Background: Fat embolism frequently occurs as a result of trauma, such as long bone fractures and orthopedic surgeries, as well as in certain non-traumatic conditions. The formation can be attributed to mechanical or biochemical processes. According to Hullman’s biochemical hypothesis, elevated C-reactive protein levels facilitate the precipitation of very-low-density lipoproteins and chylomicrons, forming fat globules that may result in fat embolism. Based on the abovementioned hypothesis, this study aims to detect fat embolism in autopsy patients (postmortem) suffering from bronchopneumonia and determine its possible role as a cause of death. Methods: A group of autopsies of deceased individuals with bacterial purulent bronchopneumonia with confirmed or presumed elevated C-reactive protein levels was rigorously selected, excluding those with other potential causes of fat embolism such as cardiopulmonary resuscitation, hypothermia, and diabetes mellitus. Multiple organs were sampled for frozen section analysis using Oil Red O fat staining and assessed for the presence and extent of fat embolism. The Falzi score, as modified by Janssen, was employed for the lung tissue. Results: In 73% of the cases, predominantly sporadic, Grade 0 or Grade I fat embolism was observed; however, in none of the cases was fat embolism identified as the cause of death or as a significant contributing factor. Furthermore, neither fat embolism syndrome nor multiorgan fat embolism were detected. Conclusions: Although an elevated C-reactive protein level facilitates the formation of fat globules and fat embolism, its role as a direct cause of mortality remains uncertain. It may predispose individuals to such conditions and potentially interact with other factors, such as minor soft tissue trauma, to exacerbate the severity of fat embolism or its clinical manifestations. These findings underscore the necessity for further comprehensive investigations within the contexts of infection/inflammation, fat embolism, and dyslipidemia.

Background: Fat embolism and fat embolism syndrome are rare but well-known consequences of long bone fractures and orthopedic surgeries. These sources support the mechanical theory of their development. On the other hand, as an alternative pathway suggested by the biochemical theory, lipase activation and fat breakdown are also a possible background for lipid droplets appearing in the vasculature. According to Hulman’s theory, elevated C-reactive protein levels can facilitate calcium-dependent agglutination of very low-density proteins and chylomicrons forming fat globules. The level of this acute-phase protein can increase mainly in advanced-stage cancers but also has predictive or indicative value in treatment success. Methods: This study focused on strictly selected patients with different histological types and origins of cancer, as well as advanced cancer in approximately 90% of the deceased. After collecting the tissue samples, the frozen sections were stained with Oil Red O to detect fat emboli. Results: Less than 50% of the cases showed punctiform, non-clinically relevant pulmonary fat embolism, and fat embolism syndrome was identified in none of the cases. In one, non-advanced cancer case, punctiform kidney fat embolism was observed. Conclusions: The end-of-life anergic state of patients may influence the procedure. In the case of osseous metastases, since the intramedullary sinuses are affected, both the mechanical and the biochemical backgrounds may prevail and mediate fat embolism formation.