Tracheal damage.

Tracheal damage. Blunt/penetrating trauma and inhalation injuries to the trachea can result in acute airway compromise, with life-threatening implications. Early assessment, identification, and prompt and appropriate management are of paramount importance in order to reduce patient morbidity and mortality. Signs and symptoms of these injuries are specific and sometimes subtle, and their seriousness may be obscured by other injuries. Diagnosis can therefore be challenging, requiring a high index of suspicion. Indeed, diagnosis and treatment are often delayed, resulting in attempted surgical repair months or even years after injury. Laryngoscopy, flexible and/or rigid bronchoscopy and computed tomography of the chest are the procedures of choice for a definitive diagnosis. Airway control and appropriate ventilation represent the key aspects of emergency management. Definitive treatment depends on the site and the extent of injury. Surgery, involving primary repair with direct suture or resection and end-to-end anastomosis, is the treatment of choice for patients suffering from tracheal injuries. A conservative approach must be considered for the paediatric population and selected patients with mainly iatrogenic damage. We present a review of the incidence, mechanisms of injury, clinical presentations, diagnosis, initial airway management, anaesthetic considerations and definitive treatment in the case of tracheal damage from blunt/penetrating trauma and inhalation injuries.

[Acute poisoning with bromine vapors of a pharmaceutical plant operator]. / Ostroe otravlenie parami broma u apparatchika khimiko-farmatsevticheskogo zavoda.

A characteristic feature of bromium acute intoxications in levomycetine production is the delayed hemorrhagic component manifestation in the clinical course of toxic bronchitis (on the 20th day after inhaling bromium vapours), and the changes in the heart in the form of myocardial toxic dystrophia, as well as the growing activity of some liver related enzymes, which is indicative of the hepatocyte membrane lesions.

Effect of high-dose cimetidine on pulmonary extravascular water after acute smoke inhalation injury.

An animal model utilizing gamma imaging was used to examine pulmonary edema of an inhalation injury model. Tests were conducted using radiolabeled tracers and a dual indicator dilution technique as well as gravimetric analysis of excised lungs to determine extravascular water formation. The effect of cimetidine (Tagamet, an H2 receptor antagonist) was investigated as a potential agent for reduction of pulmonary edema following inhalation injury. Control groups included no treatment; smoke only; fluids only; and smoke and fluids. These were compared with identical groups given the same treatments but with the addition of cimetidine (100-150 mg/kg body weight intravenously). Fluids administered were 5% body weight intravenous infusions of lactated Ringer's solution over two hours. Results show that pulmonary edema was evidenced in animals given an inhalation injury, and was markedly worsened by fluid resuscitation. Treatment with cimetidine at high doses, either before or after inhalation injury, did not protect the animals from formation of pulmonary edema.

Measurement of extravascular lung water in sheep during colloid and crystalloid resuscitation from smoke inhalation.

The pathophysiology of pulmonary inhalation injury, a major cause of morbidity and mortality from fires, is poorly understood. To examine the effects of colloid and crystalloid resuscitation on extravascular lung water (EVLW) during a standard smoke inhalation injury, we subjected 12 sheep to 8 minutes of cool pine smoke inhalation. The animals were then resuscitated to a pulmonary capillary wedge pressure (PCWP) of 10 +/- 1.5 mm Hg with either lactated Ringer's solution or plasma protein derivative. EVLW, cardiac output, vascular resistance, colloid oncotic pressure (COP), arterial and pulmonary artery pressures, PCWP, and blood gases were monitored during 4 hours of resuscitation. In colloid-treated animals, EVLW increased from 8.3 +/- 1.2 to 11.1 +/- 0.9 ml/kg with injury; it increased only to 12.5 +/- 1.3 ml/kg during resuscitation. In crystalloid-treated animals, EVLW increased from 8.0 +/- 1.0 to 10.3 +/- 0.8 ml/kg with injury and further increased to 17.4 +/- 1.6 ml/kg during resuscitation, a level significantly higher than that in the colloid group (P less than 0.05). The increases in EVLW were associated with progressive hypoxia, which was worse in the crystalloid group. In the crystalloid group, COP decreased from 27.3 +/- 0.9 to 14.2 +/- 0.4 mm Hg and intravascular driving force (COP-PCWP) dropped from 17.6 to 3.26 +/- 1.5 mm Hg; COP and COP-PCWP were maintained in the colloid group. These data demonstrate that supporting serum COP minimizes the increase in EVLW with smoke inhalation injury and suggests that smoke inhalation does not lead to a dramatic increase in alveolar capillary membrane permeability to protein.