Inhalation Injury

Original Editor - Joseph Ayotunde Aderonmu

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Introduction[edit | edit source]

Respiratory System.png

Inhalation injury happens to be one of the most challenging injuries for burn care providers. This is because it is one of the classic determinants of mortality that occurs after severe burn injury. The other determinants are age, extent of injury, as well as delay in resuscitation.[1] Inhalation injury refers to pulmonary injury resulting from inhalation of smoke or chemical products of combustion.[2]

Inhalation injury results in direct cellular damage, alterations in regional blood circulation and perfusion, obstruction of the airways, and the release of pro-inflammatory cytokine and toxin release.[3][4] Inhalation injuries also causes reduced functionality of mucociliary clearance and weakening of alveolar macrophages.[5] With this, patient is placed at a high risk of bacterial infection, especially pneumonia, which is one of the top causes of death for burn patients.[6][7]

Epidemiology[edit | edit source]

Inhalation injury is recorded in about one-third of all burn injuries and it is responsible for about 90% of all burn-related mortality.[3][8] The National Burn Repository of the American Burn Association reported up to 10.3% of burn patients to have accompanying inhalation injury.[9] Thus, 1 in 10 burn patients that survive to admission will have the inhalation injury and a corresponding increase in the mortality rate.[10]

Classes[edit | edit source]

Anatomically, inhalation injuries are divided into three classes:[11]

Heat Injury to the Upper Airway[edit | edit source]

When the room air temperature reaches 1000°F after a fire outbreak, injury is results to structures of the airway above the carina. This results due to the combination of efficient heat dissipation in the upper airway, low heat capacity of air and reflex closure of the larynx.[12]

The result of the injury to these airway structures include extensive swelling of the the tongue, epiglottis, and aryepiglottic folds and accompanying obstruction. It takes a period of hours for airway swelling to develop as fluid resuscitation is taking place. It is important to note that initial evaluation might not be the best indicator of the extent of the obstruction that may later occur.[13]

Chemical Injury to the Lower Airways[edit | edit source]

Combustion of materials leads to the the production of toxic materials to the respiratory tract. This may cause local chemical irritation in the respiratory tract.[2] Sulfur dioxide is produced by burning rubber and plastic, as well as other gases such as nitrogen dioxide, ammonia and chlorine with strong acids and alkali after combination with water in the respiratory airways and alveoli. Also, laminated furniture may contain glues that may release cyanide gas during combustion. Aldehydes are also produced when cotton or wool are burned. Furthermore, toxins produced by smoke may damage airway epithelial and capillary endothelial cells.[11][14]

Systemic Toxicity due to Carbon Monoxide or Cyanide Exposure[edit | edit source]

Fatalities result from carbon monoxide poisoning in burn-injured patients. Unfortunately, many of its fatalities happen at the scene of the fire due to its mechanism. In a closed fire space, the level of carboxyhemoglobin levels. This can result in significant injury in just a short time frame with the exposure to carboxyhemoglobin levels as minute as 10%.[11][15][16] Carbon monoxide is a competitive inhibitor of intracellular cytochrome oxidase enzyme systems, especially the cytochrome P-450 resulting in inactivation of cellular systems to make use of oxygen.[2]

On the other hand, inhaled hydrogen cyanide, which is a product of the combustion of multiple household materials also inhibits the cytochrome oxidase system. This then foster a synergy with carbon monoxide to cause tissue hypoxia with acidosis and a reduction in the consumption of oxygen by the brain tissues.[11][16]

Pathophysiology[edit | edit source]

What determines the amount of damage caused by an inhalation injury are the environment and the host. Also, other factors such as the injury source, the gases produced (temperature, concentration, and solubility), and the response of an individual to the injury.[17] The effects that follow inhalation injuries include formation of casts, reduction in the amount of available surfactants, increased airway resistance, and reduction in pulmonary compliance.[18] These culminate in acute lung injury and acute respiratory distress syndrome.[19]

This mechanism of destruction in inhalation injuries can be classified in one of four ways:

Upper Airway Injury

The course of this pathophysiology is induced by microvascular changes that result after direct thermal injury and chemical irritation.[6] Heat produced from the burn denatures protein. This causes the activation of the complement cascade that results in the release of histamine.[17][20] Furthermore, xanthine oxidase is formed, reactive oxygen species (ROS) are released which reacts with nitric oxide in the endothelium to cause upper airway edema by raising the pressure of the microvasculature and local permeability.[17][21][22] Also, pro-inflammatory cytokines, with ROS and eicosanoids bring polymorphonuclear cells to this area further causing the release of ROS and signaling proteases.[1]

This causes a remarkable increase in the pressure of the microvasculature, a reduction in interstitial hydrostatic pressure and an increase in interstitial oncotic pressure.[17] Since burn patients are administered crystalloids to be used in resuscitation, this further reduces the plasma oncotic pressure, affecting the oncotic pressure gradient in the microcirculation causing more significant airway edema.[17] Without steam inhalation and blast injuries, an efficient protection is given to the lower airway by the upper airway through heat exchange to restrict distal damage to the lower airways.[1]

Lower Airway Injury

Lower airway injury occurs as a result of the chemicals in smoke. Due to the low heat capacity of air and the efficient bronchial circulation regulating the temperature of the airway gases, most gases are at body temperature when the pass through the glottis.[23] For the induction of thermal injury to the airways, flames have to be in direct contact.[24] Burned biological materials are toxic to the airways and cause an initial response to trigger proinflammatory response. This causes up to a 10-fold increase in bronchial blood circulation within minutes after an inhalation injury. [16] This increase is sustained and results in increased permeability and damage of the bronchial epithelium.[17] An increase in pulmonary transvascular fluid results and a fall in PaO2/FiO2 ≤ 200 within 24 hours following the injury.[25] Furthermore, hyperemia of the tracheobronchial tree and lower airways occurs, which is a clinical finding very common in inhalation injury and is used to often diagnose the injury.[26][27] The copious and foamy secretions that are formed from goblet cells later solidify, resulting in the formation of casts and airway obstruction.[17]

Pulmonary parenchymal injury

The changes to lung parenchyma occur much later after the injury. The extent of this changes are dependent on the extent of the injury and the response of the patient to the injury. The occurrence of parenchymal injuries are associated with an elevation of pulmonary transvascular fluid levels and this is proportional to the period of exposure to toxins and smokes.[2] Again, it is rare for injury to the lower airways and lung parenchyma to be caused by direct thermal contact. Thus, it is only steam that can overcome the efficient heat dissipating system of the upper airway. There is a decrease to the permeability of protein, an elevation to the permeability to small particles, a reduction in pressure in the pulmonary microvasculature pressure, and hypoxic pulmonary vasoconstriction loss.[17] The major derangements that follow inhalation injury include edema, lowered pulmonary compliance following extravascular lung water and pulmonary lymph, and sudden inactivation of surfactant. In addition, a subsequent ventilation-perfusion mismatch can also occur that can lead to profound hypoxemia and ARDS.[6]

Systemic toxicity.

Inhalation of chemicals, cytotoxic liquids, fumes, mist and gases can cause systemic toxic changes. Smoke can combine with these toxins and cause increased mortality by promoting tissue hypoxia, metabolic acidosis, and reducing cerebral oxygen consumption and metabolism.[16][28]

Diagnosis[edit | edit source]

Initially, the diagnosis of inhalation injury was based on the following indirect observations:[29]

  • Facial burns
  • Singed nasal vibrissae
  • A history indicating a burn injury that occurred in an enclosed space

For each of these signs, there is a high level of false positivity. Also, when they are taken together, they are shown to underestimate the true occurrence of inhalation injury. A classic sign of smoke inhalation is also carbonaceous secretions. Although, it is a less exact predictor of either the presence or severity of inhalation injury than is widely believed. Yet, a telltale of exposure to smoke could be carbonaceous secretions but should not confirm either the diagnosis of inhalation injury or its sequela. Hypoxia, rales, rhonchi and wheezes are not often present on admission. But when they occur, they are seen in patients with the most severe injury and this may mean an extremely poor prognosis.[6]

Also, the chest X-ray of patient on admission has also been shown to be a poor indicator of inhalation injury.[6] Yet, it is observed that about two-thirds of patients may have changes of diffuse or focal infiltrates or pulmonary edema between five to ten days after injury, Therefore, the admission film is usually not used for diagnostic purposes, but is useful for making baseline evaluations.[30]

Currently, the standard for the diagnosis of inhalation injury is fiberoptic bronchoscopy.[31] It is however useful only in detecting upper airway injury. The observations may include presence of soot, mucosal necrosis, char, edema of the respiratory airways and inflammation.[32]

However, bronchoscopy alone cannot rule out the possibility of parenchyma damage. Therefore, to find out parenchyma damage, Xenon scanning has been generally utilized.[33] It is a safe, quick test which requires a minimum of patient's cooperation. It involves several chest scintiphotograms once an initial radioactive Xenon gas has been intravenously injected. The test demonstrates the locations of the decreased alveolar gas washout, revealing the sites of tiny airway obstruction that results from edema or fibrin cast formation.[6]

Management[edit | edit source]

There is generally no single standard management protocol for inhalation injury.[1] The mainstay of treatment of inhalation injury is supportive care. This is achieved by acute hospitalization and rehabilitation. [1]

Supportive Care[edit | edit source]

Inhalation injuries result in the formation of casts, they decrease the amount of surfactant available, they elevate airway resistance, and they reduce pulmonary compliance.[18]

Bronchodilators[edit | edit source]

Bronchodilators decrease airflow resistance and improve airway compliance. Albuterol and salbutamol which are β2-adrenergic  agonists reduce airway pressure by causing a relaxation of smooth muscles and inhibiting bronchospasm to increase the PaO2/FiO2 ratio.[34]

Muscarinic receptor antagonists[edit | edit source]

To reduce airway pressures and mucus secretion, muscarinic receptor antagonists like tiotropium are employed to limit cytokine release through smooth muscle constriction in the airways, and to cause a stimulation of submucosal glands.[35][36]

To reduce the inflammatory response of the host after an inhalation injury, muscarinic receptor antagonists and beta agonists can be used. Structurally, muscarinic and adrenergic receptors are in the lining of the respiratory tract, although its impact on the inflammatory and host response is not fully understood. They however have been demonstrated to reduce the activity of pro-inflammatory cytokines following stress.[37]

Inhaled (nebulized) Mucolytic agents and Anticoagulants[edit | edit source]

To address the airway obstruction that occurs following mucus, fibrin cast formation, and cellular debris after an inhalation injury, mucolytic agents are used, in particular, N Acetylcysteine (NAC).[38] NAC has anti-inflammatory properties and it is an antioxidant and free radical scavenger.[39] It acts as a strong mucolytic agent that reduces the damage caused by ROS. Inhaled anticoagulants are also employed to reduce airway obstruction from fibrin casts.

Respiratory support[edit | edit source]

Since a significant upper airway edema usually results from an inhalation injury, and the resuscitation of the burn injury often worsen the airway edema, it is often important to obtain and maintain a patent airway in the management of inhalation injury.[6] [1]

Limited trials have been carried out on the respiratory modes suitable for patients with inhalation injury. Yet, a mechanical ventilation strategy that has been demonstrated to improve morbidity and mortality from acute respiratory distress symptom and acute lung injury comes from the ARDSNET trial. This trial revealed from a large randomized controlled trial that "lung protective strategies of limited tidal volumes of 6–8mL/kg and plateau pressures of less than 30cm H2O improved outcomes".[40]

Since conventional mechanical ventilation modes such as control mode ventilation, assist-control mode, synchronized intermittent mandatory ventilation, pressure control mode and pressure support mode have been limitedly studied in the patient with inhalation injury,[18][41] non-conventional modes of ventilation modes are often employed in order to support patients with inhalation injury and apply lung-protective ventilation strategies.[42]

Common non-conventional ventilator modes that are usually used include high-frequency percussive ventilation (HFPV), high frequency oscillatory ventilation (HFOV), airway pressure release ventilation (APRV), extracorporeal membrane oxygenation (ECMO). Although HFPV has been shown to be the most promising among these modes.[1]

Physiotherapy[edit | edit source]

A number of studies have demonstrated that a techniques such as gravity-assisted bronchial drainage when combined with chest percussion and vibrations. are effective in the removal of secretions .[43][44][45]

Bronchial Drainage/Positioning[edit | edit source]

This is a modality that employs the use of gravity-assisted positioning targeted at improving the hygiene of pulmonary system in patients with inhalation injury and/or retained secretions. Due to skin grafts, donor sites, and the use of air fluid beds, clinical judgment might influence the most appropriate decisions.[6] In fact, positioning in the Trendelenburg and various other positions may acutely worsen hypoxemia. It has been shown that a patient may experience a decline in the level of arterial oxygenation positioning.[45]

Percussion[edit | edit source]

Percussion allows secretions to be removed from the tracheobronchial tree. It is essential to position a suitable padding between the patient and the physiotherapist's hands to prevent skin irritation during the process of percussion.[6] Percussion is applied over the bronchial segments to be drained using their surface landmarks. Incisions, skin grafts, and bony prominence should be avoided during percussion.[46]

Vibration/shaking[edit | edit source]

Vibration/shaking mobilizes loosened secretions into larger airways to enable easy cough up or removal through suctioning. Vibrations can be performed mechanically, and this type of vibrations have also been reported to produce good clinical results. For patients who cannot tolerate manual percussion, gentle mechanical vibration may be indicated.[6]

Early Ambulation[edit | edit source]

To prevent respiratory complications, ambulation can be commenced early for patients with inhalation injury. Patients who are on continuous ventilatory support can also be placed into a chair with appropriate use of analgesics. There are establish therapeutic effects of the sitting position which include:[6]

  • The patient can breathe with lungs regions that are normally hyperventilated
  • Muscular strength and tone can be preserved
  • Contractures are prevented and exercise tolerance is maintained

Prognosis[edit | edit source]

It is noteworthy that mortality rates for inhalation injury have not changed over the past five decades, though improvements in standards of care for severe burn injuries have.[1] Supportive strategies are vital in the management of inhalation injury, yet, more trials are needed to demonstrate sufficient evidence for many of the pharmacological agents. Also, more promising results have been achieved with unconventional modes of ventilation such as HFPV in addressing physiologic derangements from inhalation injury.[1]


Inhalation injury requires a robust knowledge of its pathophysiology to guide accurate diagnosis and drive the right therapeutic strategies. Practitioners must carefully work within available evidence for best outcomes from inhalation injuries –a classic determinant of mortality in severe burn.

References[edit | edit source]

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