Inhalation injury

Inhalation injury is damage to the respiratory tract, lungs and the body as a whole due to inhalation of combustion products during a fire.

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

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Damaging agents, pathogenesis of respiratory failure in inhalation trauma

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

1. The air is heated by the flame.
2. Chemical components of smoke that affect the respiratory tract and lung parenchyma.
3. Combustion products that have a systemic toxic effect.

Due to the reflex closure of the glottis, thermal damage to the respiratory tract usually occurs above the larynx. However, if the victim loses consciousness, the thermal effect of hot air on the lower sections is possible.

Among the chemical components of smoke that irritate the mucous membrane of the respiratory tract, the most important are acrolein, hydrochloric acid, toluene disisocyanate, and nitrogen dioxide. Under the influence of these substances, irritation, necrosis, and rejection of the mucous membrane of the respiratory tract occur. The inflammatory response following damage to the mucous membrane leads to edema of the walls of the respiratory tract, the loss of fibrin and polymorphonuclear leukocytes into the lumen of the bronchi. These processes cause obstruction of the respiratory tract. The depth of penetration of toxic irritant products into the respiratory tract depends on their solubility in water. When toxic products penetrate to the alveoli, the surfactant and alveolar epithelium are destroyed, with the development of alveolar edema and parenchymatous pulmonary insufficiency.

Among the substances that do not have a significant effect on the respiratory tract and lung parenchyma, but have a systemic toxic effect, the most dangerous are carbon monoxide (CO), which is a product of incomplete combustion of carbon, and hydrocyanic acid vapors (НСN), formed during the combustion of polyurethane. Carbon monoxide causes hemic hypoxia, forming a stable 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, several days after poisoning. The mechanisms of the neurotoxic effect of carbon monoxide are not fully understood.

Hydrocyanic acid, penetrating through 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 acute respiratory failure in inhalation trauma includes:

• obstruction of the airways due to inflammatory swelling of the bronchial walls, blockage of the lumen of the airways by necrotic masses, leukocyte conglomerates and fibrin,
• acute injury to the lung parenchyma due to toxic damage to the alveoli and destruction of surfactant,
• central respiratory failure and tissue hypoxia due to systemic poisoning with carbon monoxide and hydrocyanic acid vapors.

The victim may have one of the mechanisms of development of ARF, determining the corresponding clinical picture, or 2-3 mechanisms may be present simultaneously.

Clinical symptoms, diagnostic criteria

Signs of inhalation trauma are a dry cough, a sore throat, and multiple dry wheezing sounds during auscultation. However, these symptoms are nonspecific and do not allow for a reliable diagnosis and assessment of the severity of inhalation trauma. Impaired consciousness of the victim indicates poisoning by carbon monoxide and hydrocyanic acid vapors.

Testing the victim's blood for carboxyhemoglobin levels can provide 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 significant amount of time has passed from the moment of injury to the study, as well as the inhalation of 100% oxygen in the stage preceding the analysis, can lead to the breakdown of a significant part of the carboxyhemoglobin.

There are no specific laboratory tests to confirm poisoning with hydrocyanic acid vapors. Severe metabolic acidosis that is not amenable to correction with buffer solutions is evidence of poisoning with HCN.

Blood gas analysis may reveal hypercapnia due to airway obstruction or hypoxemia due to parenchymal lung disease.

Radiographic manifestations of inhalation trauma are non-specific. When the lung parenchyma is damaged by toxic products, a picture characteristic of ALI/ARDS is observed.

The most informative method of examination confirming the fact of smoke inhalation is fibrobronchoscopy, which allows detecting soot deposits on the mucous membrane of the respiratory tract. As a rule, primary fibrobronchoscopy does not allow assessing the severity of damage to the mucous membrane, since it is covered with a layer of soot. An indirect sign of severe inhalation injury is atony of the walls of the respiratory tract, dense fixation of soot on the walls of the trachea and bronchi.

After 1-2 days of cleaning the mucous membrane from soot, fibrobronchoscopy can assess the severity of its damage. There are four types of damage (four degrees of severity) in respiratory tract burns: catarrhal, erosive, ulcerative, necrotic.

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Criteria for suspected inhalation injury

Inhalation injury should always be suspected if there is a history of the victim being in a closed, smoky room during a fire. Physical signs that indicate possible inhalation injury include facial burns, soot deposits in the nasal passages and on the tongue. Auscultation reveals dry wheezing in the lungs. Acute respiratory failure in inhalation injury may develop late, within 12-36 hours after inhalation of combustion products. Therefore, all victims with suspected inhalation injury should be hospitalized in the intensive care unit for observation for 24-48 hours, regardless of the severity of respiratory distress.

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First aid for inhalation injury

All victims with suspected inhalation trauma, regardless of the severity of clinical manifestations, should be hospitalized in the intensive care unit. If the patient's consciousness is impaired, a blood test is required to determine the carboxyhemoglobin content. All patients should undergo chest X-ray, sanatory and diagnostic fibrobronchoscopy, arterial blood analysis for oxygen and carbon dioxide content, and determination of the acid-base balance within the first 2 hours. If catarrhal or erosive lesions of the tracheobronchial tree are detected in the patient in combination with the absence of ARF symptoms and impaired consciousness, infusion, antibacterial and nebulizer therapy are indicated for 24-48 hours. Detection of ulcerative and necrotic lesions of the respiratory tract mucosa during bronchoscopy may serve as an indication for prophylactic initiation of mechanical ventilation.

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Infusion therapy

Administration of crystalloid solutions and glucose solutions in isolated inhalation trauma is necessary for victims on artificial ventilation. Given the tendency for free water to accumulate in the walls of the bronchi and alveoli affected by smoke, the minimum possible volume of fluid should be selected to ensure diuresis of 0.5-1 ml/(kg × h), and daily X-ray monitoring should be performed to prevent hyperhydration and pulmonary edema.

Antibacterial therapy

The most common complication of inhalation trauma, which affects the severity of the disease and mortality, is bronchopneumonia. Daily X-ray examination of the lungs is necessary. Antibacterial therapy should be started from the moment of the appearance of infiltrates in the lungs and clinical signs of bronchopneumonia. Most often, pneumonias occurring in inhalation trauma are caused by gram-positive microorganisms. Gram-negative infection usually joins later and is hospital-acquired. Microbiological examination of sputum or bronchoalveolar lavage is advisable to isolate the culture of microorganisms and determine sensitivity.

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Nebulizer therapy

Nebulizer therapy should be started immediately after the victim is admitted to hospital. In some cases, inhalation therapy can relieve developing airway obstruction.

The nebulizer therapy regimen used by the authors includes an m-anticholinergic, a glucocorticoid intended for inhalation administration, and a mucolytic:

• Acetylcysteine 200 mg 2-3 times a day.
• Ipratropium bromide (Atrovent) 0.025% solution for inhalation - 2 ml.
• Budesonide (Benaport) - suspension for inhalation 0.5 mg/ml - 2 ml.
• Ambroxol - inhalation solution 7.5 mg/ml - 2 ml The use of beta-adrenergic agonists is generally ineffective. Parenteral use of glucocorticoids is ineffective, in addition, they increase the frequency of infectious complications.

Respiratory support in respiratory failure

Acute respiratory failure develops in approximately 30% of cases of inhalation injury.

The obstruction of the airways is primarily associated with the development of inflammatory edema, not bronchospasm. This explains the delay in the development of ARF up to 12-36 hours.

It is advisable to perform tracheal intubation with a large-diameter tube (at least 7.5 mm) to ensure the most convenient sanitation of the respiratory tract, reduce the likelihood of tube obstruction by detritus, and the safety of fiberoptic bronchoscopy.

The advisability of tracheostomy remains a subject of debate. Arguments in favor of tracheostomy include facilitated sanitation of the tracheobronchial tree and the exclusion of additional trauma to the larynx affected by the burn. However, tracheostomy in case of inhalation trauma is associated with a significantly higher number of complications - ruptures and stenosis of the trachea, this is caused by the extreme vulnerability of the affected mucous membrane.

When starting artificial ventilation and selecting the optimal mode, it is necessary to determine the severity of obstructive and parenchymatous changes in a specific patient. This is most conveniently done using a graphic respirator monitor. It is advisable to determine the airway resistance, the ratio of peO2/FiO2 and "latent" PEEP (auto-PEEP).

In case of severe obstructive disorders, ventilation with volume control is required, with an inhalation/exhalation ratio of 1:4-1:5 and a respiratory rate of no more than 11-12 per minute. PaCO2 control is necessary - severe obstructive disorders can lead to high hypercapnia, paradoxically increasing in response to an increase in respiratory rate and minute respiratory volume.

The principles of mechanical ventilation in parenchymal lung failure caused by inhalation injury do not differ from mechanical ventilation in ALI/ARDS.