Inhalation Injury

The classic determinants of mortality from severe burn injury are age, size of injury, delays of resuscitation, and the presence of inhalation injury. Of the major determinants of mortality, inhalation injury remains one of the most challenging injuries for burn care providers. Patients with inhalation injury are at increased risk for pneumonia (the leading cause of death) and multisystem organ failure. There is no consensus among leading burn care centers in the management of inhalation injury. This article outlines the current treatment algorithms and the evidence of their efficacy.

Key points

  • Determinants of mortality in burns are size of burn, age, and the presence of inhalation injury.

  • Inhalation injury with or without cutaneous burn increases morbidity and mortality for burn survivors.

  • Resuscitation efforts are significantly altered by the presence of inhalation injury.

  • There is no consensus among leading burn centers on the optimal mechanical ventilation modes for these patients. Supportive care remains the mainstay of treatment.

  • Despite research gains in nutrition, and the hypermetabolic response to burn injury, there remains a lack of understanding of the pathophysiology of inhalation injury and the long-term physiologic consequences.

Introduction

There is no greater trauma than a large burn. No single injury affects more organ systems than a severe burn injury. The subsequent supraphysiologic responses to that injury lead to full-body catabolism and increased morbidity and mortality. Advances in critical care management, nutrition, wound coverage, and antimicrobial therapies have substantially improved outcomes for burn survivors regardless of burn size. However, when burns are accompanied by inhalation injury, health care providers and clinical scientists have yet to make major impacts on survival.

Inhalation injury is present in up to one-third of all burn injuries; however, it accounts for up to 90% of all burn-related mortality. Inhalation injury causes localized damage via direct cellular damage, changes in regional blood flow and perfusion, airway obstruction, as well as toxin and proinflammatory cytokine release. Inhalation injuries significantly incapacitate mucociliary clearance and impair alveolar macrophages. They predispose patients to bacterial infection, specifically and primarily pneumonia, a leading cause of death for patients with burns. Burn critical care units have the highest rates of ventilator-associated pneumonia in the country, and those patients with concomitant cutaneous injuries with inhalation injury have double the rates of ventilator-associated pneumonia. Moreover, the probability of death increases from 40% to 60% when a burned patient with inhalation injury has pneumonia compared with patients with just cutaneous injuries.

Introduction

There is no greater trauma than a large burn. No single injury affects more organ systems than a severe burn injury. The subsequent supraphysiologic responses to that injury lead to full-body catabolism and increased morbidity and mortality. Advances in critical care management, nutrition, wound coverage, and antimicrobial therapies have substantially improved outcomes for burn survivors regardless of burn size. However, when burns are accompanied by inhalation injury, health care providers and clinical scientists have yet to make major impacts on survival.

Inhalation injury is present in up to one-third of all burn injuries; however, it accounts for up to 90% of all burn-related mortality. Inhalation injury causes localized damage via direct cellular damage, changes in regional blood flow and perfusion, airway obstruction, as well as toxin and proinflammatory cytokine release. Inhalation injuries significantly incapacitate mucociliary clearance and impair alveolar macrophages. They predispose patients to bacterial infection, specifically and primarily pneumonia, a leading cause of death for patients with burns. Burn critical care units have the highest rates of ventilator-associated pneumonia in the country, and those patients with concomitant cutaneous injuries with inhalation injury have double the rates of ventilator-associated pneumonia. Moreover, the probability of death increases from 40% to 60% when a burned patient with inhalation injury has pneumonia compared with patients with just cutaneous injuries.

Pathophysiology

The mechanism of destruction can be classified in 4 ways: (1) upper airway injury, (2) lower airway injury, (3) pulmonary parenchymal injury, and (4) systemic toxicity. The extent of damage from an inhalation injury depends on the environment and the host: the source of injury, temperature, concentration, and solubility of the toxic gases generated, and the response to that injury by the individual. Inhalation injuries cause formation of casts, reduction of available surfactant, increased airway resistance, and decreased pulmonary compliance, leading to acute lung injury and acute respiratory distress syndrome (ARDS).

The major pathophysiology seen in upper airway inhalation injuries is induced by microvascular changes from direct thermal injury and chemical irritation. The heat denatures protein, which subsequently activates the complement cascade causing the release of histamine. Subsequently, there is the formation of xanthine oxidase and release of reactive oxygen species (ROS), which combine with nitric oxide in the endothelium to induce upper airway edema by increasing the microvascular pressure and local permeability. Proinflammatory cytokines, ROS, and eicosanoids attract polymorphonuclear cells to the area, further amplifying ROS and signaling proteases. There is a substantial increase in microvascular hydrostatic pressure, a decrease in interstitial hydrostatic pressure, and an increase in interstitial oncotic pressure. The hallmark of burn resuscitation is the administration of large amounts of crystalloid, which reduces plasma oncotic pressure affecting the oncotic pressure gradient in the microcirculation causing significantly more airway edema. Barring steam inhalation injuries and blast injuries, the upper airway efficiently protects the lower airway via heat exchange to limit distal damage to the lower airway.

Injury to the lower airway is caused by the chemicals in smoke. The heat capacity of air is low and the bronchial circulation very efficient in warming or cooling the airway gases, so that most gases are at body temperature as they pass the glottis. In order to induce thermal injury to the airway, flames must be in direct contact. Accelerants, or burned biological materials, are caustic to the airways and induce an initial response to trigger a proinflammatory response. There is a 10-fold increase in bronchial blood flow within minutes of an inhalation injury, which is sustained and causes increased permeability and destruction of the bronchial epithelium. There is a subsequent increase in pulmonary transvascular fluid and a decrease in Pa o 2 /fraction of inspired oxygen (Fi o 2 ) ratio less than or equal to 200 nearly 24 hours after injury. There is a subsequent hyperemia of the tracheobronchial tree and lower airways, and that very prevalent clinical finding is used to diagnose the injury. Early in the injury, the secretions from goblet cells are copious and foamy. In hours to days these secretions solidify, forming casts and airway obstruction.

Changes to lung parenchyma are delayed, and depend on the severity of injury and the patient’s response to the injury. Parenchymal injuries are associated with an increase in pulmonary transvascular fluid, which is directly proportional to the duration of exposure of smoke and toxins. As stated previously, injury to the lower airways and lung parenchyma is rarely caused by direct thermal contact. Only steam can overcome the very efficient upper airway heat dissipating capabilities. There is a reduction to the permeability of protein, an increase in the permeability to small particles, an increase in pressure in the pulmonary microvasculature pressure, and a loss of hypoxic pulmonary vasoconstriction. The key pathologic derangements in inhalation injury are edema, decreased pulmonary compliance from extravascular lung water and pulmonary lymph, and immediate inactivation of surfactant. There is a subsequent ventilation-perfusion mismatch that can lead to profound hypoxemia and ARDS.

Systemic toxic changes are caused by the inhalation of chemicals and cytotoxic liquids, mists, fumes, and gases. Smoke combines with these toxins and increases mortality by increasing tissue hypoxia, metabolic acidosis, and decreasing cerebral oxygen consumption and metabolism.

Diagnosis

In the past, the diagnosis of inhalation injury has rested on both subjective and objective measures. History and physical are important factors because they may help prognosticate the host response and comorbidities. For example, the elderly population that is unable to escape from danger may have prolonged exposure to smoke and toxins. Key factors in diagnosis from history are the mechanism (flame and smoke or steam), exposure (duration), location (enclosed space), and disability. For the physical examination, facial burns, singed nasal or facial hair, carbonaceous sputum, soot, stridor, or edema. There are no changes in chest radiograph on admission. Oxygen saturation by pulse oximetry (Sp o 2 ) is usually not initially affected and may be misleading, even in the presence of carbon monoxide poisoning, in which the Sp o 2 is typically normal. Similarly, arterial blood gases are nondiagnostic. Even in the presence of carbon monoxide poisoning, the Pa o 2 is normal or increased and only the arterial oxygen saturation is decreased.

Other adjuncts used for confirming inhalation injury include carboxyhemoglobin measurements, chest computed tomography, fiberoptic bronchoscopy (FOB), radionuclide scan with 133 xenon, and pulmonary function testing. To date, these tools have substantial variability within and between institutions and lack sensitivity. Of the aforementioned studies, FOB prognosticates risk of acute lung injury, resuscitative needs, and mortality most accurately and is the focus of this article.

FOB is the standard technique for diagnosis of inhalation injury. It is readily available and allows a longitudinal evaluation. The presence of hyperemia, edema, and soot on FOB are diagnostic of inhalation injury but there remains a discordance of determining severity of injury. Severity of injury depends on the material inhaled, length of exposure, and the host response to this trauma. To further underscore the problem with grading inhalation injury, FOB, which is the most widely accepted diagnostic tool, cannot access distal airways. Hence, damage in the most distal airways is assumed and hypothesized to be the explanation of inconsistent severity of bronchoscopic findings and mortality.

The most widely used approach for grading the severity of an inhalation injury is the abbreviated injury score (AIS), popularized by Endorf and Gamelli. The AIS assigns a severity score from 0 (no injury) to 4 (massive injury) based on the findings at the initial FOB examination. The AIS grading scale for inhalation injury on bronchoscopy has shown variable results with respect to predicting outcome. Higher-grade injuries have been associated with poorer oxygenation in some studies but not others. Similarly, a higher (worse) grade of inhalation injury was associated with a longer duration of mechanical ventilation in 1 study, whereas other investigators have not been able to show this relationship. Surprisingly, the AIS grade of inhalation injury severity has not been found to be associated with fluid resuscitation requirements. In addition, the grade of inhalation injury severity does not consistently correlate with an increase in mortality. A recent study has found that clinically relevant trends toward worse oxygenation, more prolonged mechanical ventilation, and higher fluid resuscitation volumes were associated with patients with high-grade inhalation injuries (former grades 3 and 4) compared with those with low-grade inhalation injury (former grades 1 and 2). Further refinement of this approach is required and it is worth noting that serial bronchoscopic evaluations over the first 24 to 48 hours after the burn may yield more accurate information than a single examination at burn center admission.

Laboratory values used to determine severity include Pa o 2 /Fi o 2 and alveolar-arterial gradients but these can be arbitrarily high or low depending on ventilation modes and other clinical parameters.

Treatment

Although mortalities for inhalation injury have not changed significantly over the last 50 years, the improvements in standards of care for severe burn injuries have. Thus, survival is standard. There is no consensus among leading burn centers about the optimal treatment protocol for inhalation injury. The fundamental tenet of treatment of inhalation injury is supportive care through the acute hospitalization and rehabilitation. This article outlines key evidence in the literature for common treatment modalities for patients with inhalation injury.

Supportive care

Inhalation injuries cause formation of casts, reduction of available surfactant, increased airway resistance, and decreased pulmonary compliance. Patients require aggressive pulmonary toilet, chest physiotherapy, airway suctioning, therapeutic serial bronchoscopies, and early aggressive ambulation, and these define our current treatment options.

Bronchodilators

Bronchodilators decrease airflow resistance and improve airway compliance. β2-Adrenergic agonists such as albuterol and salbutamol decrease airway pressure by relaxing smooth muscle and inhibiting bronchospasm, thereby increasing the Pa o 2 /Fi o 2 ratio.

Muscarinic Receptor Antagonists

Muscarinic receptor antagonists such as tiotropium decrease airway pressures and mucus secretion and limit cytokine release by causing smooth muscle constriction within the airways, and stimulation of submucosal glands.

Both beta agonists and muscarinic receptor antagonists decrease the host inflammatory response after inhalation injury. Anatomically, there are muscarinic and adrenergic receptors lining the respiratory tract. How that affects the inflammatory response and host response is largely unknown. They have been shown to decrease proinflammatory cytokine levels after stress.

Inhaled (Nebulized) Mucolytic Agents and Anticoagulants

The airway obstruction secondary to mucus, fibrin cast formation, and cellular debris after inhalation injury are addressed by mucolytic agents, specifically, N -acetylcysteine (NAC). NAC is an antioxidant and free radical scavenger with antiinflammatory properties. It is a powerful mucolytic agent that attenuates ROS damage.

Inhaled anticoagulants are also used to mitigate airway obstruction from fibrin casts. Heparin has antiinflammatory properties, it prevents the formation of fibrin, and inhibits cast formation. The available evidence, from a limited number of human studies, is controversial. Some studies suggest that, among mechanically ventilated patients with burns with inhalation injury, 1 week of therapy with nebulized heparin (5000–10,000 units) alternating with 3 mL of 20% NAC every 4 hours is beneficial, leading to improved oxygenation and lung compliance, lower reintubation rates, and higher survival. Other studies have found no improvements in outcome with this therapeutic intervention.

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Nov 21, 2017 | Posted by in Dental Materials | Comments Off on Inhalation Injury
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