Dynamic MR Imaging Patterns of Cerebral Fat Embolism: A Systematic Review with Illustrative Cases

Kuo, Kuei-Hong; Pan, Y. J.; Lai, Yan-wei; Cheung, Wing Keung; Chang, Fan‐Ren; Jarosz, J.

doi:10.3174/ajnr.a3605

Cited by 95 publications

(91 citation statements)

References 24 publications

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“…The white matter lesions occur mainly due to venous sludging and oedema. (1) There is usually a time lag between the pulmonary and CNS symptoms whose time duration depends on the filter effect (time taken for the passage of emboli from the pulmonary to the systemic circulation). The onset of neurological symptoms is therefore faster and much worse in patients with right-to-left shunts, such as in cases of patent foramen ovale.…”

Section: Discussionmentioning

confidence: 99%

Clinics in diagnostic imaging (184)

Singh

Chawla

Peh

2018

smedj

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A 23-year-old Indian man presented to the emergency department following an injury to his right leg. Radiographs showed a fracture of the midshaft of the right femur, for which open reduction and internal fixation was subsequently performed. The patient developed shortness of breath on Postoperative Day 2, along with new-onset confusion and altered mental state. His lungs were clear on the clinical examination, but there was a new rash on the chest. The patient's condition rapidly deteriorated over the next few hours with progressive worsening of the hypoxia, and he had to be intubated. He also experienced rapid neurological decline with a worsening score on the Glasgow Coma Scale (GCS) from 15 to 11. Blood tests demonstrated mild anaemia with thrombocytopenia. Computed tomography (CT) pulmonary angiography ( Fig. 1) was performed to evaluate the cause of shortness of breath, and magnetic resonance (MR) imaging of the brain was performed to assess the rapid neurological decline (Fig. 2). What do the images show? What is the diagnosis? CMEArticleClinics in diagnostic imaging (184)

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Section: Discussionmentioning

confidence: 99%

Clinics in diagnostic imaging (184)

Singh

Chawla

Peh

2018

smedj

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“…The presence of numerous hypointensities predominantly in the white matter on susceptibilityweighted or gradient echo (GRE) sequences is considered to be pathognomic for microhemorrhages, and can also be seen in 60-88% of the acute to late stages of cerebral FES [5,[10][11][12]. These correlate with the petechial cerebral hemorrhages observed on autopsy [13].…”

Section: Discussionmentioning

confidence: 99%

“…However, in retrospect, the "starfield" pattern seen on the MRI solidifies the diagnosis of FES, rather than a TMA. In cases of cerebral FES, a "starfield" pattern on diffusion-weighted MRI is seen, consisting of numerous punctuate foci in the white and grey matter, suggesting the presence of acute microinfarcts caused by the emboli [4][5][6][7]. Given the "starfield" pattern with microhemorrhages seen on our patient's MRI, and a cardiac emboli source ruled out by echocardiogram, it is likely that his neurologic abnormalities were due to cerebral FES rather than due to cerebral vaso-occlusion from a TMA.…”

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Cerebral fat embolism syndrome mimicking thrombotic thrombocytopenic purpura in a patient with hemoglobin SC disease

2016

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A 54-year-old man with hemoglobin SC disease and a history of substance abuse presented to the Emergency Department from a nursing home with 2 days of progressive weakness, shortness of breath, and lower back pain. He developed a fever, hypoxia, and tachycardia on the day of admission. He did not have any recent changes in medications, and his family as well as the nursing home staff denied any access to illicit drugs.The patient's clinical presentation raises concern for a vaso-occlusive crisis, specifically acute chest syndrome (ACS.) ACS should be suspected when a patient with a sickle cell disorder (SCD) experiences fever, chest pain, and dyspnea, with laboratory testing demonstrating the presence of a leukocytosis and an associated decrease in hemoglobin and platelets [1]. Supportive care with hydration, oxygen, pain control, and broad-spectrum antibiotics should be initiated while awaiting hematologic, metabolic, infectious, and radiographic workups.On arrival to the hospital, his vital signs demonstrated a temperature of 39.48C, a heart rate of 140 beats per minute, and a blood pressure of 159/120 mmHg. He was hypoxic and required supplemental oxygen. Physical exam was remarkable for altered mental status (AMS) and a rapidly decreasing level of consciousness, dry mucous membranes, dilated, slightly irregular, and nonreactive pupils, and a torsional nystagmus. A later review of records from his ophthalmologist documented the presence of iris atrophy as a complication of his sickle cell disease. Upon evaluation, the patient was intubated for airway protection.ACS and the systemic inflammatory response syndrome (SIRS) remain atop the differential diagnosis. Other important considerations include severe sepsis secondary to pneumonia or meningitis, illicit drug use, metabolic disturbances, heart failure, hypertensive emergency, and embolic diseases. In general, neurologic complications are seen in 11% of patients presenting with ACS, with 31% of those patients also developing a relative thrombocytopenia [2]. While there are many etiologies that might contribute to this clinical picture, one finding that stands out is his torsional nystagmus, indicating a dysfunction in his cerebellum or brainstem. With such a finding, a metabolic or ischemic cause for his acute encephalopathy becomes more likely.Initial complete blood count showed a decrease in hemoglobin from a baseline of 13-14 to 12.4 g/dl, a decrease in platelets from a baseline of 222 to 92 k/mm 3 , and serum WBCs of 11.8 k/ml. Peripheral blood smears showed moderate amount of target cells and sickle cells, a markedly elevated number of nucleated red blood cells (65 nucleated RBCs/100 WBCs), and a slight number of schistocytes.There also was evidence of neutrophil precursors with 3% neutrophil bands, 2% metamyelocytes, and 1% myelocytes. A comprehensive metabolic panel showed an elevation of serum creatinine from a baseline of 1.2 to 1.6 mg/dl and a total bilirubin of 3.4 mg/dl. His troponin I level was 0.96 ng/ml. Further hematological work-up demonstrat...

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“…The classical starfield appearance on diffusion-weighted MRI imaging represents cytotoxic edema due to fat emboli. A recent systemic review revealed that scattered cytotoxic edema is the most common image finding of acute CFES, present in 84.6 % patients [6].…”

Section: Discussionmentioning

confidence: 99%

Favorable Outcome of Cerebral Fat Embolism Syndrome with a Glasgow Coma Scale of 3: a Case Report and Review of the Literature

et al. 2014

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Prognosis of deep coma caused by cerebral fat embolism syndrome (CFES) is rarely reported. We present a case of fulminant CFES which was induced by long bone fracture, with a Glasgow Coma Scale (GCS) of 3/15. The brain magnetic resonance imaging (MRI) revealed abnormal spotty lesions scattered over both cerebral hemispheres and the posterior fossa. Thirty days later, the patient regained consciousness with a GCS of 15/15.

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Dynamic MR Imaging Patterns of Cerebral Fat Embolism: A Systematic Review with Illustrative Cases

Cited by 95 publications

References 24 publications

Clinics in diagnostic imaging (184)

Clinics in diagnostic imaging (184)

Cerebral fat embolism syndrome mimicking thrombotic thrombocytopenic purpura in a patient with hemoglobin SC disease

Favorable Outcome of Cerebral Fat Embolism Syndrome with a Glasgow Coma Scale of 3: a Case Report and Review of the Literature

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