Correct!
4. 1 and 3

Two pathophysiologic mechanisms behind FES have been proposed which are not mutually exclusive: mechanical and biochemical. The first, mechanical theory was proposed by Gauss in 1924, and suggests that trauma of long bones causes damage to fat in the marrow and intraosseus blood vessels, subsequently releasing fat droplets into the vasculature (1,4,5). These fat droplets cause mechanical obstruction in lung capillaries, or may pass directly into the systemic circulation via a patent foramen ovale or as microglobules that can filter directly through lung capillaries. It is unclear why symptoms of FES are typically delayed in this proposed mechanism.

Lehman and Moore described an alternative biochemical theory in 1927, which proposes that symptoms of FES are attributable to a proinflammatory state. They suggest that once fat globules reach the pulmonary capillaries, they are hydrolyzed by lipase produced by pneumocytes, leading to high concentrations of free fatty acids that cause a localized inflammatory response (5). It is likely that the clinical symptoms of FES are a combination of these two theories, and occur from both mechanical vascular obstruction and the body’s inflammatory response to embolized fat.

Our patient ultimately was treated supportively, without the addition of steroids. With this, she had slow, progressive improvement in her mentation. She was extubated on hospital day 11, was discharged home on hospital day 16, and seen in neurology clinic 6 weeks later. At this follow-up visit, she was noted to have mild cognitive impairment but was otherwise thought to be doing well. She had returned to working part time.

References

  1. Duran H, Cardenas-Camarena L, Bayter-Marin JE, Ramos-Gallardo G, Robles-Cervantes JA. Microscopic and macroscopic fat embolism: solving the puzzle with case reports. Plast Reconstr Surg. 2018;142:569e-77e. [CrossRef] [PubMed]
  2. Kuo KH, Pan YJ, Lai YJ, Cheung WK, Chang FC, Jarosz J. Dynamic MR imaging patterns of cerebral fat embolism: a systematic review with illustrative cases. AJNR Am J Neuroradiol. 2014;35:1052-7. [CrossRef] [PubMed]
  3. Whalen LD, Khot SP, Standage SW. High-dose rosuvastatin treatment for multifocal stroke in trauma-induced cerebral fat embolism syndrome: a case report. Pediatr Neurol 2014;51:410-3. doi: 10.1016/j.pediatrneurol.2014.04.025. [CrossRef] [PubMed]  
  4. Bederman SS, Bhandari M, McKee MD, Schemitsch EH. Do corticosteroids reduce the risk of fat embolism syndrome in patients with long-bone fractures? A meta-analysis. Can J Surg. 2009 Oct;52(5):386-93. [PubMed]
  5. Sen RK, Tripathy SK, Krishnan V. Role of corticosteroid as a prophylactic measure in fat embolism syndrome: a literature review. Musculoskelet Surg. 2012;96(1):1-8. [CrossRef] [PubMed]
  6. Kuo KH, Pan YJ, Lai YJ, Cheung WK, Chang FC, Jarosz J. Dynamic MR imaging patterns of cerebral fat embolism: a systematic review with illustrative cases. AJNR Am J Neuroradiol. 2014;35:1052-7. [CrossRef] [PubMed]
  7. Whalen LD, Khot SP, Standage SW. High-dose rosuvastatin treatment for multifocal stroke in trauma-induced cerebral fat embolism syndrome: a case report. Pediatr Neurol 2014;51:410-3. doi: 10.1016/j.pediatrneurol.2014.04.025. [CrossRef] [PubMed]  
  8. Bederman SS, Bhandari M, McKee MD, Schemitsch EH. Do corticosteroids reduce the risk of fat embolism syndrome in patients with long-bone fractures? A meta-analysis. Can J Surg. 2009 Oct;52(5):386-93. [PubMed]
  9. Sen RK, Tripathy SK, Krishnan V. Role of corticosteroid as a prophylactic measure in fat embolism syndrome: a literature review. Musculoskelet Surg. 2012;96(1):1-8. [CrossRef] [PubMed]

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