PubMed · 13586480
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H FELTEN. 1958. [Cerebral fat embolism].. https://pubmed.ncbi.nlm.nih.gov/13586480/
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Fat embolism syndrome (FES) was first described in 1862, but its frequency today is still unclear. A diagnosis of FES is often missed because of a subclinical illness or coexisting confusing injuries or disease. Fat embolism syndrome develops most commonly after orthopedic injuries, but it has also been reported after other forms of trauma such as severe burns, liver injury, closed-chest cardiac massage, bone marrow transplantation, and liposuction. Although FES usually presents as a multisystem disorder, the most seriously affected organs are the lung, brain, cardiovascular system, and skin. Fat embolism syndrome is a self-limiting disease and treatment should be mainly supportive. Many drugs have been used to treat FES, but the results are inconclusive.
The first clinical case of fat embolism was described over 100 years ago and significant progress has been made in the understanding of this condition since then. Gurd's criteria, consisting of major and minor clinical features, is the most commonly used diagnostic tool in the literature. Due to the lack of a gold standard for diagnosis, clinical criteria cannot be validated. It is now recognized that although fat embolization occurs in the majority of patients with long bone fractures, clinical signs and symptoms occur only in 1-10% of patients with fractures.
Fat embolism (FE) and fat embolism syndrome (FES) are controversial topics, particularly regarding their clinical relevance and their independency as a clinical syndrome. FE describes the presence of fat globules within the microcirculation. FES on the other hand, is a clinical syndrome characterized by the presence of FE with the manifestation of an identifiable clinical pattern of signs and symptoms. Both experimental and clinical studies have demonstrated the occurrence and the possible harmful effects of FE. For instance, FE involving the lungs can result in adult respiratory distress syndrome (ARDS). The effects of FE are certainly mechanical, leading to capillary congestion, but are also highly likely to be of a proinflammatory and prothrombotic nature. The demarcation of FES against ARDS is mainly demonstrated by the single organ involvement of ARDS, exclusively influencing the lungs, whereas FES has a multiorgan effect with pulmonary, skin and, neurological manifestations. This article is a review of the pathophysiological mechanisms of FE and the clinical occurrence and influence of FE and FES.