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Review
. 2021 Sep;21(9):322-328.
doi: 10.1016/j.bjae.2021.04.003. Epub 2021 Jul 6.

Fat embolism syndrome

D Luff  1 , D W Hewson  1   2
Affiliations
Review

Fat embolism syndrome

D Luff et al. BJA Educ. 2021 Sep.
No abstract available

Keywords: fat embolism syndrome; femoral fracture; perioperative medicine.

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Conflict of interest statement

The authors declare that they have no conflicts of interest.

Figures

Fig 1
Fig 1
Typical clinical progression of fat embolism syndrome. (1) Long bone fracture or intramedullary instrumentation causes (2) bone marrow fat to enter the venous circulation. (3) Fat embolises to the pulmonary capillary bed causing alveolar damage and dysfunction. (4) Fat may enter the systemic circulation via a patent foreman ovale, arteriovenous shunts, the pulmonary capillary bed, or all three. (5) Fat subsequently embolises and damages other organs including neurological, dermatological, renal, hepatic, ophthalmic, cardiovascular, and haematological systems (see Table 1 for organ-specific signs and symptoms).
Fig 2
Fig 2
Pathogenesis of fat embolism. Three theories have been proposed: mechanical, coagulation, and biochemical. Fat embolisation causes local parenchymal damage after vascular occlusion (by fat or thrombus), an exaggerated inflammatory response, or both. Subsequently, pulmonary haemorrhage, consolidation, pulmonary oedema and/or alveolar collapse result in a ventilation (V˙)/perfusion (Q˙) mismatch and hypoxaemia. CRP, C-reactive protein; IL-1, interleukin-1; IL-6, interleukin-6; TNF-alpha, tumour necrosis factor-alpha.
See this image and copyright information in PMC

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