Diagnosis and management of inhalation injury

Introduction

Approximately 10–20% of patients admitted to burn centers in the U. S. are diagnosed with inhalation injury, and the incidence of inhalation injury is directly related to burn size [1]. Inhalation injury, along with age and total body surface area (TBSA) burn, is also one of the factors contributing to the morbidity and mortality of patients with burn injury; inhalation injury has been reported to increase mortality two-fold [2 – 5]. The accurate and timely diagnosis of inhalation injury is key to predicting and improving outcomes for the patient with burn injury. One of the major challenges in the diagnosis of inhalation injury is that exposure to smoke and heat result in nonhomogeneous injuries that vary by location and type of insult. Hence, inhalation injury is a term used to define multiple different types of airway injury, each of which has unique diagnostic and treatment implications. The purpose of this article is to describe the pathophysiology, diagnosis, and treatment of the different forms of inhalation injury.

In general, there are three different types of airway injury that occur after exposure to fire and smoke: 1. effects of inhaled gases, 2. upper airway injury, and 3. lower airway injury [6]. Each of the different types of smoke inhalation injury has a different cause, pathophysiology, treatment, and prognosis. As such, it is important to distinguish

Marc G. Jeschke et al. (eds.), Handbook of Burns

among the three types of injury during the initial evaluation of the patient with suspected inhalation injury.

Effects of inhaled gases

Inhalation of toxic byproducts of combustion account for 80% of fire-related deaths [7]. Several changes in the composition of gases in the environment occur as the result of combustion of flammable objects, and the person exposed to these gases is subject to their effects. When flames engulf a room, they consume oxygen. This decreases the fraction of inspired oxygen in the room to below 10%, which results in asphyxia and tissue hypoxia. Hence, the leading cause of death at the scene of a fire is due to hypoxia, not burns.

Carbon monoxide

CO is one of the leading causes of poisoning deaths in the U. S., accounting for an estimated 15,000 emergency room visits and 500 unintentional deaths yearly [8]. CO has an affinity with hemoglobin 200 – 250 times that of oxygen, which decreases both the oxygen-carrying capacity and the delivery of oxygen to tissue [9]. As such, CO shifts the oxyhemoglobin disassociation curve to the left. The morbidity and mortality associated with CO toxici-

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ty are caused by interference of oxygen transport at the cellular level and the impairment of electron transport with in the cells, resulting in tissue hypoxia [10]. Several other mechanisms have been proposed to explain the toxicity of CO, including interference with hepatic cytochromes, myoglobin binding, and peroxidation of cerebral lipids [9]. The extent of injury is dependent on the duration of exposure, the concentration of CO inhaled, and the underlying health status of the individual exposed to CO. In general, an exposure to a 0.1 % CO concentration can result in a carboxyhemoglobin level of 50% [6].

The common short and long term morbidities of CO toxicity involve the neurologic and vascular systems. Acute CO toxicity at the scene of a fire commonly results in neurologic deficits, which are related to the carboxyhemoglobin level (Table 1) [11]. In general, any patient who is confused or combative after flame burn injury should be considered to be hypoxic until proven otherwise. Neurologic sequelae are divided into two syndromes: persistent neurologic sequelae (PNS), in which the neurologic deficit improves over time, and delayed neurologic sequelae (DNS), in which a relapse of neurologic signs/ symptoms occur after a transient period of improvement. Many patients are sedated or being treated with other therapeutic adjuncts that alter level of consciousness after exposure to CO, making it difficult to differentiate to accurately assess neurologic function. CO will, in addition, interfere with the functional state of leukocytes, platelets, and vascular endothelium [12].

Table 1. Carbon monoxide levels and toxicity

Patients with isolated CO toxicity are classically described as having rosy red cheeks and nose. However, in practice, these patients often are often concomitantly hypoxic, which makes the use of skin color as a diagnostic modality problematic. Importantly, pulse oximetry does not accurately reflect systemic oxygenation, and should not be used to assess oxygenation, and pulse oximetry should NOT be used in isolation to evaluate oxygenation after burn/ smoke exposure. Cooximetry, which delineates the impact of COHb, in association with an arterial blood gas, should be used. The diagnosis of CO toxicity is made by measuring plasma carboxyhemoglobin levels. Patients should be given supplemental oxygen until the results of the COHb levels are obtained. The use of oxygen post-exposure is based upon the premise that displacing CO from the hemoglobin molecule will help return oxygen transport to normal. The duration of the hypoxic state is thought to be an important determinant of severity of CO injury; however, COHb levels do not correlate with the severity of poisoning, predict prognosis, or determine choice of a specific therapy [13].

Patients with a COHb >10% need to be treated with supplemental oxygen and COHb levels repeated every hour until the COHb level drops to >10%. Patients who are awake and alert with COHb >10% should be treated with 100% FIO2 via face mask until the COHb level drops to below 10%. Use of 100% oxygen for an additional six hours after COHb levels are >10% may help to facilitate tissue wash-out of COHb. Obtunded patients should be intubated and placed on mechanical ventilation on 100% FIO2. The half-life of COHb is dependent on the concentration of oxygen. Use of 100% FIO2 will result in a half life of COHb of 40–60 minutes [14]. If the COHb level is >25% despite aggressive oxygen therapy, then the patient may be a candidate for hyperbaric oxygen. However, the half-life of COHb remains 30 minutes with hyperbaric oxygen [15]. Four of six studies evaluating outcomes in 1335 patients randomized to either hyperbaric or normobaric oxygen found no benefit of hyperbaric oxygen in terms of neurologic sequellae [9, 16–20]. Given the potential complications of hyperbaric oxygen therapy (tympanic membrane rupture, seizure, lack of patient accessibility), it should be reserved for patients who fail to improve neurologically with documented CO exposure and COHb >25% [6, 11].