Smoke Inhalation Injury Treatment & Management
Approach Considerations
Beware that patients may appear asymptomatic on arrival but may develop significant signs and symptoms as long as 36 hours after exposure, especially in fires, which produce small particles with low water solubility. Be aware of pertinent historical risk factors when treating patients with potential smoke inhalation injury. These include closed-space fires, carbonaceous sputum, elevated carbon monoxide (CO) levels, and central facial burns.
Acute respiratory distress usually responds very well to aggressive initial management. Normal laboratory values and imaging studies, coupled with clinical improvement, can give the health care provider a false sense of security. The patient then may be discharged, only to deteriorate as delayed pulmonary edema ensues. Any patient with significant exposure to toxic smokes should be observed for 24-48 hours and imaged with serial chest radiographs. Difficulty arises in defining a significant exposure, since the clinical response is so varied.
Provide intravenous (IV) access, cardiac monitoring, and supplemental oxygen in the setting of hypoxia. A small subset of patients manifests bronchospasm and may benefit from the use of bronchodilators, although this is not well documented. This is especially true of patients with underlying chronic obstructive pulmonary disease (COPD) or asthma.
Treatment of inhalation injuries caused from toxic smokes is based on clinical presentation and involves primarily supportive care directed at the cardiopulmonary system. In some cases (eg, cyanide [CN] poisoning, methemoglobinemia), specific antidotes are available. Subcutaneous epinephrine has been used in zinc oxide (HC) exposures.
Corticosteroids are attractive for suppressing inflammation and reducing edema, but no direct data support their use in smoke inhalation. Because of the increased risk of pulmonary infection and delayed wound healing, prolonged use of steroids is discouraged. 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.
Although controlled studies assessing the effects of steroids on various forms of chemical pneumonitis are disappointing, steroids have been suggested as having some value in exposure to the following:
Oxides of nitrogen (NOx)
Zinc oxide (HC)
Red phosphorus (RP)
Sulfur trioxide (FS)
Titanium tetrachloride (FM)
Polytetrafluoroethylene (PTFE; Teflon)
In a case series by Huang et al, 25% of patients presented after HC exposure with acute lung injury requiring ventilatory support. All of these patients survived with glucocorticoids, antibiotics and lung-protective ventilatory management. However, there was no control group, so a causal link could not be made between survival and steroid treatment.[3, 45]
Smoke inhalation injuries predispose the airways to infection because of cellular injury, reduction of mucociliary clearance, and poor macrophage function. Acute bacterial colonization and invasion peaks at 2-3 days after smoke inhalation. Prophylactic antibiotics should not be used, as they are not only ineffective 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 white blood cell counts, and abnormal radiography findings. 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.
The most common organisms in secondary pneumonia after smoke inhalation injury are Staphylococcus aureus and Pseudomonas aeruginosa. Direct parenteral coverage with antibiotics to cover these bacteria if infection is suspected.
Prehospital Care
As always, prehospital care providers must do everything in their power to remove the patient from ongoing exposure without becoming casualties themselves. Although emergency department (ED) care is mostly supportive, prompt delivery to the ED should be a priority.
Secure the airway as needed, deliver high-flow oxygen by mask, and obtain IV access. Cardiac monitoring also is important for any patient with respiratory distress. Beta-agonists such as albuterol may be given as a nebulized treatment to those who demonstrate signs of bronchoconstriction.
If respiratory failure is present, the patient should have assisted ventilation and/or endotracheal intubation. Perform cricothyrotomy if airway obstruction is present or impending and an airway cannot be secured orally.
Obtain a CO level at the scene if possible. In a consecutive case series of 18 patients, cardiac arrest complicating CO toxicity was uniformly fatal, despite administration of hyperbaric oxygen (HBO) therapy after the initial resuscitation. The prognosis of this condition should be considered when making triage decisions for these patients
Emergency Department Care
Presently, no specific treatment exists to ameliorate the tissue damage and reduce the vulnerability to infection induced by smoke inhalation. Administer 100% oxygen because of the likelihood of CO inhalation in fires. Once CO toxicity, cyanide (CN) toxicity, and methemoglobinemia have been addressed, subsequent treatment is predominantly supportive.
The most urgent concern in patients is the patency of the upper airway and adequacy of ventilation. 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. The proportion of patients with an inhalation injury who require endotracheal intubation is higher for those who also have a burn injury: 62% with a burn versus 12% without a thermal injury and the incidence of inhalation injury increases with the size of the burn.[2] See the image below.
It is of vital importance that the magnitude of the swelling in the areas of the face and mandible be closely scrutinized when making decisions about the need for an artificial airway. The threshold for intubation should be lower than in other patients due to the potential of rapid development of airway edema. This is especially true of the pediatric patient. 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.
If systemic paralysis is necessary for intubation, succinylcholine can be used safely in the immediate post-burn phase and up to several days afterward, although one should be cognizant of the possibility of a rise in serum potassium. Inflate the tube cuff to minimal levels, even allowing a small leak, in order to prevent iatrogenic tracheal damage in patients with an already compromised tracheal mucosa.
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. Large-bore IV catheter access may be needed to facilitate fluid resuscitation.
Use formulas (eg, Parkland) to calculate fluid resuscitation if severe burns are present. Even minor errors in estimation of body surface area; burned surface area; and fluid, electrolyte, and protein requirements can produce profound hemodynamic and respiratory compromise. Frequent evaluation of heart rate, perfusion, and blood pressure are needed to determine stability and guide therapy.
In mass casualty scenarios, the use of fiberoptic bronchoscopy may be beneficial to rapidly triage patients to intensive care, ward, or observation status. Mobilization of otolaryngology and/or anesthesia resources may be necessary to accomplish this in a timely fashion.
Hospital Admission Criteria
Patients with smoke inhalation should be monitored for 4-6 hours in the ED. Those who are at low risk for injury and whose vital signs and physical examination findings remain normal can usually be discharged with close follow-up and instructions to return if symptoms develop.
While there are no definite criteria for admission, patients with any of the following should be strongly considered for hospitalization:
• History of closed-space exposure for longer than 10 minutes
• History of syncope
• Carbonaceous sputum production
• Arterial PO2 less than 60 mm Hg
• Metabolic acidosis
• Carboxyhemoglobin levels above 15%
• Arteriovenous oxygen difference (on 100% oxygen) greater than 100 mm Hg
• Bronchospasm
• Odynophagia
• Central facial burns
For patients with isolated smoke inhalation, treatment in an intensive care unit is appropriate. However, patients with significant cutaneous burns should be transferred to a burn center when stable, if they meet the criteria for transfer
Experimental Treatments
Studies on experimental induction of smoke inhalation confirm the presence of an acute surfactant deficiency. Instillation of artificial surfactant shortly after injury was beneficial. Larger studies are needed before instituting such therapy.
Oxidant injury eventually leads to cast formation of cellular debris in the airways, thus contributing to pulmonary failure. A pediatric study has shown that aerosolized heparin/N -acetylcysteine decreases the incidence of atelectasis, reintubation rates, and overall mortality.[52]
Acetylcysteine and L-3,4 dehydroproline and a combined regimen of hydrocortisone and penicillamine have been used to treat ARDS induced by inhalation of smoke from smoke bombs. Positive outcomes were attributed to early treatment with penicillamine.[17] In anima
Smoke Inhalation Injury Treatment & Management
Approach Considerations
Beware that patients may appear asymptomatic on arrival but may develop significant signs and symptoms as long as 36 hours after exposure, especially in fires, which produce small particles with low water solubility. Be aware of pertinent historical risk factors when treating patients with potential smoke inhalation injury. These include closed-space fires, carbonaceous sputum, elevated carbon monoxide (CO) levels, and central facial burns.
Acute respiratory distress usually responds very well to aggressive initial management. Normal laboratory values and imaging studies, coupled with clinical improvement, can give the health care provider a false sense of security. The patient then may be discharged, only to deteriorate as delayed pulmonary edema ensues. Any patient with significant exposure to toxic smokes should be observed for 24-48 hours and imaged with serial chest radiographs. Difficulty arises in defining a significant exposure, since the clinical response is so varied.
Provide intravenous (IV) access, cardiac monitoring, and supplemental oxygen in the setting of hypoxia. A small subset of patients manifests bronchospasm and may benefit from the use of bronchodilators, although this is not well documented. This is especially true of patients with underlying chronic obstructive pulmonary disease (COPD) or asthma.
Treatment of inhalation injuries caused from toxic smokes is based on clinical presentation and involves primarily supportive care directed at the cardiopulmonary system. In some cases (eg, cyanide [CN] poisoning, methemoglobinemia), specific antidotes are available. Subcutaneous epinephrine has been used in zinc oxide (HC) exposures.
Corticosteroids are attractive for suppressing inflammation and reducing edema, but no direct data support their use in smoke inhalation. Because of the increased risk of pulmonary infection and delayed wound healing, prolonged use of steroids is discouraged. 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.
Although controlled studies assessing the effects of steroids on various forms of chemical pneumonitis are disappointing, steroids have been suggested as having some value in exposure to the following:
Oxides of nitrogen (NOx)
Zinc oxide (HC)
Red phosphorus (RP)
Sulfur trioxide (FS)
Titanium tetrachloride (FM)
Polytetrafluoroethylene (PTFE; Teflon)
In a case series by Huang et al, 25% of patients presented after HC exposure with acute lung injury requiring ventilatory support. All of these patients survived with glucocorticoids, antibiotics and lung-protective ventilatory management. However, there was no control group, so a causal link could not be made between survival and steroid treatment.[3, 45]
Smoke inhalation injuries predispose the airways to infection because of cellular injury, reduction of mucociliary clearance, and poor macrophage function. Acute bacterial colonization and invasion peaks at 2-3 days after smoke inhalation. Prophylactic antibiotics should not be used, as they are not only ineffective 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 white blood cell counts, and abnormal radiography findings. 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.
The most common organisms in secondary pneumonia after smoke inhalation injury are Staphylococcus aureus and Pseudomonas aeruginosa. Direct parenteral coverage with antibiotics to cover these bacteria if infection is suspected.
Prehospital Care
As always, prehospital care providers must do everything in their power to remove the patient from ongoing exposure without becoming casualties themselves. Although emergency department (ED) care is mostly supportive, prompt delivery to the ED should be a priority.
Secure the airway as needed, deliver high-flow oxygen by mask, and obtain IV access. Cardiac monitoring also is important for any patient with respiratory distress. Beta-agonists such as albuterol may be given as a nebulized treatment to those who demonstrate signs of bronchoconstriction.
If respiratory failure is present, the patient should have assisted ventilation and/or endotracheal intubation. Perform cricothyrotomy if airway obstruction is present or impending and an airway cannot be secured orally.
Obtain a CO level at the scene if possible. In a consecutive case series of 18 patients, cardiac arrest complicating CO toxicity was uniformly fatal, despite administration of hyperbaric oxygen (HBO) therapy after the initial resuscitation. The prognosis of this condition should be considered when making triage decisions for these patients
Emergency Department Care
Presently, no specific treatment exists to ameliorate the tissue damage and reduce the vulnerability to infection induced by smoke inhalation. Administer 100% oxygen because of the likelihood of CO inhalation in fires. Once CO toxicity, cyanide (CN) toxicity, and methemoglobinemia have been addressed, subsequent treatment is predominantly supportive.
The most urgent concern in patients is the patency of the upper airway and adequacy of ventilation. 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. The proportion of patients with an inhalation injury who require endotracheal intubation is higher for those who also have a burn injury: 62% with a burn versus 12% without a thermal injury and the incidence of inhalation injury increases with the size of the burn.[2] See the image below.
It is of vital importance that the magnitude of the swelling in the areas of the face and mandible be closely scrutinized when making decisions about the need for an artificial airway. The threshold for intubation should be lower than in other patients due to the potential of rapid development of airway edema. This is especially true of the pediatric patient. 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.
If systemic paralysis is necessary for intubation, succinylcholine can be used safely in the immediate post-burn phase and up to several days afterward, although one should be cognizant of the possibility of a rise in serum potassium. Inflate the tube cuff to minimal levels, even allowing a small leak, in order to prevent iatrogenic tracheal damage in patients with an already compromised tracheal mucosa.
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. Large-bore IV catheter access may be needed to facilitate fluid resuscitation.
Use formulas (eg, Parkland) to calculate fluid resuscitation if severe burns are present. Even minor errors in estimation of body surface area; burned surface area; and fluid, electrolyte, and protein requirements can produce profound hemodynamic and respiratory compromise. Frequent evaluation of heart rate, perfusion, and blood pressure are needed to determine stability and guide therapy.
In mass casualty scenarios, the use of fiberoptic bronchoscopy may be beneficial to rapidly triage patients to intensive care, ward, or observation status. Mobilization of otolaryngology and/or anesthesia resources may be necessary to accomplish this in a timely fashion.
Hospital Admission Criteria
Patients with smoke inhalation should be monitored for 4-6 hours in the ED. Those who are at low risk for injury and whose vital signs and physical examination findings remain normal can usually be discharged with close follow-up and instructions to return if symptoms develop.
While there are no definite criteria for admission, patients with any of the following should be strongly considered for hospitalization:
• History of closed-space exposure for longer than 10 minutes
• History of syncope
• Carbonaceous sputum production
• Arterial PO2 less than 60 mm Hg
• Metabolic acidosis
• Carboxyhemoglobin levels above 15%
• Arteriovenous oxygen difference (on 100% oxygen) greater than 100 mm Hg
• Bronchospasm
• Odynophagia
• Central facial burns
For patients with isolated smoke inhalation, treatment in an intensive care unit is appropriate. However, patients with significant cutaneous burns should be transferred to a burn center when stable, if they meet the criteria for transfer
Experimental Treatments
Studies on experimental induction of smoke inhalation confirm the presence of an acute surfactant deficiency. Instillation of artificial surfactant shortly after injury was beneficial. Larger studies are needed before instituting such therapy.
Oxidant injury eventually leads to cast formation of cellular debris in the airways, thus contributing to pulmonary failure. A pediatric study has shown that aerosolized heparin/N -acetylcysteine decreases the incidence of atelectasis, reintubation rates, and overall mortality.[52]
Acetylcysteine and L-3,4 dehydroproline and a combined regimen of hydrocortisone and penicillamine have been used to treat ARDS induced by inhalation of smoke from smoke bombs. Positive outcomes were attributed to early treatment with penicillamine.[17] In anima
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