RIGHT VENTRICULAR SUPPORT IN FAT EMBOLISM SYNDROME: A ROLE FOR PULMONARY VASODILATORS AND EXTRACORPOREAL MEMBRANE OXYGENATION?

Abstract

SESSION TITLE: Clinical Conundrums in ECMO SESSION TYPE: Fellow Case Reports PRESENTED ON: 10/20/2019 01:00 pm - 02:00 pm INTRODUCTION: Pulmonary fat embolism (PFE) is a common phenomenon in the setting of orthopedic trauma. Of all patients with PFE, only a minority go on to develop the more catastrophic fat embolism syndrome (FES) that is characterized primarily by hypoxemia, altered mentation, fever, and petechiae. Thought to occur as a result of mechanical embolization of fat from the bone marrow coupled with a dysregulated inflammatory response, FES has a mortality of up to 20% with clinical decompensation primarily driven by acute cor pulmonale and RV failure [1]. CASE PRESENTATION: A 39-year old male with a history of GERD presented to the ED after suffering a traumatic femur fracture and went for operative fixation on the same day. The next day, he decompensated with fever (100.9F), tachycardia (140-150 bpm) and hypoxemia (SpO2 85% on RA). Exam was notable for moderate respiratory distress, an S3 gallop, cool extremities, and bilateral lower extremity edema. Labs were notable for leukocytosis (17,000 /mm3), hemoglobin 11.3 gm/dL, normal renal and liver function, and an A-a gradient of 192mmHg (45% FiO2) with an increased pulmonary shunt fraction. Troponin and BNP were mildly elevated. CTA demonstrated an enlarged RV, dilated PA, and bilateral interstitial infiltrates with no pulmonary embolus. Lower extremity US was negative for DVT. TTE showed a hyperdynamic and under-filled LV as well as a markedly dilated RV with severely depressed systolic function and an estimated RVSP 75 mmHg. His condition worsened, with RHC demonstrating severely elevated mPAP (60mmHg) and PVR (7.4 Wood units). He continued to deteriorate requiring increasing high flow oxygen support. The decision was made to cannulate for VA-ECMO and initiate on inotropes as well as pulmonary vasodilators. After 7 days, he was decannulated and continued on vasodilator therapy. At 1-month follow-up, RV function had normalized, and vasodilator therapy was discontinued. DISCUSSION: Management of FES in this patient was extrapolated from treatment algorithms for massive thrombotic PE with cor pulmonale, including use of extracorporeal support and pulmonary vasodilators. Treatment of FES remains relatively under-investigated and is based on data from case reports and case series. Interventions may include heparin, aspirin, corticosteroids, and albumin, but the quality of evidence supporting these therapies is low [2]. At present, there are no published descriptions of pulmonary vasodilator use in patients with FES. CONCLUSIONS: ECMO and pulmonary vasodilator therapy may help support patients with severe respiratory failure due to FES [3]. Further research into these modalities is warranted. Reference #1: Fabian TC, Hoots AV, Stanford DS, Patterson CR, Mangiante EC. Fat embolism syndrome: prospective evaluation in 92 fracture patients. Crit Care Med. 1990;18(1):42-46. Reference #2: Bederman SS, Bhandari M, McKee MD, Schemitsch EH. Do corticosteroids reduce the risk of fat embolism syndrome in patients with long-bone fractures? A meta-analysis. Can J Surg J Can Chir. 2009;52(5):386-393. Reference #3: Webb DP, McKamie WA, Pietsch JB. Resuscitation of fat embolism syndrome with extracorporeal membrane oxygenation. J Extra Corpor Technol. 2004;36(4):368-370. DISCLOSURES: No relevant relationships by Samuel McElwee, source=Web Response No relevant relationships by Takudzwa Mkorombindo, source=Web Response No relevant relationships by Raymond Wade, source=Web Response No relevant relationships by Keith Wille, source=Web Response