ABSTRACT
Systemic air embolism is a potentially lethal often unrecognised complication of severe chest trauma. We present a case of delayed diagnosis of cerebral air embolism in a patient with severe thoracic trauma. The initiation of positive pressure ventilation, systemic hypotension, intraparenchymal chest drains and aerial transfer to an intensive care unit were all factors contributing to the development of systemic air embolism. The common clinical features, diagnostic tests and management of systemic air emboli are discussed.
Subject(s)
Brain Ischemia/etiology , Drainage/adverse effects , Embolism, Air/etiology , Thoracic Injuries/therapy , Accidents, Traffic , Adult , Brain Ischemia/physiopathology , Brain Ischemia/therapy , Chest Tubes/adverse effects , Combined Modality Therapy , Critical Care/methods , Drainage/methods , Embolism, Air/physiopathology , Embolism, Air/therapy , Follow-Up Studies , Humans , Injury Severity Score , Male , Positive-Pressure Respiration , Radiography, Thoracic , Risk Assessment , Thoracic Injuries/diagnosis , Tomography, X-Ray Computed , Treatment OutcomeABSTRACT
Bacterial oropharyngeal infections in healthy young people rarely give rise to life threatening complications. Lemierre's disease, caused by Fusobacetrium necrophorum, manifests as pharyngitis, jugular venous thrombosis and septic pulmonary embolism. A previously fit young male presenting with prolonged pharyngitis, complicated by severe pneumonia and septicaemia is presented. Recognition of this syndrome and early antibiotic therapy can prevent significant morbidity in otherwise healthy people.
ABSTRACT
OBJECTIVE: To review recent studies in pathogenesis and management of ventilator-induced lung injury. DATA SOURCES: Articles and published reviews on ventilator-induced lung injury, barotrauma and acute lung injury. SUMMARY OF REVIEW: This review summarises the important differences between clinically apparent 'barotrauma' and the more subtle changes in lung structure and function associated with ventilation. Of great importance is the understanding that as the underlying lung injury worsens, the degree of injury from mechanical ventilation increases. An inflammatory process results from mechanical stimuli and this may contribute to distant organ dysfunction. A great deal of knowledge has been obtained from the use of animal models, however, one must be cautious about extrapolating these findings directly to the clinical setting without the use of adequately designed clinical trials. Tidal volume reduction and higher levels of PEEP and recruitment manoeuvres should be employed given the available evidence. The use of high frequency techniques, surfactant therapy despite their past track record, may prove to be exciting 're-discoveries'. CONCLUSIONS: Ventilator-induced lung injury is an iatrogenic disturbance that increases morbidity and mortality associated with acute respiratory distress syndrome. Tidal volume reduction and increased levels of PEEP have reduced inflammatory mediators and the mortality associated with ARDS.
