Post-Traumatic Cerebral Fat Embolism

Post-traumatic fat embolism was first reported by Zenker in 1862, Von Bergmann reported the first clinical diagnosis of the fat embolism syndrome in 1873. Fat embolism has been associated with traumatic or non-traumatic disorders. Fat embolization after long bone trauma is probably common as a subclinical event. The diagnosis of fat embolism syndrome is based on the patient's history, is supported by clinical signs of pulmonary, cerebral, and cutaneous dysfunction, and is confirmed by the demonstration of arterial hypoxemia in the abscence of other disorders. Two different mechanisms cause fat to embolize: direct entry of deposit fat into the blood stream and agglutination of endogenous or exogenous plasma fat. MRI can detect a cerebral fat embolism with a higher sensitivity than cerebral CT. We report a case of post-traumatic cerebral fat embolism without pulmonary involvement, and we present a review of the literature. A 16-year girl had a traffic accident and pelvic bone fracture. Forty eight hours later severe trauma become stuporous without a focal neurological deficit. The patient received supportive therapy, and her condition improved throughout her hospital course. She was discharged with good condition after a 30-day hospital stay.

The Incidence of Myocardial Injury in Patients with Spontaneous Subarachnoid Hemorrhage(SAH) Using Cardiac Troponin I

BACKGROUND: More than 90% of acute stroke patients have measurable cardiovascular sequelae, but we have been often overlooked in formal discussions of treatment. If we estimate the incidence of myocardial injury in patient with spontaneous SAH, we may figure the possibility of cardiac dysfunction in such patients. This study was designed to investigate the incidence of myocardial injury in patients with spontaneous SAH using cardiac troponin I(cTnI). METHODS: A prospective single emergency center study was performed to determined preoperative incidence of unrecognized cardiac injury in patients suffering spontaneous SAH. We include the spontaneous SAH patients who underwent serum measurements of the cardic troponin I immediately upon admission last six month period. ECG, CK, CK-MB and myoglobin were also performed at admission. We excluded the spontaneous SAH patients who had past history of myocardial ischemia and ECG abnormality. RESULTS: Fifty-two patients(34 females, 18 males) with spontaneous SAH were studied prospectively. 18 patients(34.6% of the total study population) had cTnI level above 0.5ng/ml. ECG was performed in 52 patients and was abnormal in 15 of the 52 patients(28.8%). CONCLUSION: The measurement of cTnI has provided physicians with a myocardial marker that has a cardiac sensitivity for cardiac injury equal to that of CK-MB yet with greater specificity. So, cardiac troponin I is useful to estimate the incidence of myocardial injury in patients with spontaneous SAH. And we may estimate the possibility of cardiac dysfunction in such patients. This knowledge will hopefully aid in the care and improve the outcome.