eMedicine Specialties > Pediatrics: General Medicine > Pulmonology
Inhalation Injury: Treatment & Medication
Updated: Jun 6, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
- 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
- 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.
- Antibiotics
- 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.
- Artificial surfactant: Although pulmonary damage includes inactivation of surfactant, the effectiveness of artificial surfactant administration has not been proven.
- Cyanide antidotes
- 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.
- Oxygen: Oxygen is used in cases with significant inhalation injury. See Medication for specific instructions.
- Bronchodilators: Bronchodilators are used in those patients with bronchoconstriction. Intravenous bronchodilators may be needed in severe cases. See Medication for specific instructions.
- Heparin: Heparin has been administered topically, subcutaneously, intravenously, or via aerosol in several studies.5 Currently, no strong evidence suggests that heparin can improve clinical outcomes in the treatment of burn injuries.
- Corticosteroids
Surgical Care
- A team experienced in caring for children with burns should evaluate children with significant cutaneous burns.
Consultations
- 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.
Diet
- 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
- Activity is performed as tolerated and as dictated by the extent of disease.
Medication
Medical gases
Oxygen is used for any suspected significant inhalation injury. Treat with high concentrations of humidified oxygen en route to the hospital.
Humidified oxygen
Use of high oxygen flow rates and a nonrebreathing-type face mask with a tight seal facilitates delivery of high levels of supplemental oxygen, which helps reverse the oxygenation defect created by ventilation-perfusion mismatch. Inhaled oxygen also helps in the displacement of CO from hemoglobin, decreasing the half-life of carboxyhemoglobin from 4-6 h in room air to 40-60 min in 100% FiO2.
Adult
Pediatric
Oxygen therapy should be continued until acidosis is corrected, the carboxyhemoglobin levels have fallen below 15%, and neurologic symptoms have resolved, which typically takes several hours
None reported
None reported
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Inspired oxygen concentrations of 50-100% carry a substantial risk of lung damage (dependent on inspired pressure and treatment duration)
Hyperbaric oxygen therapy (HBO)
This therapy also displaces CO from intracellular stores and may improve mitochondrial function. HBO requires special facilities that are not available at all centers, resulting in a delay in treatment while the patient is transported to facility with HBO. Hyperbaric therapy should be considered in those patients who have high carboxyhemoglobin levels >40%, who are unconsciousness, have other neurologic findings, or have severe metabolic acidosis (ph <7.1). Benefit of treating patients 12 h after CO exposure remains unproven.
Adult
Pediatric
The half-life of carboxyhemoglobin can be further reduced to 15-30 min in 2-3 atm of HBO
None reported
None reported
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
The potential benefits of preventing long-term neurologic sequelae from the secondary syndrome of CO poisoning should be weighed against the lack of patient access while undergoing HBO therapy; the anticipated use of hyperbaric therapy should never preclude the use of high concentrations of supplemental O2; complications include middle ear and sinus occlusion, air embolism, and seizures
Bronchodilators
These agents relieve reversible bronchospasm by relaxing smooth muscles of the bronchi. Increased resistance from airway edema and reflex bronchoconstriction from irritation of airway receptors contribute to airway obstruction.
Nebulized albuterol (Proventil, Ventolin)
Relaxes bronchial smooth muscle by action on beta2-receptors with little effect on cardiac muscle contractility.
Adult
Nebulizer: Dilute 0.5 mL (2.5 mg) of 0.5% inhalation solution in 1-2.5 mL of NS; administer 2.5-5 mg q15-20min, then space administration according to the patient's symptoms
Pediatric
<5 years (nebulizer): Dilute 0.25-0.5 mL (1.25-2.5 mg) of 0.5% inhalation solution in 1-2.5 mL of NS and administer q15-20min, then space administration according to the patient's symptoms
>5 years (nebulizer): Administer as in adults
Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation by albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, tricyclic antidepressants, and sympathomimetic agents
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hyperthyroidism, diabetes mellitus, and cardiovascular disorders; adverse effects include tachycardia, palpitations, tremor, insomnia, nervousness, nausea, and headache
Racemic epinephrine 2.25% (MicroNefrin, AsthmaNefrin, Racepinephrine)
Alleviates airway edema and reflex bronchospasm. Although it has not been directly studied, inhaled racemic epinephrine can theoretically provide relief from both airway edema and reflex bronchospasm in this setting.
Adult
Nebulizer: 0.25-0.5 mL (diluted in 3 mL of 0.9% NaCl) inhaled via nebulization q4-6h prn
Pediatric
Administer as in adults
Increases toxicity of beta- and alpha-blocking agents and that of halogenated inhalational anesthetics
Documented hypersensitivity; cardiac arrhythmias; angle-closure glaucoma
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency
Terbutaline (Brethine)
Used for severe bronchoconstriction, especially in patients with underlying reactive airways disease. Acts directly on beta2-receptors to relax bronchial smooth muscle, relieving bronchospasm and reducing airway resistance.
Adult
Loading dose: 0.25 mg IV
Maintenance dose: 0.1-0.4 mcg/kg/min IV; titrate to effect
Pediatric
Loading dose: 2-10 mcg/kg IV
Maintenance dose: 0.08-0.4 mcg/kg/min IV; titrate to effect
Concomitant use with beta-blockers may inhibit bronchodilating, cardiac, and vasodilating effects of beta agonists; concomitant administration of MAOIs with beta sympathomimetics may result in severe hypertension, headache, and hyperpyrexia, which may result in a hypertensive crisis; MAOIs may potentiate activity of beta-adrenergic agonists on the vascular system; concurrent administration of oxytocic drugs such as ergonovine with terbutaline may result in severe hypotension
Documented hypersensitivity; tachycardia resulting from cardiac arrhythmias
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Through intracellular shunting, terbutaline may decrease serum potassium levels, which can produce adverse cardiovascular effects; decrease is usually transient and may not require supplementation; paradoxical bronchoconstriction may occur with excessive use
Epinephrine (Adrenaline, EpiPen)
Used for severe bronchoconstriction, especially in patients with underlying reactive airways disease. Alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist effects of epinephrine include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.
Adult
0.1-0.5 mg (1:1000 concentration [1 mg/mL]) IM/SC q10-15min to 4 h; alternatively, 0.1-0.25 mg IV; single dose not to exceed 1 mg
Pediatric
0.01 mg/kg/dose (0.01 mL/kg of the 1:1000 concentration [1 mg/mL]); not to exceed 0.5 mg/dose
Increases toxicity of beta- and alpha-blocking agents and that of halogenated inhalational anesthetics
Documented hypersensitivity; cardiac arrhythmias or angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue; use during labor (may delay second stage of labor)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in elderly persons and patients with prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias
More on Inhalation Injury |
| Overview: Inhalation Injury |
| Differential Diagnoses & Workup: Inhalation Injury |
 Treatment & Medication: Inhalation Injury |
| Follow-up: Inhalation Injury |
| References |
| « Previous Page | Next Page » |
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Further Reading
Keywords
inhalation injury, smoke inhalation, smoke, carbon monoxide, CO, hydrogen cyanide, reflex bronchoconstriction, hydrocarbon inhalation, hypoxemia, bacterial pneumonia, airway obstruction, residual reactive airway disease, bronchiectasis, bronchiolitis obliterans, interstitial fibrosis, asthma, respiratory distress, obtundation, hyperinflation, atelectasis, air trapping, lung injury, alveolar edema, ventilation-perfusion mismatch, hypoxia, lactic acidosis, hypotension, renal tubular acidosis, hepatitis, bone marrow insufficiency, thermal burns, conjunctivitis, corneal edema, rhinitis, pharyngitis, laryngitis, tracheitis, bronchitis, alveolitis, respiratory insufficiency
