Fat embolism syndrome pathophysiology
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Fat embolism syndrome (FES) is the presence of fat globules in the circulation post traumatic insult which can lodge into the small sized capillaries in the lung, brain and skin leading to devastating clinical manifestations. The two widely accepted theories which explain the pathophysiology of FES are mechanical and biochemical theory. The mechanical theory proposes that there is mechanical obstruction by fat cells from the bone marrow in the end-capillaries after trauma. Biochemical theory attributes the clinical manifestations of FES to the pro inflammatory effect of fat emboli.
- Mechanical theory
- Biochemical 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.
- Tissue lipases break down the fat in the bone marrow, forming high levels of the following toxic intermediaries:
- Free fatty acids:
- C-reactive proteins:
- Eventually, 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.
Pathogenesis of clinical manifestations
Following pathological sequence of events occur after an orthopedic trauma such as long bone fracture.
|Microvascular obstruction and free fatty acids(FFA) mediated endothelial injury leading to proinflammatory cytokine release(IL-1,IL-6,TNF-alpha)||Acute respiratory distress syndrome|
|Arterial hypoxemia and cerebral vascular injury from FFA intermediates||Encephalopathy and focal neurological deficits|
|Vascular stasis,microinfarction and FFA mediated endothelial damage leading to rupture of thin-walled capillaries||Petechiae|
|Elevated tissue factor, excess thrombin and fibrin generation, aggregation of platelets and consumption of coagulation products||DIC, thrombocytopenia and anemia|
- There is no genetic association of FES.
There is no characteristic gross pathology associated with fat embolism.
Immunohistochemical staining shows the following changes:
- Hematoxylin and eosin staining shows fat deposits in the glomeruli.
- Fat droplets are seen in vessels.
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