Toxic Inhalational Injury

TOXIC INHALATIONAL INJURY Physical Aspects Clinical Effects Physiology Evaluation of Injury 

GENERAL THERAPEUTIC CONSIDERATIONS Further Exposure Critical Care Concepts Clinical Abnormalities Steroid Therapy 

Interactions of Pulmonary Toxic Inhalants and Exercise Therapy 

SMOKES AND OTHER SUBSTANCES Zinc Oxide Phosphorus Smokes Sulfur Trioxide-Chlorosulfonic Acid Titanium Tetrachloride Nitrogen Oxides 

Clinical Assistant Professor of Medicine, Yale University School of Medicine, New Haven, Connecticut 06510 

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Urbanetti, J. S. (1997). Toxic inhalational injury. In F. R. Sided, E. T. Takafuji, D. R. Franz (Eds.), Medical aspects of chemical and biological warfare (p. 266). Washington, DC Borden Institute. 

Parrish, J.S., Bradshaw, D.A. (2004). Toxic inhalational injury gas, vapor and vesicant exposure. Respir. Care Clin. North Am. 10 43-58. 

Urbanetti JS. Toxic inhalational injury In Textbook of Military Medicine (Zajtchuk R and Bellamy RF, Eds.), pp. 247-270, Washington, DC Office of the Surgeon General, Walter Reed Army Medical Center 1997. 

Urbanetti, J.S., Toxic inhalational injury, in Textbook of Military Medicine—Medical Aspects of Chemical and Biological Warfare, Zajtchuk, R. and Bellamy, R.E., Eds., Office of the Surgeon General, Washington, DC, 1997, 247. 

Topical damage to the respiratory tract may occur due to direct toxic inhalational injury to the airways or alveoli. Cellular damage with consequent airway obstruction, pulmonary interstitial damage, or alveolar-capillary damage ultimately compromises adequate oxygen-carbon dioxide exchange. Some substances are relatively more toxic to the central airways, whereas others are more toxic to the peripheral airways or alveoli. 

Individuals with hyperreactive airways will benefit from bronchodilator therapy and possibly from steroids after exposure to a toxic inhalant. This statement, however, does not constitute an endorsement for routine steroid use in all toxic inhalational injuries. 

Collecting historical data from the casualty is a critical aspect of assessing and treating toxic inhalational injury. Careful questioning of an exposed individual will often greatly simplify the diagnosis and therapy of the injury. 

Clinical abnormalities that may lead to respiratory failure can also be observed after pulmonary toxic inhalational injury. These include hypoxia, hypercarbia, pulmonary edema, which are all signs of possible toxic inhalant exposure and infection, which is a frequent complication, particularly in intubated patients. 

Airway resistance may increase because of toxic inhalational injury, resulting in increased work of respiration. Air trapping secondary to increased airway resistance increases intrathoracic pressure. Increased work of respiration and decreased venous return result in exercise limitation. Ventilation-perfusion abnormalities of disordered airway function limit oxygen delivery and carbon dioxide clearance, which also compromises exercise tolerance. 

An individual may remain relatively asymptomatic for up to 72 hours after inhalant exposure. During that time, dyspnea or pulmonary edema may be triggered by exertion (see the preceding section, Exertion and Toxic Inhalational Injury). 

At room temperature, white phosphorus is somewhat volatile and may produce a toxic inhalational injury. Over a period of years, repetitive exposures can result in systemic poisoning.33 At warmer temperatures, a slow oxidation to phosphorus trioxide (P2O3), which smells like garlic, can occur. At still higher temperatures (approximately 32°C [90°F]) and with adequate air exposure, dense white clouds of phosphorus pentoxide (P2O5) result from the combustion of phosphorus. 

There is no recognized prophylactic therapy for human PFIB exposure. Animal studies suggest that increasing pulmonary concentrations of oxygen free-radical scavengers containing thiol groups may be of value N-acetyl cysteine has been found effective.65,66 No postexposure medical or chemical therapy that effectively impedes or reverses the effects of this toxic inhalational injury is known. 

Toxic inhalational injury poses a 2-fold problem for military personnel ... 

Toxic inhalational injury can cause large numbers of casualties that can significantly burden medical facilities. 

C. Sequelae. Although most patients who suffer toxic inhalation injury will recover without any permanent impairment, bronchiectasis, bronchiolitis obliterans, persistent asthma, and pulmonary fibrosis can occur. 

Examples Silicosis, asbestosis, pneumonitis, pharyngitis, rhinitis or acute congestion farmer s lung, beryllium disease, tuberculosis, occupational asthma, reactive airways dysfunction S5mdrome (RADS), chronic obstructive pulmonary disease (COPD), hypersensitivity pneumonitis, toxic inhalation injury, such as metal fume fever, chronic obstructive bronchitis, and other pneumoconioses. 

John S. Urbanetti, Toxic Inhalational Injury, in Frederick R. Sidell, Ernest T. Takafuji, and David R. Franz, eds., Textbook of Military Medicine, Part I Warfare, Weaponry, and the Casualty Medical Aspects of Chemical and Biological Warfare (Washington, DC Borden Institute, Walter Reed Army Medical Center 1997) pp. 256-7. 

Traub, S., 2006. Respiratory agent attack (toxic inhalation injury). In Ciottone, G. (Ed.), Disaster Medicine, third ed. Mosby Elsevier, Philadelphia, PA, pp. 

Tuorinsky, S.D., Sciuto, A.M., 2008. Toxic inhalational injury and toxic industrial chemicals Medical Aspects of Chemical Warfare. Office of the Surgeon General and US Army Medical Department Center and School, Ft. Sam Houston, TX, pp. 339-370. 

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