Cerebral fat embolism

Cerebral fat embolism is one manifestation of fat embolism syndrome, but can also rarely occur in isolation.

Epidemiology

Cerebral fat embolism typically occurs in patients with bony fractures (usually long bones of the lower limb) or following orthopaedic or cardiac surgery ¹⁹. FatIn 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 with bone marrow fat necrosis and subsequent embolism ⁴.

Clinical presentation

Cerebral manifestations of fat embolism syndrome can be differ depending on whether the fat embolism is due to microembolism or macroembolism ¹⁹.

• microembolism

  • often occurs with fat embolism syndrome

  • highly variable and non-specific: clinical presentation

  • the symptomsclinical spectrum includes headache, lethargy, irritability, delirium, stupor, convulsions, or coma. Most cases can occur as subclinical events. Concurrent

  • concurrent pulmonary or cutaneous features may aid in diagnosis.

• macroembolism

  • often occurs without fat embolism syndrome and is a very rare entity

  • clinical presentation in-keeping with acute ischaemic 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

CT

• The microembolism

  • CT of the brain is normal in most cases ⁸. There

  • there may be evidence of diffuse oedema with scattered low-attenuating areas and haemorrhage in some situations.

• macroembolism

  • hypodense vessel sign may be present ¹⁹

  • other features in-keeping with ischaemic stroke will eventually develop ¹⁹

MRI

TheWith cerebral fat macroembolism, MRI changes are in-keeping with ischaemic stroke from other causes of large vessel occlusion¹⁹. 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-fibres, 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 embolisation is, but often has an external watershed distribution (similar to other microembolisms).​

• DWI:

  • early (most common at 1-4 days): scattered punctate foci of cytotoxic oedema (starfield pattern)¹⁷

  • later (most common at 5-14 days): confluent areas of cytotoxic oedema in the white matter ¹⁷

• SWI: profuse microhaemorrhages in the white matter (walnut kernel pattern)^12,13,16,17

• T2/FLAIR: may may show small areas of high signal intensity indicating vasogenic oedema

• 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 scattered cytotoxic oedema

• subacute (type 2)

  • type 2A: confluent cytotoxic oedema in white matter

  • type 2B: vasogenic oedema lesions that may enhance

  • type 2C: petechial haemorrhages in white matter,

• chronic (type 3): cerebral cerebral atrophy  change change, persistent gliosis

Differential diagnosis

The imaging differential to consider includes many other causes of multiple small foci of infarction or haemorrhage, 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

• watershed infarction

• diffuse axonal injury

• cardiogenic cerebral emboli or septic cerebral emboli

• cerebral vasculitis

• minute haemorrhagic cerebral metastases