What Causes Fat Embolism Syndrome?

Sickle Cell Anemia

A sickle cell anemia patient may develop fat embolism syndrome as a complication of their disease. Fat embolism syndrome develops after the affected individual has a vaso-occlusive crisis, which occurs when the sticky, malformed sickle cells obstruct small blood vessels, producing cellular injury from oxygen deprivation. Due to a vaso-occlusive crisis, bone infarction can occur or the death of bone marrow cellular elements due to ischemia or lack of blood flow. Inside the bone, the fat globular cellular material leftover from this process can diffuse into the sinusoid veins that run through the bone. Once in the venous circulation, these fat globules trigger an inflammatory response involving the accumulation of chylomicrons, fibrin, low-density lipoproteins, platelets, and other blood elements. It is thought this congregation of materials triggered by bone marrow fat globules forms the fat emboli that cause damage to the affected individual's lungs and may enter the systemic circulation. Right to left shunts or a septal defect in the patient's heart can allow the perfusion of the fat emboli into the arterial bloodstream. The fatty emboli have the potential to become lodged in the vessels of critical organs such as the brain, skin, and return to the lungs. Obstruction of blood flow to tissues of these organs by the emboli is what produces the symptoms of fat embolism syndrome.

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