Fetal Risks of Pregnancy-Induced Hypertension - Essay Example

Fetal Risks of Pregnancy-Induced Hypertension Introduction Pregnancy-induced hypertension (PIH) is a form of high blood pressure in pregnancy. It occurs in about 5 to 8 percent of all pregnancies. PIH is also called toxemia or pre-eclampsia. It occurs most often in young women with a first pregnancy. It is more common in twin pregnancies, in women with chronic hypertension, preexisting diabetes, and in women who had PIH in a previous pregnancy. Usually, there are three primary characteristics of this condition that includes (a) high blood pressure (higher than 140/90 mm Hg), (b) protein in the urine, and (c) edema or swelling. When PIH becomes severe, it is then called eclampsia in which women will have seizures resulting from the condition. This severe PIH condition occurs in about one in 1,600 pregnancies and in most cases, develops near the end of pregnancy. While the cause of PIH is by far unknown, there are some conditions that tend to increase the risk of developing PIH. These includes pre-existing hypertension or high pressure, kidney disease, diabetes, PIH with a previous pregnancy, mother’s age younger than 20 or older than 40, and twins or triplets. Thesis Pregnancy-induced hypertension is a form of hypertension which develops in pregnancy and is closely related with pre-eclampsia also known as seizure. This article contends that pregnancies involving pregnancy-induced hypertension (PIH) holds greater risk factors for the fetus and even have a long-term adverse effect on the newborn development. This text additionally puts emphasis on the influence of maternal blood pressure on fetal growth during gestation. Background Pre-eclampsia-eclampsia, also known as pregnancy-induced hypertension, is a common, multifaceted disorder of pregnancy. It occurs after twenty weeks gestation, except in the case of gestational trophoblastic disease when the syndrome can occur in the first trimester as well. Its cause is unknown. Pre-eclampsia-eclampsia is characterized by high blood pressure and the presence of protein in the urine, with or without edema (swelling) of the legs, arms, and face. Despite nearly fifty years of research, pre-eclampsia remains a major contributing factor to illness and even to death of women and babies. It affects up to 6 or 7 percent of all pregnancies and can be superimposed on the ordinary kind of hypertension (high blood pressure) that some women have prior to becoming pregnant or that develops as pregnancy progresses. Known risk factors for developing pre-eclampsia are first pregnancy, age over forty, African American background, family history of pregnancy-induced hypertension, chronic high blood pressure (hypertension), chronic kidney (renal) disease, antiphospholipid syndrome, diabetes, being pregnant with twins, and high levels of the normally present amino acid homocysteine (a genetic abnormality that can be treated with large doses of folic acid). An association between pre-eclampsia and mutations in genes that encode for blood-clotting proteins has been found. Blood pressure and urinary protein levels are routinely checked during prenatal visits to detect pre-eclampsia early. When blood pressure rises above 140 (systolic) over 85 (diastolic), or if the systolic pressure increases 30 points over the pre-pregnancy level or the diastolic pressure increases 15 or more points, pre-eclampsia is suspected. A urinary protein level of two plus or greater, as measured by the dipstick method, or the excretion of more than 500 milligrams of protein in the urine over a period of twenty-four hours, is considered significant. The accumulation of fluid (edema) in the skin of a pregnant woman, especially in the hands and face, is a sign of pre-eclampsia. Although edema, especially in the legs, is normal in pregnancy, if it is accompanied by rapid, sudden weight gain pre-eclampsia is suspected. Preeclampsia can also cause symptoms, varying in intensity, of upper-abdominal pain, nausea, and vomiting, usually with but some times without elevated blood pressure or protein in the urine. When these symptoms are present, pre-eclampsia is a consideration, particularly when blood abnormalities constituting what is known as the HELLP syndrome are also present. The HELLP syndrome has three defining characteristics, from which the term HELLP is derived: hemolysis (destruction of red blood cells), elevated liver enzymes in the blood (evidenced by inflammation of the liver), and low platelet counts. The HELLP syndrome can lead to problems of its own. A 1999 study identified as one likely cause of the HELLP syndrome a genetic defect, shared by the fetus and the pregnant woman, in the processing of fatty acids. The thinking is that fatty acids that are not metabolized by the fetus accumulate in the womans blood and are toxic to her liver because she cannot process them either. Measurement of liver enzymes, platelets, and uric acid can assist in distinguishing between preeclampsia and worsening chronic hypertension uncomplicated by preeclampsia. The risks to the fetus of preeclampsia include intrauterine growth disturbance, stillbirth, placental abruption, and prematurity, when the baby is purposely delivered early to prevent other problems and safeguard the health of the woman. Risks to the woman include convulsions (known as eclampsia when occurring in the context of pre-eclampsia); hemorrhage into the brain, with possible permanent neurological deficits; loss of vision (usually temporary); hemorrhage into the liver; kidney failure; and, at the extreme, death. Tests of fetal health in late pregnancy are used when pre-eclampsia is present. These tests help determine whether it is safe for the fetus for the pregnancy to continue. Pregnancy-Induced Hypertension and its Occurrence Pre-eclampsia is an illness which occurs in pregnancy and which can affect both the mother and her baby because it originates in their shared organ, the placenta. (Pre-eclampsia used to be known as pre-eclamptic toxemia or PET). During early pregnancy the mother’s blood vessels supplying the placenta enlarge so that they can carry a progressively increasing flow of blood to the baby as the baby grows. However, in women who later develop pre-eclampsia this adaptation does not work properly, for reasons that are not fully understood. As a result, the developing placenta may not get enough blood (becomes ischaemic). If pre-eclampsia becomes severe, the baby’s supply of oxygen and nutrients is affected, leading first to reduced growth (intrauterine growth restriction) and later to a shortage of oxygen (oxygen deficiency) (see also Placental insufficiency page 163). The mother’s own blood circulation is also disturbed and she develops raised blood pressure (pregnancy-induced hypertension), protein in her urine (proteinuria), and swelling (oedema). Severe pre-eclampsia cannot be reversed except by delivering the baby. If it becomes severe, both mother and baby are carefully monitored, ideally in hospital, with the aim of trying to delay the delivery of the baby, if possible until 36 weeks. However, sometimes the lack of nutrients and oxygen become too dangerous and it is necessary to deliver the baby urgently. The baby will be given intensive neonatal care, but if the delivery was very premature, or the baby is very small or ill, this may not succeed. Severe pre-eclampsia can also cause placental abruption, in which the placenta comes away from the womb, depriving the baby of oxygen. Doctors normally carry out an emergency caesarean section to try and save the baby but this is not always successful. Pre-eclampsia can begin at any time in the second half of the pregnancy, though it is more usual in the last few weeks. In some cases, pre-eclampsia develops into eclampsia (see below) which is extremely dangerous for both mother and baby. Some women have normal pregnancies and then develop severe pre-eclampsia during labour or immediately after delivery. In this case the baby is normally safe but the mother may be very ill. Body PIH and its Long-term Effect on Child Development With reference to fetal outcomes, again, a very small number of studies have examined the relations between maternal psychosocial factors and fetal physiology. Recently, a series of longitudinal studies were conducted by DiPietro and colleagues to study the functional development of the fetal central nervous system over the course of gestation and to identify risk factors for neuro-developmental delays (DiPietro, Hodgson, Costigan, Hilton, & Johnson, 1996a, pp.139-151, 1996b, pp. 2553-2567). In these studies, the sequence and characteristics of fetal neurobehavioral development and maturation (i.e., fetal autonomic, motoric, state, and interactive functioning) were assessed serially at six time points between 20 and 38 weeks gestation. Findings indicated that chronic maternal psycho logical distress was significantly associated with delayed and impaired neurobehavioral maturation of the fetus-that is, greater maternal stress was associated with reduced fetal heart rate variability and reduced coupling between fetal heart rate and movement (DiPietro et al., 1996a, pp. 139-151, 1996b, pp. 2553-2567). In another study of 37 women, maternal levels of trait anxiety were significantly associated with uteroplacental and fetal blood flow. Using measures of pulsatility index (PI) derived from doppler flow studies of the umbilical and fetal middle cerebral artery at from 37 to 40 weeks gestation, results indicated that fetuses of mothers with high trait anxiety had significantly higher PI values in the umbilical artery, significantly lower PI values in the fetal middle cerebral artery, and a significantly lower cerebro-umbilical PI ratio (signs of fetal hypoxia and compensatory redistribution of blood flow to the fetal brain; Sjostrom, Valentin, Thelin, & Marsal, 1997, pp. 149-155). Finally, one study with a sample of 40 low risk pregnant women examined maternal blood pressure responses to a laboratory- based behavioral stressor (interactive arithmetic task) during pregnancy. Infant birth outcomes were subsequently obtained from medical records. Results indicated that mothers with greater psychophysiological stress reactivity (in this case, larger diastolic blood pressure responses to behavioral stress) delivered infants with significantly lower birth weights and decreased gestational age (McCubbin and Read 1996, pp. 706-712). Effects of Maternal Blood Pressure Without larger samples it is impossible to perform the more penetrating statistical analyses that could better determine the independent and interactive effects of maternal pregnancy blood pressure on the newborn behavior. Nevertheless, a number of studies investigated the role of pregnancy blood pressure in neonatal irritability in more detail with larger samples. It had been reported that there is a strong positive correlation between normal maternal blood pressure during labor and newborn irritability (Chisholm, Woodson, and da Costa Woodson, 1978, pp. 171-178). The next study of Woodson (1979) came up with a conclusion that an immediate precursor of neonatal irritability was lower intrapartum fetal heart rate (pp. 127-139). Lower intrapartum fetal heart rate was associated with relative fetal growth retardation, and either oxytocin induction/augmentation of labor, or elevated maternal blood pressure during labor. Relative fetal growth retardation, in turn, was associated with greater increases in maternal blood pressure from early to mid-pregnancy. Korner and her colleagues (1980) have also recently replicated the association between normal maternal blood pressure during pregnancy and newborn irritability (pp. 35-39). Using an automatic electronic activity monitor to assess levels of irritability, they found that in a sample of 70 normal mother-infant pairs, spontaneous neonatal crying during the first 3 days of life was positively related to normal variation in maternal blood pressure during the third trimester of pregnancy. Multiple regression analyses showed that third trimester maternal blood pressure still accounted for a significant amount of the variance in spontaneous neonatal crying even after controlling for the effects of second trimester blood pressure, sex and weight of infant, length of first and second stages of labor combined, analgesic medication during labor, parity, and maternal age. However stress and/or coping mechanisms may affect blood pressure, there also exist a number of studies showing that maternal prenatal stress or anxiety affects a variety of behavior patterns in the infant. Sontag (1941), for example, found that maternal prenatal anxiety was associated with greatly increased fetal body movements during the stressful period itself (p. 996). Ottinger and Simons (1964) found that prenatal stress on mothers produced more crying in their newborns (pp. 391-394), and Stott (1973), who implicated disharmonious marital relations especially, found that maternal prenatal stress was associated with fretful and hyperactive behavior in the children at a variety of ages (pp. 770-787). Barnes work (1975) has already been mentioned; although not studying maternal prenatal stress or anxiety, she found that mothers of "poor birth status" infants were more likely to have had hypertension during pregnancy (pp. 421-433). Three years later these "poor birth status" children were more accident prone, had more trouble sleeping, showed more fear of strangers, and were more likely to be left handed or ambidextrous than were normal children. Jones and Dlugokinski (1978) report that mothers who scored higher on a test of anxiety or stress during pregnancy had newborn infants who received significantly lower APGAR scores. In a retrospective epidemiological study of psychiatric disorders in Finland, Huttunen and Niskanen (1978) compared 167 Finnish adults who had lost their fathers while their mothers were pregnant to 168 who had lost their fathers after they had been born, during their first year of life. Finding a significantly greater incidence of psychiatric disorders in the group which had lost their fathers prenatally, they suggest that maternal psychosocial stress during pregnancy increases the risk for the later development of psychiatric disorders. In another study, Turner (1956) reports that restlessness, irritability, vomiting and diarrhea, hypertonicity, and sleep problems are more commonly observed in children whose mothers were especially anxious during pregnancy (pp. 221-222). Finally, in a review of prenatal effects on neonatal behavior, Ferreira (1965) notes that several researchers have reported a link between prenatal maternal anxiety and complications of labor and delivery (pp. 108-118). The epigenesis of neonatal behaviors of all sorts begins not at birth, but at conception, and there is no good reason why anthropologists, developmental psychologists, and evolutionary biologists must let the process of delivery stand as a conceptual and disciplinary barrier to a better understanding of human epigenetics. The sensitivity of the fetus to maternal blood pressure, circulating catecholamines, and other factors could constitute an important set of mechanisms in this epigenetic process. If the fetus is sensitive to its uterine environment then it is also at least partially sensitive to the effects of the mothers larger social-physical environment on her physiology. The sensitivity of the fetus to maternal stress or anxiety could be, for example, one of the mechanisms whereby the sex ratio at birth is determined. More males than females are conceived, more males are conceived than are born, and males are known to be more susceptible to gestational insult than females; under some circumstance the maternal physiological response to stress could constitute a gestational insult that selected against males in utero (Stott, 1973, pp. 770-787). An investigation of the relationships between particular environmental factors, maternal prenatal stress, the sex ratio at birth, and the reproductive success of male and female offspring could have immense implications for socio-biological theory. Conceivably, kin selection and parent-offspring conflict could even be operating in utero; Blurton Jones (1978) suggests for example, the parent-offspring conflict may account for the fact that mean birth weight in humans is slightly less than optimum birth weight (pp. 487-489). The higher incidence of aborted male fetuses might sometimes reflect the unborn male childs "attempt" to increase its inclusive fitness by virtue of the fact that a sister might have a greater reproductive potential than he. Although completely speculative, something like this is an intriguing possibility, especially since the womb serves as a unique indicator of kinship: whether simultaneously or sequentially, inhabitants of the womb are guaranteed to be at least half-siblings. A slightly less speculative possibility is that of "pre-adaptation" taking place in utero. It seems at least possible that natural selection would favor those fetuses who were sensitive to their mothers physiology such that they could respond to their mothers physiology and thus, at the same time, to the larger environment into which they were going to be born. An irritable infant, for example, might under certain circumstances be more successful in eliciting parental investment from parents under stress than a non-irritable infant. Conclusion As a final point, pregnancies involving pregnancy-induced hypertension obviously and evidently pose greater risk to the fetus. Furthermore, maternal blood pressure also proves to have neonatal effects to the newborn. In conjunction with the other studies, which have reported strong effects of normal maternal blood pressure during pregnancy on normal neonatal behavior, similar findings on this article indicate that this prenatal environmental effect on neonatal behavior may be particularly robust. Works Cited Barnes, F. 1975. Accidents in the first three years of life. Child: Care, Health, and Development. 1 (1975): 421-433. Blurton N. G. Jones. 1978. Natural selection and birthweight. Annals of Human Biology. 5.5 (1978): 487-489. Chisholm J. S., R. H. Woodson, and E. da Costa Woodson. “Maternal blood pressure in pregnancy and newborn irritability.” Early Human Development. 2.2 (1978): 171-178. DiPieto, J. A. et al. “Development of fetal movement-fetal heart rate coupling from 20 weeks through term.” Early Human Development. 44.2 (1996a): 139-l 5 1. ---. Fetal neurobehavioral development. Child Development, 67.5 (1996b): 2553–2567. Ferreira, A. J. "Emotional factors in prenatal environment." Journal of Nervous and Mental Disease. 141 (1965): 108-118. Huttenen M. O. and P. Niskanen. Prenatal loss of father and psychiatric disorders. Archives of General Psychiatry. 35 (1978): 429-431. Jones, F. and E. Dlugokinski. The relationship of stress during pregnancy to perinatal status and maternal readiness. Paper presented at the First Biennial Meeting of the International Conference on Infant Studies, Providence, R.I., 1978. Korner, A. F., T. Gabby, and H. C. Kraemer. “Relation between prenatal maternal blood pressure and infant irritability.” Early Human Development. 4.1 (1980): 35-39. McCubbin, A., & Read, J. A. “Prenatal maternal blood pressure response to stress predicts birth weight and gestational age: A preliminary study.” American Journal of Obstetrics and Gynecology. 175.3 (1996): 706–712. Ottinger, D. and J. E. Simons. “Behavior of human neonates and prenatal maternal anxiety.” Psychological Reports. 14 (1964): 391-394. Sjostrom, K., Valentin, L., Thelin, T., & Marsal, K. “Maternal anxiety in late pregnancy and fetal hemodynamics.” European Journal of Obstetrics, Gynecology, and Reproductive Biology. 74.2 (1997): 149–155. Sontag, L. W. The significance of fetal environmental differences. American Journal of Obstetrics and Gynecology. 42 (1941): 996. Stott D. H. “Follow-up study from birth of the effects of prenatal stress.” Developmental Medicine and Child Neurology. 15 (1973): 770-787. Turner, E. K. “The syndrome in the infant resulting from maternal emotional tension during pregnancy.” Medical Journal of Australia. 43 (1956): 221-222. Woodson, R. L. et al. 1979. “Fetal mediators of the relationship between increased pregnancy and labour blood pressure and newborn irritability.” Early Human Development. 3 (1979): 127-139. Read More