**7. Conditions associated with fat embolization (Table-3)**


Table 3. Diseases related

Non-Thrombotic Pulmonary Embolism 81

stores in response to stress and catecholamine release (Lehman & Moore, 1927). Currently the most widely held view is that there is physiochemical alteration leading to degradation of embolized fat and production of toxic intermediates—mainly Free Fatty Acids (FFAs). Circulating FFAs originating from triglycerides at the fracture site may become concentrated as a result of systemic lipolysis induced by catecholamines. Alternatively, fat emboli trapped in pulmonary vessels may be metabolized to FFAs and glycerol by lipase secreted by lung parenchymal cells (P. L. Baker et al., 1971). However the exact source of FFAs remains unknown. Regardless of the source of the FFAs, circulating FFAs level is elevated in patients with fractures and in animal models of nontraumatic fat embolism. It has been postulated that decreased hepatic clearance as in shock, sepsis, or decreased plasma concentration of albumin also increase the risk of FES ( Mays, 1970; Moylan et al., 1976). FFAs have been shown in both animal and human

• interstitial hemorrhage and pulmonary edema (Herndon, 1975; Parker et al., 1974;

• C-reactive protein which is elevated in these patients appears to interact with circulating chylomicrons to form fat globules **de novo,** which can explain non traumatic

Coagulation cascade activation, disseminated intravascular coagulation (DIC), and antifibrinolytic pathways may further contribute to lung injury (E. G. King et al., 1971; Saldeen, 1970).The biochemical theory, could explain "latent period" and nontraumatic forms of FES (Schnaid et al., 1987). It must be emphasized that evidence is largely circumstantial and the exact pathophysiologic mechanism responsible for FES remains

FES usually presents as multisystem disorder in the setting of long bone fracture(s) or major trauma. The most commonly affected organs are brain and lung. The presentation is heterogeneous given diverse causes as well as multi-organ involvement. Latent period is typically 12 to 72 hours although rarely it can be as short as few hours in the setting of major trauma or as long as 2 weeks (Gary, 2004; Johnson & Lucas, 1996; M. B. King & Harmon, 1994; Mellor & Soni, 2001; Moreau, 1974; Parisi et al., 2002; Peltier, 1984; Schonfeld et al., 1983; Shier & Wilson, 1980). 85% of patients will develop signs and symptoms within 48 hours of injury (Sevitt, 1962). The classic triad of hypoxemia, neurological dysfunction and

It is uncommon to develop FES in the absence of respiratory manifestations. A great majority of patients present with varying degrees of respiratory insufficiency that can range from nearly asymptomatic hypoxemia to severe hypoxemia and ARDS requiring mechanical

• Cardiac contractile dysfunction (Dedhia & Mushambi, 2007; Hulman, 1988b)

studies to have the following systemic effects

• curtailed surfactant production

• Cerebral cortical cell damage (Parisi et al., 2002)

petechial rash is seen in only about 50% of the patients.

• Toxicity to lung parenchyma: • capillary leak

Szabo et al., 1977)

fat embolism (Hulman, 1988a).

unknown.

**11. Clinical features** 

**12. Pulmonary** 

