Fat Embolism 

  • Author: Lisa Kirkland, MD, FACP, CNSP, MSHA; Chief Editor: Vincent Lopez Rowe, MD   more...
 
Updated: Sep 8, 2011
 

Background

In 1862, Zenker first described fat embolism at autopsy. In 1873, von Bergmann clinically diagnosed fat embolism syndrome for the first time.

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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 lHaematoxylin 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.
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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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Contributor Information and Disclosures
Author

Lisa Kirkland, MD, FACP, CNSP, MSHA  Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo Clinic; ANW Intensivists, Abbott Northwestern Hospital

Lisa Kirkland, MD, FACP, CNSP, MSHA is a member of the following medical societies: American College of Physicians, Society of Critical Care Medicine, and Society of Hospital Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard M Stillman†, MD, FACS  Honorary Medical Staff, Northwest Medical Center; Former Chief of Staff and Medical Director, Wound Healing Center, Department of Surgery, Northwest Medical Center

Richard M Stillman†, MD, FACS is a member of the following medical societies: American College of Angiology, American College of Surgeons, Association for Academic Surgery, and Society of University Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Travis J Phifer, MD  Chief, Division of Vascular Surgery, Professor, Department of Surgery and Radiology, Louisiana State University Health Sciences Center in Shreveport

Travis J Phifer, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Society for Academic Emergency Medicine, Society for Vascular Surgery, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Paolo Zamboni, MD  Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy

Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences

Disclosure: Nothing to disclose.

Chief Editor

Vincent Lopez Rowe, MD  Associate Professor of Surgery, Department of Surgery, Division of Vascular Surgery, University of Southern California Medical Center

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, Pacific Coast Surgical Association, Peripheral Vascular Surgery Society, Society for Clinical Vascular Surgery, Society for Vascular Surgery, and Western Vascular Surgical Society

Disclosure: Nothing to disclose.

References

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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.
Table 1
DoseModelTimingDuration of StudyEffect on Disease Incidence
30 mg/kgDogPre-event60 minNone
10 mg/kg q8h for 24 hHuman traumaAt admissionNo dataDeclining
7.5 mg/kg q6h for 12 h or placeboHuman traumaWithin 12 h2 dDeclining
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