Causes of post-embolism syndrome

So far, there have been no reported cases of death caused solely by cardiac fat embolism, and such changes in cardiac pathology have not been seen so far. However, if fat embolism syndrome really occurs, the resistance of the pulmonary vascular bed will increase, thereby increasing the load on the right heart, so the right heart will enlarge. The heart is deprived of oxygen and therefore damaged, and generally, blood spots may appear below the epicardium. So what is the cause of post-embolism syndrome? What is the performance?

Causes

Fat embolism syndrome is caused by fat emboli entering the bloodstream and blocking small blood vessels, especially the capillaries in the lungs, causing a series of pathological changes and clinical manifestations. Due to the different affiliations of fat emboli, their clinical manifestations vary.

The source, formation and destination of fat emboli:

1. The mechanical theory (exogenous vascular theory) was proposed by Gauss in 1924. He believed that fat enters the bloodstream from the bone marrow through the torn veins at the fracture site, and then mechanically blocks the small blood vessels and capillary beds in the lungs. However, three conditions must be met to cause embolism:

(1) The adipocyte membrane ruptures, producing free lipids.

(2) Damaged and open veins.

(3) Hematoma forms at the site of injury or fracture, and local pressure increases, causing fat to enter the ruptured vein.

2. Chemical theory (endovascular theory) Since there are patients with fat embolism syndrome without bone damage in clinical practice, this situation cannot be explained by the above theory. Therefore, Lelman and Moore proposed the chemical theory in 1927. They believe that this is because certain factors hinder the natural emulsification of blood lipids, causing chylomicron particles to agglomerate with each other to form larger lipid droplets, thereby blocking small blood vessels; or in a state of traumatic stress, the sympathetic nervous system is excited, and under the action of neuro-endocrine effects, the secretion of catecholamines increases, activating adenine cyclase, increasing 3,5-cyclic adenosine monophosphate, and then activating lipase in adipose tissue, causing fat mobilization in the body.

3. Where fat emboli go

(1) When the diameter of the fat embolus is small, due to its plasticity in the blood vessels, it can directly enter the systemic circulation through the pulmonary vascular bed, deposit in tissues and organs to form systemic fat embolus, or be excreted in the urine through the glomeruli.

(2) Fat emboli can be phagocytosed by alveolar epithelial cells and fall off in the alveoli to be excreted with sputum.

(3) Sevitt believed that fat embolus could enter the systemic circulation through the right atrium, through the patent foramen ovale, or through the communicating branches of the pulmonary-bronchial precapillaries.

(4) Peltiers believed that fat emboli with larger diameters would inevitably remain in the pulmonary vascular bed and undergo hydrolysis under the action of local lipase to produce glycerol and free fatty acids.

There are many parts of the body where fat embolism may occur, such as fat in the bone marrow entering the human blood circulation, and fat in the lung capillaries forming fat embolism, which is a pathological change in the lungs. There may also be lesions in the brain, that is, the white matter of the brain can be seen directly with the naked eye, and bleeding may also occur in the cerebellum. In addition, there may be lesions in other parts of the body, such as the eyes, so you must pay attention to your body.