Smoke Inhalation Treatment & Management

• Deliver high-flow oxygen by mask.
• 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.
• Secure IV access, but do not delay transport of patient to the hospital in any way.
• Obtain 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.^[17]

Presently, no specific treatment exists to ameliorate the tissue damage and reduce the vulnerability to infection induced by smoke inhalation. Once the CO toxicity, CN toxicity, and methemoglobinemia have been corrected, subsequent treatment is predominantly supportive.

• High-flow humidified oxygen is critical to reverse or prevent hypoxia and assist displacement of CO from Hb.
• The most urgent concern in patients is the patency of the upper airway and adequacy of ventilation.

  • About 50% of patients with an inhalation injury require endotracheal intubation. The proportion of patients requiring this procedure is higher for those who also have a burn injury: 62% with a burn versus 12% without a thermal injury.
  • 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. Delays create the possibility that critical airway compromise may be unrecognized or develop quickly, making endotracheal intubation technically impossible.
• If systemic paralysis is necessary, succinylcholine can be used safely in the immediate post-burn phase and up to several days out. Inflate 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.
• Studies have shown that positive pressure ventilation with low tidal volumes (3-5 mL per kg) and positive end-expiratory pressure (PEEP) initiated immediately after the inhalation injury significantly increases short-term survival and is associated with decreased tracheobronchial cast formation. The mechanism by which PEEP works may be from "splinting" the alveoli and preventing bronchial cast formation and protein-rich fluid from entrapping the airway.^[19]
• Other studies have shown that high-frequency percussive ventilation (HFPV) also decreases mortality, pneumonia, and barotrauma. This modality generates pulsatile flow at up to 600 cycles per minute, which entrains the humidified gas by effect on molecular diffusion. Clearance of airway secretions may improve, and continued patency of the lower airways may be allowed. In patients with inhalation injury and less than 40% TBSA burns HFPV decreases both morbidity and mortality. While not as commonly used in the ED, many burn centers consider this standard therapy.^{[19, 21, 22]}
• Administer IV fluids to maintain a euvolemic state and to ensure adequate tissue perfusion. Use formulas (eg, Parkland) to calculate fluid resuscitation if severe burns are present.
• Assume elevated levels of HbCO in all fire victims.

  • The half-life of CO is 320 minutes on room air, 90 minutes on 100% oxygen, and 23 minutes in a hyperbaric chamber at 3 atmospheres absolute (ATA). Elimination of CO depends primarily on the law of mass action, so alveolar PO₂, rather than alveolar ventilation, is the critical factor in its removal.
  • CO is not only responsible for most prehospital deaths due to smoke inhalation, it is also the leading cause of injury/death from all poisons worldwide.^[23]
• The main reason for use of HBO therapy is to prevent delayed neurological sequelae.

  • Literature suggests that hypoxic encephalopathy secondary to CO poisoning results from a reperfusion injury in which the products of lipid peroxidation and free radical formation contribute to morbidity and mortality. In addition, improvement in mitochondrial oxidative metabolism, impairment of adherence of neutrophils to cerebral vasculature (decreases inflammation), and preservation of adenosine triphosphate activity was shown with HBO therapy. This partially explains why HbCO levels are poor indicators of the severity of intoxication and why patients with significant toxicity may have low levels. In fact, at the time of the initial HBO treatment, patients enrolled in most studies have normal or near-normal COHb levels.
  • A classic study demonstrated that dogs breathing 13% CO died within 1 hour after achieving CO-Hgb levels from 54% to 90%. However, exchange transfusion with blood containing 80% CO-Hgb to otherwise healthy dogs resulted in no toxic effects, despite resultant CO-Hgb levels of 57-64%. This further supports the notion that CO toxicity is not dependent on CO-Hgb formation or, in other words, solely upon a relative anemia.
  • At this time, 6 prospective, randomized controlled trials have compared HBO with normobaric oxygen (NBO) therapy for CO poisoning. Four of these studies show a benefit for CO poisoning; two do not. The data and conclusions drawn from these studies are conflicting and highlight the controversy surrounding the utility of HBO.
  • In a well-cited study, perhaps the most methodologically rigorous, Weaver et al have shown in a prospective, double blind manner that in patients with symptomatic acute CO poisoning, 3 HBO treatments, in comparison to NBO therapy, decreased the incidence of cognitive sequelae by 46% at 6 weeks.^[24] Furthermore, a benefit continued to be seen at 12-month follow-up. Essentially, for every 6 patients treated with HBO, one case of delayed neurologic sequelae could be avoided. The study had to be stopped before its completion because of the evidence.
  • Though there has been much debate regarding the accuracy of neuropsychometric testing, including the fact that patients who are depressed and who have attempted suicide with non-CO means perform as poorly as CO-exposed patients, they remain an objective means to evaluate cognitive function.
  • Neurologic abnormalities and a history of loss of consciousness are the primary clinical features used to define severe CO toxicity. HBO use is indicated in any of these patients as well as those with a base excess lower than -2 mmol/L, a CO level greater than 25% (or >15% in pregnancy as fetal hemoglobin binds CO more tightly), signs of cerebellar dysfunction, cardiovascular dysfunction, pulmonary edema, and in the extremes of age. Note that the incidence of delayed neurologic sequelae (DNS) increases with a more symptomatic initial clinical picture, in older patients, and in those with a prolonged exposure.^[23]
  • The American College of Emergency Physicians Clinical Policies Subcommittee recommended in 2008 continued use of HBO in CO poisoning, especially in children and pregnant women, due to the conflicting results of previous studies.^[25]
• Management of CN toxicity has historically involved the creation of an alternate binding site for CN to compete with cytochrome oxidase and also to provide substrate necessary to convert CN to a nontoxic metabolite.

  • Although not used universally, hydroxocobalamin (vitamin B-12), a hemelike molecule with a complexed cobalt atom, has become the preferred treatment of CN toxicity. It has been used in France for more than 30 years and was approved by the FDA in 2006 for use in the US. CN reacts with high affinity with metals such as ferric ion and cobalt and binds to numerous critical enzymes in the body. The mechanism of action is direct binding to CN to form cyanocobalamin that is excreted renally.
  • In vitro studies indicate that hydroxocobalamin penetrates cells and can act intracellularly. Side effects are chromaturia and reddening of the skin. Empiric administration to patients subsequently confirmed to have CN poisoning has been shown to be associated with 67% survival. It has a rapid onset of action, is easy to administer, does not interfere with cellular oxygen use, is well tolerated, and is safe for smoke inhalation patients. Additionally, it is not associated with hypotension or the formation of a dyshemoglobinemia found in previous antidote kits.^{[2, 26, 27]}
  • The traditional CN antidote kit contains amyl and sodium nitrite to create a methemoglobin level of 3% and 20-30%, respectively, which, in turn, has a higher affinity for CN than for cytochrome a₃. Also included is sodium thiosulfate, which provides substrate for the enzyme rhodanese, which combines thiosulfate and CN to form a nontoxic compound, thiocyanate, which is excreted renally.
  • Induction of methemoglobinemia is theoretically dangerous in the setting of HbCO, due to an even greater reduction in oxygen carrying capacity, and the clinician should consider withholding the nitrite portion of the kit. Another drawback of this treatment is the delayed onset of thiosulfate. Finally, this treatment may be more preventative rather than curative.
  • Methemoglobinemia in smoke inhalation is relatively rare and rarely requires treatment with methylene blue. This antidote is reduced by the nicotinamide adenine dinucleotide phosphate (NADPH) methemoglobin reductase enzyme and in return reduces methemoglobin to normal hemoglobin. Indications for treatment are a change in mental status, acidosis, ECG changes, and ischemic chest pain. Levels lower than 30% may not require treatment, depending on the patient's cardiorespiratory reserve.
• 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 COPD or asthma.
• Although the pathophysiology of smoke inhalation involves irritants setting off the inflammatory response, no benefit has been shown with corticosteroid therapy. In fact, many studies report an increased rate of pulmonary infection.^[28]
• Inhalation injuries clearly predispose the airways to infection after several days because of cellular injury, reduction of mucociliary clearance, and poor macrophage function. Despite this, prophylaxis with parenteral antibiotics has not shown any benefit. Acute bacterial colonization and invasion peaks at 2-3 days after smoke inhalation injury. Consider cultures and possible treatment at this time.
• 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-acetylcystine decreases the incidence of atelectasis, reintubation rates, and overall mortality.^[29]
• In the animal model, whole-body hypothermia has recently been shown to suppress oxidant bronchoalveolar damage and pulmonary inflammation.^[30] Mechanistically, this appears to halt the progression of bronchoalveolar-capillary permeability.

Obtain trauma surgery or burn specialist consultation in patients with significant exposure.