PLACENTA IN PREGNANCY-INDUCED HYPERTENSION- HISTOPATHOLOGY AND FOETAL OUTCOMEA CORRELATIVE STUDY
Journal Title: Journal of Evolution of Medical and Dental Sciences - Year 2018, Vol 7, Issue 23
Abstract
BACKGROUND Placenta is an organ specially formed for the purpose of supplying oxygen and nutrition to the foetus. In addition, it accomplishes the functions of excretion and haematopoiesis and secretes a number of hormones all directly related to foetal nutrition and aimed at preparing the foetus for extrauterine life.1 Pregnancy-induced hypertension (PIH) is one among the most common complications in pregnancy. Severe pregnancy-induced hypertension is a serious health hazard to both the mother and her foetus. Various studies undertaken on placenta in PIH have revealed increased incidence of certain typical, but not pathognomonic lesions.2 The most consistent findings were cytotrophoblastic proliferation, thickening of the villous basement membrane and paucity of vasculosyncytial membrane.3 These are suggestive of a reduced uteroplacental blood flow, which may be predicted by Doppler studies.4 Also the technique of placental bed biopsy enables a more precise assessment of the uteroplacental vasculature.5 Regarding the foetal outcome, the incidence of intrauterine growth restriction and perinatal mortality has been found to be more in PIH compared to normal pregnancy. The hypertension alone may not affect the foetal outcome, but its coexistence with the placental lesions result in growth restriction and/or foetal loss.6 The present study was undertaken to assess the pattern of histopathological changes in the placenta and the foetal outcome in relation to the severity of pregnancy-induced hypertension. The Aims and Objectives of our study were1. To study the gross and histological changes in the placenta in pregnancy-induced hypertension. 2. To correlate the placental changes with the severity of pregnancy-induced hypertension. 3. To correlate the placental changes with the foetal outcome. MATERIALS AND METHODS Our study was a cross-sectional study conducted at the Department of Pathology, Medical College, Thiruvananthapuram and Department of Obstetrics and Gynaecology, SAT Hospital, Thiruvananthapuram for a period of 2 years. Fifty placentas from patients with pregnancy-induced hypertension and an equal number from normal pregnancy were studied. Cases with multiple pregnancy, anaemia, past history of hypertension, history of renal disease, history of chronic vascular disease and diabetes mellitus were excluded from the study. The relevant clinical details regarding the mother and the baby were obtained as per the structured proforma. The placentas were collected soon after delivery, fixed whole in 10% formalin for two weeks and then examined grossly and microscopically. The paraffin sections were stained with Haematoxylin and Eosin, PAS and Van Gieson stain. The villous lesions noted were1. Cytotrophoblastic proliferation. 2. Basement membrane thickening. 3. Paucity of vasculosyncytial membrane. 4. Fibrinoid necrosis. 5. Excessive syncytial knots. 6. Stromal fibrosis. RESULTS In the present study, 50 placentas from patients with pregnancy-induced hypertension and an equal number from normal pregnancy were studied. The placental histopathology was correlated with the foetal outcome. Depending on the blood pressure, presence of oedema, albuminuria and convulsions the study group was divided into1. Mild PIH, 25 cases. 2. Severe PIH, 18 cases. 3. Eclampsia, 7 cases. The peak incidence of pregnancy-induced hypertension was in the age group of 20 - 29 years (82%). The incidence of PIH was more in primigravidae (58%). Only 6% in the study group were G3 or above. The mean placental weight in the control group was 464 grams, while it was 415 grams in the study group. In the normal group and mild PIH, the mean weight was comparable whereas it was significantly lower in cases of severe PIH and eclampsia. Considering the grade of PIH the mild group showed no appreciable difference from the control group, whereas the mean infarction (Percentage) in the severe and eclampsia group was significantly higher. The incidence of retroplacental clot was higher in the study group compared to the control group, which was statistically highly significant. There was no significant difference in the incidence of calcification and intervillous thrombus between the study group and the control group. The incidence of cytotrophoblastic proliferation and basement membrane thickening was much higher in the study group than in the control group. The other lesions which showed an increased incidence in the study group were paucity of vasculosyncytial membrane, fibrinoid necrosis of the villi, excessive syncytial knots and villous stromal fibrosis. In the present study the incidence of the following placental lesions was found to be directly related to the severity of PIH, infarction, retroplacental clot, cytotrophoblast proliferation, basement membrane thickening, paucity of vasculosyncytial membrane, excessive syncytial knots and stromal fibrosis. The incidence of preterm delivery in the study group was more than 2 times higher than that in the control group. Thus, the observations in the present study indicate that the placental histopathology is directly related to the severity of PIH and the adverse foetal outcome is well correlated with the extent of infarction and the villous lesions in the placenta. CONCLUSION The placental histopathological findings observed in this study suggest the existence of a reduced uteroplacental blood flow in pregnancy-induced hypertension. The abnormal placentation in PIH has been well established by many workers by their studies on the placental bed vasculature. As a response to the uteroplacental ischaemia there is vasoconstriction of the foetal stem arteries in the placenta, manifesting histologically as sclerosis of vessels and increased number of syncytial knots. The intrauterine growth retardation and foetal loss observed in PIH are also attributable to the defective uteroplacental perfusion. The fact that the placental bed vessels, which harbour the important pathological processes are not usually available for study is particularly distressing. However, placental histopathology with more emphasis on the technique of placental bed biopsy could compliment the clinical diagnosis or support the clinical suspicion in cases, in which the blood pressure values do not meet the criteria for a diagnosis of preeclampsia.
Authors and Affiliations
Kavitha Ravi, Santha Sadasivan
Keywords
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- EP ID EP439342
- DOI 10.14260/jemds/2018/624
- Views 63
- Downloads 0
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