Thromboembolism and PE
The most frequent scenario of the pathology is the detachment of a thrombus or its fragment (tail, body). The source can be veins, arteries, or heart chambers.
A special place is occupied by pulmonary embolism (PE). Risk groups include immobile patients, individuals with malignant neoplasms, and cardiovascular diseases.
- Sources: most often, thrombi originate from deep veins of the lower extremities and the pelvic adipose tissue. Less frequently from hepatic veins, the inferior vena cava, or the right heart chambers.
- Thanatogenesis (causes of death): death occurs not so much due to mechanical lumen occlusion (acute right ventricular failure) as due to the pulmonocoronary reflex. The thrombus irritates receptors in the intima of the pulmonary trunk, triggering a reflex spasm of the coronary arteries and cardiac arrest.
The consequences depend on the caliber of the vessel. Small emboli cause a hemorrhagic pulmonary infarction, while a massive occlusion leads to collapse (acute drop in blood pressure). If multiple thrombi disseminate into the systemic circulation (e.g., in endocarditis or myocardial infarction), thromboembolic syndrome develops.
Exogenous Embolisms
Sometimes the vessel lumen is blocked by substances entering from outside or altering their physical state:
- Air embolism: occurs during trauma to large neck veins (due to negative pressure), gaping uterine veins after placental detachment, pneumothorax, or medical errors (injections, infusions). Air accumulates in the right heart chambers, giving the blood a foamy appearance.
- Gas embolism: associated with rapid decompression (in divers, during airplane depressurization). Gases dissolved in the blood (nitrogen, less commonly helium) transition into a gaseous state due to pressure drop. This is the basis of decompression sickness. It also occurs as a complication of anaerobic gangrene.
- Foreign body embolism: entry of shrapnel, fragments of medical catheters, or particles of eroded calcified atherosclerotic plaques into the bloodstream.
Endogenous Non-Thrombotic Embolisms
The body itself can become a source of dangerous particles during severe trauma or disease:
- Fat embolism: fat droplets enter the bloodstream during fractures of long tubular bones, crushing of adipose tissue, severe fatty liver disease, or accidental intravenous administration of oil solutions. In the lungs, they cause hemodynamic disorders and pneumonia, while penetrating into the systemic circulation, they damage the brain and kidneys. A small amount of fat may emulsify and resolve spontaneously.
- Cellular (tissue) embolism: circulation of tumor cells (the basis of metastasis), amniotic fluid in laboring women, or destroyed tissues in newborns with birth trauma. It threatens pulmonary vessel spasm, heart failure, and disseminated intravascular coagulation (DIC).
- Microbial embolism: clusters of bacteria, fungi, or parasites (Alveococcus) during septicopyemia or purulent melting of a thrombus. It leads to multiple necroses and metastatic abscesses.
Dynamics of Emboli Movement
The direction of particle movement determines which specific organ will be damaged. Three pathways are distinguished:
- Orthograde (antegrade): classic movement along the normal blood flow. Most common.
- Retrograde: movement against blood flow. Occurs if a foreign body has a high mass, or during reverse lymph flow (such as retrograde lymphogenic metastasis in gastric cancer).
- Paradoxical: transition from systemic veins to arteries (or vice versa), bypassing the pulmonary filter. Possible only with anatomical cardiac septal defects (patent foramen ovale) or the presence of arteriovenous anastomoses (ductus arteriosus).