Acute inhalation injury can occur due to frequent and widespread use of household cleaning agents and industrial gases (including chlorine and ammonia). The airways and lungs receive continuous first-pass exposure to non-toxic and irritating or toxic gases through inhalation. Irritant gases are gases that, when inhaled, dissolve in the respiratory tract mucosa and trigger an inflammatory response, usually from the release of an acid or alkali radical. Smoke, chlorine, phosgene, sulfur dioxide, hydrogen chloride, hydrogen sulfide, nitrogen dioxide, ozone, and ammonia are common irritants.
Depending on the type and amount of inhaled irritant gas, the victim may experience symptoms ranging from mild respiratory discomfort to acute respiratory and lung injury and even death. Common responses to various types of irritant gases include inflammation, edema and epithelial decay, which, if left untreated, can lead to scar tissue formation and lung and airway remodeling. Currently, mechanical ventilation remains a therapeutic mainstay for pulmonary dysfunction after acute inhalation injury.
Video Acute inhalation injury
Cause
Inhaling smoke
Inhalation injury of smoke, either by itself but rather because of burns on the surface of the body, can cause severe morbidity and lung mortality. The most common cause of death in burn centers now is respiratory failure. The September 11 attacks of 2001 and forest fires in US states such as California and Nevada are examples of incidents that have led to inhalation of smoke injuries. Injuries to the lungs and airways are not only due to fine particulate soot deposition but also because of the smoke gas component, which includes phosgene, carbon monoxide, and sulfur dioxide.
Chlorine
Chlorine is a relatively common gas in the industry with various uses. It is used to disinfect water as well as become part of the sanitation process for industrial wastes and wastes. Chlorine is also used as a bleaching agent during paper and cloth production. Many household cleaning products, including bleach, contain chlorine. Given the volume and ease of chlorine for industrial and commercial use, exposure can occur from accidental spills or deliberate attacks. The National Institute for Occupational Safety and Health recommends that a person wear anti-splash goggles, face shields and a respirator mask while working around chlorine gas. Since chlorine is a gas at room temperature, most of the exposure occurs through inhalation. Exposure may also occur through skin or eye contact or by ingestion of food or water contaminated with chlorine. Chlorine is a strong oxidizing element that causes hydrogen to split from water in moist tissue, producing newborn oxygen and hydrogen chloride which causes corrosive tissue damage. In addition, chlorine oxidation can form hypochlorite acid, which can penetrate cells and react with cytoplasmic proteins that destroy cell structures. The smell of chlorine provides early warning signs of exposure but causes fatigue or olfactory adaptation, reducing awareness of exposure to low concentrations. With increased exposure, symptoms can develop into difficult breathing, severe cough, chest tightness, wheezing, dyspnea, and bronchospasm associated with decreased oxygen saturation levels.. Severe exposure can cause changes in the upper and lower airways that result in acute lung injury, which may not appear until several hours after exposure. A recent chlorine gas leak in Pune, India, landed 20 people in the hospital. Although it was an accidental exposure, chlorine gas has been used as a weapon of war since World War I, the last in 2007 in Iraq.
Phosgene
Phosgene, mainly used as a chemical weapon during World War I, is also used as industrial reagents and building blocks in the synthesis of drugs and other organic compounds. Due to safety concerns, phosgene is almost always produced and consumed in the same plant and extraordinary steps are made to contain this gas. In low concentrations, the smell of phosgene resembles grass or freshly cut grass. Because of this, the gas may be unnoticed and symptoms may appear slowly. Phosgene directly reacts with amines, sulfhydryls, and alcohol groups, affecting macromolecules and cell metabolism. Direct toxicity to cells leads to increased capillary permeability. Furthermore, when the phosgene hydrolyzes to form hydrochloric acid, which can damage the cell surface and cause cell death in the alveoli and bronchioles. Hydrochloric acid triggers an inflammatory response that attracts neutrophils to the lungs, leading to pulmonary edema.
Ammonia
Ammonia is commonly used in household cleaning products, as well as in farmland and in some industrial and commercial locations, and this facilitates the occurrence of accidental or intentional exposure. Ammonia interacts with a moist surface to form ammonium hydroxide, which causes tissue necrosis. Exposure to high concentrations may cause bronchiolar and alveolar edema and airway damage resulting in respiratory failure or failure. Although ammonia has a strong odor, it also causes fatigue or olfactory adaptation, reducing awareness of prolonged exposure.
Sulfur mustard
Sulfur mustard was used as a chemical weapon in World War I and more recently in the Iran-Iraq War. Sulfur mustard is a vesical alkylation agent with strong cytotoxic, mutagenic, and carcinogenic properties. After exposure, the victim shows skin irritation and blisters. These agents also cause respiratory tract lesions, bone marrow depression, and eye damage, the epithelial tissues of these organs are largely affected. Inhalation of high doses of this gas causes lesions in the larynx, trachea, and large bronchi with inflammatory and necrotic reactions. Alkylation agents affect more of the upper respiratory tract, and only very open victims show signs such as distal bronchiolitis obliterans. Secondary effects of exposure to sulfur mustard cause chronic lung disease such as chronic bronchitis.
Chloramine
General exposure involves the unintentional mixing of household ammonia with a cleanser containing bleach, causing irritant chloramine gas to be released.
Gas mustard
Mustards, vesicating agents, have been used primarily in warfare. They damage the upper airway mucosa. Pulmonary edema is rare because mustard rarely affects the lung parenchyma and alveoli.
Methyl isocyanate
Methyl isocyanate is an intermediate chemical in the production of carbamate pesticides (such as carbaryl, carbofuran, methomyl, and aldicarb). It has also been used in rubber and adhesive production. As a very poisonous and irritating material, it is harmful to human health, and is involved in the Bhopal disaster - which killed nearly 8,000 people initially and about 17,000 people in total. When breathing steam produces a direct inflammatory effect on the respiratory tract.
Maps Acute inhalation injury
Pathophysiology
Respiratory damage related to gas concentration and solubility. Exposure to irritating gases primarily affects the airways, causing tracheitis, bronchitis, and bronchiolitis. Other inhalation agents may be directly toxic (eg cyanide, carbon monoxide), or cause harm only by transferring oxygen and producing asphyxia (eg methane, carbon dioxide). The effects of inhalation of irritant gases depend on the extent and duration of exposure and to the specific agent Chlorine, phosgene, sulfur dioxide, hydrogen chloride, hydrogen sulfide, nitrogen dioxide, ozone and ammonia are one of the most important irritant gases. Hydrogen sulfide is also a powerful cell poison, blocking the cytochrome system and inhibiting cellular respiration. More water-soluble gases (eg chlorine, ammonia, sulfur dioxide, hydrogen chloride) dissolve in the upper airways and immediately irritate mucous membranes, which can remind people of the need to escape exposure. Permanent damage to the upper respiratory tract, distal airway, and pulmonary parenchyma occurs only when out of the gas source is inhibited. Less soluble gases (eg nitrogen dioxide, phosgene, ozone) can not dissolve until they enter the respiratory tract, often reaching the lower airways. These agents tend not to produce early warning signs (phosgene in low concentrations have a pleasant odor), are more likely to cause severe bronchiolitis, and often have lag >> 12 hours before symptoms of pulmonary edema develop.
Acute pulmonary injury
Acute lung injury (ALI), also called non-cardiogenic pulmonary edema, is characterized by sudden onset of hypoxemia and a significant diffuse pulmonary infiltration in the absence of heart failure. Core pathology is a disorder of the capillary-endothelial interface: this actually refers to two separate constraints - the endothelium and the basement membrane of the alveoli. In the acute phase of ALI, there is an increased permeability of this barrier and protein-rich fluid leaking out of the capillaries. There are two types of alveolar epithelial cells - type 1 pneumocytes represent 90% of the cell surface area, and are easily damaged. Type 2 pneumocytes are more resistant to damage, which is important because these cells produce surfactants, transmit ions and proliferate and differentiate into Type 1 cells. Damage to the endothelium and alveolar epithelium causes the creation of an open interface between the lungs and blood, facilitating the spread of micro- organism from the lungs systemically, triggering a systemic inflammatory response. In addition, injury to epithelial cells defects the ability of the lungs to pump fluid out of the air space. Liquid-filled air space, loss of surfactant, microvascular thrombosis and irregular repair (leading to fibrosis) reduced resting lung volume (decreased adherence), increased ventilation-perfusion mismatch, right-to-left shunting and respiratory work. In addition, lymphatic drainage of lung units appears to be limited - stunned by acute injuries - that contribute to extravascular fluid buildup. Some patients recover quickly from ALI and have no permanent residual symptoms. Prolonged pneumatic inflammation and destruction leads to fibroblastic proliferation, hyaline membrane formation, tracheal remodeling and pulmonary fibrosis. This fibrosing alveolitis may become apparent as early as five days after the initial injury. Subsequent recovery may be characterized by a reduction in physiological reserves, and increased susceptibility to further lung injury. Broad microvascular thrombosis can lead to pulmonary hypertension, myocardial dysfunction and systemic hypotension.
Acute respiratory distress syndrome
Clinically, the most serious and immediate complication is acute respiratory distress syndrome (ARDS), which usually occurs within 24 hours. Those with significant lower airway involvement may develop bacterial infections. Importantly, victims suffering from surface burns and smoke inhalation are the most vulnerable. Thermal injury combined with an inhalation injury compromised lung function, resulting in microvascular hyperpermeability leading to a significant increase in lung flow of lymphatics and pulmonary edema. The terrorist attacks on the World Trade Center on September 11, 2001 caused many people with impaired lung function. A study of firefighters and EMS workers enrolled in the FDNY WTC Medical Monitoring and Treatment Program, whose lung function was tested before 9/11, documented a sharp decline in lung function in the first year after 9/11. A new study involving a thousand additional workers shows that the decline continues over time. Before 9/11, 3% of firefighters had below normal lung function, one year after 9/11 nearly 19% did so, and six years later stabilized at 13%. Ten to 14 days after acute exposure to some agents (eg ammonia, nitrogen oxide, sulfur dioxide, mercury), some patients develop obliterans developed into ARDS bronchiolitis. Bronchiolitis obliterans with organized pneumonia can occur when granulation tissue accumulates in the terminal airways and alveolar ducts during the body's reparative process. A small proportion of these patients develop late pulmonary fibrosis. Also at increased risk are people with comorbidities. Several studies have reported that both parents and smokers are particularly vulnerable to the adverse effects of inhalation injuries.
Care strategy
Specific precautions, drugs to prevent lung injury that is chemically induced due to respiratory airway toxicity, are not available. Analgesics, oxygen, humidification, and ventilator support are currently standard therapies. In fact, mechanical ventilation remains a therapeutic mainstay for acute inhalation injury. The cornerstone of treatment is to keep PaO2 & gt; 60 mmHg (8.0 kPa), without causing injury to the lungs with excessive O2 or volutrauma. Pressure control ventilation is more flexible than volume control, although the breath should be limited in volume, to prevent injury to the alveoli strain. The positive end-expiratory pressure (PEEP) is used in patients with mechanical ventilation with ARDS to improve oxygenation. Bleeding, indicating substantial damage to the lining of the airways and lungs, may occur with exposure to highly corrosive chemicals and may require additional medical intervention. Corticosteroids are sometimes given, and bronchodilators to treat bronchospasm. Drugs that reduce the inflammatory response, promote tissue healing, and prevent the onset of pulmonary edema or secondary inflammation can be used after severe injury to prevent chronic scarring and airway narrowing.
Although current treatment can be provided in controlled hospital settings, many hospitals are not suitable for situations involving mass casualties among civilians. Inexpensive positive pressure apparatus that can be used easily in mass casualty situations, and drugs to prevent inflammation and pulmonary edema are needed. Some drugs that have been approved by the FDA for other indications promise to treat chemical-induced pulmonary edema. This includes? 2-agonists, dopamine, insulin, allopurinol, and non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen. Ibuprofen is very interesting because it has an established security record and can be easily given as an early intervention. The inhaled and systemic forms of 2-agonists used in the treatment of asthma and other commonly used drugs, such as insulin, dopamine, and allopurinol have also been effective in reducing pulmonary edema in animal models but require further study. A recent study documented in the AANA Journal discusses the use of volatile anesthetic agents, such as sevoflurane, for use as a bronchodilator that lowers peak air pressure and increases oxygenation. Other promising drugs in earlier developmental stages act on various steps in the complex molecular pathways that underlie pulmonary edema. Some of these potential drugs target inflammatory responses or specific sites of injury. Others modulate ion channel activity that controls the transport of fluids across the lung membrane or the target surfactant, a substance that lines the air sacs in the lungs and prevents them from collapsing. Mechanistic information based on toxicology, biochemistry, and physiology may play a role in setting new targets for therapy. Mechanical studies can also assist in the development of new diagnostic approaches. Some chemicals produce metabolic byproducts that can be used for diagnosis, but detection of these byproducts may not be possible until several hours after initial exposure. Additional research should be directed towards developing sensitive and specific tests to identify individuals quickly after they are exposed to varying levels of toxic chemicals into the respiratory tract.
There are currently no clinically approved agents that can reduce pulmonary and airway dropleting and prevent transition to lung and/or airway fibrosis.
Preclinical development of lung protection strategies
Given the constant threat of bioterror-related events, there is an urgent need to develop pulmonary protection and reparative agents that can be used by first responders in mass casualty settings. Use in such an arrangement would require administration through a convenient route to eg. intramuscularly through epipens. Other administrative routes that may be inhaled and possibly at lower levels of oral ingestion can be difficult in various forms of injury especially if accompanied by secretions or if the victim is nauseated. A number of in vitro and in vivo models allow for preclinical evaluation of new lung therapies.
In vitro
In vitro, exposure of human epithelial bronchial cells or human lung epithelial epithelial cells to agents such as hydrogen peroxide or bleach results in time and dose-dependent dose-toxins in cellular viability. The cells affected by these agents show significant decreases in ATP, DNA damage, and lipid peroxidation, followed by possible deaths for evaluation of new cytoprotective agents. Potential tissue reparative agents can be evaluated in vitro by determining their effect on the stimulation of pulmonary and airway epithelial cell proliferation.
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Test articles received in vitro can be evaluated in a number of in vivo models (usually in mice) of ALI including chlorine inhalation, intratracheal bleomycin instillation and in changing growth factors? 1 (TGF 1) transgenic mice expressed excessively exposed to high doses of doxycycline. Acute exposure to high concentrations of chlorine gas induces pathological and functional changes in rodent lung. Histologic changes consist of epithelial necrosis and detachment, increased smooth muscle area, epithelial regeneration and mucosal cell hyperplasia. Most of these disorders disappear over time. Functional changes (increased RL and/or bronchial response to inhaled methacholine) last for an average interval of 3 and 7 days after exposure, but can last up to 30 and 90 days, respectively. Functional changes are associated with overall abnormal airway epithelial damage and there is a significant correlation between RL and bronchoalveolar lavage (BAL) neutrophilia. Bleomycin is an antineoplastic antibiotic drug isolated in 1966 from actinomycete Streptomyces verticillus. Bleomycin forms complexes with oxygen and metals such as Fe2, leading to the production of oxygen radicals, DNA breaks, and finally cell death. Doxycycline pushed overexpression from TGF? 1 in transgenic rat lung produces a time dependent inflammatory response characterized by large infiltration of F4/80 monocytic/macrophage-like cells and apoptotic lung cell death waves. Rats that survive from this onslaught show elevated levels of lung collagen, and decreased lung compliance. The great animal model of ALI is a model of body surface moistened by the body. It has been established that combined burns and inhalation injuries damage the hypoxic pulmonary vasoconstriction (HPV), vasoconstriction response to hypoxia, resulting in incompatibility of ventilation with perfusion. Gas exchange is influenced by increased spread of both alveolar ventilation and cardiac output because bronchial and vascular functions are altered by injury-related factors, such as the effects of inflammatory mediators on the respiratory tract and vascular smooth muscle tone. As a rule of thumb, all of these models are characterized by high mortality, inflammation of the airways and pulmonary parenchyma, edema and alveolar space floods by protein exudates, airway decay and pulmonary epithelium, scarring and transition to the airways and lungs. remodeling.
References
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