**42.1 Silicone embolism**

98 Pulmonary Embolism

Fig. 6. a: Chest radiograph showing radio-opaque density in right main pulmonary artery

Fig. 6. b: CT Chest revealing bright intravascular densities in segmental and subsegmental

In venous GE, manifestations include cough, dyspnea, tachypnea and a hypoxemic ''gasp'' reflex when 10% or more of the pulmonary vessels are occluded (Souders, 2000; Sviri et al., 2004). Arterial embolization into the coronary arteries induces a specific drum-like or ''millwheel'' murmur along with electrocardiographic changes of ischemia (Rossi et al., 2000). The key to controlling air embolism lies in prevention. First line of treatment includes administration of 100% oxygen, placing the patient in left lateral decubitus position to prevent right ventricular outflow obstruction by airlock. Hyperbaric Oxygen (HBO) may be used. 100% oxygen decreases the size of the gas bubbles by increasing the ambient pressure and by establishing a diffusion gradient that favors the elimination of gas from the bubbles and by increasing the gradient for the egress of nitrogen from

pulmonary arteries

Silicone is thought to be an immunological inert substance and a component of many implantable medical devices. Silicone emboli (SIE) were first reported in trans-sexual males in 1970's and then later in young healthy women seeking low cost enhancements. Silicone implants are approved and widely used for breast augmentation, however liquid silicone used for aesthetic purposes cause significant morbidity when injected in the hips and buttocks, face, breasts, and vagina and is illegal in the US (Bartsich & Wu, 2010). Clinical features are similar to fat embolism with majority of patients meeting Schonfeld criteria (Schmid et al., 2005). The most common presentation is hypoxemia (92%) (Bartsich & Wu, 2010). Silicone embolic syndrome (SES) is a constellation of mainly pulmonary symptoms including dyspnea, fever, cough, hemoptysis, chest pain, hypoxia, alveolar hemorrhage, and altered consciousness presenting in patients shortly after silicone injection (within the first few hours) (Schmid et al., 2005). Later sequelae may occur within a few days and the possibility of delayed-onset pneumonitis or local inflammation at injection sites can occur up to years after administration (Chastre et al., 1987). Several factors have been implicated in leading to silicone emboli, including large volume injections, high-pressure infiltration, particle migration, and intravascular injection (Villa & Sparacio, 2000). It is thought that alveolar macrophages ingest silicone and fat to provoke an inflammatory response by increasing vascular permeability, activating endothelial cells, inducing the accumulation of activated neutrophils and modulating immunoregulatory responses in the lung. Imaging is usually suggestive of an embolic, congestive, pneumonitis or diffuse alveolar damage pattern. Treatment is supportive, consisting mainly of supplemental oxygen and steroid therapy.
