Inhalation injuries happen to be one of the most challenging injuries for burn caregivers. This is because it is one of the typical determinants of mortality that occurs after severe burns. Other determining factors are the age of injury and delay in recovery.  inhalation Injuries are lung injuries from inhalation of fumes or burning chemical products. 
Inhalation injury results in direct cellular alterations in local blood circulation and airway perfusion obstruction, as well as the release of pro-inflammatory cytokines and toxins.  Inhalation injury can also lead to decreased mucociliary clearance and Alveolar macrophages  This patient is at high risk for bacterial infections, especially pneumonia, which is one of the leading causes of death in burn patients. 
Inhalation injuries account for approximately one-third of all burn injuries and approximately 90% of all burn-related mortality.  The American Burn Society National Burn Database reports that up to 10.3% of burn patients have associated inhalation injuries.  Therefore, one-tenth Burn patients who survive to hospital admission develop inhalation injury, with a commensurate increase in mortality. 
Inhalation injuries are anatomically divided into three categories:
Heat Injury to the Upper Airway
When the room temperature reaches 1000°F after a fire breaks out, it can cause damage to the airway structures above the carina. This is due to the combination of the low heat capacity of the air in the upper airway and the efficient heat dissipation from the reflective closure of the larynx. 
Consequences of damage to these airway structures include extensive swelling of the lingual and aryepiglottic folds with concomitant obstruction. Airway swelling takes hours to develop as fluid resuscitation progresses. It is important to note that the initial Evaluation may not be the best indicator of the degree of blocking that may occur later. 
Chemical Injury to the Lower Airways
Combustion of material can cause respiratory release of toxic substances. This may cause local chemical irritation of the respiratory tract.  Sulfur dioxide is produced by burning rubber and plastic, as well as other gases such as nitrogen dioxide, ammonia, and chlorine Strong acids and bases combined with water in the airways and alveoli. Laminated furniture may also contain glue, which may release cyanide gas during combustion. Aldehydes are also produced when cotton or wool is burned. Additionally, toxins from smoke may damage the airways Epithelial cells and capillary endothelial cells. 
Systemic toxicity from carbon monoxide or cyanide exposure
Burn victims died from carbon monoxide poisoning. Unfortunately, due to its mechanism, many of its deaths occurred at the scene of fires. In an enclosed fire, damage is affected by carboxyhemoglobin levels. Major damage can be done in a short period of time Exposure to carboxyhemoglobin levels frame a minimum of 10%.  Carbon monoxide is a competitive inhibitor of intracellular cytochrome oxidase systems, especially cytochrome P-450, which inactivates cellular systems to utilize oxygen. 
On the other hand, inhalation of hydrogen cyanide, a product of combustion of various household materials, also inhibits the cytochrome oxidase system. This then promotes a synergistic effect with carbon monoxide leading to tissue hypoxia with acidosis and reduced consumption of oxygen by the brain Tissue
It is the environment and the host that determine the size of the inhalation injury. Other factors such as the source of the injury, the gases produced (temperature concentration and solubility), and the individual’s response to the injury determine the extent of the injury.  This Effects following inhalation injury include cast formation, reduced amount of surfactant available, increased airway resistance, and reduced lung compliance.  These eventually lead to acute lung injury and acute respiratory distress syndrome. 
The mechanism of destruction of this inhalation injury can be classified in one of four ways:
Upper Airway Injury
This pathophysiological process results from microvascular changes following direct thermal injury and chemical stimulation.  The heat from combustion denatures proteins. This leads to the activation of the complement cascade, which leads to the release of histamine.  In addition Xanthine oxidase releases reactive oxygen species (ROS), which react with nitric oxide in endothelial cells, causing upper airway edema by increasing microvasculature stress and local permeability.  Pro-inflammatory cytokines with ROS and eicosanoids also brought The entry of polymorphonuclear cells into this area further leads to the release of ROS and signaling proteases. 
This results in a marked increase in microvascular pressure, a decrease in interstitial hydrostatic pressure, and an increase in interstitial osmotic pressure.  As burn patients are resuscitated with crystalloid fluids, which further reduces plasma colloid permeability Pressure affects the osmotic pressure gradient in the microcirculation, leading to more severe airway edema.  There is no steam inhalation and explosion injury, and the upper respiratory tract provides effective protection to the lower respiratory tract through heat exchange to limit the distal damage to the lower respiratory tract airway
Lower Airway Injury
Chemicals in smoke can cause lower airway damage. Due to the low heat capacity of air and efficient bronchial circulation regulating the temperature of airway gases, most gases are at body temperature as they pass through the glottis.  for inducing thermal injury There must be direct contact with the airway flame.  Burning biomaterials are toxic to the airways, causing an initial response to trigger a pro-inflammatory response. This results in a 10-fold increase in bronchial blood circulation within minutes of an inhalation injury.  This It continues to increase and leads to increased permeability and damage of bronchial epithelial cells.  Increased transvascular fluid in the lungs and a decrease in PaO2/FiO2 ≤ 200 within 24 hours after injury.  Furthermore the tracheobronchial tree is hyperemic and The presence of an airway is a very common clinical finding in inhalation injury and is often used to diagnose the injury.  The copious foamy secretions formed by goblet cells subsequently solidify, leading to cast formation and airway obstruction. 
Pulmonary Parenchymal Injury
Changes in the lung parenchyma occur long after injury. The extent of this change depends on the extent of the injury and the patient’s response to the injury. The occurrence of parenchymal injury is associated with elevated levels of pulmonary transvascular fluid, and This is directly proportional to the time of exposure to toxic substances and fumes.  Likewise, there is very little damage to the lower respiratory tract and lung parenchyma from direct thermal exposure. Therefore, only steam can overcome the efficient cooling system of the upper airway. There is a decrease Permeability of proteins Increased permeability of small particles Reduced pulmonary microvascular pressure and loss of hypoxic pulmonary vasoconstriction.  Major disturbances after inhalation injury include edema, decreased lung compliance Following sudden inactivation of extravascular lung water and pulmonary lymph and surfactant. In addition, a ventilation-perfusion mismatch ensues, leading to severe hypoxemia and ARDS. 
Inhalation of chemical cytotoxic liquid fumes and gases can cause systemic toxic changes. Smoke can bind to these toxins and lead to increased mortality by promoting hypoxic metabolic acidosis, reducing brain oxygen consumption and metabolism .
The initial diagnosis of inhalation injury is based on the following indirect observations:
- Facial burns
- Singed nasal vibrissae
- Medical history indicating burns occurred in an enclosed space
For each of these signs, there is a high level of false positives. Furthermore, when taken together, they were shown to underestimate the true incidence of inhalation injury. A classic sign of smoke inhalation is also carbonaceous secretions. Although it is a less accurate predictor The presence or severity of inhalation injury is higher than generally believed. However, signs of smoke exposure may be carbonaceous secretions, but should not confirm the diagnosis of inhalation injury or its sequelae. Hypoxic crackles and wheezing were infrequent on admission. but when They occur in the most severely injured patients, which can mean a very poor prognosis. 
In addition, chest x-rays on admission have also been shown to be poor indicators of inhalation injury.  However, it has been observed that approximately two-thirds of patients may develop diffuse or focal infiltrates or changes in pulmonary edema between five and ten days after injury. therefore admitted Films are not usually used for diagnostic purposes, but can be used for baseline assessment. 
The current standard for diagnosing inhalation injury is fiberoptic bronchoscopy . However, it is only useful for detecting upper airway damage. Observations may include soot mucosal necrosis, charring edema, and inflammation of the airways. 
However, bronchoscopy alone cannot exclude the possibility of parenchymal injury. Therefore, xenon scanning is commonly used to identify parenchymal damage . It is a safe rapid test that requires minimal cooperation from the patient. It involves several boob flashing pictures, once The initial radioactive xenon has been injected intravenously. This test demonstrates locations of reduced alveolar gas flushing, revealing locations of microscopic airway obstructions caused by edema or fibrin cast formation. 
There is generally no single standard management protocol for inhalation injuries.  Treatment of inhalation injury is primarily supportive care. This is achieved through acute hospitalization and rehabilitation. 
Inhalation injuries lead to the formation of casts, which reduce the amount of surfactant available, increase airway resistance and reduce lung compliance. 
Bronchodilators reduce airflow resistance and improve airway compliance. Albuterol and albuterol are β2-adrenergic agonists that increase the PaO2/FiO2 ratio by relaxing smooth muscle and inhibiting bronchospasm, thereby reducing airway pressure. 
Muscarinic Receptor Antagonists
To reduce airway pressure and mucus secretion, muscarinic receptor antagonists such as tiotropium bromide are used to limit the release of cytokines through airway smooth muscle contraction and to stimulate submucosal glands. 
To reduce host inflammatory responses following inhalational injury, muscarinic receptor antagonists and beta agonists can be used. Structurally, muscarinic and adrenergic receptors are located in the lining of the airways, although their influence on inflammation and host response is incomplete Understood. However, they have been shown to reduce the activity of pro-inflammatory cytokines after stress. 
Inhaled (nebulized) mucolytics and anticoagulants
Address airway obstruction that occurs following mucofibrin cast formation and cellular debris following the use of inhaled injury mucolytics; specifically N-acetylcysteine (NAC).  NAC has anti-inflammatory properties and is an antioxidant and free radical scavenger.  it Acts as a strong mucolytic, reducing damage from ROS. Inhaled anticoagulants are also used to reduce airway obstruction from fibrin casts.
Achieving and maintaining a patent airway is often important in the management of inhalation injury, as severe upper airway edema is often caused by inhalation injury, and resuscitation of burns often worsens airway edema.  
There have been limited trials of breathing patterns suitable for patients with inhalation injuries. However, the ARDSNET trial has demonstrated a mechanical ventilation strategy that reduces morbidity and mortality in acute respiratory distress symptoms and acute lung injury. This trial revealed from a large randomized controlled trial that a lung protective strategy of limiting tidal volumes to 6-8 mL/kg and plateau pressures below 30 cm H2O improves outcomes. 
Due to the limited research of conventional mechanical ventilation modes such as control mode ventilation assist control mode synchronized intermittent mandatory ventilation pressure control mode and pressure support mode in patients with inhalation injury non-traditional modes Ventilation patterns are often employed to support patients with inhalation injury and apply lung-protective ventilation strategies. 
Commonly used unconventional ventilator modes include high-frequency percussive ventilation (HFPV), high-frequency oscillatory ventilation (HFOV), airway pressure release ventilation (APRV), and extracorporeal membrane oxygenation (ECMO). Although HFPV has been shown to be the most Very promising in these modes. 
Numerous studies have shown techniques such as gravity-assisted bronchial drainage combined with chest percussion and vibration. Effectively removes secretions. 
Bronchial Drainage / Positioning
This is a gravity-assisted positioning modality designed to improve the hygiene of the pulmonary system in patients with inhalational injury and/or retained secretions. Clinical judgment may be most influenced by skin graft donor site and use of air fluidized bed appropriate decision.  In fact, head-down positions and various other postures may dramatically worsen hypoxemia. It has been shown that patients may experience a decrease in localized levels of arterial oxygenation. 
Tapping can remove secretions in the tracheobronchial tree. It is important to place suitable padding between the patient’s and physical therapist’s hands to prevent skin irritation during percussion.  Percussion applied to bronchial segments Drain using their surface landmarks. Avoid incision skin grafts and bony protrusions when tapping. 
Vibration / Shaking
Vibration/shaking mobilizes loose secretions into the larger airways for easy coughing or clearing of secretions with suction. Vibration can be performed mechanically, and this type of vibration has also been reported to produce good clinical results. For patients who cannot tolerate manual manipulation A slight mechanical vibration can be indicated by tapping. 
In order to prevent respiratory complications, patients with inhalation injury can start activities on the ground as soon as possible. Patients receiving continuous ventilatory support may also be placed in a chair with the appropriate use of analgesics. There is a definite therapeutic effect of sitting posture Including: 
- Patient can breathe in areas of the lungs that are normally hyperventilated
- May maintain muscle strength and tone
- Prevent contractures and maintain exercise tolerance
Notably, despite improvements in the standard of care for severe burns, the mortality rate from inhalation injuries has not changed over the past five years.  Supportive strategies are critical in the management of inhalation injury. More experiments are needed to prove Adequate evidence for many drugs. Unconventional modes of ventilation, such as HFPV, have also had more promising results in addressing the physiological disturbances caused by inhalation injury. 
Inhalation injury requires an in-depth understanding of its pathophysiology to guide accurate diagnosis and develop the right treatment strategy. Practitioners must work carefully within the available evidence to achieve optimal outcomes from inhalation injury – a typical determinant of mortality in critically ill patients burn.
- ↑ Jump up to:1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Jones SW, Williams FN, Cairns BA, Cartotto R. Inhalation injury: pathophysiology, diagnosis, and treatment. Clinics in plastic surgery. 2017 Jul 1;44(3):505-11.
- ↑ Jump up to:2.0 2.1 2.2 2.3 Dries and EndorfScandinavian Journal of Trauma, Resuscitation and Emergency Medicine2013,21:31
- ↑ Jump up to:3.0 3.1 Kadri SS, Miller AC, Hohmann S, Bonne S, Nielsen C, Wells C, Gruver C, Quraishi SA, Sun J, Cai R, Morris PE. Risk factors for in-hospital mortality in smoke inhalation-associated acute lung injury: data from 68 United States hospitals. Chest. 2016 Dec 1;150(6):1260-8.
- ↑ Reper P, Heijmans W. High-frequency percussive ventilation and initial biomarker levels of lung injury in patients with minor burns after smoke inhalation injury. Burns. 2015; 41:65–70. [PubMed: 24986596]
- ↑ Al Ashry HS, Mansour G, Kalil AC, Walters RW, Vivekanandan R. Incidence of ventilator associated pneumonia in burn patients with inhalation injury treated with high frequency percussive ventilation versus volume control ventilation: A systematic review. Burns. 2016 Sep 1;42(6):1193-200.
- ↑ Jump up to:6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 Mlcak RP, Suman OE, Herndon DN. Respiratory management of inhalation injury. burns. 2007 Feb 1;33(1):2-13.
- ↑ Pruitt BA, McManus AT. The changing epidemiology of infection in burn patients. World journal of surgery. 1992 Jan 1;16(1):57-67.
- ↑ Tan A, Smailes S, Friebel T, Magdum A, Frew Q, El-Muttardi N, Dziewulski P. Smoke inhalation increases intensive care requirements and morbidity in paediatric burns. Burns. 2016 Aug 1;42(5):1111-5.
- ↑ Burn Incidence Fact Sheet. American Burn Association; 2016 National Burn Repository. American Burn Association; 2017.
- ↑ Foncerrada G, Culnan DM, Capek KD, González-Trejo S, Cambiaso-Daniel J, Woodson LC, Herndon DN, Finnerty CC, Lee JO. Inhalation injury in the burned patient. Annals of plastic surgery. 2018 Mar;80(3 Suppl 2):S98.
- ↑ Jump up to:11.0 11.1 11.2 11.3 McCall JE, Cahill TJ. Respiratory care of the burn patient. Journal of Burn Care & Rehabilitation. 2005 May 1;26(3):200-6.
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- ↑ Palmieri TL. Inhalation injury: research progress and needs. Journal of burn care & research. 2007 Jul 1;28(4):549-54.
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- ↑ Jump up to:16.0 16.1 16.2 16.3 Traber, D., Herndon, David, Enkhbaatar, Perenlei, Maybauer, Marc, Maybauer, Dirk. The pathophysiology of inhalation injury. In: Herndon, D., editor. Total Burn Care. Fourth. Saunders Elsevier; 2012. p. 219-28
- ↑ Jump up to:17.0 17.1 17.2 17.3 17.4 17.5 17.6 17.7 Sousse LE, Herndon DN, Andersen CR, Ali A, Benjamin NC, Granchi T, Suman OE, Mlcak RP. High tidal volume decreases adult respiratory distress syndrome, atelectasis, and ventilator days compared with low tidal volume in pediatric burned patients with inhalation injury. Journal of the American College of Surgeons. 2015 Apr 1;220(4):570-8.
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