Inhalation trauma

Inhalation trauma - the defeat of the respiratory tract, lungs and the body as a whole with the inhalation of combustion products during a fire.

Inhalation trauma can be isolated or combined with skin burns, significantly weighting the course of the burn disease and worsening the prognosis.

[1], [2], [3], [4], [5], [6]

Impact agents, pathogenesis of respiratory failure with inhalation trauma

The damaging agents of smoke can be divided into three groups:

1. The hot air from the flames.
2. Chemical components of smoke, affecting the respiratory tract and lung parenchyma.
3. Combustion products with systemic toxic effects.

Due to the reflex closure of the glottis, thermal damage to the respiratory tract occurs, as a rule, above the larynx. However, in the event of a loss of consciousness, the affected person may be exposed to the thermal effects of hot air on the lower parts.

Among the chemical components of smoke, which irritate the mucous membrane of the respiratory tract, the most important are acrolein, hydrochloric acid, toluene dizisocyanate, nitrogen dioxide. Under the influence of the listed substances, irritation, necrosis and rejection of the mucous membrane of the respiratory tract occurs. Inflammatory response following a lesion of the mucous membrane leads to swelling of the walls of the respiratory tract, proliferation of fibrin and polymorphonuclear leukocytes into the lumen of the bronchi. These processes cause a violation of airway patency. The depth of penetration of toxic products of irritant action in the respiratory tract depends on their solubility in water. With the penetration of toxic products to the alveoli, the surfactant breaks down, the epithelium of the alveoli develops with the development of alveolar edema and parenchymal pulmonary insufficiency.

Among substances that do not have a significant effect on the respiratory tract and lung parenchyma, but have a systemic toxic effect, carbon monoxide (CO), which is a product of incomplete combustion of carbon, and pairs of hydrocyanic acid (NSN), formed during the combustion of polyurethane, are the most dangerous. Carbon monoxide causes hemic hypoxia to form a persistent compound with hemoglobin - carboxyhemoglobin. In addition, carbon monoxide has a direct toxic effect on the central nervous system, causing severe encephalopathy. CNS damage due to carbon monoxide poisoning can develop delayed, a few days after poisoning. The mechanisms of the neurotoxic effect of carbon monoxide are not completely clear.

Cyanic acid, penetrating inhalation in the form of vapors, blocks the mitochondrial enzyme cytochrome oxidase, causing severe tissue hypoxia accompanied by metabolic acidosis.

The mechanism of development of ODN in inhalation trauma includes:

• violation of airway patency due to inflammatory edema of bronchial walls, obstruction of airway clearance by necrotic masses, leukocyte conglomerates and fibrin,
• acute damage to the lung parenchyma due to toxic damage to the alveoli and destruction of the surfactant,
• disturbances of respiration of the central genesis and tissue hypoxia due to systemic poisoning by carbon monoxide and vapors of hydrocyanic acid.

The victim may be dominated by one of the mechanisms of development of ODN, determining the appropriate clinical picture, or at the same time there are 2-3 mechanisms.

Clinical symptoms, diagnosis criteria

Signs of inhalation trauma - dry cough, a feeling of sore throat, the identification of multiple dry wheezes in auscultation. However, these symptoms are nonspecific and do not allow to reliably diagnose and assess the severity of inhalation trauma. Violation of consciousness of the victim testifies in favor of poisoning with carbon monoxide and vapors of prussic acid.

The study of the blood of the victim for the content of carboxyhemoglobin can give an idea of the severity of carbon monoxide poisoning:

• 10-20% - mild poisoning,
• 20-50% - moderate poisoning,
• more than 50% - severe poisoning.

However, the detection of low concentrations of carboxyhemoglobin in the blood does not exclude carbon monoxide poisoning, since a considerable time elapsed from the time of trauma to examination, as well as inhalation of 100% oxygen in the pre-analysis stage, can lead to the decay of a significant part of carboxyhemoglobin.

Specific laboratory studies that confirm the poisoning with vapors of hydrocyanic acid do not exist. In favor of HCN poisoning is evidence of severe metabolic acidosis, which can not be corrected by buffer solutions.

When examining the gas composition of blood, hypercapnia due to airway obstruction or hypoxemia due to parenchymal lung disease can be identified.

Radiological manifestations of inhalation trauma are nonspecific. When lesions with toxic products of the lung parenchyma, a pattern is observed that is characteristic of OPL / ARDS.

The most informative method of research, confirming the fact of inhalation of smoke, is a fibrobronchoscopy that allows detecting a smear of soot on the mucous membrane of the respiratory tract. As a rule, with primary fibrobronchoscopy, it is not possible to assess the severity of mucosal lesions, since it is covered with a layer of soot. Indirect sign of severe inhalation trauma - atony of the walls of the respiratory tract, dense fixation of soot on the walls of the trachea and bronchi.

After 1-2 days after cleansing the mucous membrane from the soot with fibrobronchoscopy, the severity of its lesion can be assessed. There are four types of lesions (four degrees of severity) with burns of the respiratory tract, catarrhal, erosive, ulcerative, necrotic.

[7], [8], [9], [10], [11]

Criteria of suspicion of inhalation trauma

Suspicion of inhalation trauma should always occur with anamnestic information about the victim's presence in a closed smoke-filled room during a fire. Physical signs indicating a possible inhalation trauma - face burns, soot stains in the nasal passages and in the tongue Auscultatory reveal dry wheezing in the lungs. Acute respiratory failure with inhalation trauma can develop delayed, within 12-36 hours after inhalation of combustion products. Therefore, all victims with suspected inhalation damage should be admitted to the intensive care unit for observation within 24-48 hours, regardless of the severity of respiratory disorders.

[12], [13], [14], [15], [16], [17]

First Aid for Inhalation Trauma

All victims with suspected inhalation trauma, regardless of the severity of the clinical manifestations, should be hospitalized in the ICU. When the patient's consciousness is disturbed, a blood test is needed to determine the carboxyhemoglobin content. All patients during the first 2 hours should be performed lung radiography, sanation-diagnostic fibrobronchoscopy, analysis of arterial blood for oxygen and carbon dioxide content, determination of the acid-base state. When a patient finds a catarrhal or erosive lesion of the tracheobronchial tree in combination with the absence of ODN phenomena and impaired consciousness, infusion, antibacterial and nebulizer therapy is shown within 24-48 hours. Detection of ulcerative and necrotic lesions of the mucous membrane of the respiratory tract during bronchoscopy can serve as an indication to the preventive onset IVL.

[18], [19], [20],

Infusion therapy

The introduction of crystalloid solutions and glucose solutions with an isolated inhalation trauma is necessary for those affected by mechanical ventilation. Given the tendency to accumulation of free water in the walls of the bronchi and alveoli affected by smoke, the minimum possible volume of fluid providing diuresis of 0.5-1 ml / (kg-hr) should be selected, and daily radiographic monitoring should be used to prevent hyperhydration and pulmonary edema.

Antibiotic therapy

The most common complication of inhalation injury, which affects the severity of the disease and lethality, is bronchopneumonia. Every day a radiologic examination of the lungs is necessary. Antibiotic therapy is advisable to begin with the emergence of infiltrates in the lungs and clinical signs of bronchopneumonia. Most often pneumonia, occurring with inhalation trauma, is caused by gram-positive microorganisms. Gram-negative infection usually joins later and is hospitalized. It is expedient to microbiological examination of sputum or bronchoalveolar flushing to isolate the culture of microorganisms and determine sensitivity.

[21], [22], [23], [24]

Nebulizer therapy

Nebulizer therapy should be started immediately after the patient is admitted to hospital. In some cases, with the help of inhalation therapy, it is possible to stop developing airway obstruction.

The scheme of nebulizer therapy used by the authors includes m-holinoblokator, glucocorticoid, intended for inhalation, and mucolytic:

• Acetylcysteine 200 mg 2-3 times a day.
• Ipratropium bromide (atrovent) 0.025% solution for inhalation - 2 ml.
• Budesonide (Benaport) - suspension for inhalations 0.5 mg / ml - 2 ml.
• Ambroxol - solution for inhalation 7.5 mg / ml - 2 ml The use of beta-adrenomimetics, as a rule, is ineffective. Parenteral administration of glucocorticoids is ineffective, in addition, they increase the incidence of infectious complications.

Respiratory support for respiratory failure

Acute respiratory failure develops in about 30% of cases of inhalation trauma.

Violation of airway patency is associated primarily with the development of inflammatory edema, and not with bronchospasm. This explains the delay in the development of ODN to 12-36 hours.

Intubation of the trachea is advisable to perform a large diameter tube (at least 7.5 mm) to ensure the most comfortable sanitation of the airways, reduce the likelihood of obturation of the detritus tube and the safety of fibrobronchoscopy.

The feasibility of tracheostomy remains the subject of discussion. Arguments in favor of tracheostomy are a facilitated sanation of the tracheobronchial tree, exclusion of additional trauma to the larynx affected by the burn. However, tracheostomy with inhalation trauma is associated with a significantly greater number of complications - ruptures and stenoses of the trachea, this is caused by the extreme vulnerability of the affected mucous membrane.

At the beginning of ventilation and the selection of the optimal regimen, it is necessary to determine the severity of obstructive and parenchymal changes in a particular patient. The easiest way to do this is with the graphic monitor of a respirator. It is advisable to determine the resistance of the airways, the ratio of pO2 / FiO2 and "hidden" PEP (auto-PEEP).

In severe obstructive disorders, ventilation with volume control, ventilation / expiration ratio 1 4-1 5, and respiratory rate no more than 11-12 per minute is necessary. It is necessary to control pCO2 - severe obstructive disorders can lead to high hypercapnia, paradoxically increasing in response to an increase in respiratory rate and minute volume of respiration.

The principles of mechanical ventilation in case of parenchymal pulmonary insufficiency caused by inhalation trauma do not differ from artificial lung ventilation in APL / ARDS.