Eclampsia pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

While multiple theories have been proposed to explain preeclampsia and eclampsia, it occurs only in the presence of a placenta and is resolved by its removal. E. W. Page suggested that placental hypoperfusion is a key feature of the process. It is accompanied by increased sensitivity of the maternal vasculature to pressure agents leading to vasospasm and hypoperfusion of multiple organs. Further, an activation of the coagulation cascade leads to microthombi formation and aggravates the perfusion problem. Loss of plasma from the vascular tree with the resulting edema additionally compromises the situation. These events lead to signs and symptoms of toxemia including hypertension, renal, pulmonary, and hepatic dysfunction, and - in eclampsia specifically - cerebral dysfunction. Preclinical markers of the disease process are signs of increased platelet and endothelial activation.

Pathophysiology

Anatomy and Physiology of placenta

The formation of the placenta commences with the development of trophoblast. After the fertilization of the ovum in the fallopian tubes, it travels towards the uterus and by the time it reaches the uterus it has already become a morula. The morula is still surrounded by the zona pellucida which prevents it from sticking to the walls of the tube. The zona pellucida disappears soon after the blastocyst reaches the uterine cavity. Now the cells lining the blastocyst constitute the trophoblast whose function is to invade the surrounding uterine tissues to provide nutrition to the developing blastocyst. When the trophoblast attaches to the endometrium, it is known as implantation, which begins on the sixth day after fertilization in humans. This process is additionally enhanced by the proteolytic enzymes produced by the trophoblast and the interaction between the receptors present uterine epithelium and L-selectin and integrins produced by the trophoblast cells. Hence, implantation is a result of mutual exchange between the endometrium of the uterine cavity and the trophoblastic cells surrounding the blastocyst.

Decidua

After the implantation, the uterine endometrium is termed the Decidua. Once the implantation has occurred the stromal cells undergo a decidual reaction which consists of enlargement of the cells, vacuolisation and storage of glycogen and lipids.

Decidua basalis

• The area of the endometrium or decidua that is deep to the blastocyst, where the placenta is to be formed is inferred as decidua basalis. It consists of the terminally differentiated large stromal cells which encompass largely lipids and glycogen that acts as a source of nutrition for the embryo. It also comprises of maternal vascular cells and maternal blood cells inside and outside those vessels.
• This area is also known as the decidual plate and it is firmly united to the chorion.
• The stromal cells also produce a variety of humoral proteins such as insulin-like growth factor binding proteins and prolactin and its family proteins.

Chorionic villi

These consist of the fetal portion of the placenta. They are offshoots or very small finger-like processes, hence called the villi, from the surface of the trophoblast cells. Within the substance of these villi are fetal blood capillaries and fetal blood cells which arise from the extra-embryonic mesoderm. Since the trophoblast and the extra-embryonic mesoderm constitutes the chorion, these villi are also known as chorionic villi.

Chorion fundosum

Originally the villi are formed all over the trophoblast and commence invading the surrounding decidua. Nevertheless gradually the villi related to the decidua capsularis degenerate and in contrast, those associated with the decidua basalis undergo further differentiation and substantial growth and helps form the placenta. This part is known as chorion fundosum. During the differentiation process, the trophoblast which is originally a single layer of cells multiplies into two distinct layers. The cells in the superficial layer, that is the layer which is in proximity with the decidua, lose their cell boundaries and mould into one consecutive layer of cytoplasm and several nuclei, known as the syncytiotrophoblast. The second layer cells, which rest on extra-embryonic mesoderm, however retain their cell walls and are known as the cytotrophoblast.

Placenta

• The tissues of desidua basalis and chorion fundosum jointly form a disc-shaped structure called the placenta.
• Various septa start growing into the intervillous space from the maternal side and subdivide the placenta into 15-20 lobes known as the maternal cotyledons.
• Each lobe homes several anchoring villi and their branches. One such villus along with its branches constitute a fetal cotyledon.
• The maternal vessels empty into the intervillous space and the maternal blood circulates through the intervillous space and the fetal blood travels through the fetal blood vessels in the villi. At any given time, the maternal and fetal blood do not mix and all exchanges take place via the placental membrane or the placental barrier.
• The layers of the placental membrane(from the fetal side):
  1. The endothelium and the basement membrane of the fetal blood vessels
  2. Surrounding connective tissue(mesoderm)
  3. Cytotrophoblast
  4. Syncytiotrophoblast
• The functions of the placenta include:
  • The transport of water, electrolytes, oxygen, and nutrition from mother to the baby
  • Excretion of waste products such as carbon dioxide, urea, etcetera produced by the fetus into the maternal blood
  • Passage for the maternal IgG to reach the fetus and give immunity against some infections
  • A barrier against many bacteria, certain viruses, and harmful substances
  • Synthesis of several hormones such as oestrogen(estriol), progesterone, human chorionic gonadotropin (hCG), somatomammotropin (hCS)

Spinal artery remodelling

Spinal artery remodelling of the maternal blood vessels, one of the physiological changes of pregnancy, is a process that begins in the first few weeks of pregnancy and modifies the low-flow, high-resistant arteries to high-flow, low-resistance blood vessels which are capable of meeting the demands of the growing fetus.

Pathophysiology

Placental hypoperfusion is linked to abnormal modeling of the fetal-maternal interface that may be immunologically mediated The invasion of the trophoblast appears to be incomplete. Adrenomedullin, a potent vasodilator, is produced in diminished quantities by the placenta in preeclampsia (and thus eclampsia). Other vasoactive agents are at play including prostacyclin, thromboxane A2, nitric oxide, and endothelins leading to vasoconstriction. Many studies have suggested the importance of a woman's immunological tolerance to her baby's father, whose genes are present in the young fetus and its placenta and which may pose a challenge to her immune system.

Eclampsia is seen as form of a hypertensive encephalopathy in the context of those pathological events that lead to preeclampsia. It is thought that cerebral vascular resistance is reduced, leading to increased blood flow to the brain. In addition to abnormal function of the endothelium, this leads to cerebral edema. Typically an eclamptic seizure will not lead to lasting brain damage; however, intracranial hemorrhage may occur.

Histopathology

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References