Fat embolism syndrome pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Feham Tariq, MD [2]

Pathophysiology

Two major theories have been described to explain the pathophysiology of fat embolism syndrome(FES):

• Mechanical theory
• Biochemical theory

Mechanical theory:

The theory proposes that there is mechanical obstruction by fat cells from the bone marrow in the end-capillaries after trauma.

• Post traumatic insult, the fat cells travel via venous sinusoids to the capillaries.
• These cells have potent prothrombotic and proinflammatory potential.
• They trigger rapid aggregation of platelets and accelerated fibrin generation as they travel through the venous system, eventually lodging in the pulmonary arterial circulation.
• Pulmonary capillary obstruction leads to interstitial hemorrhage and edema, alveolar collapse, and reactive hypoxemic vasoconstriction.
• Massive fat emboli may also lead to macrovascular obstruction and shock.
• Fat cells may also enter the arterial circulation via a patent foramen ovale or directly through the pulmonary capillary bed, causing the characteristic neurological and dermatologic findings of FES

Biochemical theory:

Bone marrow fat is broken down by tissue lipases, resulting in high concentrations of glycerol and toxic free fatty acids. These intermediate products lead to end-organ dysfunction. In the lung, toxic injury to pneumocytes and pulmonary endothelial cells causes vasogenic and cytotoxic edema as well as hemorrhage. The damaged pulmonary endothelium triggers a proinflammatory cytokine cascade, leading to the development of acute lung injury or acute respiratory distress syndrome

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The pathogenesis of FES is not completely defined. It is thought to be caused by blockage of vessels from systemic embolization of fat globules. Echocardiographic reports have demonstrated echogenic material passing through the right atrium followed by increased pulmonary pressures and right heart pressures and subsequent paradoxical embolization of this material through a patent foramen ovale (PFO).

The fat induces a toxic, inflammatory reaction. This inflammatory reaction is thought to be related to the production of free fatty acids. Studies have shown that neutral fatty acids are not toxic , however, they are hydrolyzed over many hours to substances proven to cause ARDS in animal models. Not surprisingly, C-reactive protein is usually elevated in these patients. Levels of lipoprotein lipase, and free fatty acids (FFA) are noted in animal models.