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Management of Blast and Inhalation Injury

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review blast injury.qxd 17/05/2007 15:29 Page 2 Key points k All patients with facial burns may be suspected of having "difficult-to-control" airways owing to smoke inhalation injury (SII). Many of them either have an incorrect diagnosis, or mild-to-moderate injury with unrecognised aggravating respiratory failure. k For a diagnosis of inhalation injury, it is necessary to follow the patient closely for >48 h. k Inhalation injury is a condition with different clinical presentations. Clinical follow-up is necessary to improve patient care, to help guide treatment and to provide clues for therapeutic interventions. k Notwithstanding intensive care treatment including airway intubation and mechanical ventilation, many patients with severe inhalation injury remain under-treated. review blast injury.qxd 17/05/2007 15:30 Page 3 REVIEW C. Gregoretti1 D. Decaroli2 Management of blast and M. Stella3 A. Mistretta4 inhalation injury F. Mariano4 L. Tedeschi1 1Dipartimento Emergenza Accettazione, 2Dipartimento di Educational aims Chirurgia Plastica, S.C. Chirurgia Plastica Indirizzo Grandi Ustionati, 4Dipartimento di Area k To discuss the initial approach and assessment of a patient with SII. Medica, S.C. Nefrologia e Dialisi, k To help the reader recognise different clinical pictures of inhalation injury. ASO CTO-CRF-Maria Adelaide, and k To outline management and discuss treatment. 3Dipartimento di Anestesiologia e Rianimazione, Università di Torino, Ospedale S. Giovanni Summary Battista-Molinette, Turin, Italy, "Inhalation injury" describes a variety of insults caused by the aspiration of superheated gases, steam or noxious products of incomplete combustion. Inhalation injury involves the entire respiratory system. Early diagnosis based on history and physical examination, in addition to careful monitoring for respiratory complications, is mandatory. As there is no specific treatment for inhalation injury, management involves providing the necessary Correspondence: degree of support required to compensate for upper airway swelling and impairment in C. Gregoretti gas exchange. Airway intubation and mechanical ventilation may be required while the Dipartimento Emergenza endobronchial and alveolar mucosa are regenerating. Accettazione Primary blast injury (BI) is caused by immediate pressure variations, which are the prod- ASO CTO-CRF-Maria Adelaide Via Zuretti, 29 uct of rapid sequences of compression and decompression. Secondary and tertiary BI 10129 Torino include lesions caused when the subject is thrown against rigid structures or is hit by fly- Italy ing objects. Its diagnosis and therapy follows guidelines for emergency care. E-mail: [email protected] A major burn is one of the most devastat- In the past 20 years, burn-related mortality j ing physiological and psychological has decreased in western countries. This is the insults known. Severe burns involve a skin result of primary prevention of all causes of injury accompanied by a serious systemic ill- burns and the introduction of specific treat- ness with consequences in different distant ment protocols for burn shock. This includes organs. early fluid resuscitation as well as an early Major burns are a serious clinical chal- diagnosis of suspected smoke inhalation or lenge and have a high mortality rate. Patient blast injury. Thereafter, primary prevention age, the percentage of total burned surface also includes an immediate admission to the area (TBSA) and the presence of multi-organ care of a specialised burns team. A team dysfunction syndrome (MODS) are the main approach including all caregivers (intensivist, factors influencing outcome. MODS is the surgeon, nurses, respiratory therapist and psy- leading cause of death (from one-third to two- chologist) is mandatory. thirds of deaths in the burn population), and Respiratory care, independent of the type among organs, the lungs are invariably of injury is as important as other major com- affected (100%), followed in frequency by the ponents of burn care, such as fluid manage- Main image ©Shaun Lowe/istock- gut and kidneys (68%) [1]. ment, wound coverage and infection control. photo Breathe | June 2007 | Volume 3 | No 4 365 review blast injury.qxd 17/05/2007 15:30 Page 4 REVIEW Management of blast and inhalation injury Table 1 Involvement of the respiratory system in burns the gut, a few hours after burn injury, an patients increased mesenteric vascular resistance and decreased gut perfusion can be observed lead- Early airway involvement (up to 48–72 h) Late airway involvement (after 48–72 h) ing to bacterial translocation and endotox- Upper airway injuries Lower airway injuries aemia. Hormonal effects include increased levels Lower airway injuries of cortisol, glucagon and catecholamines, affect- ing several metabolic functions and causing neg- In the present review, only respiratory ative nitrogen and calcium balance, lipolysis, involvement (including that caused by smoke massive peripheral muscle wasting and hepatic inhalation or blast injury) will be tackled. Major fat deposition. burn management, carbon monoxide poisoning Acute lung injury (ALI) or acute respiratory and cyanide exposure are beyond the scope of distress syndrome (ARDS) are likely to occur at this article. any time during the clinical course of the burns patient [4]. DANCEY et al. [5] estimated that the inci- Respiratory system dence of ARDS among mechanically ventilated burn patients is as high as 54%. As a conse- involvement quence, pulmonary injury is a major source of morbidity and mortality for the burns patient [6]. Burns can be the result of thermal, chemical, electrical or inhalation injury. Although many organ systems may be affected by a burn, the Smoke inhalation respiratory system often sustains the most dam- age. The severity of this insult may range from injury mild to life-threatening. Injury of the respiratory system in major burns patients may assume SII is defined as a clinical picture including a many forms. Table 1 summarises the involve- variety of insults that are attributable to the ment of the respiratory system in burns patients. inhalation of superheated gases, steam or gases Lung injury may result directly from smoke resulting from incomplete combustion of nox- inhalation injury to the lungs or indirectly from ious products. It has an incidence of approxi- inflammatory mediators associated with infec- mately 20% in patients admitted to major burn tion, sepsis, the burn itself or blast injury [2]. centres. It has been estimated that a patient aged A diagnosis of SII may double mortality from >60 years, with >40% TBSA and with inhalation that predicted based on age and burn size injury, has a >90% probability of death [3]. alone [3]. Thermal and chemical injuries cause coagu- The mechanism of inhalation injury consists lative necrosis of the skin and underlying subcu- of a combination of [7]: taneous tissue. The major determinants of burns • direct thermal injury to the upper airway severity are the extension of injury (as % TBSA) from the inhalation of hot gases and its thickness (partial or full thickness). Burns • damage to cellular and oxygen transport elicit a time-dependent (from minutes to hours) mechanisms by inhalation of carbon sustained local and systemic release of inflam- monoxide and cyanide matory mediators and changes in hormonal and • chemical injury to the lower airways immunological responses, proportional to their caused by inhalation of toxic products of extent and thickness. Circulating and local medi- combustion. ators include cytokines (interleukin (IL)-1, IL-2, The clinically important problems include: IL-6, IL-8, IL-12 and tumour necrosis factor), • loss of airway patency secondary to growth factors, activation products of coagula- mucosal oedema tion and contact phase cascades, complement • bronchospasm factors, nitric oxide, platelet activating factor, • intrapulmonary shunting with decreased prostaglandins and leukotrienes. These lung compliance secondary to alveolar molecules, present at high concentrations for flooding and collapse days, lead to marked vasodilation, generalised • pneumonia secondary to loss of ciliary increased microvascular permeability and clearance extravascular fluid loss, as well as hypotension if • bronchiectasis. hypovolaemic shock is not properly treated. In 366 Breathe | June 2007 | Volume 3 | No 4 review blast injury.qxd 17/05/2007 15:30 Page 5 Management of blast and inhalation injury REVIEW Although air temperature in a room con- Table 2 Toxins produced by burning materials taining a fire may exceed 550°C [8], super- heated air usually causes thermal injury only to Burning substance Toxins produced airway structures above the carina. This is Rubber and plastic products May produce sulphur dioxide, nitrogen dioxide, because of the combination of efficient heat dis- ammonia and chlorine, which form strong sipation in the upper airway, the low heat acids and alkalis when combined with water in capacity of air and reflex closure of the larynx. the airways and alveoli The combustion of most substances may gener- Glues in laminated furniture and wall panelling May release cyanide gas ate toxic materials. Toxins generated by smoke- Cotton or wool May produce toxic aldehydes related products damage both epithelial and increased risk of pulmonary BI. Enclosed envi- capillary endothelial cells of the airway. Table 2 ronments also increase the risk of air and fat summarises the toxins produced by burning embolism and pleural tearing as a result of materials [9]. trauma
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