Fat Embolism Syndrome (FES)
Maxime J-M Coles MD, FICS, FRCS
Orthopedic Surgeon and Traumatologist

For long time Orthopedic Traumatologists were suspicious of the fact that every fracture of long bone produces a leakage of fat in the blood stream, which at time can cause morbidity.  The last decade 2002-2011 was declared The Bone and Joint decade by George W Bush and Resources were allocated to research on Trauma.
The Orthopedist clinician / scientist play an important role in bridging the essential links between basic Sciences and the development on new therapy. Fat Embolism Syndrome (FES), first described in 1873 may require a high level of suspicion to be diagnosed.  It is most commonly associated with long bone and pelvic fractures, more often in closed than open injuries. A patient with one long bone fracture has 3% chances to develop FES while the one with bilateral femur fractures may develop the syndrome in 33 % of the cases. It is rarely seen in children and adolescents. FES can be fatal in up to 15% of the cases.
Generally, 24 to 72 hours after a significant trauma involving long bones fractures, symptoms related to the dissemination of fat in the bloodstream can manifest, usually coming from the fat marrow or the adipose tissue or through the production of fat toxins (Chylomicrons or infused lipids). Many studies have demonstrated the passage of echogenic fatty material during orthopedic procedures creating a micro-embolism (venous System) or a paradoxical embolism ( foramen ovale to the arterial circulation ).
The classic symptoms of FES include Tachypnea, Tachycardia, Hypoxemia and Dyspnea as early findings.  Mental status changes and confusion state will follow with occasionally seizures disorders but those signs are transient and fully reversible. Finally Petechial rashes (pathognomonic sign) may be the last part of the triad in almost half of the time around the sub-conjunctiva, neck, anterior chest, axilla due to the occlusion of the dermal capillaries by fat. Some minor signs like Scomata ( Purtscher’s Retinopathy), lipiduria and myocardial depression can also be present.
Chest X-Rays are often in the normal limits, or can reveal air space disease due to edema or alveolar hemorrhage. Ventilation/Perfusion scans may demonstrate mottled pattern of sub-segmental perfusion with a normal ventilator pattern. CT scan will show a ground glass opacification with interlobar septal thickening. MRI of the brain may reveal high intensity signal on T2 signal.
It is a misconception to believe that finding fat globules in the sputum, urine, blood drawn will necessary confirm the diagnosis of FES because some studies have shown such with 50% of patients with fractures in general. There is evidence that bronchio-alveolar lavage can detect and diagnose FES.
FES can be prevented with early immobilization of long bone fractures and operative stabilization. Intra-osseus pressure during orthopedic procedures can be monitored by the use of reamers with venting holes or by avoiding cement fixation of the prosthesis.  Finally, prophylactic corticosteroids althrough controversial has been used in high risk patients at a low regimen 1.5mg/kg IV each 8 hours for six doses.
The treatment of FES is supportive with Intubation and Ventilation under high positive and respiratory pressure levels. Risk of FES is markedly decreases if fractures stabilization can be done in the 24 hours although major complications can also arrive when excessive reaming and fracture stabilization itself is performed. Most patients with FES will recover.
A syndrome associated to the embolization of the Silicone is also identical to FES. Other conditions like soft tissue injuries, burns, liposuction and bone marrow transplant are known to inject fatty substances in the bloodstream. Diseases unrelated to trauma like Pancreatitis, Diabetes Mellitus, Sickle cell disease, Lipid infusion, Bone tumor Lysis or alcoholic liver disease can mimic the same situation.
Similar clinical findings are found in Adult Respiratory Distress Syndrome (ARDS) which often is complicated by a chest injury so, it is better to wait for 24 to 48 hours prior to stabilize the long bone fractures. Thoracic injury and Hypovolemic shock will complicate the picture, necessitating more mechanical ventilation because of the loss of lung compliance. Tachycardia, Tachypnea, Hypoxemia will be present. In spite of the supportive ventilator management, the mortality can reach easily 50%. It is still debatable to believe that early fixation of long bone fracture can be beneficial in the survival and in the less chance of ARDS.
Some clinical findings can be as well seen in Pulmonary Thromboembolism with chest pain, low grade temperature, mental changes, tachypnea, tachycardia, hypoxia. Low molecular Heparin will be used to to keep the INR between 2 and 3 followed by warfarin for 3 months.

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