Fat Embolism
- Author: Lisa Kirkland, MD, FACP, CNSP, MSHA; Chief Editor: Vincent Lopez Rowe, MD more...
Background
In 1862, Zenker first described fat embolism at autopsy. In 1873, von Bergmann clinically diagnosed fat embolism syndrome for the first time.
Pathophysiology
Two theories about fat embolism 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.
Second, the biochemical theory states that hormonal changes caused by trauma and/or sepsis induce systemic release of free fatty acids as chylomicrons. Acute-phase reactants, such as C-reactive proteins, cause chylomicrons to coalesce and create the physiologic reactions described above. The biochemical theory helps explain nontraumatic forms of fat embolism syndrome.[1]
Haematoxylin and eosin stain of a section of the lungs showing a blood vessel with fibrinoid material and an optical empty space indicative of the presence of lipid dissolved during the staining process. This 55-year-old woman died of massive fat embolism after developing pancreatitis due to endoscopic retrograde cholangiopancreaticography. Image source: Pancreatitis with an unusual fatal complication following endoscopic retrograde cholangiopancreaticography: a case report. Journal of Medical Case Reports. 2008;2:215. Epidemiology
Frequency
United States
Frequency is estimated to be 3-4%. Fat embolism is a clinical diagnosis. Many patients are likely to have a missed diagnosis because of subclinical illness or confounding injury or illness.
Mortality/Morbidity
The mortality rate of fat embolism is 10-20%. Patients with increased age, multiple underlying medical problems, and/or decreased physiologic reserves have worse outcomes than other patients.
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| Dose | Model | Timing | Duration of Study | Effect on Disease Incidence |
| 30 mg/kg | Dog | Pre-event | 60 min | None |
| 10 mg/kg q8h for 24 h | Human trauma | At admission | No data | Declining |
| 7.5 mg/kg q6h for 12 h or placebo | Human trauma | Within 12 h | 2 d | Declining |

