FROM FAT EMBOLUS TO FAT-EMBOLISM SYNDROME

The occurrence of a fat embolism syndrome (FES) can be explained by tw o hypothetic mechanisms. In the mechanical hypothesis, bone marrow ent ers into the cardiovascular system during an intramedullary peak press ure. This peak could occur during either long bone fracture and/or int ramedullary nailing or cemented or noncemented arthroplasty. According to the biochemical hypothesis, the FES could occur in nontraumatic co nditions such as lipid emulsion infusion or sickle cell disease. The C -reactive protein is a possible factor for destabilizing plasma fat (c hylomicrons or Intralipid(R) liposomes). Treatment with heparin has be en reported to interfere with lipid metabolism through a << creaming > > phenomenon. Plasma fatty acids increase lipid peroxidation, with pot ential severe oxidative stress of lung. Vascular lung injury is increa sed by granulocytes and the clotting cascade is activated by neutral f at. After a symptom-free period, the full clinical picture is characte rized by pulmonary insufficiency with hypoxaemia, neurological impairm ent, pyrexia and petechial haemorrhages. The accurate incidence cannot be assessed as many subclinical forms remain unrecognized. Transoesop hageal echocardiography with color-flow Doppler allows considerable in sight into the sequence of embolic events and patent foramen ovale (PF O). A PFO induces an increase in right-to-left shunt in case of an ele vated intrapulmonary pressure. PFO might elicit systemic manifestation s of the FES, particularly with neurological impairment. Carotid ultra sonography helps to visualize embolism. Magnetic resonance imaging of cerebral fat emboli is a better diagnostic tool for detecting brain em bolism than computerized tomography. Quantification of cells containin g fat droplets in bronchoalveolar lavage material could also be helpfu l. Pulmonary microvascular cytology analysis of capillary blood sample s obtained through a pulmonary artery catheter in combination with blo od gas changes are of value for earlier stage FES. Prophylactic and th erapeutic measures are aimed to counteract the various mechanisms lead ing to FES. The decrease in time delay of fracture management is proba bly 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 externa l fixation have several advantages. Albumin infusion is recommended fo r restoration of blood volume and binding of fatty acids. Among pharma cologic measures, only corticosteroids have a proven benefit, not only for prophylaxis but also for therapy. Aprotinin and heparin are benef icial in counteracting blood cell aggregation. A prophylactic use of v ena cava filters has been advocated. Prevention or early treatment of hypovolaemia and hypoxaemia are essential.