Table 1. Gurd’s and Wilson criteria for FES

The highest incidence of FES is among closed, long bone fractures of the lower extremities, especially the femur, and pelvis. Severe burns, infection, kidney transplant, liposuction, cardiopulmonary bypass, and transfusions are other possible causes. Males Age: 10–40 years, multiple fractures, and unstable bone fracture movement are the common risk factors. In our case, a closed long bone fracture of the tibia and fibula followed by joint manipulation makes the patient a high-risk candidate for FES. [2,3]

The onset of clinical symptoms can occur within 12 hours, but symptoms mostly present after 24–72 hours. The classic triad of respiratory manifestations (95 %), cerebral symptoms (60 %), and petechiae (33 %) are seen among patients with FES and are seen in our case [7,8]. Cerebral emboli cause neurological signs in up to 86 % of cases and mainly occur after the onset of respiratory distress, as observed in our patient’s clinical manifestation. Neurological manifestations of FES can vary from mild cognitive changes to coma, as evidenced by our patient’s Glasgow Coma Scale score of E4V2M6 [9]. Petechial rash, as seen in our patient’s conjunctiva, is considered pathognomonic of FES and is reportedly present in up to 60 % of patients [10]. Neurological symptoms are typically accompanied by respiratory failure and skin eruptions. Several cases of isolated cerebral fat embolism have also been reported [11,12]. In our case, respiratory system, skin, and eye examinations were abnormal. The main initial symptom was respiratory distress followed by an alteration in consciousness.

Brain CT showed normal findings in most cases. On the other hand, MRI is more sensitive and can show small high-signal-intensity lesions scattered in the cerebral white matter, cerebellum, and brainstem on T2-weighted or diffusion-weighted images [13,14]. In our case, CT Brain was unremarkable, whereas brain MRI showed bilateral symmetrical punctate foci with restricted diffusion “star field” pattern and mottled fluid-attenuated inversion recovery (FLAIR) signals. Also, a Chest CT scan of the patient showed diffuse bilateral pulmonary infiltrates with consolidation and ground glass opacities. A study by Gupta et al. evaluated 1692 patients with long bone and pelvic fractures and found that 12 patients met the diagnosis of FES. Three were diagnosed with CFE, whereas five suffered multiple bone fractures. Neurological status alterations were seen among all the patients with CFE with T2 and FLAIR hyperintense lesions in the bilateral cerebral hemisphere, basal ganglia, thalamus, pons, and cerebellum [15].

Despite changes in sensorium and respiratory distress, the symptoms resolved with supportive care. Although the initial presentation of CFE may be moderate to severe, most case reports on CFE demonstrate that the cerebral deterioration associated with CFE is amendable [16].

Even though the pathophysiology of FES remains poorly known, mechanical and biochemical theories are the two main proposed theories to explain pathology. Gossling et al. [17] described a mechanical theory, which states that a rise in intramedullary pressure after an injury forces marrow to pass into the injured venous sinusoids causing large fat droplets to be released into the venous system. These fat droplets that travel to the lungs and occlude pulmonary capillaries and systemic vasculature may enter the arterial circulation via a patent foramen ovale or directly through the pulmonary capillary bed, causing the characteristic neurological and dermatologic findings of FES. Similarly, Baker et al. [18] described the biochemical theory, which states that the clinical manifestations of FES are attributable to a pro-inflammatory state. The intermediate products, such as glycerol and toxic-free fatty acids, because of local hydrolysis of triglyceride emboli by tissue lipase, may lead to an injury to pneumocytes and pulmonary endothelial cells, causing vasogenic and cytotoxic edema, leading to the development of acute lung injury or respiratory distress syndrome.

Prevention, early detection, and appropriate treatment are critical parameters in FES.  Intracranial pressure and cerebral tissue oxygenation monitoring help maintain optimal perfusion, as suggested by Kumar et al. [19]. Traumatic patients have improved outcomes with splinting and fixation of orthopedic fractures in an early phase, and supportive care remains the mainstay of treatment for FES [20, 21].

Adequate supportive treatment and improved care can help the majority of the patients of FES recover completely. The severity of respiratory problems is a close indicator of the risk of death, with overall mortality for this condition 5–15 % [22]. Most case reports on CFE demonstrate that the cerebral deterioration associated with CFE is amendable [23-25,16].