CT diagnosis of fat embolism

Eventual bronchoalveolar lavage (BAL) yielded 63% lipid containing macrophages and transbronchial biopsy revealed diffusely damaged alveoli, consistent with FE.18,19 Trauma patients and patients undergoing orthopedic procedures (especially total hip arthroplasty, total knee arthroplasty, and intramedullary nailing of the femoral shaft) are at increased risk for FE, a relatively rare diagnosis that carries a mortality rate of up to 20%.13,20 The diagnosis of FE is multifactorial, and requires identification of a distinct radiopathologic correlation in a specific clinical setting.16,17,21 The underlying pathophysiological mechanism responsible for the radiographic manifestations of FE begins with bone injury, resultant increased intramedullary pressure, and introduction of marrow fat fragments into the circulation through disrupted vessels.22 Once lodged in the pulmonary vasculature, hydrolysis of these fragments produces free fatty acids that activate a local inflammatory response and are directly toxic to the lung parenchyma.22 The temporal nature of these events and resultant chemical pneumonitis with secondary damage (microhemorrhage, edema) account for the classic onset of multiple, diffuse, bilateral opacities, and interlobular septal thickening on CT 1 to 3 days after a traumatic event or intervention.17,23,24 These findings often resemble pulmonary edema without pleural effusion or cardiomegaly, demonstrate a predilection for the basilar and peripheral lung regions, coincide with the appearance of symptoms, and have been shown to positively correlate with clinical severity.21,23 Clinically, patients present along a spectrum of severity, ranging from subclinical fat embolism (tachycardia, tachypnea, fever) to fulminant acute fat embolism syndrome (cor pulmonale, neurological signs, [confusion, stupor, coma], and diffuse petechiae).18 Hypoxemia and respiratory alkalosis are early indicators of FE.