A fat embolism occurs when fat macroglobules or fat tissue circulates through the bloodstream and ultimately lodge within a blood vessel. It is most often a result of trauma to the long bones of the body (e.g., femur, humerus).
Symptoms from a fat embolism (commonly called fat embolism syndrome) typically onset 24 to 72 hours after the insult  . In some cases symptoms appear as soon as 12 hours and as late as 2 weeks following injury. The severity of symptoms depends on the location of the blocked vessels. Patients present with the "classic triad" of symptoms, which consists of respiratory distress, petechial rash, and neurological abnormalities.
Less common symptoms of fat embolism include: pyrexia, cardiac depression, Purtscher's retinopathy, fever, coagulopathy (resembling disseminated intravascular coagulation), and kidney dysfunction (e.g., lipiduria, oliguria, proteinuria, hematuria)  .
The diagnosis of fat embolism syndrome can be made based on clinical presentation; for example, when the "classic" petechial rash occurs alongside hypoxemia and neurologic impairment, fat embolism syndrome should be suspected. A recent history of trauma resulting in the fracture of or surgery on a large bone (e.g., femur or humerus) should raise the index of suspicion for a fat embolism .
Staining of bronchoalveolar lavage (BAL) contents (alveolar macrophages for fat) will demonstrate fat droplets, allowing diagnosis of a fat embolism . Findings should be interpreted with caution since fat droplets in BAL may also be present in patients with sepsis, hyperlipidemia, and patients on lipid feeding infusions. The use of BAL for diagnosis of fat embolism is controversial and its sensitivity and specificity are not well studied .