Magnetic Resonance Imaging of Fat
Departments of Neurosurgery and *Neuroradiology, Institute of Neurosciences, **Department of Orthopedics , St. Mary's Hospital, Kurume, Fukuoka
Abstract The authors
a case of fat embolism
in a 20-year-old
(MR) imaging demonstrated multiple small cerebral infarcts suggesting this is the cause of the associ ated cerebral dysfunction. He underwent chemotherapy and hyperbaric oxygen therapy and recovered rapidly. MR imaging can provide prognostic indications in fat embolism syndrome. Key words:
pulmonary insufficiency and hypoxemia, neuro logical dysfunction, and petechiae. It develops after trauma, and in particular after long bone fractures and is sometimes incorrectly diagnosed as intra cranial hematoma. Many clinical and pathological investigations of this syndrome have been reported, but the pathogenesis of the neurological dysfunction is still controversial. Various authors ascribe the neurological symptoms to hypoxemia,9'10) intra cranial hypertension and fat emboli.',') We report a patient with fat embolism syndrome. Magnetic resonance (MR) imaging displayed numerous infarcts in bilateral thalami and the periventricular deep white matter, suggesting that in farcts caused by circulating fat droplets caused the neurological dysfunction. Case
A 20-year-old male suffered a motorcycle accident on September 16, 1989. After the accident, he had been in a stable condition with open fractures of the right fibula and tibia until a sudden seizure and subse quent Received
on the May
Computed tomographic (CT) scanning failed to demonstrate any intracranial lesions, and he was referred to our hospital for further investigation. On admission, he was semicomatose and assumed a decerebrate posture. Petechiae were noted on the anterior chest wall and conjunctivae. Hyper-reflexic deep tendon reflexes and positive Babinski signs were noted bilaterally. The rest of the neurological and general physical examination was noncontributory. The peripheral white blood cell count was 10,900/ mm3, and the platelet count 63,000/mm3. The ar terial blood during inhalation of 50% oxygen from a face mask demonstrated: pH 7.44, partial pressure of carbon dioxide (PCO2) 32.6, and partial pressure of oxygen (P02) 56.3. Increased serum transaminase levels were noted. A chest x-ray film revealed a fine diffuse veiling over the left lung field with moderately increased peri bronchial markings. A precontrast CT scan revealed no abnormal finding, including evidence of intra cranial hypertension (Fig. 1). T1-weighted MR image (field strength 1.5 T) 12 hours after seizure onset showed multiple low-intensity lesions in the peri ventricular deep white matter bilaterally (Fig. 2A). T2-weighted MR images demonstrated multiple high intensity regions in the bilateral thalami, putamen, and periventricular deep white matter (Fig. 2B, C). Administration of Trasylol (400,000 IU/day), methylprednisolone (1000 mg/day) and low mole
of lateral ventricles normal intracranial
finding. and cortical pressure.
Discussion cular weight dextran, and hyperbaric oxygen therapy were begun. He recovered rapidly, with verbal responses on the 5th hospital day and absence of neurological deficits by the 15th hospital day. A T2-weighted MR image 20 days after the seizure showed fewer multiple high-intensity lesions in the periventricular deep white matter, and those in the thalamus had disappeared (Fig. 3). His clinical course was thereafter uneventful. He was discharged without any neurological deficit after orthopedic treatments.
The fat embolism syndrome is a rare but serious com plication of trauma to the long bones due to systemic intravascular dissemination of neutral fat globules.') After a time interval, usually of 24 hours, patients develop pulmonary insufficiency with hypoxemia, petechiae, and neurological insufficiency.') Bone mar row fat entering the venous circulation at fractures most commonly causes serious pulmonary dysfunc tion, but neurological manifestations occur in as many as 80% of cases.s) Three hypotheses for the pathogenesis of neuro
A: Axial T,-weighted MR image (TR 0.6 sec, TE 15 msec) demonstrating patchy low-intensity lesions in periventricular deep white matter. B,C: T2-weighted MR images (TR 3.0 sec, TE 90 msec) showing high-intensity lesions in periventricular deep white matter (B), bilateral thalami and putamen (C).
logical dysfunction in fat embolism syndrome have been proposed. Sproule et al.") and Ross') suggested that hypoxia secondary to the adult respiratory distress syndrome is important in producing the neurological disorders. However, Findlay and DeMajo2) and Font et al.') have reported cases with cerebral dysfunction but no evidence of pulmonary involvement. Meeke et al.') emphasized intracranial hyperten sion caused by the cerebral edema secondary to microinfarcts. Murillo-Cabezas et al.' measured the intracranial pressure (ICP) in a 21-year-old female with fat embolism syndrome. The pressure was over 40 mmHg during ventilation or endotracheal suc tion, but the resting pressure was below 20 mmHg. These values were not high enough to disturb con sciousness. CT scanning is considered valuable for detecting increased ICP in fat embolism syndrome,') but can only reveal indicators such as CT number changes and narrowing of the extracerebral and/or intracerebral cerebrospinal fluid (CSF) spaces. However, in young patients especially true narrow ing of the CSF spaces is quite difficult to distinguish. The third mode of pathogenesis proposed is multi ple infarcts caused by fat globules which have en tered the circulation at the fracture site. The typical neuropathology reported is widespread distribution of fat embolisms in both gray and white matter, with diffuse petechial hemorrhagic infarcts and less frequent focal pale infarcts in the white matter.") Kamenar and Burger') reported that a more widespread distribution of fat embolisms throughout the deeper gray matter, pons, and medulla occurs in a small percentage of cases. MR imaging findings of cerebral fat embolism have not been previously reported. In our patient, MR imaging showed multiple le sions, especially in the bilateral thalami and periven tricular deep white matter. Kamenar and Burger') reported the same autopsy findings, suggesting that diffuse microemboli are involved in the pathogenesis of the fat embolism syndrome. Further, the CT and MR imaging appearance of the subarachnoid spaces and ventricles in our case showed no evidence of intracranial hypertension. These pathological and
clinical observations support the idea that ischemic cerebral anoxia caused by cerebral fat emboli, rather than hypoxemic anoxia or intracranial hypertension, produce the neurological dysfunction associated with fat embolism syndrome in most patients. MR imaging can provide prognostic indications in pa tients with fat embolism syndrome.
References 1) 2) 3)
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S. Anegawa, Institute
St. Mary's Hospital, 422 Kurume, Fukuoka 830, Japan.