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Athens, Greece
Dr. Georgopoulos is Associate Professor, Head Intensive Care Unit, Medical School University of Crete and University Hospital. Dr. Bouros is Professor of Pneumonology, Head Department of Pneumonology, Medical School University of Thrace and University Hospital.
Correspondence to: Demosthenes Bouros, MD, FCCP, 1A Achilleos St, Agia Paraskevi, Athens 15342, Greece; e-mail: bouros{at}med.uoc.gr
Fat embolism develops in nearly all patients with bone fractures or during orthopedic procedures.1 2 Rarely, fat embolism may occur in other nontrauma-related pathologic conditions such as pancreatitis and sickle cell disease. Fat embolism is usually asymptomatic, but in the minority of the patients symptoms and signs develop as a result of dysfunction of several organs, notably of the lungs, brain, and skin, in which case the term fat embolism syndrome (FES) is reserved. FES most commonly is associated with long-bone and pelvic fractures, and is more frequent in closed, rather than open, fractures. Patients with long-bone fractures have a 1 to 20% chance of acquiring the syndrome. However, the true incidence of FES is rather unknown because mild cases may be unnoticed.
FES typically manifests 24 to 72 h after the initial insult (trauma or orthopedic operation).1 2 Affected patients present with a classic triad of hypoxemia, neurologic abnormalities, and a petechial rash. Respiratory system dysfunction occurs frequently, and its severity may vary ranging from mild, manifested only with dyspnea and/or tachypnea, to severe, characterized by symptoms and signs indistinguishable from ARDS. It has been shown that approximately 50% of patients with FES caused by long-bone fractures acquire severe hypoxemia and require mechanical ventilation. Neurologic abnormalities, consisting of altered levels of consciousness, seizures, or focal deficits, develop in the majority of patients with FES and often occur after the development of respiratory system dysfunction.3 4 The characteristic petechial rash is usually observed on the head, neck, anterior thorax, subconjunctiva, and axillae.1 2
The pathogenesis of FES remains controversial, and several theories have been proposed.5 It is believed that the organ dysfunction in FES is the result of the direct entry of depot fat globules from disrupted tissue into the bloodstream, or of the production of toxic intermediaries of plasma-derived fat such as chylomicrons or infused lipids.2 5 The 24- to 72-h delay in syndrome appearance after the insult indicates the production of toxic intermediaries as the predominant pathogenetic mechanism.
Clinical diagnosis of cerebral FES can be aided by noting the presence of respiratory failure, hypoxemia, and cutaneous petechiae. Cerebral CT scan results are usually negative, while MRI, especially diffusion-weighted MRI, is more sensitive.6 7 8 Mild cases of respiratory system dysfunction may be associated with normal chest radiographic findings, and this may complicate the interpretation of symptoms and signs reflecting the lung function. BAL has been proposed to detect fat droplets in alveolar macrophages as a means to diagnose FES.9 10 11 However, the invasive nature of the procedure limits the usefulness of this technique. In addition, the diagnostic criteria vary considerably between studies while the sensitivity and specificity are unknown. The diagnostic value of noninvasive methods, like induced sputum, have not been evaluated and compared with BAL.
Malagari et al in this issue of CHEST (see page 1196) reported the high-resolution CT (HRCT) findings of the lungs in patients with mild FES. They observed that in these patients HRCT revealed bilateral ground-glass opacities and thickening of the interlobular septa, whereas in some cases centrilobular nodular opacities were present. In most patients, chest radiographic findings were reported normal. The clinical significance of these findings, however, is not clear. FES is a clinical diagnosis; currently, it is not known to what extent high-cost diagnostic tests such as HRCT may improve the accuracy of the clinical examination. Although the authors suggest that HRCT in mild cases of FES may aid in diagnosis prior to development of clinical manifestations,12 the design of their study does not permit firm conclusions regarding the clinical value of HRCT. HRCT was performed in patients in whom a clinical diagnosis of FES had been made. This precludes any statement as far as the diagnostic role of HRCT is concerned. Furthermore, the specificity and sensitivity of HRCT is not known. At present, the existing data in the literature do not support the routine use of HRCT as a tool to diagnose the respiratory system dysfunction in FES. Further studies with appropriate designs are needed to resolve this issue. Even in the current era of high technology, FES is one of the few pathologic entities that are diagnosed based on readily available clinical criteria. Nevertheless, the study of Malagari et al may serve as a useful framework to further assess the role of HRCT in diagnosing mild cases of FES. Until the appropriate studies are available, careful clinical examination remains the "gold standard" for diagnosing FES.
References
This article has been cited by other articles:
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  T. C. Lee, E. S. Bartlett, A. J. Fox, and S. P. Symons The Hypodense Artery Sign AJNR Am. J. Neuroradiol., September 1, 2005; 26(8): 2027 - 2029. [Abstract] [Full Text] [PDF]
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 A. Schmid, A. Tzur, L. Leshko, and B. P. Krieger Silicone Embolism Syndrome: A Case Report, Review of the Literature, and Comparison With Fat Embolism Syndrome* Chest, June 1, 2005; 127(6): 2276 - 2281. [Abstract] [Full Text] [PDF]
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