[From fat emboli to fat embolism syndrome]

The occurrence of a fat embolism syndrome (FES) can be explained by two hypothetic mechanisms. In the mechanical hypothesis, bone marrow enters into the cardiovascular system during an intramedullary peak pressure. This peak could occur during either long bone fracture and/or intramedullary nailing or cemented or noncemented arthroplasty. According to the biochemical hypothesis, the FES could occur in nontraumatic conditions such as lipid emulsion infusion or sickle cell disease. The C-reactive protein is a possible factor for destabilizing plasma fat (chylomicrons or Intralipid liposomes). Treatment with heparin has been reported to interfere with lipid metabolism through a "creaming" phenomenon. Plasma fatty acids increase lipid peroxidation, with potential severe oxidative stress of lung. Vascular lung injury is increased by granulocytes and the clotting cascade is activated by neutral fat. After a symptom-free period, the full clinical picture is characterized by pulmonary insufficiency with hypoxaemia, neurological impairment, pyrexia and petechial haemorrhages. The accurate incidence cannot be assessed as many subclinical forms remain unrecognized. Transoesophageal echocardiography with color-flow Doppler allows considerable insight into the sequence of embolic events and patent foramen ovale (PFO). A PFO induces an increase in right-to-left shunt in case of an elevated intrapulmonary pressure. PFO might elicit systemic manifestations of the FES, particularly with neurological impairment. Carotid ultrasonography helps to visualize embolism. Magnetic resonance imaging of cerebral fat emboli is a better diagnostic tool for detecting brain embolism than computerized tomography. Quantification of cells containing fat droplets in bronchoalveolar lavage material could also be helpful. Pulmonary microvascular cytology analysis of capillary blood samples obtained through a pulmonary artery catheter in combination with blood gas changes are of value for earlier stage FES. Prophylactic and therapeutic measures are aimed to counteract the various mechanisms leading to FES. The decrease in time delay of fracture management is probably the most effective prophylactic means. A reaming procedure can be noxious, particularly in a patient with a severe thoracic trauma. The insertion without reaming of a small diameter nail, plating or external fixation have several advantages. Albumin infusion is recommended for restoration of blood volume and binding of fatty acids. Among pharmacologic measures, only corticosteroids have a proven benefit, not only for prophylaxis but also for therapy. Aprotinin and heparin are beneficial in counteracting blood cell aggregation. A prophylactic use of vena cava filters has been advocated. Prevention or early treatment of hypovolaemia and hypoxaemia are essential.