Teaching Case

A 64-year-old female was admitted to the emergency department for multiple trauma. The neurologic, pulmonary and abdominal examination was unremarkable. The patient was hemodynamically stable. Plain-film radiography showed a fracture of right femur. Abdominal CT revealed multiple fractures in pelvis and a fat density image measuring 1 cm into the right femoral vein.

Noteworthy items in the patient's medical history included dyslipemia, deep vein thrombosis in lower limbs, with pulmonary thromboembolism and laparoscopic cholecystectomy. Neurologic, pulmonary and abdominal examination was unremarkable. The patient was hemodynamically stable. Plain-film radiography showed a fracture of right femur. There was a small focus of subaracnoid hemorrhage on cranial CT. Abdominal CT only revealed multiple fractures in the pelvis and a fat density image measuring 1 cm into the right femoral vein that was diagnosed as fat embolism [1, 2]. The patient was admitted to the intensive car unit, where external fixation was applied to improve the stability of the femoral fracture as the insertion of an intramedullary pin was considered unfeasible because of the fractured rami. Follow-up US of the right femoral vein showed a hyperechogenic tubular intravascular image that had clearly increased in size with respect to the previous CT examination; at this point in time, the embolism measured 6 cm and extended from the level of the saphenofemoral junction and into the superficial femoral vein. Another CT examination was confirmed the US findings and determining that it consisted entirely of fatty tissue and did not correspond to a possible fibrin thrombus forming over the initial fat embolism. A temporary filter was placed in the vena cava and the patient underwent vascular surgery with removal of the intraluminal material. Histological study of the material removed found a thrombus formed by fibrin-lined adipose tissue. The patient evolved favourably and the vena cava filter was withdrawn one month later.

Fat embolism occurs in nearly 90% of patients after long-bone or pelvis fractures; however, it is usually asymptomatic. It has also occurred in association with non-traumatic conditions [3]. Only about 4% of patients develop Fat Embolism Syndrome (FES), which sometimes leads to adult respiratory distress syndrome and multiple organ failure. The mortality rate of FES is 10-33%. FES is a clinical diagnosis that is likely to be missed. The signs of FES include persistent tachycardia, tachypnea, dysnea and hypoxia due to ventilation-perfusion abnormalities12-72 hours after injury, fever, petechial over the upper body, subconjuntival and oral hemorrhages and neurological disfunction. Laboratory findings are increase in pulmonary shunt fraction alveolar-to-arterial oxygen tension difference, hypocalcemia, anemia, thrombocytopenia and hyofibrinogenemia; however, these are non-specific [4, 5]. The pathophysiology of FES remains unclear [6, 7, 8]. Two major theories have been proposed. The biochemical theory suggests that hormonal changes caused by trauma induce systemic release of free fatty acids as chylomicrons. Chylomicrons show calcium- dependent agglutination by C-reactive protein which directly affects the pneumonocytes. This theory helps to explain nontraumatic forms of FES. The mechanical theory holds that bone marrow contents enter the venous system through intramedullary veins damaged by trauma. Fat droplets are deposited in the pulmonary capillary beds and may travel to systemic circulation. The imaging work-up can include chest radiography, head CT, ventilation/perfusion scintigraphy, transcranial Doppler US and transesophageal echocardiography; however, the findings are non-specific [9]. Abdominal CT can demonstrated intravenous fat emboli on rare occasions. To our knowledge, there are only two reports in the literature that describe this finding. In the present case, CT not only was able to demonstrate the presence of fat embolism in the femoral vein but also the increase in size. Early immobilization of long-bone fractures have been reported to reduce the amount of intramedullary fat released into the venous flow. In our patient, the impossibility of fixing the fracture of the femur with an intramedullary pin probably contributed to a degree of movement of the fragments and the continued release of intraosseous fat that was deposited in the initial embolism, increasing its size. The treatment of trauma patient with long-bone and/or pelvis fractures with FES or fat embolism consists of definitive fixation of the fractures, the prophylactic administration of heparin, respiratory support, correct hydratation, and monitoring the patient [10, 11, 12]. The definitive treatment in our patient was femoral venotomy with the removal of the emboligenic material. Histological examination demonstrated the presence of intravenous fatty material surrounded by fibrin, and a newly formed endothelium lining the fibrin in a reparative attempt. US is highly sensitive in the diagnosis of venous thrombosis but non-specific. Both, fatty and fibrin emboli are hyperechogenic at US. The CT demonstration of intravenous fatty material in an asymptomatic traumatic patient is very useful alerting clinicians to the potential risk of FES and enabled appropriated action to be undertaken. In our patient, the growth of the embolism led to the placement of a temporary filter of vena cava.