Review Question - QID 218949

This patient presents with fat embolism syndrome after long bone fixation. The release of free fatty acids secondary to lipoprotein lipase activation has been implicated as one of the underlying etiologies of this condition (Answer B).

Fat embolism syndrome (FES) is diagnosed with the classic triad of respiratory distress, neurologic decline, and petechial rash 24-72 hours after traumatic injury. It more commonly occurs in males, aged 10-40 years, and in the setting of closed long bone fractures (particularly femoral shaft). The two presiding theories for FES involve (1) mechanical or (2) biochemical causation. The mechanical theory involves disruption of intraosseous blood vessels (shear forces with reaming) where intramedullary fatty marrow can easily enter the circulation and eventually create a mechanical embolus with focal ischemia. The biochemical theory involves fat emboli traveling to the lungs where it activates a high local concentration of lipoprotein lipase resulting in the release of free fatty acids and glycerol. The fatty acids are highly toxic to surrounding endothelial cells causing a massive influx of proinflammatory cytokines resulting in acute respiratory distress syndrome (ARDS). FES is likely a combination of both theories and the treatment involves supportive measures with respiratory support if needed.

Rothberg and Makarewich presented an overview of fat embolism and fat embolism syndrome with implications in orthopaedic surgery. They discuss that early fracture stabilization in stable trauma patients and slow advancement with fast revolutions on reamer advancement can collectively negate the production of fat emboli in the circulatory system. The authors conclude that the best treatment of FES is prevention by minimizing the modifiable risk factors.

Akhtar provided a similar overview of fat embolism highlighting its detrimental multi-system effects. They discuss that FES can appear almost identical to ARDS, which can be potentially life-threatening to the polytrauma patient with low physiologic reserve. They also highlight the decreasing incidence of FES with earlier fracture fixation protocols adopted by hospitals throughout the country. The author concludes that any cardiorespiratory and neurologic deterioration following orthopaedic trauma should bring fat embolism to the forefront of clinicians’ differential diagnosis.

Incorrect Answers:
Answer 1: Exposure of localized subendothelial collagen and tissue factor induce activation of the extrinsic and intrinsic coagulation cascades, respectively. Collectively, these cascades form blood clots that can result in pulmonary emboli with acute onset of dyspnea, tachypnea, and tachycardia.
Answer 2: Type 1 hypersensitivity reactions can result in sudden onset anaphylaxis secondary to an IgE mediated response. The acute respiratory collapse is not gradual with neurologic decline and a rash, as seen in this patient.
Answer 4: Tranexamic acid inhibits plasmin production, thus encouraging clot stabilization and decreasing perioperative bleeding. It has been shown to be safe and effective, even in orthopaedic trauma settings, without a significant increase in thromboembolic events.
Answer 5: Fat embolism syndrome and ARDS are nearly indistinguishable and many believe fat embolism syndrome is just one etiology for ARDS. In either case, both result in increased capillary permeability and DECREASED production of lung surfactant which exacerbates alveolar edema and contributes to collective respiratory failure.