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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Osteomyelitis

An individual's osteomyelitis may cause them to develop fat embolism syndrome as a complication of their condition. Osteomyelitis describes the infection or inflammation of bone marrow or bone. This type of inflammation or infection is caused by a pathogenic infection entering the bone from the bloodstream or direct injury. When this process happens, immune components like neutrophils are summoned to the bone to try and eradicate the causative pathogen. If the infection overcomes the neutrophils in the bone, these dead cells begin to build at the infection site. This buildup can obstruct the flow of blood to the tissues and can result in bone death. While the exact mechanism has not been pinpointed, the development of fat emboli in affected individuals is known to be associated with the effects of elevated c-reactive protein. The liver produces and releases this protein in response to inflammation caused by numerous processes, including osteomyelitis and its associated bone tissue damage. C-reactive protein has a high potential to cause clumping or congregation of low-density lipoproteins, chylomicrons, and liposomes of nutritional fat compounds. It is an excessive provocation of this inflammatory process that causes the formation of fat emboli in the venous capillaries traveling to the lungs, producing symptoms of fat embolism syndrome.

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