Fat embolism syndrome should be considered in the differential diagnosis of cardiorespiratory
and neurological deterioration after trauma and orthopaedic surgery but though the first case was diagnosed in the year 1873 by Von Bergman, target treatment towards this syndrome has not come up without controversies. The incidence can vary from 0.25% to 35 % [1
] (Table 1,2).
Causes of Fat embolism syndrome are [1
2) Non-Traumatic: a) Disease (pancreatitis, crush injury, alcoholic fatty liver etc.)
b) Drug (lipids > 3.8 gm/kg/day)
c) Procedure related (intraosseous fluid and drug administration)
Exact pathophysiology of fat embolism syndrome is not known but two theories have been put forwarded-
1) Mechanical Hypothesis: Increased intramedullary pressure forces marrow particles, fat or bone fragments into the circulation via the open sinusoids causing obstruction of the small pulmonary (20 micrometer in diameter) and systemic vessels [3
2) Biochemical Hypothesis : Fat globules being acted upon by lipoprotein lipase releases free fatty acids causing direct injury to pneumocytes and lung endothelial cells through their inflammatory effects Chemical mediators including platelet activating factor, phospholipase A2, cGMP, serotonin, nitric oxide have been implicated in the pathogenesis of fat embolism syndrome [1
Clinical presentations are multi systemic involving pulmonary system, CNS, CVS, skin, eyes, renal and circulatory systems [7
]. Diagnostic aids are mainly laboratory based and image based parameters as stated in case summary [8
]. Fat embolism is basically a diagnosis of exclusion.
Immunomodulation is defined as modulation of the immune respone with naturally occurring nutrients in order to limit tissue injury, reduce infection rates and morbidity [9
Koji Ito demonstrated that ulinastatin is a human urinary trypsin inhibitor which inhibits the production of TNF-α involved in potentiating the leukocyte activation having a role in development of oleic acid induced lung injury [10
Pacht ER et al. demonstrated that enteral diet enriched in eicosapentaenoic acid and gamma linolenic acid for at least 4-7 days significantly reduced BAL fluid interleukin (IL-8), TNF- α, total proteins, neutrophils and significantly improved oxygenation and reduced vascular permeability. Hence it can be an essentially helpful aid in acute respiratory distress syndrome (ARDS) [11
Role of Glutamine:
A) In systemic inflammatory response syndrome (SIRS):
1) Decreases Simplified Acute Physiology Score (SAPS) II Scores, leukocytes and natural killer (NK) cell count, which might be associated with suppressing inflammation and improving clinical recovery.
2) B and T lymphocytes increased → Improves immune system.
3) Decreases infection related complications and length of hospital stay [12
B) As stress handler: Glutamine is an essential precursor of glutamate for the synthesis of glutathione (GSH) which is a tripeptide protecting cells from oxidative stress.
C) As an immunonutrient and immunomodulator: Glutamine is essential for immune nutrition in the critically ill. Impairment of immune system functioning contributes to the development of sepsis. Glutamine is required by the cells of the immune system both as a primary fuel and as a carbon and nitrogen donor for nucleotide precursor synthesis. Glutamine is essential for optimal immune cell functioning for monocytes, lymphocytes and neutrophils. It helps in nitrogen transport maintaining cellular redox state [13