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].