Inhalational injuries

Baron-Marano, F.L. and M.C. Izard. 1968. Observation d anomalies ultrastructurales dans la descendance d algues traitees par l acroleine. Compt. Rend. Hebdom. Sean. Acad. Sci. D, Sci. Natur. 267 2137-2139. Barrow, R.E., C-Z. Wang, R.A. Cox, and M.J. Evans. 1992. Cellular sequence of tracheal repair in sheep after smoke inhalation injury. Lung 170 331-338. 

Sinclair JS, McManus DT, O Hara MD, et al Fatal inhalation injury following an industrial accident involving acetic anhydride. Burns 20(5) 469M70, 1994... 

Pathophysiology and Treatment of Inhalation Injuries, edited by J. Loke... 

Seinfeld, J.H. 1986. Atmospheric Chemistry and Physics of Air Pollution. New York Wiley. Sheppard, D. 1988. Mechanisms of airway responses to inhaled sulfur dioxide. Pp. 49— 65 in Pathophysiology and Treatment of Inhalation Injuries, Lung Biology in Health and Disease, Vol. 34., J.Loke, ed. New York, NY Marcel Dekker. 

Although burns are cutaneous injuries, the effects can influence nearly all systems of the body. The overall morbidity associated with a burn injury will be determined by burn depth, percentage total body surface area (TBSA) involved, patient age, and presence of inhalation injury. Children and older adults have thinner skin and are more likely to sustain a deeper burn injury. Patients at the age extremes are also less likely to tolerate the stress of burn shock. The presence of an inhalation in-... 

Second- or third-degree burns greater than 10%-20% TBSA or patients with significant smoke inhalation injury will require fluid resuscitation. Peripheral IV catheters can be used, but placement of a central venous catheter is optimal. An indwelling urine catheter should be placed so that output measures can he used to monitor the status of fluid resuscitation. 

Morbidity and mortality associated with wildfires include burns, inhalation injuries, respiratory complications, and stress-related cardiovascular events (exhaustion and myocardial infarction while fighting or fleeing the fire). 

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. 

Chisholm, C.D., Singletary, E.M., Okerberg, C.V. (1989). Inhaled sodium bicarbonate therapy for chlorine inhalation injuries (Abstract). Ann. Emerg. Med. 18 466. 

Urbanetti, J. S. (1988). Battlefield chemical inhalation injury. In J. Loke (Ed.), Pathophysiology and treatment of inhalation injuries (pp. 281-348). New York Marcel Dekker. 

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. 

Meyer, G.W., Hart, G.B., and Strauss, M.B., Hyperbaric oxygen therapy for acute smoke inhalation injuries. Postgrad. Med., 89, 221-223, 1991. 

Urhanetti, J.S., Battlefield chemical inhalation injury, in Pathophysiology and Treatment of Inhalation Injuries., Loke, 1., Ed., Marcel Dekker, New York, 1988. 

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. 

TOXIC INHALATIONAL INJURY Physical Aspects Clinical Effects Physiology Evaluation of Injury... 

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). 

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