Treatment Of Smoke Inhalation Injury Research Articles

Respiratory Management in Smoke Inhalation Injury.

Smoke inhalation injury (SII) is a major morbidity and cause of mortality in patients with burns. Damage caused by inhalation of thermal or chemical irritants, including toxic fumes and chemicals, leads to respiratory cilia and epithelial cell injuries, which turn to severe bronchospasm and alveolar damage and results in acute respiratory distress syndrome. Respiratory management plays a vital role in the treatment of SII. In this review, we provide an overview of SII with emphasis on respiratory management, including aerosol therapy, bronchial hygiene therapy, advanced ventilation modes, and heated humidified high-flow nasal cannula. In summary, the information may be helpful for further improvements in outcomes.

Smoke Inhalation Injury: Etiopathogenesis, Diagnosis, and Management.

Smoke inhalation injury is a major determinant of morbidity and mortality in fire victims. It is a complex multifaceted injury affecting initially the airway; however, in short time, it can become a complex life-threatening systemic disease affecting every organ in the body. In this review, we provide a summary of the underlying pathophysiology of organ dysfunction and provide an up-to-date survey of the various critical care modalities that have been found beneficial in caring for these patients. Major pathophysiological change is development of edema in the respiratory tract. The tracheobronchial tree is injured by steam and toxic chemicals, leading to bronchoconstriction. Lung parenchyma is damaged by the release of proteolytic elastases, leading to release of inflammatory mediators, increase in transvascular flux of fluids, and development of pulmonary edema and atelectasis. Decreased levels of surfactant and immunomodulators such as interleukins and tumor-necrosis-factor-α accentuate the injury. A primary survey is conducted at the site of fire, to ensure adequate airway, breathing, and circulation. A good intravenous access is obtained for the administration of resuscitation fluids. Early intubation, preferably with fiberoptic bronchoscope, is prudent before development of airway edema. Bronchial hygiene is maintained, which involves therapeutic coughing, chest physiotherapy, deep breathing exercises, and early ambulation. Pharmacological agents such as beta-2 agonists, racemic epinephrine, N-acetyl cysteine, and aerosolized heparin are used for improving oxygenation of lungs. Newer agents being tested are perfluorohexane, porcine pulmonary surfactant, and ClearMate. Early diagnosis and treatment of smoke inhalation injury are the keys for better outcome.

A rat model of smoke inhalation injury

Context: Smoke inhalation injury is the leading cause of acute respiratory failure in critical burn victims. Advances in the treatment of smoke inhalation injury have been limited in the past years. To further explore the pathogenesis, stable and practical animal models are necessary.Objective: To develop a rat model of smoke inhalation injury.Materials and methods: The smoke composition including the particulate matters, irritant gases, chemical carcinogens was measured. The blood gas values, pro-inflammatory and protein concentration in bronchoalveolar lavage fluid and lung wet to dry weight ratio were assayed. Pathological evaluations of pulmonary were performed at 24 h, 96 h, 7 days and 28 days post-injury. Masson–Goldner trichrome staining was performed on day 7 and 28 post-injury, along with the measurement of hydroxyproline and collagen I and III.Results: In our present animal model, smoke inhalation caused a significant hypoxemia and CO poisoning. A surge of pro-inflammatory response and microvascular hyperpermeability with neutrophils accumulations were also found in our animal model. At 24 h post-smoke inhalation, the hematoxylin and eosin results exhibited that there were inflammatory exudates and diffuse hemorrhage in the lung tissue with significant edema. With the time going, the lung injuries appeared at alveolar collapse and alveolar septum thickening, which indicated that smoke inhalation further induced damage to lung parenchyma. Specially, the markedly collagen deposition appeared at 28 days post-injury indicated that pulmonary fibrosis happened.Discussion and conclusion: In conclusion, this rat smoke inhalation injury model induced by our novel self-made smoke generator could be used for acute and chronic lung injury experiments.

Pathophysiology, management and treatment of smoke inhalation injury

Smoke inhalation injury continues to increase morbidity and mortality in burn patients in both the third world and industrialized countries. The lack of uniform criteria for the diagnosis and definition of smoke inhalation injury contributes to the fact that, despite extensive research, mortality rates have changed little in recent decades. The formation of reactive oxygen and nitrogen species, as well as the procoagulant and antifibrinolytic imbalance of alveolar homeostasis, all play a central role in the pathogenesis of smoke inhalation injury. Further hallmarks include massive airway obstruction owing to cast formation, bronchospasm, the increase in bronchial circulation and transvascular fluid flux. Therefore, anticoagulants, antioxidants and bronchodilators, especially when administered as an aerosol, represent the most promising treatment strategies. The purpose of this review article is to provide an overview of the pathophysiological changes, management and treatment options of smoke inhalation injury based on the current literature.

Steroids in the Treatment of Smoke Inhalation Injury

Steroids have been used for decades to treat many chronic lung diseases. The key hypothesis for the use of steroids is to reduce a prolonged and destructive inflammatory response. In addition, glucocorticoids may enhance the responsiveness to beta-agonists (which themselves reduce airway reactivity and mucosal edema).1 The anti-inflammatory effects not only reduce the destructive effects of persistent inflammation, but they may also reduce mast cells and thus inhibit the response to allergens. In smoke inhalation injury the response to the insult may be as damaging as the original injury—so it makes sense that steroids may improve the outcome of inhalation injury. Glucocorticoids may have theoretic advantages but their use is not without risk. A major concern is increased potential for infections in patients already at risk for sepsis. The well-known side effects of systemic treatment have led to the common use of inhaled steroids. The concept is that the drugs are delivered to the site of activity while minimizing the ill effects. There are both local and systemic side effects of inhaled steroids.2,3 Local effects include pharyngitis, dysphonia, reflex cough, bronchospasm, and oropharyngeal candidiasis. Because the lungs are a highly efficient avenue for drug delivery (such as delivery of nicotine in cigarettes) it is not surprising that there are systemic side effects of inhaled corticosteroids (ICS). Inhaled ICS can suppress the hypothalamic-pituitary-adrenal (HPA) axis function even to the point of causingadrenal crisis. In children, suppressed growth velocity (as measured by lower leg length) has been well documented. The delayed growth velocity is reversed with the cessation of the ICS. Patients of all ages may have reduced bone mineral density that increases the risk for fractures and osteoporosis. There are potentialchanges to the skin (thinning and increased bruising) and eyes (increased risks for cataracts and glaucoma) that result from inhaled steroids.

Use of Nebulized Heparin in the Treatment of Smoke Inhalation Injury

Use of Nebulized Heparin in the Treatment of Smoke Inhalation Injury

Use of β-Agonists in Inhalation Injury

Damage to the pulmonary parenchyma from smoke represents a second cause of inhalation injury. To date, the treatment of lung injury due to smoke has been largely supportive in nature. Patients are intubated, placed on mechanical ventilation, and maintained on support until pulmonary status improves, permanent airway access obtained, or the patient dies. Given that the insult associated with inhalation injury causes direct pulmonary damage and that the lungs have the ability of absorb drugs, the use of inhaled therapies for inhalation injury is appealing. The goal of this chapter is to describe the potential role of inhalation therapies in the treatment of smoke inhalation injury.

Delayed partial liquid ventilation shows no efficacy in the treatment of smoke inhalation injury in swine.

In an earlier neonatal porcine model of smoke inhalation injury (SII), immediate postinjury application of partial liquid ventilation (PLV) had dramatic beneficial effects on lung compliance, oxygenation, and survival over a 24-h period. To explore the efficacy of PLV following SII, we treated animals at 2 and 6 h after SII and followed them for 72 h. Pigs weighing 8-12 kg were sedated and pharmacologically paralyzed, given a SII, and placed on volume-cycled, pressure-limited ventilation. Animals were randomized to three groups: group I (+SII, no PLV, n = 8), group II (+SII, PLV at 2 h, n = 6), and group III (+SII, PLV at 6 h, n = 7). Ventilatory parameters and arterial blood gasses were obtained at scheduled intervals. The PLV animals (groups II and III) followed a worse course than group I (no PLV); PLV groups had higher peak and mean airway pressures, oxygenation index, and rate-pressure product (a barotrauma index) and lower lung compliance and arterial partial pressure of oxygen-to-inspired oxygen fraction ratio (all P < 0.05). PLV conferred no survival advantage. The reported beneficial effects of PLV with other models of acute lung injury do not appear to extend to the treatment of SII when PLV is instituted in a delayed manner. This study was not able to validate the previously reported beneficial effects of PLV in SII and actually found deleterious effects, perhaps reflecting the predominance of airway over alveolar disease in SII.

THERMAL INJURY

Intensive care management of severely burned patients demands expertise in several areas. These include airway management, fluid resuscitation, support of the hypermetabolic response, infection control, and treatment of smoke inhalation injury. Surgical management of the burn wound, plastic reconstruction, and long-term rehabilitation are also essential aspects of modern burn care.

Smoke Inhalation Injury In A Pony

SummaryA seven year old Welsh pony stallion was admitted to the Veterinary Medicine Teaching Hospital for treatment of smoke inhalation injury (SII) sustained in a barn fire. The pony was severly affected and demonstrated the three clinical phases typically described with SII. A nuclear pulmonary perfusion scan demonstrated multiple areas of unperfused lung suggesting reflex hypoxic pulmonary vasoconstriction, while thoracic radiographs showed only a mild increase in broncho‐interstitial pattern. The pony responded well to treatment with oxygen, diuretics, intravenous fluids, bronchodilators, non‐steroidal antiinflammatory agents and antibiotics. A tracheostomy was done to relieve upper airway obstruction and to facilitate removal of tracheobonchial pseudomembranous casts. Ultrasonic nebulization and to facilitate removal of tracheobonchial pseudomembranous casts. Ultrasonic nebulization was utilized to moisturize and break up secretions and casts and to deliver bronchodilatory agents. The pony recovered and seven months following the fire was pasture breeding mares. The pathophysiology and treatment of SII in the equine is discussed.

Dimethylsulfoxide With Heparin in the Treatment of Smoke Inhalation Injury

Recent studies suggest that lung lesions occurring in inhalation injury result from actions of oxygen-free radicals released from polymorphonuclear leukocytes marginating in the pulmonary microcirculation and tracheobronchial region. Peroxide and hydroxyl ions have been implicated as mediators in the increased microvascular permeability and pulmonary edema noted after inhalation injury. In this study we evaluated the use of an O2-free radical scavenger, dimethylsulfoxide (DMSO), and heparin in the treatment of smoke inhalation. Ewes (N = 26) that had been surgically prepared five days earlier were insufflated with smoke from burning cotton. There were four groups: controls (n = 7), DMSO (n = 6), heparin (n = 6), and DMSO plus heparin (n = 7). All animals were given ventilatory support to maintain their PO2 above 60 mmHg and their PCO2 below 45 mmHg. There was a significant difference in survival rates between groups. By 72 hours all seven of the control group were dead. All animals in the DMSO plus heparin group survived, four of the DMSO group died, and two of the heparin group died. Lung lymph flow was not as high in the DMSO plus heparin group as in the heparin-only group. DMSO was proved effective in reducing the lung injury associated with smoke inhalation.

Corticosteroid treatment of experimental smoke inhalation.

The effect of four corticosteroid analogs was evaluated in the treatment of smoke inhalation injury. Rats were exposed to white pine smoke for 15 minutes at 25 C, in a specially designed smoke apparatus. Methylprednisolone, 10 mg bid x 2d, starting one hour post exposure, was most effective in reducing expectant mortality (22.6%). A single injection of methylprednisolone, 20 mg, at one hour, resulted in a 76.7% reduction. There was no significant difference between the single injection of methylprednisolone and dexamethasone, 4 mg, but the administration of analogs with primarily mineralocorticoid activity, cortisone and hydrocortisone, actually increased mortality. In the control rats, marked interstitial edema occurred by 24 hours, the absence of which following treatment correlated closely with the results of the mortality study. This suggests that post exposure death due to white pine smoke is a result of direct lung injury, with increased endothelial and alveolar membrane permeability and edema, and that administration of glucosteroids in massive doses was effective in reducing this permeability and resultant edema.