Supportive Medical Care
Specific medical therapy for fat embolism and fat embolism syndrome (FES) does not exist at this time, and supportive measures have not been tested in adequate randomized, controlled trials. Treatments such as heparin, dextran, and steroids have not been shown to help reduce morbidity and mortality, but methylprednisolone given prophylactically may have beneficial effects. [28]
Current care of patients with fat embolism is aimed at supporting physiologic derangements and includes the following:
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Maintenance of adequate oxygenation and ventilation with open lung strategies such as the use of airway pressure release ventilation (APRV)
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Maintenance of hemodynamic stability
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Administration of blood products as clinically indicated
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Hydration
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Prophylaxis of deep venous thrombosis and stress-related gastrointestinal bleeding
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Nutrition
Judicious use of crystalloids, colloids, and diuretics is necessary; volume depletion may precipitate shock and organ dysfunction, but volume overload may worsen the hypoxia.
Continuous pulse oximetry monitoring in at-risk patients (eg, patients with long-bone fractures and multiple trauma), may facilitate early detection of desaturation, allowing prophylactic administration of oxygen and possibly steroids, thereby decreasing the chances of hypoxic injury and systemic complications of FES. [29]
At-risk patients should be placed in a monitored setting, and appropriate services should be consulted. If a patient has sustained major traumatic injuries, transfer to the nearest trauma center with 24-hour in-house surgical intensive care is essential.
Surgical Management
Early stabilization of long-bone fractures is recommended to minimize bone marrow embolization into the venous system. [30] Rigid fixation within 24 hours has been shown to yield a fivefold reduction in the incidence of FES. [9]
Appropriate surgical technique, particularly in reaming or nailing the marrow, may help reduce the volume of fat embolization. Utilization of a vacuum or venting during reaming has been shown to decrease the incidence of fat embolization. [9]
Prophylactic placement of inferior vena cava filters may help reduce the volume of fat that reaches the heart in at-risk patients.
Prevention
Several studies performed in the late 1970s attempted to show that use of methylprednisolone as a “membrane stabilizer” would reduce the incidence of FES, but follow-up work has yet to reproduce these findings. [31, 32]
A meta-analysis of randomized trials studying corticosteroid use as a preventive adjunct in patients with long-bone fractures uncovered 104 studies, of which only seven met the authors' eligibility criteria for analysis. [33] Although the pooled analysis of 389 patients found that corticosteroids reduced the risk of FES by 78%, the authors warned that these studies were of poor quality and held to standards of the 1970s. [33, 34]
The use of heparin has been shown to reduce the degree of pulmonary comprise and intravascular coagulation despite the risk of hemorrhage and intravascular lipolysis; however, this practice has not been shown to yield a statistically significant benefit.
Ethanol (which decreases lipolysis) and dextrose (which decreases free fatty acid mobilization) have been used as prevention modalities, but at present, there is little to no evidence to support the use of these agents in FES. [34]
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Hematoxylin-eosin stain of section of lungs showing blood vessel with fibrinoid material and optical empty space indicative of presence of lipid dissolved during staining process. This 55-year-old woman died of massive fat embolism after developing pancreatitis due to endoscopic retrograde cholangiopancreatography. Image courtesy of Wikimedia Commons. Originally published in Kanen BL, Loffeld RJLF. Pancreatitis with an unusual fatal complication following endoscopic retrograde cholangiopancreaticography: a case report. Journal of Medical Case Reports. 2008;2:215.
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Frozen section of lung stained with oil red O showing multiple orange red fat globules of varying sizes in septal vasculature. Image courtesy of Dr AVC Rao, Senior Lecturer in Pathology, The University of the West Indies at St Augustine, Trinidad and Tobago. Originally published in Journal of Orthopaedics (http://www.jortho.org/2008/5/4/e8/).
