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Table of Contents    
Year : 2017  |  Volume : 65  |  Issue : 6  |  Page : 1420-1422

Nonconvulsive status in the trauma centre: Think of cerebral fat embolism

Department of Medicine, Grant Medical College and Sir JJ Hospital, Mumbai, Maharashtra, India

Date of Web Publication10-Nov-2017

Correspondence Address:
Dr. Vidya S Nagar
Department of Medicine, Grant Medical College and Sir JJ Hospital, Mumbai - 400 008, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.217950

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How to cite this article:
Chatterjee R, Nagar VS, Sajjan B, Patel K. Nonconvulsive status in the trauma centre: Think of cerebral fat embolism. Neurol India 2017;65:1420-2

How to cite this URL:
Chatterjee R, Nagar VS, Sajjan B, Patel K. Nonconvulsive status in the trauma centre: Think of cerebral fat embolism. Neurol India [serial online] 2017 [cited 2019 Nov 12];65:1420-2. Available from:


A 22-year old male patient presented to the Orthopedic emergency facility after a road traffic accident with pain and swelling of the right thigh. On examination, his vital parameters were stable. His systemic examination was also normal. The Glasgow Coma Scale (GCS) score was 15/15. There was a fracture of shaft of the femur of the right leg, which was splinted for stabilization after radiographic confirmation [Figure 1]. A routine computed tomography (CT) scan of the brain revealed no evidence of head trauma, and an abdominal ultrasound revealed no significant abnormality [Figure 2]. His chest X-ray was also normal [Figure 3]. The patient was planned for emergency nailing and internal fixation of the right femur. He had an episode of generalized tonic–clonic convulsion 2 hours post-admission. There was no return of consciousness after the seizure. His GCS score deteriorated to 8/15. His blood sugar level was normal. A fresh CT scan of the brain revealed no significant change from the one previously undertaken. Endotracheal intubation was prophylactically undertaken, and the patient was shifted to the critical care unit and started on mechanical ventilation. There was tachycardia with a heart rate of 124/min with a blood pressure of 106/70 mm Hg. There was a diffuse petechial rash all over the upper extremities. A thorough neurological evaluation was carried out. His consciousness was impaired and, therefore, higher mental functions could not be tested. His tone was normal in all extremities. The muscle stretch reflexes were preserved, and Babinski's reflex was present. His pupils were reacting to light, and persistent flickering eye movements were noted. His fundoscopy was within normal limits. His routine investigations revealed no significant derangements in the complete blood count and renal or liver functions. There was no evidence of thrombocytopenia. His cerebrospinal fluid analysis was normal. The electroencephalogram (EEG) revealed multifocal epileptiform discharges consistent with nonconvulsive status epilepticus. The patient was sedated utilizing injectable midazolam as his status epilepticus was uncontrollable despite the use of multiple antiepileptics including levetiracetam, sodium valproate, and lacosamide. Magnetic resonance imaging (MRI) of the brain revealed multiple punctate areas of restricted diffusion involving both cerebral hemispheres, predominantly present in bilateral periventricular regions, midbrain, as well as the cerebellum, which were suggestive of cerebral fat embolism [Figure 4]a, [Figure 4]b, [Figure 4]c,[Figure 4]d. The splinting of the fracture was rechecked and found to be adequate. There was no evidence of any structural heart defect on two-dimensional echocardiogram done as a part of the routine hemodynamic monitoring. His sedation was eventually tapered with continuous vital parameter monitoring and serial EEGs to assess his response. The patient regained full consciousness on day 8 of his admission. He was maintained on supportive management only and was weaned off mechanical ventilation. Definitive management of fracture of the shaft of femur was then carried out by performing an internal fixation of the bony fragments. Following a prolonged rehabilitation, he had a complete recovery with no residual disability. The patient was discharged with no significant neurological sequelae and his antiepileptic medication was tapered off. At a follow up of 2 months, he was asymptomatic and was continued on two antiepileptics, lacosamide and levetiracetam. No follow-up CT scan or EEG were performed, as subsequently, the patient remained asymptomatic.
Figure 1: Plain radiograph of the right thigh showing fracture of the shaft of femur of the right leg

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Figure 2: Contrast enhanced CT scan of the brain showing no significant abnormality

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Figure 3: Chest radiograph showing no active infiltrates

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Figure 4: (a) T2-weighted axial MR images showing multiple punctate hyperintensities arranged in the characteristic “starfield” pattern. (b) T1-weighted axial MR images at the same level showing discrete hypointense lesions. (c) T2-weighted coronal MR images showing the periventricular hyperintensities. (d) T2-weighted axial MR images showing bilateral cerebellar hyperintensities

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The criteria for diagnosing the fat embolism syndrome were first elucidated in 1974 and include three major criteria and six minor criteria.[1] A triad of respiratory insufficiency, neurological deficit, and diffuse petechial rash is typical. In addition, patients may have derangements in their hematological profile that may include persistent thrombocytopenia and anemia, disproportionate to the amount of blood loss incurred; and, which is usually refractory to blood transfusion. Neurological involvement may include focal neurological deficits, altered sensorium, dementia, a confused state, convulsions, and coma.[2] Neurological involvement without respiratory insufficiency is rare as it implies the passage of emboli through the pulmonary vasculature and systemic circulation.[3] The neurological effects routinely resolve with correct identification and treatment of the condition; however, the generalised presentation of altered sensorium and seizures often lead to a misdiagnosis that may result in a significant morbidity and mortality. Though fat embolism is more common after a breach of the long bone medulla in the postoperative period following the procedure of intramedullary nailing, preoperative cases have been reported and have been caused by the primary fracture itself.

There are no diagnostic CT findings of cerebral fat embolism.[2] Diffusion-weighted magnetic resonance (MR) images are more sensitive and may be used for an early diagnosis.[4],[5] Diffuse cerebral deep white and gray matter involvement with multiple non-confluent areas of hyperintensity on T2-weighted images, and iso- or hypointense areas on T1-weighted images at the boundaries of different regions of circulation are characteristic features of cerebral fat embolism.[3],[4] A striking “starfield” pattern of scattered white spots on a dark background may be evident.[5],[6] A grading of the lesions on the basis of their size and distribution has been proposed.[3]

The 2013 Salzburg criteria for diagnosing non-convulsive status epilepticus include: (1) More than 25 epileptiform discharges (ED) per 10s epoch, that is, >2.5/s, (2) patients with EDs ≤2.5/s or rhythmic delta/theta activity (RDT) exceeding 0.5/s accompanied by at least one of the additional criteria: (2a) Clinical and EEG improvement following the administration of antiepileptic drugs (AEDs); (2b) the presence of a subtle clinical phenomena; or, (2c) a typical spatiotemporal evolution.[7] These were based on the recommendations of the American Clinical Neurophysiology Society's Standardized Critical Care EEG Terminology, 2012 version.[8] Nonconvulsive status epilepticus as a result of cerebral fat embolism is rare.

Cerebral fat embolism without other systemic involvement may present with a diagnostic challenge and may lead to an unwarranted morbidity and mortality. An early MRI brain and EEG evaluation would be helpful in the management of patients who often present with seizures.[9],[10]

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There are no conflicts of interest.

  References Top

Gurd AR, Wilson RE. The fat embolism syndrome. J Bone Joint Surg Br 1974;56:408-16.  Back to cited text no. 1
Jacobson DM, Terrence CF, Reinmuth OM. The neurologic manifestations of fat embolism. Neurology 1986;36:847-51.  Back to cited text no. 2
Takahashi M, Suzuki R, Osakabe Y, Asai JI, Miyo T, Nagashima G, et al. Magnetic resonance imaging findings in cerebral fat embolism: Correlation with clinical manifestations. J Trauma 1999;46:324-7.  Back to cited text no. 3
Guillevin R, Vallie JN, Demeret S, Sonneville R, Bolgert F, Mont'alverne F, et al. Cerebral fat embolism: Usefulness of magnetic resonance spectrometry. Ann Neurol 2005;57:434-9.  Back to cited text no. 4
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 2001;32:2942-4.  Back to cited text no. 5
Ryu CW, Lee DH, Kim TK, Kim SJ, Kim HS, Lee JH, et al. Cerebral fat embolism: Diffusion-weighted magnetic resonance imaging findings. Acta Radiol 2005;46:528-33.  Back to cited text no. 6
Leitinger M, Beniczky S, Rohracher A, Gardella E, Kalss G, Qerama E, et al. Salzburg Consensus Criteria for Non-Convulsive Status Epilepticus-approach to clinical application. Epilepsy Behav 2015;49:158-63.  Back to cited text no. 7
Murthy J. Refractory status epilepticus. Neurol India 2006;54:354-8.  Back to cited text no. 8
[PUBMED]  [Full text]  
Hirsch LJ, LaRoche SM, Gaspard N, Gerard E, Svoronos A, Herman ST, et al. American Clinical Neurophysiology Society's Standardized Critical Care EEG Terminology: 2012 version. J Clin Neurophysiol 2013;30:1-27.  Back to cited text no. 9
Dubey D, Kalita J, Misra UK. Status epilepticus: Refractory and super-refractory. Neurol India 2017;65, Suppl S1:12-7.  Back to cited text no. 10


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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