INTRODUCTION: Fat embolism syndrome (FES) secondary to the release of fat into the pulmonary and systemic circulations, classically manifests with the trio of progressive respiratory insufficiency, deteriorating mental status and petechial rash. These symptoms develop 12-72 hours after trauma and are often associated with a benign course requiring only supportive care. Mortality from FES ranges from 5-15% due to cardiopulmonary collapse despite intensive supportive care. We report the case of a patient admitted with traumatic femur and olecranon fracture, who, after intramedullary fixation, developed FES with cardiopulmonary collapse and was subsequently treated with inhaled nitric oxide.
CASE PRESENTATION: A 33-year-old man with no significant past medical history was brought into the hospital after a motor vehicle accident (motorcycle versus auto) complaining of right elbow and leg pain. Initial radiographs confirmed a displaced right mid-femur fracture and right olecranon fracture. Chest radiograph on admission showed clear lungs and the patient was breathing at a rate of 20 per minute with an oxygen saturation of 98% on room air. On hospital day #2, the patient underwent an open reduction and internal fixation of his complex right olecranon fracture. On hospital day #3, he returned to the operating room for intramedullary fixation of the right femur fracture. On the following day, a “Rapid Response” was called for respiratory distress, and the patient was placed on 100% supplemental oxygen and transferred to the intensive care unit. Repeat chest radiograph showed worsening aeration with bilateral parenchymal lung opacities. Computed tomography with pulmonary artery angiography showed no evidence of pulmonary embolus but patchy ground-glass opacities and interlobular septal thickening. Subsequent transthoracic echocardiogram showed signs of acute right heart strain with an estimated right ventricular systolic pressure of 75mmHg. The patient's condition rapidly deteriorated with acute mental status changes marked by hallucinations, followed by worsening hypoxemia and hypotension. He was emergently intubated and started on multiple vasopressor/inotropic infusions for refractory hypotension. Given the patient's impending cardiopulmonary arrest, a trial of inhaled nitric oxide was started. The patient showed immediate improvement in both oxygenation and hemodynamics and he was gradually weaned off all vasopressor/inotropic infusions over the next 48 hours. He was weaned off inhaled nitric oxide over the course of a week and was subsequently extubated, transferred out of the ICU and eventually discharged home approximately six weeks after his initial presentation.
DISCUSSIONS: FES is a known complication of long bone trauma as well as intramedullary nailing, secondary to increased pressure in the medullary cavity forcing fat, marrow and bone fragments into the venous channels. The exact pathophysiologic mechanism of FES is unknown, but it is thought to be secondary to mechanical obstruction of the pulmonary microvasculature by fat globules as well as direct inflammatory and endothelial damage by free fatty acids. Inhaled nitric oxide therapy has been postulated to be helpful in multiple pulmonary conditions with elevated right-sided pressures including pulmonary embolism and acute respiratory distress syndrome, by selectively vasodilating the pulmonary vasculature as well as redistributing pulmonary blood flow to ventilated parts of the lung. In this case, where the patient was acutely hypotensive on multiple vasopressor/inotropic medications with signs of right heart strain on echocardiogram, inhaled nitric oxide was used as a successful rescue therapy.
CONCLUSION: In near fatal cases of FES with severe hypoxemia and hypotension not responding to conventional respiratory and hemodynamic support, inhaled nitric oxide may have utility as a rescue therapy. Further research is warranted.
DISCLOSURE: Tomio Miyai, No Financial Disclosure Information; No Product/Research Disclosure Information