Inhalation injury is a topic well studied and strongly associated with high rates of morbidity and mortality. The temperature and composition of the toxins that result from combustion rapidly attack tissues and disseminate quickly to the cellular level. This lethality has been exploited throughout the history of warfare. In 423 BC, Spartan general Thucydides recorded the earliest use of a toxic inhalant.1 Later, Pliny the Younger used inhalation as a form of execution, subjecting caged victims to smoke from burning greenwood. His uncle, Pliny the Elder, died in 79 AD in the eruption of Mount Vesuvius.2 His body was found two days later beneath the ash, with no apparent external injuries.
Assault on the respiratory system
The assault of inhalation injury first begins in the oral cavity and oropharynx with microvascular changes that lead to edema. The cascading inflammatory process involves complement histamine and reactive oxygen and nitrogen species. The ensuing edema with absent capillary integrity is compounded by increased microvascular pressure and decreased plasma oncotic pressure from large volume resuscitations.3 Airway patency is soon compromised and can quickly lead to death if the health care provider does not anticipate these changes.
Although less common, thermal injuries to the tracheobronchial tree can occur with explosions or with forceful entry of steam pushing past the glottis. Gases are typically cooled before entering the larynx and more distal areas.4 More commonly, injuries to these areas are secondary to chemical irritants and toxins. The caustic materials trigger additional inflammatory responses, resulting in hyperemia and shedding of columnar epithelium.5 Similarly, changes in bronchial microvasculature, along with hyper-secretion of goblet cells, form exudative casts that can block already edematous, constricted, and inflamed airways.6 Changes to the lung parenchyma are delayed, typically seen 18–24 hours after injury with worsening edema, compliance, and PaO2/FiO2 ratios.7
Systemic toxicity results from the smoke’s components; the destructive array can vary depending on the industrial compounds involved. For example, combustion of ubiquitous materials such as cellulose and polyvinyl chloride produce carbon monoxide (CO). The affinity of CO for hemoglobin is 200 times greater than that of oxygen, creating carboxyhemoglobin (COHb).8 Not only does the oxygen-hemoglobin dissociation curve shift to the left, but CO also inhibits cytochrome-a and P-450 enzyme systems.9 Ultimately, less oxygen is available to the tissues, and cellular systems are also prevented from using oxygen.
There are special considerations with this pathology. To achieve resuscitation, thermal injuries accompanied by inhalation injury will require increased volumes of fluid by as much as 50 percent above those predicted through standard formulas.10 The concern for worsening pulmonary edema should not prompt clinicians to restrict intravenous fluids; on the contrary, the lung microvascular permeability changes seen with inhalation injury are worsened by inadequate fluid resuscitation.11 Furthermore, conventional pulse oximeters cannot distinguish between oxyhemoglobin and COHb; therefore, COHb must be measured via arterial or venous CO oximetry.12 A quantitative level can assess the severity of injury and dictate the urgency and aggressiveness of treatment and intervention.
Inhalation injury is an independent risk factor for mortality. Mortality indices, such as the revised Baux score, include burn size, age, and inhalation injury. The presence of inhalation injury adds the equivalent of 17 years to a patient’s age or an additional burn surface area of 17 percent.13 Ultimately, smoke inhalation is the leading cause of death due to fires. For those patients who do survive, long-term sequela can result from laryngeal damage causing persistent hoarseness and dysphonia,3 and some patients may show obstructive and restrictive patterns on pulmonary function tests as many as eight years after injury.14
To examine the occurrence of inhalation injuries in the National Trauma Data Bank® (NTDB) research dataset for 2013, admissions medical records were searched using the International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis codes. Specifically searched were records that contained one of the following external cause of injury codes (E-code): E890.1 (fumes from combustion of polyvinylchloride [pvc] and similar material in conflagration in private dwelling), E890.2 (other smoke and fumes from conflagration in private dwelling), E891.1 (fumes from combustion of polyvinylchloride [pvc] and similar material in conflagration in other and unspecified building or structure), or E891.2 (other smoke and fumes from conflagration in other and unspecified building or structure). A total of 1,258 records were found. Of these records, 988 contained a discharge status, including 668 patients discharged to home, 148 to acute care/rehab, and 78 sent to skilled nursing facilities; 95 died. These patients were 56.6 percent male, on average 45.9 years of age, had an average hospital length of stay of 9.8 days, an average intensive care unit length of stay of 10.2 days, an average injury severity score of 9.6, and were on the ventilator for an average of 8.5 days. Of those patients tested for alcohol (625), more than half (52 percent) tested positive (see figure).
Activities that generate smoke, such as a campfire, barbecues, or an old-fashioned fish boil, may be tantalizing to watch. However, being confined in an enclosed space with all smoke and no fire can lead to a devastating and potentially fatal injury.
Throughout the year, we will be highlighting these data through brief reports that will be found monthly in the Bulletin. The NTDB Annual Report 2014 is available on the ACS website as a PDF file. In addition, information is available on our website about how to obtain NTDB data for more detailed study. If you are interested in submitting your trauma center’s data, contact Melanie L. Neal, Manager, NTDB, at email@example.com.
Statistical support for this article has been provided by Chrystal Caden-Price, Data Analyst, NTDB.
- Thucydides. The Peloponnesian War. Crawley R, trans. New York, NY: Random House; 1951.
- Margotta R. An Illustrated History of Medicine. Middlesex, England: Hamlyn; 1967:86.
- Traber DL, Herndon DN, Enkhbaatar P, Maybauer MO, Maybauer DM. The pathophysiology of inhalation injury. In: Herndon DN, ed. Total Burn Care, Fourth Edition. Philadelphia, PA: W. B. Saunders; 2012.
- Baile EM, Dahlby RW, Wiggs BR, Paré PD. Role of tracheal and bronchial circulation in respiratory heat exchange. J Appl Physiol. 1985;58(1):212-222.
- Linares HA, Herndon DN, Traber DL. Sequence of morphologic events in experimental smoke inhalation. J Burn Care Rehab. 1989;10(1):27-37.
- Cox RA, Burke AS, Soejima K, et al. Airway obstruction in sheep with burn and smoke inhalation injuries. Am J Respir Cell Mol Biol. 2003;29(3):295-302.
- Soejima K, Schmalstieg FC, Sakurai H, Traber LD, Traber DL. Pathophysiological analysis of combined burn and smoke inhalation injuries in sheep. Am J Physiol Lung Cell Mol Physiol. 2001;280(6):L1233-L1241.
- West JB. Pulmonary Pathophysiology: The Essentials. 6th ed. Baltimore, MD: Lippincott, Williams & Wilkins; 2003.
- Smith RP. Chapter 14. Toxic responses of the blood. In Doull J, Klaassen CD, Amdur MO, eds. Casarett and Doull’s Toxicology, The Basic Science of Poisons. 1st ed. New York, NY: Macmillan Company; 1986:223-244.
- Navar PD, Saffle JR, Warden GD. Effect of inhalation injury on fluid resuscitation requirements after thermal injury. Am J Surg. 1985;150(6):716-720.
- Herndon DN, Traber DL, Traber LD. The effect of resuscitation on inhalation injury. Surgery. 1986;100(2):248-251.
- Piatkowski A, Ulrich D, Grieb G, Pallua N. A new tool for the early diagnosis of carbon monoxide intoxication. Inhal Toxicol. 2009;21(13):1144-1147.
- Osler T, Glance LG, Hosmer DW. Simplified estimates of the probability of death after burn injuries: Extending and updating the Baux score. J Trauma. 2010;68(3):690-697.
- Mlcak R, Desai MH, Robinson E, Nichols R, Herndon DN. Lung function following thermal injury in children—an 8-year follow up. Burns. 1998;24(3):213-216.