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Neuroradiology Case of the Week
Case 447
October 2009
Shawn Rosen, Balasubramanya Kolar, MD, and P-L Westesson, MD, PhD, DDS
Clinical
Presentation: Patient is a 19-year-old male with muscular dystrophy presenting with seizure, and pelvic and femur fractures after falling from his wheelchair while riding a bus.
Imaging Findings: See below.
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Figure 1: Axial T2 MR image of the head demonstrates bilateral punctuate hyperintensities in the caudate nucleus and deep and periventricular gray matter. Bilateral scalp hematomas are also identified. |
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Figure 2: Axial MR of the head with diffusion-weighted imaging (DWI) shows multiple punctuate lesions in the deep and periventricular gray matter. |
Figure 3: Axial apparent diffusion coefficient (ADC) map MR image demonstrates low-signal intensity lesions in the deep white matter and basal ganglionic regions suggesting restriction of diffusion. |
Diagnosis: Cerebral fat embolism (CFE)
Discussion: For CFE, MR findings include small, scattered, hyperintense lesions on long-TR images. These appear predominantly in periventricular, subcortical, and deep white matter, the basal ganglia, and the cerebellum. White matter lesions may or may not be associated with focal hemorrhage and may enhance with contrast [1]. T2-weighted images seem to be the most sensitive for diagnosing CFE [2]. Contrast-enhanced T1-weighted imaging is useful to demonstrate breakdown of the blood-brain barrier [1] and diffusion-weighted imaging (DWI) can confirm the presence of embolic cytotoxic edema [1]. On ADC map the hyperintense signals on DWI present with dark signal intensity [4]. In the acute phase, high-intensity T2 signals have been identified as early as 4 hours after onset of CFE [2]. Also, DWI may be useful acutely [4]. If initial MR images are negative, changes may appear days after the precipitating event [1].
Other imaging differential diagnosis may include common white matter etiologies of this age group that may have pre-existed. Examples include multiple sclerosis and acute disseminated encephalomyelitis [1].
Fat embolism syndrome is commonly associated with severely displaced multiple fractures of long bones of the lower extremities and is thought to occur with a frequency of 0.5% to 3.5% in long bone fractures. It develops typically between 12 hours and 3 days after the trauma. The major clinical features are respiratory distress, encephalopathy, and petechial rash [4]. Symptoms frequently diminish or resolve over time [1-3].
Yet, CFE need not exist concurrently with respiratory failure [1]. Although emboli may reach the systemic circulation through a patent foramen ovale or other arteriovenous communication, fat emboli may also transverse pulmonary capillaries [1]. CFE’s pathogenesis remains largely unexplained. Theories contrast “mechanical” and “chemical” causes of injury. The mechanical theory proposes that bones’ intramedullary veins are damaged in trauma, allowing fat to embolize to the lungs. In contrast, the “chemical” hypothesis suggests fat emboli are composed of aggregated chylomicrons and very-low-density lipoproteins that coalesce in the vasculature after trauma [5]. Classic microscopic findings show fat globules in microvessels with surrounding extravasated blood. Fat globules are more common in the gray matter than in those of white matter. Infarcts from occlusion and cytotoxic edema may occur. Some have suggested that the likelihood of infarct and hemorrhage depends on the size of the fat globules.
The patient’s recent transthoracic echocardiogram did not demonstrate a patent foramen ovale (PFO) and he has no known pulmonary arteriovenous (AV) shunts. This case is similar to that reported in a case report in 2003 [1] and seems to support the passage of fat across pulmonary capillaries or the chemical theory of CFE’s pathogenesis.
References:
- Simon AD, Ulmer JL, Strottmann JM. Contrast-enhanced MR imaging of cerebral fat embolism: case report and review of the literature. AJNR Am J Neuroradiol. 2003 Jan;24(1):97-101. PMID: 12533333 [PubMed]
- Takahashi M, Suzuki R, Osakabe Y, Asai JI, Miyo T, Nagashima G, Fujimoto T, Takahashi Y. Magnetic resonance imaging findings in cerebral fat embolism: correlation with clinical manifestations. J Trauma. 1999 Feb;46(2):324-7. PMID: 10029041 [PubMed]
- Butteriss DJ, Mahad D, Soh C, Walls T, Weir D, Birchall D. Reversible cytotoxic cerebral edema in cerebral fat embolism. AJNR Am J Neuroradiol. 2006 Mar;27(3):620-3. PMID: 16552005 [PubMed]
- Ryu CW, Lee DH, Kim TK, Kim SJ, Kim HS, Lee JH, Choi CG, Suh DC. Cerebral fat embolism: diffusion-weighted magnetic resonance imaging findings. Acta Radiol. 2005 Aug;46(5):528-33. PMID: 16224931 [PubMed]
- Pell AC, Hughes D, Keating J, Christie J, Busuttil A, Sutherland GR. Brief report: fulminating fat embolism syndrome caused by paradoxical embolism through a patent foramen ovale. N Engl J Med. 1993 Sep 23;329(13):926-9. PMID: 8123102 [PubMed]
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