Toxemia of pregnancy (gestosis)

This is a disease of the placenta that manifests itself in the mother through arterial high blood pressure. Normally, pregnancy toxicosis occurs in the 3rd trimester in those who are pregnant for the first time. A triad of edemas, high blood pressure and proteinuria are involved that can be accompanied by consumption coagulopathy, NaCl retention, hyperreflexia (pre-eclampsia) and, when untreated, leads to cramping (eclampsia).

Three kinds of gestosis are distinguished:

  • The gestosis that is found during the 3rd trimester in young women who are pregnant for the first time
  • The gestosis that results from another disease, such as hypertonia (multipara with a hypertonia or a kidney ailment)
  • The recurring gestosis (generally vessel and kidney damage is seen here)

Common to these 3 gestosis types is the risk of severe complications such as eclampsia, retro-placental hematoma or the intra-uterine death of the fetus.

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Reminders about physiology:
During pregnancy, kidney perfusion as well as glomerular function increases from 30% to 50%. The systolic and diastolic arterial blood pressures normally fall around 10 to 15 mmHg, when compared to the values preceding the pregnancy. The vasodilatation in the uterus, the kidneys and the skin, as well as the release of vasodilatating prostaglandins and a reduced arteriolar sensibility to angiotensin II play a role in the sinking of blood pressure during pregnancy.
In the third trimester the arterial diastolic blood pressure should not exceed 85 mmHg.
The rise of the arterial blood pressure in the course of a pregnancy is nevertheless a common complication and is potentially dangerous. A blood pressure that exceeds 140/90 mmHg is pathological.

Eclampsia: pathogenic mechanisms
The pathogenesis of this disease is still unclear. The lesion that lies at its base seems to be a utero-placental ischaemia.
Various circumstances that promote it can be mentioned, namely the over-stretching of the uterus in the case of a twin pregnancy, vessel lesions in connection with diabetes, or a villus hypoxia. Coagulopathies and the hormonal factors causing them, possibly also immunologic processes, are also thought to be responsible.

Fetal erythroblastosis (morbus haemolyticus fetalis)

The feto-maternal blood incompatibility indicates the transplacental passage of antibodies.
Through lesions in placental vessels or hemorrhages during delivery, small amounts of fetal blood can enter into the maternal circulation. Contamination of the maternal blood can also occur with a miscarriage or a previous transfusion. When the baby is Rhesus-positive (Rh+) and the mother Rh-, the passage of fetal blood into the maternal circulation system can lead to the formation of antibodies against Rh+ antibodies in the mother (agglutinin anti D of type IgM then IgG).

With a subsequent pregnancy the IgG antibodies that are now present in the maternal blood can pass through the placental barrier and thus get into the fetal blood. When the fetus is Rh+, the antibodies bind to the surface of the fetal erythrocytes and destroy them (hemolysis).
This happens in roughly 5% of all pregnancies where the mother is Rh- and the father is Rh+.

The destruction of the red blood corpuscles is responsible for the morbus haemolyticus neonatorum (fetal erythroblastosis) with the following symptoms:

  • anemia (due to the hemolysis)
  • splenomegaly (location of the macrophages that destroy the erythrocytes)
  • hepatomegaly (intensive hematopoesis in order to compensate the hemolysis)
  • icterus (transformation of hemoglobin of the destroyed erythrocytes into bilirubin)

The systematic check for Rh antibodies in women in whom such a risk is present permits a prevention of this feto-maternal immunization. When at birth it is established that the newborn is Rh+ , anti-D agglutinin is injected into the Rh- mother, thus neutralizing the fetal erythrocytes that have entered the maternal circulation system.

It is still to be emphasized that feto-maternal immunization reactions can also happen against other surface features of the erythrocytes, e.g., at the ABO system.