caring for children with burns should evaluate children with significant cutaneous burns.

A pediatric pulmonologist, surgeon, or otolaryngologist should be consulted to perform direct laryngoscopy or bronchoscopy if needed. A pediatric pulmonologist is needed for children suspected of having residual pulmonary disease.

Do not feed children by mouth until significant respiratory or hemodynamic compromise clearly does not require tracheal intubation.

Even with extensive burns, most patients can tolerate enteral feedings at the end of the first 24 hours. Begin enteral feedings as soon as possible. As enteral intake increases, decrease intravenous fluids accordingly. Patients may demonstrate marked hypermetabolism. Therefore, providing adequate nutritional support is important.

Activity is performed as tolerated and as dictated by the extent of disease.