Abstract:Nearly all long-bone fractures are accompanied by some form of fat embolism. The rare complication of clinically significant fat embolism syndrome, however, occurs in only 0.9-2.2% of cases. The clinical triad of fat embolism syndrome consists of respiratory distress, altered mental status, and petechial rash. Cerebral fat embolism causes the neurologic involvement seen in fat embolism syndrome. A 19-year-old African-American male was admitted with gunshot wounds to his right hand and right knee. He had diffus… Show more
“…Most patients with CFE show complete neurological recovery despite initial cerebral dysfunction and prolonged coma. (6,8,14) This is also true in our patient, who was discharged from the hospital one month later without any neurological sequelae.…”
Fat embolism to the lungs and brain is an uncommon complication following fractures. Few reports with descriptions of computed tomographic (CT) findings of emboli to the brain or cerebral fat embolism are available. We report a case of cerebral fat embolism following multiple skeletal fractures and present its CT findings here.
“…Most patients with CFE show complete neurological recovery despite initial cerebral dysfunction and prolonged coma. (6,8,14) This is also true in our patient, who was discharged from the hospital one month later without any neurological sequelae.…”
Fat embolism to the lungs and brain is an uncommon complication following fractures. Few reports with descriptions of computed tomographic (CT) findings of emboli to the brain or cerebral fat embolism are available. We report a case of cerebral fat embolism following multiple skeletal fractures and present its CT findings here.
“…Characteristic findings on diffusion-weighted and susceptibility-weighted MR images provide valuable supporting evidence for the diagnosis of cerebral fat embolism syndrome. The starfield pattern, which consists of innumerable bright punc-tate foci of restricted diffusion against the dark background of brain parenchyma, has a limited differential diagnosis including diffuse axonal injury; cardiogenic, septic, or fat emboli; vasculitis; and minute hemorrhagic metastases (11)(12)(13)(14). In cerebral fat embolism syndrome, this pattern is thought to represent numerous sites of cytotoxic edema related to hemorrhage and infarction due to cerebral vessel occlusion by fat emboli.…”
Section: Discussionmentioning
confidence: 99%
“…In a number of reported cases, patients with cerebral fat embolism due to trauma experienced neurologic changes that were transient and eventually followed by a full recovery (11)(12)(13)15). In patients with sickle cell disease, the clinical course of fat embolism is more often fulminant.…”
A 57-year-old African American woman with a history of sickle cell b-thalassemia presented to the hospital with a 3-day history of chest and back pain unresponsive to oxygen and analgesic therapy. Her medical history included multiple painful crises due to sickle cell-induced vaso-occlusion, multiple blood transfusions, hypertension, and diabetes mellitus. The evening of her admission, she developed a fever and hypotension, and a sepsis evaluation was initiated. She was treated with empirical antimicrobial agents and received oxygen, a red blood cell transfusion, and medications for pain. Two nights later, she became mildly confused. Unenhanced computed tomography (CT) of the head was performed. The following morning, magnetic resonance (MR) imaging of the brain and MR angiography of the head and neck were performed. Later that day, the patient's hypotension worsened, and she became difficult to arouse. Intubation was performed to protect her airway, and she was transferred to the intensive care unit. Thrombocytopenia was diagnosed, and the prophylactic antithrombotic therapy initiated at admission was temporarily withheld. Multiple studies for infectious agents returned negative results. The patient's status continued to deteriorate with the development of respiratory failure, renal failure, and ischemic hepatitis ("shock liver"). Sedation was discontinued, and 48 hours later, with the patient still unresponsive, comfort measures were instituted. The patient died on the 10th day of her hospitalization.
“…Many researchers have reported that diffusion weighted cranial MRI is a useful adjunct in recognizing cerebral FES. [9][10][11] In our patient, cranial MRI was consistent with cerebral involvement. He had many scattered small lesions of limited diffusion within both cerebral hemispheres, basal ganglia, centrum semiovale and corpus callosum (Figure 1).…”
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