Inhalation injury

Introduction to inhalation injury Inhalation injury refers to the chemical damage caused by inhaling toxic fumes or chemicals to the respiratory tract. In severe cases, the lung parenchyma can be directly damaged. It occurs mostly in large areas, especially in patients with head and face burns. Inhalation injury is related to the environment in which the injury occurs. It often occurs in an environment that is not ventilated or sealed, especially in an explosive atmosphere. In this environment, the concentration of the hot flame is high, the temperature is high, and it is not easy to spread rapidly. The patient cannot immediately leave the fire source; in addition, in a confined space, the combustion is incomplete, resulting in A large amount of carbon monoxide and other toxic gases make patients toxic and coma, and suffocate and die. When combined with explosive combustion, high temperature, high pressure, high flow rate of air and thick toxic gases can cause damage to the deep respiratory tract and lung parenchyma. In addition, the patient stands or rushes to shout, causing the heat to inhale, which is also one of the causes of injury. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific population Mode of infection: non-infectious Complications: hypoxic ischemic encephalopathy

Cause of inhalation injury

Cause

The main cause of inhalation injury is thermal action, but at the same time, a large amount of unburned smog, carbon particles, and irritating chemicals are also inhaled, which also damages the respiratory tract and alveoli. Therefore, inhalation damage is a mixed damage of heat and chemicals.

Inhalation injury is related to the environment in which the injury occurs. It often occurs in an environment that is not ventilated or sealed, especially in an explosion. In this environment, the concentration of the hot flame is high, the temperature is high, and it is not easy to spread rapidly. The patient cannot immediately leave the fire; in addition, in a confined space, the combustion is incomplete, resulting in A large amount of carbon monoxide and other toxic gases make patients toxic and coma, and suffocate and die. When combined with explosive combustion, high temperature, high pressure, high flow rate of air and thick toxic gases can cause damage to the deep respiratory tract and lung parenchyma. In addition, the patient stands or rushes to shout, causing the heat to inhale, which is also one of the causes of injury.

Injury mechanism

1. Direct damage to the respiratory tract by heat

The heat includes both dry heat and hot heat. Flames and hot air are dry heat, and hot steam is hot and humid. When inhaling hot air, the vocal cords can be reflectively closed, while the heat transfer capacity of the dry hot air is poor. The upper respiratory tract has a water-heat exchange function, which can absorb a large amount of heat to cool it; the dry hot air reaches the bronchial bifurcation At the time of the department, the temperature can be reduced to 1/5 to 1/10 of the original. Therefore, dry heat often causes damage to the upper respiratory tract. The hot and humid air is about 2000 times larger than the heat capacity of dry hot air, and the conduction capacity is about 4000 times larger than that of dry air, and the heat dissipation is slow. Therefore, in addition to causing upper respiratory tract injury and tracheal damage, moist heat can also cause damage to the bronchi and lung parenchyma.

2. Damage to the respiratory tract by harmful substances

In addition to particles in the inhalation of smoke, there are a large number of harmful substances, including carbon monoxide, nitrogen dioxide, sulfur dioxide, nitrogen peroxide, hydrochloric acid, hydrogen cyanide, aldehydes, ketones and the like. These substances can cause direct damage to the respiratory tract through thermal action. Toxic gases can irritate the throat and bronchospasm and cause chemical damage to the respiratory tract. Water-soluble substances such as ammonia, chlorine, sulfur dioxide and the like are synthesized with water as an acid or a base, which can cause chemical burns. Nitride reacts with water and salt on the respiratory mucosa to form nitric acid and nitrite. The former directly corrodes the respiratory tract, and the latter absorbs with hemoglobin to form methemoglobin, which causes tissue hypoxia. Hydrogen cyanide can cause cytochrome oxidase to lose oxygen and inhibit intracellular respiration. Aldehydes can reduce cilia activity, reduce the activity of alveolar macrophages, and damage capillary blood vessels and cause pulmonary edema. The acrolein content of the smoke produced by the combustion of polyurethane is about 50ppm. Chemical respiratory damage and pulmonary edema can occur when inhaled with 5.5ppm of acrolein, and 10ppm will cause death within a few minutes. Hydrogen cyanide and carbon monoxide are additive. When the temperature is raised to 1000 °C, the polyurethane foam decomposes to produce a large amount of hydrogen cyanide. When the concentration of cyanide in the serum reaches 100 mol/L, it can cause death.

When carbon monoxide is inhaled in the smoke, it will cause people to be poisoned by carbon monoxide, and the heavy ones may die on the spot. When inhaled air containing 5% carbon monoxide, it can cause poisoning.

Its toxic effects are:

(1) The combination of carbon monoxide and hemoglobin to form carboxyhemoglobin and carboxyhemoglobin is equivalent to 1/3600 of the dissociation rate of oxyhemoglobin, and the affinity of carbon monoxide with blood albumin is 200-300 times greater than that of oxygen. Therefore, blood oxygenation dysfunction, resulting in systemic tissue hypoxia.

(2) Reduce the ability of the cellular enzyme system to utilize oxygen. Carbon monoxide competes with oxygen for receptors in the cytochrome oxidase system, directly inhibiting cellular respiration.

(3) Carbon monoxide combines with myoglobin to reduce oxygen transport in tissues.

In addition, in the event of fire, the simultaneous production of high concentrations of carbon dioxide and carbon dioxide can aggravate the symptoms of carbon monoxide poisoning and aggravate tissue hypoxia.

Inhalation injury prevention

The main method is to prevent disasters. In addition, special workers should have escape skills in dangerous situations such as fires. In patients with inhalation injury, infections need to be prevented.

Prevention and treatment of infection: After inhalation injury, due to airway and lung damage, cilia function is destroyed, airway secretions and foreign bodies can not be discharged in time, local and systemic resistance is reduced, etc., often cause airway and lung infection, once infected If the treatment is not timely, it can be complicated by acute respiratory failure and become an important lesion of systemic infection, which induces sepsis.

Thoroughly remove foreign bodies in the airway and exfoliated necrotic mucosa, and circulate smoothly, which is the basic measure for prevention and treatment of infection, followed by strict aseptic technique and disinfection and isolation, strictly control wound-pulmonary-cranial bacterial cross-infection; regular airway secretion Smear and culture, use sensitive antibiotics, in addition, systemic support therapy should be strengthened to improve the body's immune function, which is reasonable for prevention and treatment of infection.

Complications of inhalation injury Complications hypoxic ischemic encephalopathy

The combination of carbon oxide and hemoglobin to form carboxyhemoglobin and carboxyhemoglobin is equivalent to 1/3600 of the dissociation rate of oxyhemoglobin, and the affinity of carbon monoxide and blood play protein is 200-300 times larger than that of oxygen. Therefore, blood oxygenation dysfunction, resulting in systemic tissue hypoxia.

Inhalation injury symptoms Common symptoms Breathing difficulty Heart rate increased Mucosal congestion above the tracheal carina burst Moderate inhalation injury Sound hoarseness wheezing Airway obstruction Laryngeal edema Breathing sound weakened

Clinical manifestation

Medium, severe inhalation injury, with different clinical and pathological changes as the course progresses, is divided into three periods.

1, respiratory insufficiency

Severe inhalation injury, respiratory insufficiency within 2 days after injury, which mainly manifests dyspnea, usually lasts for 4 to 5 days, gradually deteriorates or worsens to cause respiratory failure and death, dyspnea is due to extensive bronchial injury or contains lung parenchymal injury , causing ventilation, ventilation disorders, ventilation and blood perfusion ratio imbalance, leading to progressive hypopemia, blood PaC2 <7.8kPa, lung auscultation can be heard and dry, wet rales and wheezing.

2, pulmonary edema

Pulmonary edema can occur within an hour after injury, most of which occurs within 4 days after injury. Clinically, there are obvious symptoms of pulmonary edema, which are mainly pulmonary capillary permeability, airway obstruction, ventilatory disorder, resulting in tissue deficiency. Oxygen, there is no left heart failure at this time, if the early treatment is not appropriate, the amount of fluid infusion is more likely to cause pulmonary edema.

3. Infection period

3 to 14 days after the injury, the course of the disease enters the infection period. Due to the damage of the trachea and bronchial mucociliary, the airway mechanically removes the dysfunction of the foreign body, and the local and systemic immune function decreases, and the damage of the lung to the bacteria is enhanced. Necrotic mucosal necrosis, can form ulcers, long-term unhealed, become a lung infection, lung infections are often secondary to mechanical obstruction and atelectasis, severe infection can induce systemic infection.

Clinical classification

The classification criteria for inhalation injury are not uniform, and some are classified into three categories: light, medium and heavy, light or heavy according to the severity of the disease; some are divided into upper, lower airway and lung parenchymal damage according to the injury site. At present, most of the domestic use of the three-degree classification.

1. Mild inhalation injury

Above the glottis, including nasal, pharyngeal and glottic injuries, clinical manifestations of nasopharyngeal pain, cough, increased saliva, dysphagia; local mucosal congestion, swelling or blisters, mucosal erosion, necrosis, patient hoarseness And breathing difficulties, lung auscultation no abnormalities.

2, moderate inhalation injury

Refers to tracheal carina above, including throat and tracheal injury, clinical manifestations of irritating cough, hoarseness, difficulty breathing, sputum can smash carbon particles and exfoliated tracheal mucosa, laryngeal edema leading to airway obstruction, aspiration asthma Hearing, the auscultation of the lungs is weakened or rough, and occasionally can be heard and wheezing and dry rales. Patients often have bronchitis and aspiration pneumonia.

3. Severe inhalation injury

Refers to the area below the bronchus, including the damage of the bronchus and muscle parenchyma. The clinical manifestation is severe dyspnea immediately or within a few hours after the injury. The tracheal incision can not be relieved; progressive hypoxia, cyanosis, increased heart rate, swaying, sputum Or coma; cough and phlegm, early pulmonary edema, hemoptysis-like phlegm; necrotic endometrial shedding, can cause atelectasis or suffocation, lung auscultation, low breath, rough, audible and wheezing, then appear Dry, wet rales, severe lung parenchymal injury patients, within a few hours after injury can be caused by extensive alveolar damage and severe bronchospasm caused by acute respiratory failure.

Inhalation injury examination

1, X-ray inspection

In the past, X-rays were considered to have no diagnostic significance for invasive injury, but Wang Tianyi et al. (1980) and Yang Zhiyi et al. (1982) observed that the right anterior oblique X-ray film was taken from 2 to 6 hours after injury by animal experiments and clinical observations. The trachea is narrow, the trachea shows the effect of spotted yin, the transmittance is reduced, the mucosa is irregular, and the characteristics of tracheal stenosis are shown early. It can be used as the X-ray change of the absorption. The pulmonary edema shows diffuse, slide-like shadow, leaf. Interimage, hilar enlargement, linear or crescent-shaped image; central infiltrates or diffuse and dense infiltrates in pulmonary infection; sometimes visible balloons due to compensatory emphysema Increased transparency and pneumothorax images due to alveolar rupture or emphysema-like vesicle rupture.

2, special inspection

(1) Fiberoptic bronchoscopy:

Fiberoptic bronchoscopy can directly observe the degree of damage of the throat, vocal cords, trachea, bronchial mucosa, determine the injury site, because it can be taken in the airway, drainage, washing, it is a therapeutic tool, through the dynamic observation of fiberoptic bronchoscopy, Can understand the outcome of the evolution of the lesion.

Inhalation injury seen under the microscope: upper airway inhalation injury can be seen pharyngeal edema, congestion, vesicle formation, ulceration or hemorrhage, generally visible glottis, severely damaged mucosa, high edema, piriform sinus disappeared, ventricular sinus close, Can not see the glottis, lower airway inhalation injury can be seen in the wall mucosa congestion, edema, a large vascular network, the lumen is obviously narrow, the cartilage ring is blurred or exposed, the mucosa can gradually fall off to form ulcers and hemorrhage, bronchial opening redness Or closed, the opening can be blocked by the detached mucous membrane or secretion, there are foreign bodies in the lumen, such as smoke particles, secretions, blood, necrotic mucosa or purulent secretions, in addition, trachea, bronchial dysfunction can also be found Changes: the trachea during normal inhalation, the transverse diameter of the bronchus becomes wider, the long diameter becomes longer, and the opposite is the exhalation. When the injury occurs, the lumen is narrow to closed when exhaled, and the cough is slow or disappears.

When performing fiberoptic bronchoscopy, depending on the condition, oral or nasal insertion, and tracheotomy can be directly inserted into the tracheotomy. Bronchial bronchoscopy can cause hypoxia due to stimulation, grade 3 bronchus This test cannot be performed when the airway and alveolar unit damage is below the level. In addition, this test may cause an exogenous infection.

(2) 133 lung scan continuous blinking photography check:

Moylan first used the 133 scan method to diagnose inhalation injury in 1972. It is considered to be a safe and reliable early diagnosis method. The error between the result and the autopsy result is only 13%. This test is generally 48 hours after injury. Internally, the radioactive isotope 13322×10774×107 (6×10-320×10-3 Curie) is placed in physiological saline for peripheral intravenous injection, and scintillation photography is performed every 15 seconds. Until 133 is completely removed, under normal circumstances, 133 after 90150 seconds after injection, it can be completely removed from the lungs, which is called normal scanning; if it is not cleared after 150 seconds, it is called scanning abnormality, delayed clearing, clearing Incomplete or 133 presented segmental retention, indicating inhalation injury, there is a focal area with increased radioactivity density on scintigraphy.

Patients with chronic obstructive pulmonary disease such as bronchitis and bronchiectasis before injury may have false positive results. The false negative rate of hyperventilation is about 5%. On the 14th day after injury, about 80% of abnormal scans at the time of admission can be recovered. Normal, so this test can not be used as a means of early diagnosis after the third day after injury. The accuracy of this test can reach 87%. It can only determine whether there is inhalation injury or damaged part, and can not judge the severity of the damage.

(3) Exfoliated cell scoring method:

Ambiavagar first reported in 1974 on the observation of changes in the morphology and structure of various cells in bronchial secretions, as well as the presence or absence of smoke particles, and the diagnosis of inhalation injury. After inhalation injury, the morphology and structure of ciliated cells are mutated including cilia. Shedding, the endplate disappeared, the cytoplasm was stained with waxy stone blue, the nucleus was pyknosis, and severe rupture or dissolution.

3, lung function test

(1) Blood gas analysis:

After inhalation injury, PaO2 has different degrees of decline, most of which are lower than 8kPa (60mmHg), the burn area is similar without inhalation injury, generally PaO2>10.67kPa (80mmHg), PaO2/FIO2 ratio is reduced (normal>53.2kPa ), A-aDO2 is elevated early, and its increase can be used as a predictor of prognosis. If the progressive PaO2 is low, A-aDO2 is significantly increased, suggesting a serious condition and a poor prognosis.

(2)) Determination of lung function:

It is sensitive to low-level inhalation injury, including first-second time vital capacity (FEV1), maximum vital capacity (FVC), J maximum expiratory flow rate-volume curve (MEFV), peak flow rate (Peakflow), flow rate at 50% vital capacity, and Respiratory dynamics (lung compliance, airway force, lung resistance, etc.), after severe inhalation injury, involving small airways and lung pumping, airway resistance increases, peak flow rate can be reduced to 41.6 ± 14.3% when 50% of vital capacity, The lung compliance decreased, the lung resistance increased significantly, MEFV was significantly lower than the normal value, and both FEV1 and FVC showed abnormalities earlier. The above changes were caused by airway obstruction. Therefore, the lung function test has certain significance for the expected disease development.

Diagnosis of inhalation injury

Fiberoptic bronchoscopy should be performed to determine the location and extent of damage to the trachea and bronchus. Regular chest X-rays, timely blood gas analysis and carboxyhemoglobin determination to understand respiratory function and lung lesions.

diagnosis

The diagnosis of inhalation-induced injury is mainly based on the time of injury and clinical manifestations, combined with laboratory tests, X-rays and special examinations to determine whether there is inhalation injury, the location and extent of the injury.

1, medical history

The situation at the time of injury should be asked in detail. If there is a history of close space burns and the main irritant, the history of corrosive gases, the possibility of inhalation injury should be suspected.

2, clinical manifestations

The patient has a head, neck burn wound, especially a burn wound around the nose and mouth, nasal hair burnt, oral, pharyngeal mucosa congestion, edema, blisters; cough, cough, sputum with carbon particles; difficulty breathing, lack of Oxygen, irritability; hoarseness, endotracheal detachment; hemoptysis-like sputum in pulmonary edema, low suffocation in the lungs, rough or dry, wet rales, etc., inhalation injury, stenosis due to laryngotracheal edema When breathing difficulties occur, the breath sounds of the throat gas become high-profile, sometimes a sharp whistle sounds. At this time, tracheal opening should be performed. In the early stage of severe inhalation injury, progressive dyspnea occurs, but in the case of extensive burns, Even if there is no inhalation injury, acute muscle dysfunction may occur in the early stage and dyspnea may occur. This should be noted.

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