Teaching Case

20-year-old male patient presented with decreasing level of consciousness, mild hypoxaemia, tachycardia and seizures 18 hours after being involved in a motor vehicle accident resulting in displaced fractures of left humerus, left tibia, left fibula and right iliac bone.

Chest radiography, contrast-enhanced chest CT and head CT were normal.
Head MRI showed numerous punctate T2 and FLAIR (Fig. 1) hyperintensities in subcortical and deep white matter of the cerebrum as well as in the basal ganglia and in the cerebellum. Most of the lesions were hyperintense on diffusion-weighted imaging (Fig. 2 - DWI), with hypointensity on corresponding apparent diffusion coefficient (Fig. 3 - ADC) maps, suggesting restriction of water diffusion. Additionally, multiple hypointense foci were scattered throughout the cerebral white matter on susceptibility weighted imaging (Fig. 4 & 5 - SWI), representing microbleeds. Findings are consistent with cerebral fat embolism.

Clinical Perspective:
Cerebral fat embolism (CFE) has been traditionally associated with displaced long bone fracture [1], but may also occur in nontraumatic disorders such as collagen disease, diabetes, burns, severe infections, neoplasms, osteomyelitis, blood transfusion, cardiopulmonary bypass, suction lipectomy and renal transplantation [2]. Fat embolism syndrome is characterised by respiratory distress, petechial skin rash and various neurological deficits, ranging from headache and confusion to seizures and coma [1], with reported incidence of 0.9 - 2.2% [3]. However, this triad may not be present in all patients [4]. Features of traumatic brain injury such as cerebral contusions and/or hypoxic-ischaemic injury often coexist in the setting of trauma, making the diagnosis of CFE even more challenging [1].

Imaging Perspective:
MRI is the method of choice in the diagnosis of CFE [5]. Five distinct MRI patterns have recently been proposed: scattered embolic ischaemia, confluent symmetric cytotoxic oedema, vasogenic oedematous lesions, petechial haemorrhages and chronic sequelae [1]. In the acute setting, scattered cytotoxic oedema is the most common finding. It is characterised by multiple hyperintense spot lesions on diffusion-weighted imaging (DWI), a so called "starfield pattern" [6]. Another characteristic feature is confluent symmetric T2 hyperintense lesions with restricted diffusion on DWI, found predominantly at the subacute stage. Lesions are located in periventricular and subcortical white matter, but cerebellar peduncles, corpus callosum, and posterior internal capsule may be involved [1]. Pathognomonic finding of CFE is petechial haemorrhage of white matter [1]. Susceptibility weighted imaging (SWI) is superior to gradient-echo sequence in detecting haemorrhage of CFE [7]. Minute hypointense foci on SWI are located predominantly in the white matter and share the same distribution as the confluent cytotoxic oedema pattern. Diffuse axonal injury also presents with petechial haemorrhagic lesions but these are mainly located in the grey-white matter junction and corpus callosum [1].

Outcome:
Prevention of secondary brain damage due to hypoxia is essential to avoid permanent neurologic sequelae. With early diagnosis, intensive care and rehabilitation, the prognosis is favourable even in cases with a poor clinical picture at presentation [8].

Teaching Points:
In the setting of neurologic deterioration after long bone or pelvic fracture, the scattered SWI hypointensities are indicative of cerebral fat embolism. In the acute stage, scattered cytotoxic oedema on DWI and T2 weighted images may be identified. In the subacute stage, confluent cytotoxic and/or vasogenic oedema may be present.