Smoke Inhalation Injury: Etiopathogenesis, Diagnosis, and Management

IntRoductIonIn major fire disasters such as 9/11 bombing of the World Trade Centre in New York, smoke inhalation injury was an important cause of mortality.[1] Smoke inhalation injury increases the mortality by 24 times in fire-related injuries [2] and is highlighted to be one of the most important risk factors increasing the morbidity and mortality.[2] The objective of this article is to review the etiopathogenesis, early diagnosis, and latest management guidelines of smoke inhalation injury.This knowledge is important for anesthesiologists, emergency physicians, and critical care specialists, who are frequently involved in the care of these patients. pathophysIologySmoke inhalation injury is caused by the inspiration of steam, superheated gases, or toxic, often incomplete products of combustion.The heating capacity of steam is 4000 times that of hot dry air and thus causes tissue damage, even with momentary contact.[3] The various toxic compounds present in smoke are carbon monoxide (CO), hydrogen cyanide (HCN), phosgene, ammonia, sulfur dioxide, hydrogen sulfide (H 2 S), formaldehyde, and acrylonitriles.[3] Some of these superheated products of combustion are inhaled, causing thermal burns to the airway mucosa.[4] Particles larger than 10 μ in size are retained in the nasopharynx, but 1-2 μ sized particles can pass into the alveoli.[5] Smoke inhalation results in three physiological types of injury: (a) thermal injury predominantly to the upper 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.

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