Fat embolism and fat embolism syndrome (FES) are clinical phenomena characterized by the systemic dissemination of fat emboli within the systemic circulation. The dissipation of fat emboli disrupts the capillary bed and affects microcirculation, causing a systemic inflammatory response syndrome.[1][2][3][4] End-organ manifestation typically involves the skin, the central nervous system, the lungs, and the retina. FES is most common in patients with orthopedic trauma. It also can occur in nontraumatic conditions such as acute or chronic pancreatitis, bone marrow transplant, or liposuction. In most instances, diagnosis is usually established during the autopsy. Fat embolism is the presence of fat globules in microcirculation, whereas FES is a systemic manifestation of the dissemination of fat molecules or globules in microcirculation. FES is a continuum of fat embolism. Zenker first described the clinical presentation of FES in 1863 in a patient suffering from a crush injury. In 1873, Von Bergmann clinically diagnosed the condition for the first time. Since the initial description by Zenker and Von Bergmann, several articles and studies have been published on this disease entity. In the early 1970s, Gurd proposed a clinical criterion for diagnosing FES. This was later modified by Wilson in 1974 in conjunction with Gurd and is the most commonly used clinical criteria for diagnosis. Since the majority of reported cases of fat embolism are seen in patients with orthopedic trauma, most research on this condition is in orthopedic patients. Even though the clinical criteria proposed by Gurd et al and Wilson can help or aid in the diagnosis, FES still poses a major diagnostic challenge to most clinicians.