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Cerebral Fat Embolism with Multiple Rib and Thoracic Spinal Fractures

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Cerebral Fat Embolism with Multiple Rib and Thoracic Spinal Fractures KISEP J Korean Neurosurg Soc 36 : 408-411, 2004 Case Report 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. Introduction erebral fat embolism(CFE) may be seen in polytr- C 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 A B bone fractures. Their brain computed tomography(CT) shows multiple low density lesions in white matter, subcortical gray Fig. 1. Plain x-ray(A) and chest computed tomography(B) showing matter and magnetic resonance(MR) imaging reveals well multiple rib fractures(1st-2nd, 7th-9th) and multiple thoracic transverse process fractures(2nd-8th) on right side, and bilateral enhanced multiple lesions, a decrease intensity on the T1- clavicle fractures. weighted image and an increase intensity on the T2-weighted image. diagnosed as cerebral concussion, bilateral clavicle fractures, In this report, we describe a case of CFE with multiple hemothorax, pneumothorax, brachial plexus injury, multiple enhancing brain parenchymal lesions in a patient with rib fractures, and multiple thoracic transverse process fract- multiple rib and transverse process fractures along with a ures at the emergency room. review of the relevant literatures. After admission, he complained of headache, posterior neck pain, right shoulder and chest pain. On the physical exam- Case Report ination, he showed tachypnea and tenderness on the bilateral clavicles and the chest wall. The grunting sound was audible 24-year-old young male was referred to our emergency on the both lung field. There were moderate respiratory A room from a local hospital with right arm monoplegia distress, but not dermal petechiae, fever, or fat globules in the and abrasion on chest wall after a motor car accident. At the urine. On the neurological examination, he was in a confused accident, he had a transient loss of consciousness. He was state and had severe flaccid grade 0 monoplegia on the right arm. The deep tendon reflex and sensation of pain and Received：May 10, 2004 Accepted：June 28, 2004 temperature of the right arm were absent. On laboratory Address for reprints：Seong-Hyun Park, M.D., Department of Neurosurgery, School of Medicine, Kyungpook National University, examination, arterial blood gas analysis showed arterial 50 Samduk-2-ga, Jung-gu, Daegu 700-721, Korea oxygen saturation 88%, blood cell counts showed a hemog- Tel : 053)420-5649, Fax : 053)423-0504 lobin level of 14.1g/dl a platelet count of 293000mm3. E-mail : [email protected] One day after trauma, hemoglobin suddenly decreased to 408 J Korean Neurosurg Soc 36 YS Lee, et al. to an alert mentality and no further neurological disturbance was seen. Discussion is an uncommon, but pot- CFE entially lifethreatening, co- mplication of the long bone fra- ctures. The condition occurs pred- A B C 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). D E F The mortality associated with fat embolism has been reported to be Fig. 2. On admission, non-enhanced computed tomography(CT) showing no abnormality(A, B ,C). 13% to 87%1,4,7,10,12). But this rate 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). has been decreased with recent medical progress in respiratory 8.8g/dl, platelet to 124000mm3. Plain radiograph and chest and intensive care1,7,12). CT showed bilateral clavicle fractures, hemothorax, The pathogenesis of CFE remains controversial, and is pneumothorax, multiple rib(1st-2nd, 7th-9th) fractures and thought to be multietiologic. The cause of neurological thoracic transverse process(2nd-8th) fractures(Fig. 1A, B). dysfunction induced by fat embolism was previously thought Brain CT at the emergency room revealed no abnorm- to be secondary to hypoxia due to respiratory distress or ality(Fig. 2A, B, C). Cervical MRI for the evaluation of right intracranial hypertension. More recently, however, several arm monoplegia also showed non-specific findings. theories have been proposed to explain the cause of neurol- Three days after the trauma, he was still intermittently ogical dysfunction. 1) Mechanical : intraluminal fat globules confused, restless, and disoriented to the place, and brain CT smaller than 7㎛ in diameter can pass through the pulmonary was again performed. Brain CT revealed multiple hypodense arteriolar network which enter directly into the brain causing a lesions on the left occipital pole, and paracentral lobule, right blockage of capillary blood vessels7) 2) Toxic : fat globules cerebellar paravermian area(Fig. 2D, E, F). One week after activate chemical mediators that alter capillary permeability13). trauma, brain MRI revealed increased signal intensity on T2- Microscopically, fat embolisms are observed mainly in the weighted images, iso to low signal intensity on T1-weighted gray matter because of its abundant capillary network, and the images, and multiple enhancing lesions were seen in the left pathologic changes are predominant in the white matter calcarine sulcus, precentral and postcentral gyrus, right because of its poor collateral circulation and susceptibility to cerebellar vermis and paravermian area(Fig. 3). But the ischemia6). cerebellar signs or visual disturbance was not seen. Two Manifestations of CFE are highly variable and nonspecific : weeks after trauma, electromyography(EMG) and nerve headache, lethargy, delirium, confusion, convulsion, coma8). conduction velocity(NCV) showed whole arm typed right Subclinical CFE probably occurs more often and its clinical brachial plexus palsy. assessment has been difficult because brain CT does not show Three weeks after trauma, follow up brain MR imaging specific findings of CFE in the acute stage. revealed decreased edema on T2-weighted images and high Diagnosis of CFE has been made on the basis of clinical signal intensity along the cortical surface on T1-weighted features and Gurd's diagnostic criteria has been commonly images(Fig. 4). Four months after the discharge, he improved used5). In our case, based on various symptoms and signs, VOLUME 36 November, 2004 409 Cerebral Fat Embolism A B C D E 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. 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 A B injury(DAI), areas of vasogenic edema associated with microinfarcts, foci of gliosis, dilatated perivascular Virchow- Fig. 4. Three weeks after trauma, axial T1-weighted MR imaging(A) Robin spaces, and demyelinating disease15). In our patient, reveals high signal intensity on the precentral and postcentral gyrus. diffusion-weighted(DW) MRI was performed one week after Postcontrast sagittal T1-weighted MR imaging(B) shows decreased enhancement. injury and revealed low-signal lesions. But, in some cases, when DW-MRI was perfomed earlier, it showed high including hypoxemia, cerebral signs unrelated to head injury intensity lesions in the brain and may give an early-appearing or any other condition, and sudden drop in hemoglobin level, and more sensitive indicator of the diagnosis of CFE in the sudden thrombocytopenia, we made the diagnosis of CFE. As clinical context of long bone injury without head trauma12). for the diagnostic imaging of CFE, there are several reports Alternative diagnostic methods for revealing decreased regarding CT and MRI. The findings of all imaging methods cerebral blood flow in the acute stage of CFE are 99mTc including MRI appear to be non-specific for CFE. The hexamethyl propylene amine oxine single photon emission localization of the spotty cerebral lesions which are char- computed tomography(HMPAO SPECT) or transcranial acteristically located along the watershed zones of the major Dopper sonography(TCD). vascular territories can be a useful indicator for diffe- Fracture mangement and supportive pulmonary care are the rentiating CFE from primary intra-axial brain injury14). Brain cornerstones of fat embolism treatment. No specific treatment CT findings of the acute phase include multiple low-density has been proven to be effective : only corticosteroids used areas or normal despite of clinical encephalopathy or focal prophylactically have been shown to reduce the incidence of deficits. Therefore its principal role is to exclude other causes fat embolism4). CFE also can be complicated by anemia, and of neurological dysfunction2).
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