Fat embolism

Frequency estimated to be 3-4%.

The incidence is estimated to range from 0.54% in patient with an isolated femoral fracture to 1.29% in patients with multiple fractures.

Fat embolism syndrome develops after delay in primary bone reduction in fixation at twice the rate in the absence of such a delay.

Suspected that fat droplets are deposited into the pulmonary capillary beds and travel through arteriovenous shunts to the brain.

It is characterized by a clinical pattern that develops after an insult associated with the release of fat into the circulation.

It is most often observed following a traumatic injury, typically a long bone fracture of the leg.

Lodging of fat droplets produces local ischemia and inflammation in the microvasculature with release of inflammatory mediators, vasoactive amines and associated with platelet aggregation.

A second hypothesis for this process suggests it is caused by hormonal changes related to trauma and sepsis induced release of free fatty acids as chylomicrons.

Non-orthopedic causes are exceedingly rare and include pancreatitis, sickle cell disease,  alcoholic liver disease, bone marrow harvest or transplantation, and liposuction.

Liposuction is increasingly common cosmetic surgery.

With liposuction, rupture of small blood vessels may allow lipid micro fragments to reach the venous circulation and in some cases the arterial circulation with end organ injury.

Coronary artery occlusion caused by fat embolism after liposuction has been reported.

Chylomicrons can be coalesced by C reactive proteins elevated during stress.

In the presence of advanced age, multiple medical processes and decreased reserve have poorer outcomes compared to other patients.

May be related to trauma to long bones, pelvis or from surgical orthopedic procedures.

May be secondary to parenteral lipid infusions.

Associated with recent corticosteroid administration.

Patients typically present with multi organ dysfunction within 12 to 72 hours after the initial event.

Its classic triad of hypoxemia, neurologic abnormalities and petechiae occur.

Patients may manifest dyspnea and tachypnea due to respiratory failure.

Neurologic manifestations of fat embolus include: focal defects, confusion, lethargy, and ultimately coma.

fat embolism hematologic findings include: petechiae, thrombocytopenia, anemia, and DIC.

Patients with fulminant fat embolism may have right ventricular or biventricular heart failure, acute respiratory distress syndrome, shock, or death.

The diagnosis can be made often, on the basis of clinical recognition of appropriate predisposing insults, compatible symptomatology and physical findings supported by imaging and laboratory studies.

Chest x-rays in fat embolism may appear normal or show interlobular septal thickening, groundglass with nodular opacities, or diffuse bilateral infiltrates consistent with acute respiratory distress syndrome.

MRI of the brain can reveal diffuse punctate hyperintense lesion with a starfield pattern on the fusion weighted sequences.

On BAL sampling, staining of more than 30% of alveolar cells for fat strongly supports a clinical diagnosis.

Overall major criteria include: petechial rash, respiratory symptoms with abnormalities on imaging studies, and signs involving the CNS.

Minor criteria include: tachycardia fever, retinal changes due to fat with petechiae, renal abnormalities of anuria, lipiduria, or oliguria, acute thrombocytopenia, acute anemia, increased ESR, and fat globules in the sputum.

The primary treatment for fat embolism is supportive care.


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