pathogenesis

Last reviewed 05/2021

Fat Embolism Syndrome (FES) was first diagnosed in 1873. Today, there are two theories as to the mechanism of the damage to the pulmonary capillary epithelium seen in FES - the mechanical theory and the biochemical theory.

Whilst it is assumed that all of these mechanisms are involved to some degree in producing the clinical picture of FES it is not understood why certain trauma patients develop FES while others develop fat emboli without FES.

• two theories:
  • the mechanical theory by Gassling et al.which states that large fat droplets are released into the venous system; these droplets are deposited in the pulmonary capillary beds and travel through arteriovenous shunts to the brain
    • microvascular lodging of the droplets produces local ischemia and inflammation, with concomitant release of inflammatory mediators and vasoactive amines and platelet aggregation
      
      
  • biochemical theory states that hormonal changes caused by trauma and/or sepsis induce systemic release of free fatty acids as chylomicrons
    • acute-phase reactants, such as C-reactive proteins, cause the chylomicrons to coalesce and create the physiologic reactions described above
    • Baker et al. blame the fatty acids for FES; the local hydrolysis of fat emboli by pneumocytes generates free fatty acids, which migrate to other organs via the systemic circulation, causing multiorgan dysfunction

An explanation of the occurrence of FES without trauma can only be hypothesised - Emboli may be aggregated chylomicrons?

Notes:

• FES is commonly associated with traumatic fracture of femur, pelvis, and tibia, and, postoperatively, after intramedullary nailing and pelvic and knee arthroplasty
  • other forms of trauma that may be rarely responsible for FES include:
    • massive soft tissue injury, severe burn, bone marrow biopsy, bone marrow transplant, cardiopulmonary resuscitation, liposuction, and median sternotomy
  • non-traumatic conditions are very uncommon causes of FES and include:
    • acute pancreatitis, fatty liver, corticosteroid therapy, lymphography, fat emulsion infusion and haemoglobinopathies.
• risk factors for the development of FES are:
  • young age, closed fractures, multiple fractures, and conservative therapy for long-bone fractures
  • factors which increase the risk of FES after intramedullary nailing are over-zealous nailing of the medullary cavity, reaming of the medullary cavity, increased velocity of reaming and increase in the gap between nail and cortical bone

Reference:

• Bulger EM, Smith DG, Maier RV, Jurkovich GJ. Fat embolism syndrome: A 10 years review. Arch Surg. 1997;132:435-9.
• Fabian TC, Hoots AV, Stanford DS, Patterson CR, Mangiante EC. Fat embolism syndrome, prospective evaluation in 92 fractured patients. Crit Care Med. 1990;18:42-6.
• Shapiro MP, Hayes JA. Fat embolism in sickle cell disease: Report of a case with brief review of literature. Arch Intern Med. 1984;14:181-2.
• Glossing HR, Pellegrini VD., Jr Fat embolism syndrome: A review of pathology and physiological basis of treatment. Clin Orthop Relat Res. 1982;165:68-82.