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Inhalation Injury Emergency Files Inhalation injury Bryan Wise MD CCFP Zachary Levine MD CCFP(EM) Case description mask, and starting intravenous fluids as indicated by the Mr B. is a 46-year-old man who is brought to your patient’s circulatory status.2 emergency department one night after being rescued Once that is complete, a brief history should be from a fire in his apartment complex. He thinks he obtained from the patient or any witnesses. Details of might have briefly lost consciousness while he was the exposure, including the type and location of the fire, trapped in a smoke-filled room before firefighters the duration of smoke exposure, any loss of conscious- were able to free him. He is fully awake and breathing ness, and the condition of any other victims, can provide comfortably upon arrival. Measurement of his vital information about potential inhalation injury.3,4 signs reveals the following: heart rate of 85 beats/min, A targeted physical examination should evaluate for blood pressure of 124/76 mm Hg, respiratory rate of any signs suggestive of inhalation injury, such as face 20 breaths/min, oxygen saturation of 100% on room and neck burns, singed nasal hairs, carbonaceous spu- air, temperature of 36.8°C, and a glucose level of tum, soot in the upper airways, voice changes, or wheez- 6.5 mmol/L. A brief examination reveals only superfi- ing.3,4 It is important to note that the absence of these cial burns to his face and neck. He says that he feels signs does not rule out inhalation injury.2 Additionally, fine now and he wants to return home. How would the patient should be fully exposed, and the extent and you manage Mr B.? Is there anything concerning depth of any cutaneous burns should be noted. about Mr B.’s story? To intubate or not to intubate? Inhalation injury after a fire is a very serious condi- The decision of when to definitely secure the patient’s tion, with very high rates of morbidity and mortality. airway is among the most challenging in manag- Inhalation injury complicates 20% of burns, particu- ing inhalation injury. While any sign of airway com- larly facial burns, leads to respiratory failure in 70% of promise during the primary assessment (eg, stridor, patients, and is fatal in 30% of cases.1 It accounts for respiratory distress, hypoventilation, or decreased more than 80% of all fire-related mortality, with carbon mental status) clearly necessitates intubation, even monoxide (CO) being responsible for most deaths.1 patients who are well initially can rapidly deterio- Inhalation injury encompasses 3 different types of rate.4 Furthermore, as airway edema worsens, intu- insult to respiratory function. Thermal injury to supra- bation becomes technically more difficult. However, glottic structures results in edema and can rapidly lead there is no reliable indicator of which patients will to upper airway obstruction in the initial hours after go on to need intubation, and intubation is neither exposure.2,3 Chemical injury develops over the first 36 without harm to patients nor practical for every burn hours when small particles contained in smoke travel victim.2 A reasonable approach is to consider prophy- to the alveoli and trigger inflammatory reactions that lactic intubation for patients with evidence of seri- lead to bronchospasm and impaired gas exchange in ous cutaneous burns, soot in the oropharynx, or deep the distal airways.3 Finally, systemic oxygenation is burns to the face, neck, or oropharynx, and to closely impaired by toxic gases released in most fires, specifi- observe those without such signs for 24 hours while cally CO and cyanide.3 maintaining a low threshold for intervention.4 It is While advances in burn care have resulted in sub- important to properly secure the endotracheal tube, stantial improvements in the management of cuta- particularly during transfer, as loss of the airway could neous burns, the same cannot be said for inhalation be catastrophic.1 injury. Some of the reasons for this are the lack of clear diagnostic criteria and the absence of specific disease- Further management modifying treatments.1 That is why a high level of There is very little available in terms of specific thera- clinical suspicion and aggressive supportive care remain pies for inhalation injury, so treatment continues to the mainstays of management. focus on supportive care. Regardless of the patient’s oxygen saturation on pulse oximetry, 100% supplemen- Initial assessment tal oxygen should be administered owing to potential The initial assessment of inhalation injury begins with CO exposure. Additionally, if there is any sign of bron- the rapid evaluation and stabilization of the airway, chospasm, inhaled β-agonists can be helpful.3 breathing, and circulation. In a burn patient, this means Fluid replacement can be difficult to manage in ensuring a patent airway, administering 100% oxygen by patients with inhalation injury. While it has been VOL 61: JANUARY • JANVIER 2015 | Canadian Family Physician • Le Médecin de famille canadien 47 Emergency Files shown that inhalation injury in the context of severe smokers).3 Supplemental 100% oxygen will accelerate CO cutaneous burns greatly increases fluid requirements, clearance and is the treatment of choice. Hyperbaric aggressive fluid replacement in isolated inhalation oxygen treatment is thought to clear the CO more injury can be harmful by worsening airway edema quickly, but whether it improves outcomes is contro- and obstruction in the initial hours, and increas- versial.5 Owing to the difficulty of managing critically ill ing the risk of developing adult respiratory distress patients in a hyperbaric chamber, it is not universally syndrome.2 Optimal rehydration requires frequent recommended, but you can discuss this with your local reassessment with adjustments as indicated by the hyperbaric medicine centre.5 patient’s status. Cyanide is produced by the combustion of vari- Efforts to expand the therapeutic arsenal have ous synthetic materials often found in house fires. It largely been directed at interrupting the inflamma- causes hypoxemia by blocking the electron trans- tory and coagulation cascades in the distal airways.1 port chain in the mitochondria and inducing anaero- The most promising results were seen with nebulized bic metabolism.1 Symptoms of cyanide poisoning (eg, anticoagulants, such as heparin; however, there is not restlessness, dyspnea, headache, and dizziness) can yet enough evidence to recommend them as standard be very nonspecific, but toxicity should be suspected in treatment.1 Other treatment strategies being studied any patient with a history of exposure and depressed include modulating pulmonary blood flow or using sur- level of consciousness or respiration.6-8 Cyanide lev- factants and anti-inflammatory agents.1 Notably, anti- els are rarely available in the acute setting, but a lac- biotics and corticosteroids are not effective in the tate level greater than 10 mmol/L is highly predictive treatment of inhalation injury.2,4 of poisoning.6-8 Hydroxocobalamin has replaced the combination of amyl nitrite and sodium thiosulfate Investigations as the antidote of choice and should be considered in While inhalation injury remains largely a clinical diag- severe cases.9 Discussion with your local poison cen- nosis, there are several studies that can provide valu- tre is recommended. able information. Measurement of arterial blood gas is necessary for a true assessment of oxygen saturation, What next? as pulse oximetry is inaccurate in the context of CO poi- After the primary evaluation and treatment, the next soning.5 Blood gas testing with co-oximetry can also step will depend on the patient’s condition and your demonstrate the presence of carboxyhemoglobin or lac- centre’s capabilities. Patients with minimal exposure, tic acidosis.5 Imaging is rarely helpful acutely, as findings a physical examination with normal findings, and no of a chest x-ray scan will usually be unremarkable.4 If evidence of CO or cyanide poisoning can likely be dis- available, bronchoscopy can be used to help diagnose charged home with instructions to return if any symp- and determine the severity of inhalation injury. Different toms develop.1,2 Patients with severe inhalation injury bronchoscopic grading systems exist, which might offer requiring intubation or with other concerning burns prognostic information; however, none can reliably pre- should be transferred to a burn centre intensive care dict which patients will develop respiratory failure, and unit as early as possible after stabilization. Long-term the absence of findings on bronchoscopic investigation concerns for these patients include pneumonia, atel- cannot rule out inhalation injury.3 ectasis, and acute respiratory distress syndrome.4 Patients who are well but in whom inhalation injury Systemic poisoning is suspected represent a more difficult decision, and In addition to direct pulmonary injury in inhalation should be managed in consultation with your local injury, patients are also at risk of hypoxemia from CO burn centre.2 and cyanide inhalation, particularly if the fire occurred in an enclosed space. Back to Mr B. Carbon monoxide is formed by the incomplete com- Because the fire was in an enclosed space, he lost bustion of hydrocarbons and binds to hemoglobin with consciousness, and there were burns to his face, 200 times more affinity than oxygen. This causes an Mr B. was kept in the emergency department for effective anemic state by decreasing the oxygen-car- investigation and monitoring. Further examination rying capacity of hemoglobin and shifting the oxygen did not reveal any burns or soot in the oropharynx dissociation curve to the left.5 Symptoms of CO poison- and blood tests showed no sign of CO or cyanide ing, such as headache, nausea, malaise, dyspnea, and poisoning. He remained asymptomatic and was dis- decreased level of consciousness, can be nonspecific.5 charged home 24 hours later.
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