Thromboembolism and pulmonary embolism
The most frequent scenario for the development of the pathology is the detachment of a thrombus or its fragment (tail, body). Sources can include veins, arteries, or heart cavities.
A special place is occupied by pulmonary embolism (PE). Risk groups include bedridden patients, individuals with malignant neoplasms, and cardiovascular diseases.
- Sources: most commonly, thrombi originate from the veins of the lower extremities and the pelvic adipose tissue. Less frequently, they arise from the hepatic veins, inferior vena cava, or the right side of the heart.
- Thanatogenesis (causes of death): death occurs not so much due to mechanical lumen closure (acute right ventricular failure) as due to the pulmonocoronary reflex. The thrombus irritates the receptors of the pulmonary trunk intima, causing reflex spasm of the coronary arteries and cardiac arrest.
Consequences depend on the caliber of the vessel. Small emboli cause hemorrhagic infarction of the lung, while massive occlusion leads to collapse (acute blood pressure drop). 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 the outside or altering their physical state:
- Air: occurs during wounds of 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: associated with rapid decompression (in divers, during aircraft depressurization). Gases dissolved in the blood (nitrogen, less frequently 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 bodies: entry of shrapnel, fragments of medical catheters, or particles of destroyed calcified atherosclerotic plaques into the bloodstream.
Endogenous non-thrombotic embolisms
The body itself can become a source of dangerous particles during severe trauma or diseases:
- Fat: fat droplets enter the bloodstream in 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, and upon penetrating the systemic circulation, they affect the brain and kidneys. A small amount of fat can emulsify and resolve independently.
- Cellular (tissue): circulation of tumor cells (the basis of metastasis), amniotic fluid in postpartum women, or destroyed tissues in newborns with birth trauma. It threatens with pulmonary vessel spasm, heart failure, and DIC syndrome.
- Microbial: clusters of bacteria, fungi, or parasites (*Alveococcus*) in septicopyemia or purulent dissolution of a thrombus. It leads to the appearance of multiple necroses and metastatic abscesses.
Dynamics of embolus migration
The direction of particle movement determines which specific organ will be affected. Three pathways are distinguished:
- Orthograde (antegrade): classical movement along the natural blood flow. Occurs most frequently.
- Retrograde: movement against the flow. Occurs if the foreign body has a large mass, or during retrograde lymph flow (this is how retrograde lymphogenic metastasis occurs in gastric cancer).
- Paradoxical: transition from systemic veins to arteries (or vice versa), bypassing the pulmonary filter. Possible only with anatomical defects of the cardiac septa (patent foramen ovale) or the presence of arteriovenous anastomoses (ductus arteriosus).
Briefly: answers to topical questions
What histological stains are used to detect fat embolism in tissues at autopsy?
To detect fat embolism at autopsy, stains of frozen sections with Sudan III or osmic acid are used.
- Sudan III stains fat droplets orange-red (orange).
- Osmic acid stains fat droplets black.
Additionally, for histochemical detection of fats in tissues, the following may be used:
| Dye | Staining color |
|---|---|
| Sudan IV, Oil Red O, Scharlach R | Red |
| Sudan Black B | Black |
| Nile blue sulfate | Dark blue (fatty acids) or red (neutral fats) |
Routine histological processing is not used, as fat dissolves during passage through alcohols and xylene.
What stages of DIC syndrome occur as a complication of tissue embolism?
Cellular (tissue) embolism can be complicated by DIC syndrome. The sources describe the following stages for DIC syndrome:
- Stage I — hypercoagulation and thrombosis: intravascular clotting and microthrombus formation.
- Stage II — progressive consumption coagulopathy: depletion of procoagulants and platelets, development of hypofibrinogenemia.
- Stage III — profound hypocoagulation and activation of fibrinolysis: lysis of previously formed microthrombi and proteolysis of clotting factors.
The sources indicate that DIC syndrome includes four stages, but the content of stage IV is not presented in the provided materials.
The ORP rule helps memorize the directions of embolus movement: Orthograde — Ordinary (along the bloodstream), Retrograde — Rotation (against the bloodstream), Paradoxical — Passage (through a cardiac defect).
Class and exam questions
What is the main cause of death in PE?
The pulmonocoronary reflex plays the main role. Mechanical irritation of pulmonary artery receptors by a thrombus causes reflex coronary vasospasm and cardiac arrest.
How to prove air embolism at autopsy?
A special test is used: the heart is opened under water. If air bubbles are released from the right ventricle, the diagnosis is confirmed.
How does gas embolism differ from air embolism?
Air embolism occurs when atmospheric air enters veins from the outside (trauma, injections). Gas embolism is the transition of gases dissolved in the blood itself (nitrogen) into bubbles due to a sharp drop in pressure (decompression).
Does embolism always lead to organ infarction?
No. In organs with well-developed collateral circulation (skeletal muscles, liver, kidneys), occlusion may be asymptomatic. Damage to the brain, heart, and pulmonary trunk is most dangerous.
What else to study on this topic
- Pathogenesis and stages of development of hemorrhagic pulmonary infarction in PE
- Mechanisms of DIC syndrome development in amniotic fluid embolism
- Features of systemic and pulmonary forms of fat embolism
- Thromboembolic syndrome: connection with endocarditis and heart defects
- Microbial embolism as a key mechanism in the development of septicopyemia
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