Inhalation Injury

2018 ◽  
Author(s):  
Madhu Subramanian ◽  
Erica I Hodgman ◽  
Steven E Wolf

Among those who have been burned in fires, inhalation injury is common from high-temperature air in the upper airway and inhaled toxins in smoke, causing metabolic poisoning and chemical burns in the trachea and lower airways. The diagnosis of inhalation injury is difficult as it is often based on qualitative measures in the history and physical examination, although measurement of carboxyhemoglobin and untoward acidosis are effective indirect measures. The use of CT for diagnosis is also playing a greater role. Treatment is generally supportive with airway and ventilator support, including the use of volumetric diffuse respiration and occasionally hydrogen cyanide antidotes. Inhalation injury is contributory to morbidity and mortality in the severely burned but is often a signal of the severity of the burns as well. This review discusses the pathophysiology, diagnosis, and treatment of inhalation injury, with an emphasis on potential complications.    This review contains 1 figure, 4 tables and 159 references Key words: airway pressure release ventilation, bronchodilator therapy, carbon monoxide poisoning, cyanide poisoning, inhalation injury

Author(s):  
Silvia Coppola ◽  
Franco Valenza

Inhalation injury represents one of the most serious associated injuries complicating the care of thermally-injured patient. It can result in severe respiratory failure and acute respiratory distress syndrome (ARDS) by three mechanisms—thermal or chemical injury, and impairment of systemic oxygen supply. Thermal injury can cause erythema, ulceration, and progressive, life-threatening oedema, particularly of the upper airways. Chemical injury is due to irritants or cytotoxic compounds, and depends on the material burned, the temperature of the fire, and the amount of oxygen present in the fire environment. It is responsible for irritation, ulceration, and oedema of the mucosal surface, and the initiation of a lung inflammatory reaction when small particles reach the alveoli. Moreover, the increased vascular permeability, and the reduced surfactant production carry a significant risk in the development of pneumonia and ARDS. Bronchospasm and upper airway oedema can occur rapidly, while lower airway oedema can be asymptomatic for up to 24 hours. Lung imaging techniques may not reveal injured areas for the first 24–48 hours. Fibre optic bronchoscopy is considered to be the most direct diagnostic method for the definitive diagnosis of inhalation injury. The patient management includes airways assessment, adequate fluid resuscitation, and mechanical ventilation when required. All victims of smoke inhalation should be always evaluated for cyanide and carbon monoxide poisoning.


2013 ◽  
Vol 39 (3) ◽  
pp. 373-381 ◽  
Author(s):  
Ana Carolina Pecanha Antonio ◽  
Priscylla Souza Castro ◽  
Luiz Octavio Freire

In view of the tragic fire at a nightclub in the city of Santa Maria, Brazil, which culminated in the sudden death of 232 young people, we decided to review the literature regarding smoke inhalation injury caused by enclosed-space fires, which can be divided into direct thermal damage, carbon monoxide poisoning, and cyanide poisoning. Such injuries often call for immediate orotracheal intubation, either due to acute airway obstruction or due to a reduced level of consciousness. The diagnosis and the severity of the thermal injury can be determined by fiberoptic bronchoscopy. The levels of gases and gas by-products in the bloodstream should be assessed as rapidly as possible, even while still at the scene of the incident. First responders can also treat carbon monoxide poisoning, with immediate administration of oxygen at 100%, as well as cyanide poisoning, with oxygen therapy and hydroxocobalamin injection


2009 ◽  
Vol 18 (1) ◽  
pp. 3-12
Author(s):  
Andrea Vovka ◽  
Paul W. Davenport ◽  
Karen Wheeler-Hegland ◽  
Kendall F. Morris ◽  
Christine M. Sapienza ◽  
...  

Abstract When the nasal and oral passages converge and a bolus enters the pharynx, it is critical that breathing and swallow motor patterns become integrated to allow safe passage of the bolus through the pharynx. Breathing patterns must be reconfigured to inhibit inspiration, and upper airway muscle activity must be recruited and reconfigured to close the glottis and laryngeal vestibule, invert the epiglottis, and ultimately protect the lower airways. Failure to close and protect the glottal opening to the lower airways, or loss of the integration and coordination of swallow and breathing, increases the risk of penetration or aspiration. A neural swallow central pattern generator (CPG) controls the pharyngeal swallow phase and is located in the medulla. We propose that this swallow CPG is functionally organized in a holarchical behavioral control assembly (BCA) and is recruited with pharyngeal swallow. The swallow BCA holon reconfigures the respiratory CPG to produce the stereotypical swallow breathing pattern, consisting of swallow apnea during swallowing followed by prolongation of expiration following swallow. The timing of swallow apnea and the duration of expiration is a function of the presence of the bolus in the pharynx, size of the bolus, bolus consistency, breath cycle, ventilatory state and disease.


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