Fat embolism syndrome pathophysiology: Difference between revisions
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==Microscopic pathology== | ==Microscopic pathology== | ||
Hematoxylin and eosin staining shows the following changes in the lungs, kidneys and brain: | Hematoxylin and eosin staining shows the following changes in the lungs, kidneys and brain: | ||
Lung: | |||
*Alveolar haemorrhagic edema | *Alveolar haemorrhagic edema | ||
*Fat droplet deposition | *Fat droplet deposition | ||
*Fibrin thrombi | *Fibrin thrombi | ||
*Multiple fat droplets | *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== | ==References== | ||
Revision as of 22:39, 22 February 2018
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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
Gross pathology
Microscopic pathology
Hematoxylin and eosin staining shows the following changes in the lungs, kidneys and brain: 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
- ↑ Parisi DM, Koval K, Egol K (2002). "Fat embolism syndrome". Am J Orthop (Belle Mead NJ). 31 (9): 507–12. PMID 12650535.
- ↑ Robert JH, Hoffmeyer P, Broquet PE, Cerutti P, Vasey H (1993). "Fat embolism syndrome". Orthop Rev. 22 (5): 567–71. PMID 8316420.
- ↑ 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.
- ↑ Estèbe JP (1997). "[From fat emboli to fat embolism syndrome]". Ann Fr Anesth Reanim. 16 (2): 138–51. PMID 9686075.
- ↑ 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.