These GW786034 cell line are associated with vascular congestion and hypersensitivity pneumonitis resulting in extensive diffuse alveolar damage and ultimately ARDS.3 Most patients develop clinical signs within the first 24 h of silicone administration and the onset of symptoms has been linked to a higher mortality rate (20%).4 The most frequent symptoms include hypoxemia, dyspnea, fever, chest pain, cough and hemoptysis.1 Bronchoalveolar lavage (BAL) commonly reveals alveolar hemorrhage, and a restrictive

pattern is usually observed on pulmonary function studies. While the acute presentation is typical for the majority of patients, delayed-onset pneumonitis and injection-site inflammation occurring years after silicone administration has been described. Migration of micro-droplets of silicone could also assume a delayed presentation in the form of pulmonary fibrosis.4 Occasionally, pulmonary toxicity has been described to lag behind CNS manifestations especially when initial chest radiography and pulmonary LY2109761 cell line examinations are benign in the presence of lethargy. Increasing release of silicone emboli from the source results in a slow progression to ARDS similar to the manifestation of heroin induced pulmonary

edema.5 Neurologic sequelae of silicone embolism vary from mild alteration in levels of consciousness to frank coma. Interestingly, the absence of underlying cardiac septal defects does not preclude the occurrence of neurologic manifestations, as microinfarcts in white matter

following cerebral silicone embolism has been described in these individuals and pheromone observed to be uniformly fatal.2 Large volume injections, high pressure infiltrations and prior exposure to silicone have been associated with a worse prognosis and increased rapidity of symptom onset.2 The presence of an IgG polydimethylsiloxane antibody which selectively binds to the silicone polymers has been implicated in this inflammatory process. Histology typically reveals multi-organ involvement with granulomas diffusely dispersed within the cardiopulmonary, renal, hepatic and gastrointestinal organ systems. Histopathologic analysis with the aid of infrared spectrophotometry and atomic absorption reveals these granulomas to consist of silicone vacuoles, tissue macrophages, neutrophils, eosinophils and fibrin deposits. Pulmonary silicone embolism characteristically results in a consistent chest CT imaging pattern of bilateral peripheral ground-glass opacities and interlobular septal thickening as portrayed by the present patient.4 The mechanism of silicone injury to pulmonary capillaries closely mimics fat embolism with the occurrence of bilateral alveolar hemorrhages and diffuse presence of silicone droplets in pulmonary alveolar macrophages and lung capillaries.