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]

Overview

Pathophysiology

Two major theories have been described to explain the pathophysiology of fat embolism syndrome(FES):[1][2]

  • 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:

This theory attributes the clinical manifestations of FES to the pro inflammatory effect of fat emboli.[3][4][5]

  • Tissue lipases break down the fat in the bone marrow, forming high levels 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.
  • Acute lung injury or acute respiratory distress syndrome. results from damaged pulmonary endothelium that triggers a proinflammatory cytokine cascade.

Video

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Genetics

  • There is no genetic association of FES.

Gross pathology

Microscopic pathology

Hematoxylin and eosin staining shows the following changes in the lungs, kidneys and brain:[6]

Lung:

  • Alveolar haemorrhagic edema
  • Fat droplet deposition
  • Fibrin thrombi
  • Multiple fat droplets

Immunohistochemical staining shows the following changes:

  • Raised levels of iNOS in the alveolar macrophages.

Kidney:

  • Hematoxylin and eosin staining shows fat deposits in the glomeruli

Brain:

References

  1. Parisi DM, Koval K, Egol K (2002). "Fat embolism syndrome". Am J Orthop (Belle Mead NJ). 31 (9): 507–12. PMID 12650535.
  2. Robert JH, Hoffmeyer P, Broquet PE, Cerutti P, Vasey H (1993). "Fat embolism syndrome". Orthop Rev. 22 (5): 567–71. PMID 8316420.
  3. Husebye EE, Lyberg T, Røise O (2006). "Bone marrow fat in the circulation: clinical entities and pathophysiological mechanisms". Injury. 37 Suppl 4: S8–18. doi:10.1016/j.injury.2006.08.036. PMID 16990064.
  4. Estèbe JP (1997). "[From fat emboli to fat embolism syndrome]". Ann Fr Anesth Reanim. 16 (2): 138–51. PMID 9686075.
  5. Hofmann S, Huemer G, Kratochwill C, Koller-Strametz J, Hopf R, Schlag G; et al. (1995). "[Pathophysiology of fat embolisms in orthopedics and traumatology]". Orthopade. 24 (2): 84–93. PMID 7753543.
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