Cerebral fat embolism is one manifestation of fat embolism syndrome, but can also rarely occur in isolation.
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Epidemiology
Cerebral fat embolism typically occurs in patients with bony fractures (usually long bones of the lower limb) or following orthopedic or cardiac surgery 19. In particular, fat embolism syndrome has an incidence of 1-3% following long bone fractures and 33% in patients with bilateral long bone fractures 18.
Rarely it has been described as part of a sickle cell crisis with bone marrow fat necrosis and subsequent embolism 4.
Clinical presentation
Cerebral manifestations of fat embolism syndrome differ depending on whether the fat embolism is due to microembolism or macroembolism 19.
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microembolism
often occurs with fat embolism syndrome
highly variable and non-specific clinical presentation
the clinical spectrum includes headache, lethargy, irritability, delirium, stupor, convulsions, or coma
concurrent pulmonary or cutaneous features may aid in diagnosis
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macroembolism
often occurs without fat embolism syndrome and is a very rare entity
clinical presentation in-keeping with acute ischemic stroke due to a large vessel occlusion
Pathology
Fat emboli usually reach the brain through either right-to-left cardiac shunt or through intact pulmonary circulation in those without a shunt 3.
Radiographic features
Radiographic features vary depending on whether cerebral fat embolism is due to microembolism or macroembolism.
CT
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microembolism
CT of the brain is normal in most cases 8
there may be evidence of diffuse edema with scattered low-attenuating areas and hemorrhage in some situations
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macroembolism
hypodense vessel sign may be present 19
other features in-keeping with ischemic stroke will eventually develop 19
MRI
With cerebral fat macroembolism, MRI changes are in-keeping with ischemic stroke from other causes of large vessel occlusion 19. However, cerebral fat microembolism has distinct radiographic features on MRI. In cerebral fat microembolism, the distribution of changes in the brain is bilaterally symmetric and predominantly in the subcortical and deep white matter, including subcortical U-fibers, corpus callosum, and internal capsule. SWI and DWI are the most sensitive sequences 17. The distribution and pattern are variable and depends on how extensive embolization is, but often has an external watershed distribution (similar to other microembolisms).
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DWI:
early (most common at 1-4 days): scattered punctate foci of cytotoxic edema (starfield pattern) 17
later (most common at 5-14 days): confluent areas of cytotoxic edema in the white matter 17
SWI: profuse microhemorrhages in the white matter (walnut kernel pattern) 12,13,16,17
T2/FLAIR: may show small areas of high signal intensity indicating vasogenic edema
T1: corresponding focal regions may show low T1 signal 9
T1 C+: some of the areas of vasogenic may enhance 17
Classification of MRI features
These patterns have been divided into three main types based on chronicity, although the classification system has not been widely adopted in clinical practice 17.
acute (type 1): scattered cytotoxic edema
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subacute (type 2)
type 2A: confluent cytotoxic edema in white matter
type 2B: vasogenic edema lesions that may enhance
type 2C: petechial hemorrhages in white matter
chronic (type 3): cerebral atrophy, persistent gliosis
Differential diagnosis
The imaging differential to consider includes many other causes of multiple small foci of infarction or hemorrhage, although generally, only fat emboli will result in a very large number of tiny lesions on both SWI and DWI. Other diagnoses to consider 6:
disseminated intravascular coagulation due to systemic causes other than fat embolisms, such as infection/sepsis
cardiogenic cerebral emboli or septic cerebral emboli
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