408 J Korean Neurosurg Soc 36 Introduction C erebral fat embolism(CFE) may be seen in polytr- aumatized patients who present with neurological impairments. The pathogenesis of these lesions is still unclear and remains a source of considerable controversy. It is well known that CFE is a poten-tially serious complication of long bone fractures and it is important to consider the possibility of CFE in patients with neurological symptoms and multiple bone fractures. Their brain computed tomography(CT) shows multiple low density lesions in white matter, subcortical gray matter and magnetic resonance(MR) imaging reveals well enhanced multiple lesions, a decrease intensity on the T1- weighted image and an increase intensity on the T2-weighted image. In this report, we describe a case of CFE with multiple enhancing brain parenchymal lesions in a patient with multiple rib and transverse process fractures along with a review of the relevant literatures. Case Report A 24-year-old young male was referred to our emergency room from a local hospital with right arm monoplegia and abrasion on chest wall after a motor car accident. At the accident, he had a transient loss of consciousness. He was diagnosed as cerebral concussion, bilateral clavicle fractures, hemothorax, pneumothorax, brachial plexus injury, multiple rib fractures, and multiple thoracic transverse process fract- ures at the emergency room. After admission, he complained of headache, posterior neck pain, right shoulder and chest pain. On the physical exam- ination, he showed tachypnea and tenderness on the bilateral clavicles and the chest wall. The grunting sound was audible on the both lung field. There were moderate respiratory distress, but not dermal petechiae, fever, or fat globules in the urine. On the neurological examination, he was in a confused state and had severe flaccid grade 0 monoplegia on the right arm. The deep tendon reflex and sensation of pain and temperature of the right arm were absent. On laboratory examination, arterial blood gas analysis showed arterial oxygen saturation 88%, blood cell counts showed a hemog- lobin level of 14.1g/dl a platelet count of 293000mm 3 . One day after trauma, hemoglobin suddenly decreased to Cerebral Fat Embolism with Multiple Rib and Thoracic Spinal Fractures Yoon-Soo Lee, M.D., Seong-Hyun Park, M.D., In-Suk Hamm, M.D. Department of Neurosurgery, School of Medicine, Kyungpook National University, Daegu, Korea Cerebral fat embolism(CFE) is a rarely reported and usually underestimated disease entity. It is important to consider the possibility of CFE when intracranial lesions on brain magnetic resonance(MR) imaging without direct relation to the trauma are seen in patients with multiple bone fractures. The authors report a case of CFE caused by trauma with multiple enhancing lesions on the enhanced T1-weighted MR images and high signal intensity on T2-weighted images in a 24-year-old-man with multiple bone fractures. KEY WORDS : Fat embolism·Multiple injuries·Magnetic resonance imaging. Received：May 10, 2004 Accepted：June 28, 2004 Address for reprints ：Seong-Hyun Park, M.D., Department of Neurosurgery, School of Medicine, Kyungpook National University, 50 Samduk-2-ga, Jung-gu, Daegu 700-721, Korea Tel : 053)420-5649, Fax : 053)423-0504 E-mail : [email protected] Case Report Fig. 1. Plain x-ray(A) and chest computed tomography(B) showing multiple rib fractures(1st-2nd, 7th-9th) and multiple thoracic transverse process fractures(2nd-8th) on right side, and bilateral clavicle fractures. A B J Korean Neurosurg Soc 36 : 408-411, 2004 KISEP
Cerebral Fat Embolism with Multiple Rib and Thoracic Spinal Fractures
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³í11Introduction
Cerebral fat embolism(CFE) may be seen in polytr- aumatized patients who present with neurological
impairments. The pathogenesis of these lesions is still unclear and remains a source of considerable controversy. It is well known that CFE is a poten-tially serious complication of long bone fractures and it is important to consider the possibility of CFE in patients with neurological symptoms and multiple bone fractures. Their brain computed tomography(CT) shows multiple low density lesions in white matter, subcortical gray matter and magnetic resonance(MR) imaging reveals well enhanced multiple lesions, a decrease intensity on the T1- weighted image and an increase intensity on the T2-weighted image.
In this report, we describe a case of CFE with multiple enhancing brain parenchymal lesions in a patient with multiple rib and transverse process fractures along with a review of the relevant literatures.
Case Report
A 24-year-old young male was referred to our emergency room from a local hospital with right arm monoplegia
and abrasion on chest wall after a motor car accident. At the accident, he had a transient loss of consciousness. He was
diagnosed as cerebral concussion, bilateral clavicle fractures, hemothorax, pneumothorax, brachial plexus injury, multiple rib fractures, and multiple thoracic transverse process fract- ures at the emergency room.
After admission, he complained of headache, posterior neck pain, right shoulder and chest pain. On the physical exam- ination, he showed tachypnea and tenderness on the bilateral clavicles and the chest wall. The grunting sound was audible on the both lung field. There were moderate respiratory distress, but not dermal petechiae, fever, or fat globules in the urine. On the neurological examination, he was in a confused state and had severe flaccid grade 0 monoplegia on the right arm. The deep tendon reflex and sensation of pain and temperature of the right arm were absent. On laboratory examination, arterial blood gas analysis showed arterial oxygen saturation 88%, blood cell counts showed a hemog- lobin level of 14.1g/dl a platelet count of 293000mm3.
One day after trauma, hemoglobin suddenly decreased to
Cerebral Fat Embolism with Multiple Rib and Thoracic Spinal Fractures
Yoon-Soo Lee, M.D., Seong-Hyun Park, M.D., In-Suk Hamm, M.D. Department of Neurosurgery, School of Medicine, Kyungpook National University, Daegu, Korea
Cerebral fat embolism(CFE) is a rarely reported and usually underestimated disease entity. It is important to consider the possibility of CFE when intracranial lesions on brain magnetic resonance(MR) imaging without direct relation to the trauma are seen in patients with multiple bone fractures. The authors report a case of CFE caused by trauma with multiple enhancing lesions on the enhanced T1-weighted MR images and high signal intensity on T2-weighted images in a 24-year-old-man with multiple bone fractures.
KEY WORDS : Fat embolism·Multiple injuries·Magnetic resonance imaging.
ReceivedMay 10, 2004 AcceptedJune 28, 2004 Address for reprintsSeong-Hyun Park, M.D., Department of Neurosurgery, School of Medicine, Kyungpook National University, 50 Samduk-2-ga, Jung-gu, Daegu 700-721, Korea Tel : 053)420-5649, Fax : 053)423-0504 E-mail : [email protected]
C ase R
A B
J Korean Neurosurg Soc 36 : 408-411, 2004K I S E P
VOLUME 36 November, 2004 409
YS Lee, et al.
8.8g/dl, platelet to 124000mm3. Plain radiograph and chest CT showed bilateral clavicle fractures, hemothorax, pneumothorax, multiple rib(1st-2nd, 7th-9th) fractures and thoracic transverse process(2nd-8th) fractures(Fig. 1A, B). Brain CT at the emergency room revealed no abnorm- ality(Fig. 2A, B, C). Cervical MRI for the evaluation of right arm monoplegia also showed non-specific findings.
Three days after the trauma, he was still intermittently confused, restless, and disoriented to the place, and brain CT was again performed. Brain CT revealed multiple hypodense lesions on the left occipital pole, and paracentral lobule, right cerebellar paravermian area(Fig. 2D, E, F). One week after trauma, brain MRI revealed increased signal intensity on T2- weighted images, iso to low signal intensity on T1-weighted images, and multiple enhancing lesions were seen in the left calcarine sulcus, precentral and postcentral gyrus, right cerebellar vermis and paravermian area(Fig. 3). But the cerebellar signs or visual disturbance was not seen. Two weeks after trauma, electromyography(EMG) and nerve conduction velocity(NCV) showed whole arm typed right brachial plexus palsy.
Three weeks after trauma, follow up brain MR imaging revealed decreased edema on T2-weighted images and high signal intensity along the cortical surface on T1-weighted images(Fig. 4). Four months after the discharge, he improved
to an alert mentality and no further neurological disturbance was seen.
Discussion
CFEis an uncommon, but pot- entially lifethreatening, co-
mplication of the long bone fra- ctures. The condition occurs pred- ominantly in patients with the long bone fractures or in those who have undergone orthopedic mani- pulations. CFE may also occur with the nondisplaced fractures and fractures of the smaller bo- nes5). In patients with long bone fractures, fat embolism is enco- untered in 0.9~2.2% of all cases10). The mortality associated with fat embolism has been reported to be 13% to 87%1,4,7,10,12). But this rate has been decreased with recent medical progress in respiratory
and intensive care1,7,12). The pathogenesis of CFE remains controversial, and is
thought to be multietiologic. The cause of neurological dysfunction induced by fat embolism was previously thought to be secondary to hypoxia due to respiratory distress or intracranial hypertension. More recently, however, several theories have been proposed to explain the cause of neurol- ogical dysfunction. 1) Mechanical : intraluminal fat globules smaller than 7 in diameter can pass through the pulmonary arteriolar network which enter directly into the brain causing a blockage of capillary blood vessels7) 2) Toxic : fat globules activate chemical mediators that alter capillary permeability13). Microscopically, fat embolisms are observed mainly in the gray matter because of its abundant capillary network, and the pathologic changes are predominant in the white matter because of its poor collateral circulation and susceptibility to ischemia6).
Manifestations of CFE are highly variable and nonspecific : headache, lethargy, delirium, confusion, convulsion, coma8). Subclinical CFE probably occurs more often and its clinical assessment has been difficult because brain CT does not show specific findings of CFE in the acute stage.
Diagnosis of CFE has been made on the basis of clinical features and Gurd's diagnostic criteria has been commonly used5). In our case, based on various symptoms and signs,
Fig. 2. On admission, non-enhanced computed tomography(CT) showing no abnormality(A, B ,C). Three days after trauma, brain CT reveals low density lesions on the right cerebellar vermis and paravermian area, left occipital pole, paracentral lobule(D, E, F).
A B C
D E F
Cerebral Fat Embolism
including hypoxemia, cerebral signs unrelated to head injury or any other condition, and sudden drop in hemoglobin level, sudden thrombocytopenia, we made the diagnosis of CFE. As for the diagnostic imaging of CFE, there are several reports regarding CT and MRI. The findings of all imaging methods including MRI appear to be non-specific for CFE. The localization of the spotty cerebral lesions which are char- acteristically located along the watershed zones of the major vascular territories can be a useful indicator for diffe- rentiating CFE from primary intra-axial brain injury14). Brain CT findings of the acute phase include multiple low-density areas or normal despite of clinical encephalopathy or focal deficits. Therefore its principal role is to exclude other causes of neurological dysfunction2). Typical MRI findings in the acute stage of CFE consist of diffuse patchy lesions throughout the brain, most commonly in the white matter and subcortical gray matter. These lesions are demonstrated by low signal on T1-weighted images and high signal on T2- weighted images in the cerebrum, cerebellum, and brain stem9). And multiple enhanced lesions are shown on enhanced T1-weighted images due to disruption of blood- brain barrier(BBB). Erdem et al3) have reported to reveal hyperintensive areas on T1-weighted images corresponding
to hemorrhagic infarcts or hyperintensive area on T2-weig- hted images corresponding to anemic infarcts. Follow-up MRI after 2 weeks in our case revealed hyperintense lesions in the subcortical white matter on T1-weighted images and we supposed that hypoperfusion zones became hemorrhagic infarcts. Differential diagnoses of disseminated hyperintense lesions on T2-weighted images include diffuse axonal injury(DAI), areas of vasogenic edema associated with microinfarcts, foci of gliosis, dilatated perivascular Virchow- Robin spaces, and demyelinating disease15). In our patient, diffusion-weighted(DW) MRI was performed one week after injury and revealed low-signal lesions. But, in some cases, when DW-MRI was perfomed earlier, it showed high intensity lesions in the brain and may give an early-appearing and more sensitive indicator of the diagnosis of CFE in the clinical context of long bone injury without head trauma12). Alternative diagnostic methods for revealing decreased cerebral blood flow in the acute stage of CFE are 99mTc hexamethyl propylene amine oxine single photon emission computed tomography(HMPAO SPECT) or transcranial Dopper sonography(TCD).
Fracture mangement and supportive pulmonary care are the cornerstones of fat embolism treatment. No specific treatment has been proven to be effective : only corticosteroids used prophylactically have been shown to reduce the incidence of fat embolism4). CFE also can be complicated by anemia, and coagulopathy or DIC due to enhanced coagulation defects, and the treatment must be focused on prophylaxis of DIC as well as on treatment for pulmonary injury.
The impairment of consciousness and focal neurological signs must be differentiated from other complications of the trauma such as cerebral contusion, DAI, anoxic brain injury, extra or intracerebral hematoma and from coma of metabolic, toxic or infectious origin associated with the trauma4). DAI may resemble images of CFE, but in the case of DAI, the average number of the MRI lesions is usually fewer than
Fig. 3. Axial T2-weighted magnetic resonance(MR) images(A, B) show high signal intensity in the right cerebellar vermis and paravermian area, and left paracentral lobule. Axial T1-weighted MR images(C, D) reveal iso to low signal intensity. Postcontrast sagittal T1-weighted MR imaging(E) reveals marked enhancement.
A B C D E
Fig. 4. Three weeks after trauma, axial T1-weighted MR imaging(A) reveals high signal intensity on the precentral and postcentral gyrus. Postcontrast sagittal T1-weighted MR imaging(B) shows decreased enhancement.
A B
YS Lee, et al.
three, and numerous, bilaterally distributed, spotty lesions are uncommon11). Anoxic states affect primarily the cerebral cortex and basal ganglia resulting in cortical laminar necrosis and white matter dysfunction2). CFE is quite different from ischemic infarction in that the lesion shows hyperintensity on T2-weighted images earlier than ischemic infarction and also in parenchymal enhancement. Theses findings may be caused by the early appearance of vasogenic edema and disruption of BBB by fat emboli in the hyperacute stage9).
CFE can be suspected if patients experience alteration of the mental status that cannot be referred to a primary cerebral trauma and it is important to recognize CFE in early stage because it may be occasionally lethal although complete recovery from CFE is frequent1).
Conclusion
We report a case of CFE in a patient with the multiple bone fractures. It is sometimes difficult to find out
exact causes of the neurological manifestations in polytrau- matized patients. When the brain lesions are seen on the brain MRI without direct head injury from trauma, the possibility of CFE should be considered. In order to make correct diagnosis, it is important to have careful considerations about clinical symptoms, neuroimage finding, and pathophysiology of CFE and it deserves a certain interest due to differential diagnosis. It is necessary to recognize the possible occurrence of CFE associated with the multiple bone fractures and to diagnose and treat as soon as possible.
References 1. Bouaggard A, Harti A, Elmouknia M, Bouderka MA, Barrou H,
Abassi O, et al : Neurologic manifestations of fat embolism. Cah Anesthesiol 5: 441-443, 1995
2. Chrysikopoulos H, Maniatis V, Pappas J, Filalithis P, Gogalis C, Sfyras D : Case report : post-traumatic cerebral fat embolism : CT and MR fingdings. Report of two cases and review of the literature. Clin Radiol 51 : 728-732, 1996
3. Erdem E, Namer IJ, Saribas O, Aras T, Tan E, Bekdik C, et al : Cerebral fat embolism studied with MRI and SPECT. Neuroradiology 35 : 199-201, 1993
4. Finlay ME, Benson MD : Case report : magnetic resonance imaging in cerebral fat embolism. Clin Radiol 51 : 445-446, 1996
5. Gurd AR : Fat embolism : an aid to diagnosis. J Bone Joint Surg 52B: 732-737, 1970
6. Herndon JH : The syndromes of fat embolism. South Med J 68: 1577- 1584, 1975
7. Jacobson DM, Terrence CF, Reinmuth OM : The neurologic manifestations of fat embolism. Neurology 36: 847-851, 1986
8. Johnson MJ, Lucas GL : Fat embolism syndrome. Orthopedics 19: 41-49, 1996
9. Kim HJ, Lee CH, Lee SH, Moon TY : Magnetic resonance imaging and histologic findings of experimental cerebral fat embolism.Invest Radiol 38 : 625-634, 2003
10. Muller C, Rahn BA, Rfister U, Meinig RP : The incidence, pathogenesis, diagnosis, and treatment of fat embolism. Orthop Rev 23 : 107-117, 1997
11. Oh KS, Ha SI, Suh BS, Lee HS, Lee JS : The correlation of MRI findings to outcome in diffuse axonal injury patients. J Korean Neurosurg Soc(Suppl I) 30: 20-24, 2001
12. Parizel PM, Demey HE, Veeckmans G, Verstreken F, Cras P, Jorens PG, et al : Early diagnosis of cerebral fat embolism syndrome by diffusion-weighted MRI(starfield pattern). Stroke 32 : 2942-2944, 2001
13. Peltier LF : Fat embolism, III : toxic properties of neutral fat and free fatty acids. Surgery 40: 665-670, 1956
Cerebral fat embolism(CFE) may be seen in polytr- aumatized patients who present with neurological
impairments. The pathogenesis of these lesions is still unclear and remains a source of considerable controversy. It is well known that CFE is a poten-tially serious complication of long bone fractures and it is important to consider the possibility of CFE in patients with neurological symptoms and multiple bone fractures. Their brain computed tomography(CT) shows multiple low density lesions in white matter, subcortical gray matter and magnetic resonance(MR) imaging reveals well enhanced multiple lesions, a decrease intensity on the T1- weighted image and an increase intensity on the T2-weighted image.
In this report, we describe a case of CFE with multiple enhancing brain parenchymal lesions in a patient with multiple rib and transverse process fractures along with a review of the relevant literatures.
Case Report
A 24-year-old young male was referred to our emergency room from a local hospital with right arm monoplegia
and abrasion on chest wall after a motor car accident. At the accident, he had a transient loss of consciousness. He was
diagnosed as cerebral concussion, bilateral clavicle fractures, hemothorax, pneumothorax, brachial plexus injury, multiple rib fractures, and multiple thoracic transverse process fract- ures at the emergency room.
After admission, he complained of headache, posterior neck pain, right shoulder and chest pain. On the physical exam- ination, he showed tachypnea and tenderness on the bilateral clavicles and the chest wall. The grunting sound was audible on the both lung field. There were moderate respiratory distress, but not dermal petechiae, fever, or fat globules in the urine. On the neurological examination, he was in a confused state and had severe flaccid grade 0 monoplegia on the right arm. The deep tendon reflex and sensation of pain and temperature of the right arm were absent. On laboratory examination, arterial blood gas analysis showed arterial oxygen saturation 88%, blood cell counts showed a hemog- lobin level of 14.1g/dl a platelet count of 293000mm3.
One day after trauma, hemoglobin suddenly decreased to
Cerebral Fat Embolism with Multiple Rib and Thoracic Spinal Fractures
Yoon-Soo Lee, M.D., Seong-Hyun Park, M.D., In-Suk Hamm, M.D. Department of Neurosurgery, School of Medicine, Kyungpook National University, Daegu, Korea
Cerebral fat embolism(CFE) is a rarely reported and usually underestimated disease entity. It is important to consider the possibility of CFE when intracranial lesions on brain magnetic resonance(MR) imaging without direct relation to the trauma are seen in patients with multiple bone fractures. The authors report a case of CFE caused by trauma with multiple enhancing lesions on the enhanced T1-weighted MR images and high signal intensity on T2-weighted images in a 24-year-old-man with multiple bone fractures.
KEY WORDS : Fat embolism·Multiple injuries·Magnetic resonance imaging.
ReceivedMay 10, 2004 AcceptedJune 28, 2004 Address for reprintsSeong-Hyun Park, M.D., Department of Neurosurgery, School of Medicine, Kyungpook National University, 50 Samduk-2-ga, Jung-gu, Daegu 700-721, Korea Tel : 053)420-5649, Fax : 053)423-0504 E-mail : [email protected]
C ase R
A B
J Korean Neurosurg Soc 36 : 408-411, 2004K I S E P
VOLUME 36 November, 2004 409
YS Lee, et al.
8.8g/dl, platelet to 124000mm3. Plain radiograph and chest CT showed bilateral clavicle fractures, hemothorax, pneumothorax, multiple rib(1st-2nd, 7th-9th) fractures and thoracic transverse process(2nd-8th) fractures(Fig. 1A, B). Brain CT at the emergency room revealed no abnorm- ality(Fig. 2A, B, C). Cervical MRI for the evaluation of right arm monoplegia also showed non-specific findings.
Three days after the trauma, he was still intermittently confused, restless, and disoriented to the place, and brain CT was again performed. Brain CT revealed multiple hypodense lesions on the left occipital pole, and paracentral lobule, right cerebellar paravermian area(Fig. 2D, E, F). One week after trauma, brain MRI revealed increased signal intensity on T2- weighted images, iso to low signal intensity on T1-weighted images, and multiple enhancing lesions were seen in the left calcarine sulcus, precentral and postcentral gyrus, right cerebellar vermis and paravermian area(Fig. 3). But the cerebellar signs or visual disturbance was not seen. Two weeks after trauma, electromyography(EMG) and nerve conduction velocity(NCV) showed whole arm typed right brachial plexus palsy.
Three weeks after trauma, follow up brain MR imaging revealed decreased edema on T2-weighted images and high signal intensity along the cortical surface on T1-weighted images(Fig. 4). Four months after the discharge, he improved
to an alert mentality and no further neurological disturbance was seen.
Discussion
CFEis an uncommon, but pot- entially lifethreatening, co-
mplication of the long bone fra- ctures. The condition occurs pred- ominantly in patients with the long bone fractures or in those who have undergone orthopedic mani- pulations. CFE may also occur with the nondisplaced fractures and fractures of the smaller bo- nes5). In patients with long bone fractures, fat embolism is enco- untered in 0.9~2.2% of all cases10). The mortality associated with fat embolism has been reported to be 13% to 87%1,4,7,10,12). But this rate has been decreased with recent medical progress in respiratory
and intensive care1,7,12). The pathogenesis of CFE remains controversial, and is
thought to be multietiologic. The cause of neurological dysfunction induced by fat embolism was previously thought to be secondary to hypoxia due to respiratory distress or intracranial hypertension. More recently, however, several theories have been proposed to explain the cause of neurol- ogical dysfunction. 1) Mechanical : intraluminal fat globules smaller than 7 in diameter can pass through the pulmonary arteriolar network which enter directly into the brain causing a blockage of capillary blood vessels7) 2) Toxic : fat globules activate chemical mediators that alter capillary permeability13). Microscopically, fat embolisms are observed mainly in the gray matter because of its abundant capillary network, and the pathologic changes are predominant in the white matter because of its poor collateral circulation and susceptibility to ischemia6).
Manifestations of CFE are highly variable and nonspecific : headache, lethargy, delirium, confusion, convulsion, coma8). Subclinical CFE probably occurs more often and its clinical assessment has been difficult because brain CT does not show specific findings of CFE in the acute stage.
Diagnosis of CFE has been made on the basis of clinical features and Gurd's diagnostic criteria has been commonly used5). In our case, based on various symptoms and signs,
Fig. 2. On admission, non-enhanced computed tomography(CT) showing no abnormality(A, B ,C). Three days after trauma, brain CT reveals low density lesions on the right cerebellar vermis and paravermian area, left occipital pole, paracentral lobule(D, E, F).
A B C
D E F
Cerebral Fat Embolism
including hypoxemia, cerebral signs unrelated to head injury or any other condition, and sudden drop in hemoglobin level, sudden thrombocytopenia, we made the diagnosis of CFE. As for the diagnostic imaging of CFE, there are several reports regarding CT and MRI. The findings of all imaging methods including MRI appear to be non-specific for CFE. The localization of the spotty cerebral lesions which are char- acteristically located along the watershed zones of the major vascular territories can be a useful indicator for diffe- rentiating CFE from primary intra-axial brain injury14). Brain CT findings of the acute phase include multiple low-density areas or normal despite of clinical encephalopathy or focal deficits. Therefore its principal role is to exclude other causes of neurological dysfunction2). Typical MRI findings in the acute stage of CFE consist of diffuse patchy lesions throughout the brain, most commonly in the white matter and subcortical gray matter. These lesions are demonstrated by low signal on T1-weighted images and high signal on T2- weighted images in the cerebrum, cerebellum, and brain stem9). And multiple enhanced lesions are shown on enhanced T1-weighted images due to disruption of blood- brain barrier(BBB). Erdem et al3) have reported to reveal hyperintensive areas on T1-weighted images corresponding
to hemorrhagic infarcts or hyperintensive area on T2-weig- hted images corresponding to anemic infarcts. Follow-up MRI after 2 weeks in our case revealed hyperintense lesions in the subcortical white matter on T1-weighted images and we supposed that hypoperfusion zones became hemorrhagic infarcts. Differential diagnoses of disseminated hyperintense lesions on T2-weighted images include diffuse axonal injury(DAI), areas of vasogenic edema associated with microinfarcts, foci of gliosis, dilatated perivascular Virchow- Robin spaces, and demyelinating disease15). In our patient, diffusion-weighted(DW) MRI was performed one week after injury and revealed low-signal lesions. But, in some cases, when DW-MRI was perfomed earlier, it showed high intensity lesions in the brain and may give an early-appearing and more sensitive indicator of the diagnosis of CFE in the clinical context of long bone injury without head trauma12). Alternative diagnostic methods for revealing decreased cerebral blood flow in the acute stage of CFE are 99mTc hexamethyl propylene amine oxine single photon emission computed tomography(HMPAO SPECT) or transcranial Dopper sonography(TCD).
Fracture mangement and supportive pulmonary care are the cornerstones of fat embolism treatment. No specific treatment has been proven to be effective : only corticosteroids used prophylactically have been shown to reduce the incidence of fat embolism4). CFE also can be complicated by anemia, and coagulopathy or DIC due to enhanced coagulation defects, and the treatment must be focused on prophylaxis of DIC as well as on treatment for pulmonary injury.
The impairment of consciousness and focal neurological signs must be differentiated from other complications of the trauma such as cerebral contusion, DAI, anoxic brain injury, extra or intracerebral hematoma and from coma of metabolic, toxic or infectious origin associated with the trauma4). DAI may resemble images of CFE, but in the case of DAI, the average number of the MRI lesions is usually fewer than
Fig. 3. Axial T2-weighted magnetic resonance(MR) images(A, B) show high signal intensity in the right cerebellar vermis and paravermian area, and left paracentral lobule. Axial T1-weighted MR images(C, D) reveal iso to low signal intensity. Postcontrast sagittal T1-weighted MR imaging(E) reveals marked enhancement.
A B C D E
Fig. 4. Three weeks after trauma, axial T1-weighted MR imaging(A) reveals high signal intensity on the precentral and postcentral gyrus. Postcontrast sagittal T1-weighted MR imaging(B) shows decreased enhancement.
A B
YS Lee, et al.
three, and numerous, bilaterally distributed, spotty lesions are uncommon11). Anoxic states affect primarily the cerebral cortex and basal ganglia resulting in cortical laminar necrosis and white matter dysfunction2). CFE is quite different from ischemic infarction in that the lesion shows hyperintensity on T2-weighted images earlier than ischemic infarction and also in parenchymal enhancement. Theses findings may be caused by the early appearance of vasogenic edema and disruption of BBB by fat emboli in the hyperacute stage9).
CFE can be suspected if patients experience alteration of the mental status that cannot be referred to a primary cerebral trauma and it is important to recognize CFE in early stage because it may be occasionally lethal although complete recovery from CFE is frequent1).
Conclusion
We report a case of CFE in a patient with the multiple bone fractures. It is sometimes difficult to find out
exact causes of the neurological manifestations in polytrau- matized patients. When the brain lesions are seen on the brain MRI without direct head injury from trauma, the possibility of CFE should be considered. In order to make correct diagnosis, it is important to have careful considerations about clinical symptoms, neuroimage finding, and pathophysiology of CFE and it deserves a certain interest due to differential diagnosis. It is necessary to recognize the possible occurrence of CFE associated with the multiple bone fractures and to diagnose and treat as soon as possible.
References 1. Bouaggard A, Harti A, Elmouknia M, Bouderka MA, Barrou H,
Abassi O, et al : Neurologic manifestations of fat embolism. Cah Anesthesiol 5: 441-443, 1995
2. Chrysikopoulos H, Maniatis V, Pappas J, Filalithis P, Gogalis C, Sfyras D : Case report : post-traumatic cerebral fat embolism : CT and MR fingdings. Report of two cases and review of the literature. Clin Radiol 51 : 728-732, 1996
3. Erdem E, Namer IJ, Saribas O, Aras T, Tan E, Bekdik C, et al : Cerebral fat embolism studied with MRI and SPECT. Neuroradiology 35 : 199-201, 1993
4. Finlay ME, Benson MD : Case report : magnetic resonance imaging in cerebral fat embolism. Clin Radiol 51 : 445-446, 1996
5. Gurd AR : Fat embolism : an aid to diagnosis. J Bone Joint Surg 52B: 732-737, 1970
6. Herndon JH : The syndromes of fat embolism. South Med J 68: 1577- 1584, 1975
7. Jacobson DM, Terrence CF, Reinmuth OM : The neurologic manifestations of fat embolism. Neurology 36: 847-851, 1986
8. Johnson MJ, Lucas GL : Fat embolism syndrome. Orthopedics 19: 41-49, 1996
9. Kim HJ, Lee CH, Lee SH, Moon TY : Magnetic resonance imaging and histologic findings of experimental cerebral fat embolism.Invest Radiol 38 : 625-634, 2003
10. Muller C, Rahn BA, Rfister U, Meinig RP : The incidence, pathogenesis, diagnosis, and treatment of fat embolism. Orthop Rev 23 : 107-117, 1997
11. Oh KS, Ha SI, Suh BS, Lee HS, Lee JS : The correlation of MRI findings to outcome in diffuse axonal injury patients. J Korean Neurosurg Soc(Suppl I) 30: 20-24, 2001
12. Parizel PM, Demey HE, Veeckmans G, Verstreken F, Cras P, Jorens PG, et al : Early diagnosis of cerebral fat embolism syndrome by diffusion-weighted MRI(starfield pattern). Stroke 32 : 2942-2944, 2001
13. Peltier LF : Fat embolism, III : toxic properties of neutral fat and free fatty acids. Surgery 40: 665-670, 1956
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