Two theories about the syndrome exist. First, the mechanical theory states that large fat droplets are released into the venous system. These droplets are deposited in the pulmonary capillary beds and travel through arteriovenous shunts to the brain. Microvascular lodging of droplets produces local ischemia and inflammation with concomitant release of inflammatory mediators, platelet aggregation, and vasoactive amines. Acute phase reactants, such as C-reactive proteins, cause chylomicrons to coalesce and create the physiologic reactions described above.
Fat embolism is a clinical diagnosis.
It is likely that many patients have missed diagnoses due to subclinical illness or confounding injury or illness. Patients with an increased age, multiple underlying medical problems, and less physiologic reserves have worse outcomes. Patients become febrile with high-spiking temperatures. Subconjunctival and oral hemorrhages and petechiae also appear. Central nervous system dysfunction initially manifests as agitated delirium but may progress to stupor, seizures, or coma and frequently is unresponsive to correction of hypoxia.