General cascade of complications and ischemia outcomes
Vascular occlusion by an embolus triggers a chain of pathological reactions. Hypoxia and metabolite accumulation become the primary damaging factors. Initially, functional complications occur: the specific function of the tissue drops (for example, filtration in the kidneys or myocardial contractility decreases).
Then, with increasing severity, structural changes develop:
- Appearance of dystrophies (this stage is reversible if the cause is eliminated and blood flow is restored);
- Hypotrophy, atrophy, and hypoplasia of the parenchyma;
- Infarction — tissue necrosis, which is the most severe outcome.
Dead tissue undergoes organization. First, macrophages resorb necrotic masses, then granulation tissue proliferates at the periphery. Ultimately, sclerosis occurs—replacement of the defect with a scar (for example, cardiosclerosis or a gliomesodermal scar in the brain). If the focus in the brain was large, a cavity—a cyst—forms in its place. The scar tissue may subsequently undergo hyalinosis.
A natural outcome is a persistent impairment of organ function. As compensation, intact tissue areas undergo working hypertrophy.
Systemic thromboembolic syndrome
Detachment of thrombotic masses in the left heart chambers (in endocarditis, myocardial infarction, aneurysm) or from the valves leads to systemic thromboembolism. The branches of the aorta carry the emboli, causing acute infarcts of the retina, myocardium, kidneys, brain, and spleen.
Spleen involvement is a clear example. Due to the main-type blood supply and weak anastomoses, a classic wedge-shaped (white) infarct forms here. Splenic artery occlusion can develop not only in cardiogenic embolism, but also against the background of hypercoagulation (polycythemia, sickle cell anemia leading to autosplenectomy, antiphospholipid syndrome). If, however, venous outflow suffers while arterial inflow is preserved, hemorrhagic imbibition develops—forming a red (venous) splenic infarct.
Complications in the pulmonary artery system
Complications of embolism in the pulmonary circulation depend on the caliber of the affected vessel. Blockage of small branches is accompanied by severe bronchospasm and the formation of a hemorrhagic pulmonary infarct.
In massive pulmonary embolism (PE), collapse develops—an acute drop in blood pressure. The mechanism of patient death (thanatogenesis) in this case is associated with acute right ventricular failure, but of primary importance is the pulmono-coronary reflex. Irritation of the pulmonary trunk intima receptors by the thrombus causes a powerful reflex spasm of the coronary arteries and immediate cardiac arrest.
Peripheral complications: extremities and intestine
In acute arterial insufficiency of the extremities, occlusion is accompanied by a reflex spasm of collateral pathways. The main symptom is severe pain capable of causing pain shock. In a subacute course, the clinical picture is different: incomplete occlusion initially causes numbness, paresthesias ("pins and needles"), and coldness. Pain appears only when secondary thrombosis joins and complete occlusion occurs. The outcome without blood flow restoration is gangrene.
Chronic ischemia, for example, in the intestinal wall, proceeds gradually: necrosis of the superficial mucosa, acute erosions, local hemosiderosis. The process descends into the deep layers, granulations proliferate, and the result is fibrosis and strictures (narrowing). With collateral decompensation, the chronic process turns into arterial or venous infarction and intestinal gangrene.
The stages of organization of a necrotic focus are easy to remember by the acronym RSGH: Resorption by macrophages → Granulation tissue → Sclerosis (scar) → Hyalinosis of the scar.
Class and exam questions
What factors determine the severity of ischemia outcome in embolism?
The spectrum of complications depends on the rate of blood flow cessation, the sensitivity of a particular tissue to hypoxia, the degree of collateral development, and the timeliness of restoring vessel patency.
Why does instantaneous death occur in pulmonary trunk embolism?
Irritation of pulmonary artery receptors causes the pulmono-coronary reflex—an acute spasm of the heart's own arteries, leading to cardiac arrest, aggravated by right ventricular failure.
How to distinguish a subacute course of arterial obstruction of the extremity from an acute one?
In acute occlusion, pain appears immediately and can cause shock. In subacute occlusion (when blockage is incomplete), numbness, coldness, and paresthesias appear first, and pain joins later when a secondary thrombus grows on the embolus.
What happens to organ function after the infarction zone has scarred?
The specific function in the lesion focus is lost forever. However, the healthy part of the organ can compensatorily increase in volume (working hypertrophy) to take over part of the lost functions.
What else to study on this topic
- Pathogenesis of autosplenectomy in sickle cell anemia
- Formation of a gliomesodermal cyst in the brain
- Mechanisms of compensatory myocardial hypertrophy in cardiosclerosis
- The role of hemosiderosis in ischemic intestinal injury
- Variants of circulatory disorders of the venous (hemorrhagic) type
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