Cerebral fat embolism syndrome after long bone fracture due to gunshot injury
A 20-year-old male patient was admitted to the emergency department with sudden change in consciousness and muscle contractions after 1 day follow-up in a hospital for long bone fractures of femur and tibia due to gun-shot injury. On admission, he had generalised tonic clonic seizures and his Glascow Coma Scale was seven with localization of painful stimuli, incomprehensible muttering, and no eye opening. In the physical examination, blood pressure was 130/80 mmHg, pulse was 128/min, breath rate was 22/min and body temperature was 38°C. His pupils were isocoric and bilaterally responsive to light. He had decorticated posture in response to noxious stimulus. No lateralising motor deficit was found. There was a long bone splint on the left lower extremity. Examination of other systems were normal. The patient was intubated and respiration was supported by mechanical ventilation.\nThe results of hematologic and biochemical parameters of the patient with the range of normal values of our laboratory in the paranthesis were as follows at first admission: Hemoglobine: 11.1 gr/dl (13,6-17,2), platelet count: 75000/μl (156000-373000), glucose: 189 mg/dl (70-110), aspartate aminotransferase (AST): 143 IU/L (0-46), alanine aminotransferase (ALT): 53 IU/L (0-46), and creatine phosphokinase (CPK): 7866 IU/L (35-195). Other biochemical findings and blood gas analysis were normal. There were no abnormalities on a postero-anterior chest X-ray cervical and thoracic computed tomography (CT). An initial CT of the head was unremarkable for intracranial abnormalities. Magnetic resonance imaging (MRI) was performed diffusion weighted MRI trace images with a 2 mm slice gap, 5 mm slice thickness, Echoplanar imaging (EPI) sequence type, b value of 1000 mm/s2, signal intensity dots on a dark background. This resulted in a “starfield” appearance of the cerebral hemispheres [Figures and ]. Diffusion coefficient map slice of the patient revealed the hypointense punctuate to lesions in centrum semiovale and periventricular regions [Figures and ].\nAn electroencephalogram was performed and diffuse bioelectrical delay on the right hemisphere was found. With the above findings, the diagnosis of the case was cerebral diffuse FES. Antiepileptic therapy with phenytoin (2 × 150 mg) and low molecular weighted heparin therapy with enoxaparin sodium (2 × 4000 U) were administered.\nThe patient had hypoxemia and the arterial blood gas analysis revealed PaO2 as 65 mmHg, and saturation of arterial oxygen as 82% requiring mechanical ventilation, disturbance of conscioussness and sudden drop in hemoglobin and platelet count. Hemoglobin was 7.1 gm/dl and platelet count had decreased to 53000/μl at that time. The patient was rehydrated and administered with sulbactam/ampicillin (4 × 1 g i.v.) for fever and a possible infection due to open injuries. Three units of erhthrocyte suspension and 3 units of fresh frozen plasma were given to patient to replace blood loss. On the 5th day of hospitalization, the level of consciousness of the patient improved and mechanical ventilatory support could be discontinued.\nThe bone fractures were multi-fragmental in left tibia with articular defects. The fragments were inernally fixed. He subsequently had uncomplicated recovery and was discharged home after 27 days of hospitalization.