Gestoses

Pathogenesis and development of multiple organ dysfunction syndrome

The pathogenesis of the disease is complex. The trigger for the cascade of reactions is vascular endothelial injury combined with systemic hypertension. Endothelial dysfunction provokes prolonged vasospasm, which naturally causes ischemia of the myocardium, liver, and kidneys.

Placental ischemia is of particular significance. Experiencing severe hypoxia, the placenta begins to release thromboplastic substances into the maternal circulation. The combination of this substance release and initial endothelial injury initiates disseminated intravascular coagulation (DIC syndrome). The formation of multiple microthrombi in the capillary bed further exacerbates the degeneration of vital organs. The presence of genetic mutations in clotting factors or platelet abnormalities in the pregnant woman serves as a predisposing background for severe DIC syndrome.

Concurrently, due to fluid retention and transudation of the fluid portion of blood into surrounding tissues, hypovolemia develops and edema forms. The culmination of this pathological cascade is the development of multiple organ dysfunction syndrome.

Clinical presentation and its features

Traditionally, several sequential stages of the pathology are distinguished:

1. Basic gestosis: manifests with the classic triad including progressive edema, elevated blood pressure, and proteinuria (protein in the urine).
2. Preeclampsia: the patient's condition worsens, with symptoms of cerebral circulation impairment—severe headache and visual disturbances—joining the aforementioned triad.
3. Eclampsia: a critical condition with extremely high mortality. The main sign is the development of clonic-tonic seizures. The seizure may be triggered by the slightest external stimulus or begin completely spontaneously (the term translates from Greek as "suddenness").

The modern clinical course of gestoses exhibits marked polymorphism. The complete classic triad is observed today in only 15% of patients. Atypical and monosymptomatic forms have become prevalent in obstetric practice, requiring heightened diagnostic vigilance. Severe complications with high mortality also include acute fatty liver of pregnancy and HELLP syndrome.

Pathological anatomy of target organs

Morphological changes in gestosis reflect the pattern of widespread ischemia and intravascular thrombus formation.

• Liver: macroscopically, subcapsular hematomas form, the rupture of which threatens massive intraperitoneal hemorrhage. Pale yellow necrosis foci (single or confluent) and hemorrhages are visible in the parenchyma. Histologically, fibrin thrombi are identified in the portal tract vessels.
• Kidneys: swelling of the capillary endothelium in renal glomeruli is noted, with fibrin deposits settling on the basement membrane. A morphological picture of immune complex mesangial glomerulonephritis is possible. A severe course leads to necrotizing nephrosis and acute renal failure.
• Brain: microscopic and macroscopic foci of hemorrhage, as well as thrombosis of small vessels, are revealed. Massive cerebral hemorrhages (especially in the basal ganglia) are a major cause of death.
• Placenta and uterus: physiological transformation is absent in the spiral arteries of the placental bed, and atherosis develops (appearance of a broad layer of fibrinoid containing large foam cells, clearly visible with hematoxylin and eosin staining). In the placenta, ischemia causes thickening of the trophoblast basement membrane, cytotrophoblast hyperplasia, infarctions, and an excess of syncytial knots. Premature detachment is possible.

The fetus suffers severely from hypoxia and intrauterine growth restriction due to placental damage. Children are born premature. In eclampsia, intrauterine fetal death is frequently recorded.

Trophoblastic disease

A group of pathologies originating from placental tissues. These diseases are rare, but the risk of their development is significantly higher in pregnant women under 16 and over 35 years of age. This group includes hydatidiform mole (occurring in 1 per 1,000 births), its invasive form, choriocarcinoma (2 per 100,000), and placental site trophoblastic tumor.

Hydatidiform mole macroscopically presents as an enlarged uterus where chorionic villi are transformed into vesicles filled with clear fluid, resembling clusters of grapes. These structures may lie freely in the uterine cavity and be discharged from the vagina. Microscopically (with hematoxylin and eosin staining), marked edema of villi of varying sizes is determined, with the formation of fluid-filled spaces—"cisterns"—in their centers.

Two variants of the pathology are distinguished:

• Complete hydatidiform mole: has a 46, XX diploid karyotype of exclusively paternal origin. It occurs either upon fertilization of an "empty" (anucleate) oocyte by a 23, X sperm followed by chromosome duplication, or via dispermic fertilization. The entire placental tissue is affected, and the fetus is absent.
• Partial hydatidiform mole: characterized by a triploid karyotype due to an extra set of paternal chromosomes. Edematous villi are distributed focally among normal placental tissue. A fetus is initially formed but inevitably dies in early gestation.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of dispermic fertilization in hydatidiform mole
• Histological picture of the kidneys in necrotizing nephrosis
• Choriocarcinoma and placental site trophoblastic tumor
• Morphology of subcapsular liver hematomas and bleeding risks

Other topics in "Chapter 21. Pathology of Pregnancy"

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