Cerebral fat embolism

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Cerebral fat embolism is one manifestation of fat embolism syndrome.

Epidemiology

Cerebral fat embolism typically occurs in patients with bony fractures (usually long bones of the lower limb). 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 can be highly variable and non-specific: the symptoms spectrum includes headache, lethargy, irritability, delirium, stupor, convulsions, or coma. Most cases can occur as subclinical events. Concurrent pulmonary or cutaneous features may aid in diagnosis.

Pathology

Fat emboli usually reach the brain through either right-to-left cardiac shunt or through an intact pulmonary circulation in those without a shunt 3.

Radiographic features

CT 

The CT of the brain is normal in most cases 8. There may be evidence of diffuse oedema with scattered low-attenuating areas and haemorrhage in some situations.

MRI 

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 isand 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 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 oedema
  • subacute (type 2)
    • type 2A: confluent cytotoxic oedema in white matter 
    • type 2B: vasogenic oedema lesions that may enhance 
    • type 2C: petechial hemorrhages in white matter,
  • chronic (type 3): cerebral atrophy  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 thea very large number of tiny lesions on both SWI and DWI. Other diagnoses to consider 6:

  • -<p><strong>Cerebral fat embolism </strong>is one manifestation of <a href="/articles/fat-embolism-syndrome">fat embolism syndrome</a>.</p><h4>Epidemiology</h4><p>Cerebral fat embolism typically occurs in patients with bony fractures (usually long bones of the lower limb). Rarely it has been described as part of a <a href="/articles/sickle-cell-disease-cerebral-manifestations-1">sickle cell crisis</a> with bone marrow fat necrosis and subsequent embolism <sup>4</sup>.</p><h4>Clinical presentation</h4><p>Cerebral manifestations of fat embolism syndrome can be highly variable and non-specific: the symptoms spectrum includes headache, lethargy, irritability, <a href="/articles/delirium">delirium</a>, stupor, convulsions, or coma. Most cases can occur as subclinical events. Concurrent pulmonary or cutaneous features may aid in diagnosis.</p><h4>Pathology</h4><p>Fat emboli usually reach the brain through either right-to-left cardiac shunt or through an intact pulmonary circulation in those without a shunt <sup>3</sup>.</p><h4>Radiographic features</h4><h5>CT </h5><p>The CT of the brain is normal in most cases <sup>8</sup>. There may be evidence of diffuse oedema with scattered low-attenuating areas and haemorrhage in some situations.</p><h5>MRI </h5><p>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 <sup>17</sup>. The distribution is variable and depends on how extensive embolisation is, but often has an external <a title="Watershed cerebral infarction" href="/articles/watershed-cerebral-infarction">watershed distribution</a> (similar to other microembolisms). </p><ul>
  • +<p><strong>Cerebral fat embolism </strong>is one manifestation of <a href="/articles/fat-embolism-syndrome">fat embolism syndrome</a>.</p><h4>Epidemiology</h4><p>Cerebral fat embolism typically occurs in patients with bony fractures (usually long bones of the lower limb). Rarely it has been described as part of a <a href="/articles/sickle-cell-disease-cerebral-manifestations-1">sickle cell crisis</a> with bone marrow fat necrosis and subsequent embolism <sup>4</sup>.</p><h4>Clinical presentation</h4><p>Cerebral manifestations of fat embolism syndrome can be highly variable and non-specific: the symptoms spectrum includes headache, lethargy, irritability, <a href="/articles/delirium">delirium</a>, stupor, convulsions, or coma. Most cases can occur as subclinical events. Concurrent pulmonary or cutaneous features may aid in diagnosis.</p><h4>Pathology</h4><p>Fat emboli usually reach the brain through either right-to-left cardiac shunt or through intact pulmonary circulation in those without a shunt <sup>3</sup>.</p><h4>Radiographic features</h4><h5>CT </h5><p>The CT of the brain is normal in most cases <sup>8</sup>. There may be evidence of diffuse oedema with scattered low-attenuating areas and haemorrhage in some situations.</p><h5>MRI </h5><p>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 <sup>17</sup>. The distribution and pattern are variable and depends on how extensive embolisation is, but often has an external <a href="/articles/watershed-cerebral-infarction">watershed distribution</a> (similar to other microembolisms). ​</p><ul>
  • -</ul><h4>Differential diagnosis</h4><p>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 the very large number of tiny lesions on both SWI and DWI. Other diagnoses to consider <sup>6</sup>:</p><ul>
  • +</ul><h6>Classification of MRI features</h6><p>These patterns have been divided into three main types based on chronicity, although the classification system has not been widely adopted in clinical practice <sup>17</sup>. </p><ul>
  • +<li>acute (type 1): scattered cytotoxic oedema</li>
  • +<li>subacute (type 2)<ul>
  • +<li>type 2A: confluent cytotoxic oedema in white matter </li>
  • +<li>type 2B: vasogenic oedema lesions that may enhance </li>
  • +<li>type 2C: petechial hemorrhages in white matter,</li>
  • +</ul>
  • +</li>
  • +<li>chronic (type 3): cerebral atrophy  change, persistent gliosis</li>
  • +</ul><h4>Differential diagnosis</h4><p>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 <sup>6</sup>:</p><ul>
  • -<a href="/articles/disseminated-intravascular-coagulation">disseminated intravascular coagulation</a> due to systemic causes other than fat embolism, such as infection/sepsis</li>
  • +<a href="/articles/disseminated-intravascular-coagulation">disseminated intravascular coagulation</a> due to systemic causes other than fat embolisms, such as infection/sepsis</li>

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