Traumatic vs non-traumatic fat embolism
My first thought here was that both liposuction and long bone fractures involve tissue trauma, which allows fat particles to enter the circulation, whereas lipolysis in exercise is purely a biochemical process.
However, there are non-traumatic causes of fat embolism:
- Fatty Liver
- Acute or chronic pancreatitis
- Therapy with corticosteroid
- Infusion of fat emulsion
- Sickle cell disease
From Fat Embolism (Adebayo and Louisdon):
There are two theories of the pathophysiology of fat embolism.
Large fat droplets are released into the venous system. Elevation of the intramedullary from trauma or surgery leads to the release of fat into the venous sinusoids. From the venous system, these fat globules are deposited in the pulmonary capillary bed where they travel to the brain via the arteriovenous shunt.
According to this theory, the precipitating event, whether traumatic or nontraumatic, triggers a hormonal change. This leads to release of free fatty acid (FFA) and chylomicrons. The presence of acute phase reactants, such as C-reactive protein, causes the chylomicron to coalesce and migrate. Baker et al. attribute the development of fat embolism syndrome to FFA. Pneumocyte hydrolysis of fat particles generates FFA which migrate to other organs, causing multiple organ dysfunction syndromes. The biochemical theory helps to explain the development of fat embolism syndrome in nontraumatic patients.
Liposuction and long bone fractures are likely accounted for by the mechanical theory, due to trauma.
The non-traumatic causes listed above involve conditions that disrupt metabolic pathways, leading to release of free fatty acids and fat embolism.
However, biochemical lipolysis is a normal physiological response to exercise and does not seem to increase the risk of fat embolism.
I cannot find any reports of purely exercise-induced fat embolism. This case report demonstrates fat embolism triggered by exertion but two months after hip replacement surgery.