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#61
25.07.2006, 00:03
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Бредятина.Вы это к чему?Я,честно говоря,в словопрениях не силён,скрытый смысл улавливаю плохо...
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#62
25.07.2006, 15:25
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Цитата:
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#63
25.07.2006, 16:33
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Kidney Int Suppl. 1997 Jun;59:S90-6.
Edema in pregnancy.Davison JM. Department of Obstetrics and Gynaecology, University of Newcastle upon Tyne, Royal Victoria Infirmary, England, United Kingdom. During normal pregnancy total body water increases by 6 to 8 liters, 4 to 6 liters of which are extracellular, of which at least 2 to 3 liters are interstitial. At some stage in pregnancy 8 out of 10 women have demonstrable clinical edema. There is also cumulative retention of about 950 mmol of sodium distributed between the maternal extracellular compartments and the product of conception. Thus, changes in factors governing renal sodium and water handling accompany alterations in local Starling forces whereby there is a moderate fall in interstitial fluid colloid osmotic pressure (COPi) and a rise in capillary hydrostatic pressure (Pc), as well as changes in hydration of connective tissue ground substance. Edema is a traditional criterion for diagnosing pre-eclampsia, but should no longer be used as its detection is not clinically useful. The role of diuretics in obstetric practice should be restricted to the management of pulmonary edema in pre-eclampsia. Volume expansion therapy in pregnancy runs the risk of pulmonary or cerebral edema, particularly in the immediate puerperium. Vulval edema and erythematous edema associated with deep venous thrombosis are rare but dangerous complications of pregnancy. Williams Obstetrics > Section II. Anatomy and Physiology > Chapter 5. Maternal Physiology Water Metabolism Increased water retention is a normal physiological alteration of pregnancy. This retention is mediated, at least in part, by a fall in plasma osmolality of approximately 10 mOsm/kg induced by a resetting of osmotic thresholds for thirst and vasopressin secretion (Heenan and colleagues, 2003; Lindheimer and Davison, 1995). At term, the water content of the fetus, placenta, and amnionic fluid amounts to about 3.5 L. Another 3.0 L accumulates as a result of increases in the maternal blood volume and in the size of the uterus and the breasts. Thus, the minimum amount of extra water that the average women accrues during normal pregnancy is about 6.5 L. Clearly demonstrable pitting edema of the ankles and legs is seen in most pregnant women, especially at the end of the day. This accumulation of fluid, which may amount to a liter or so, is caused by an increase in venous pressure below the level of the uterus as a consequence of partial occlusion of the vena cava. A decrease in interstitial colloid osmotic pressure induced by normal pregnancy also favors edema late in pregnancy (Øian and co-workers, 1985). Longitudinal studies of body composition have shown a progressive increase in total body water and fat mass during pregnancy. It has been known for decades that both initial maternal weight and the weight gained during pregnancy are highly associated with birthweight. It is unclear, however, what role maternal fat or water have in fetal growth. Studies in well-nourished term women suggest that maternal body water, rather than fat, contributes more significantly to infant birthweight (Lederman and co-workers, 1999; Mardones-Santander and associates, 1998). Electrolyte and Mineral Metabolism During normal pregnancy, nearly 1000 mEq of sodium and 300 mEq of potassium are retained (Lindheimer and colleagues, 1987). Although the glomerular filtration of sodium and potassium is increased, the excretion of these electrolytes is unchanged during pregnancy as a result of enhanced tubular resorption (Brown and colleagues, 1986, 1988). Although pregnancy is associated with increased total accumulations of sodium and potassium, the serum concentrations of these electrolytes are decreased slightly as a result of the expanded plasma volume, however, they remain very near the range of normal for nonpregnant women (Kametas and colleagues, 2003b). Nutrition Sodium Deficiency during pregnancy is unusual unless diuretics are prescribed or dietary sodium intake is reduced drastically. A normal diet provides an abundance of sodium. Although pregnancy is associated with increased total accumulation of sodium, the serum concentration decreases slightly due to the expanded plasma volume. Sodium excretion remains unchanged, and averages 100 to 110 mEq/day (Brown and colleagues, 1986). Pragmatic Nutritional Surveillance Although the science of nutrition continues in its perpetual struggle to identify the ideal amounts of protein, calories, vitamins, and minerals for the pregnant woman and her fetus, those directly responsible for their care may best discharge their duties as follows. In general, advise the pregnant woman to eat what she wants in amounts she desires and salted to taste. Make sure that there is ample food to eat in the case of socioeconomically deprived women. Monitor weight gain, with a goal of about 25 to 35 pounds in women with a normal BMI. Periodically explore food intake by dietary recall to discover the occasional nutritionally absurd diet. Give tablets of simple iron salts that provide at least 27 mg of iron daily. Give folate supplementation before and in the early weeks of pregnancy. Recheck the hematocrit or hemoglobin concentration at 28 to 32 weeks to detect any significant decrease.
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#64
25.07.2006, 16:35
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Яна, Вы нарушаете авторские права
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#66
25.07.2006, 17:18
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Хотела сказать, делайте это почаще, но рука дрогнула.. И все же упоминается мониторинг прибавки массы тела и целевые значения ее.
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#68
25.07.2006, 17:32
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Тогда была бы только нижняя граница целевых значений
 Но голодать, конечно, хуже. Интересно, а с ожирением целевые значения, значит, другие - ниже?
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#69
25.07.2006, 18:05
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WEIGHT GAIN AND PREGNANCY
An infant's birth weight is affected by many factors, including the mother's prepregnancy weight-for-height value and weight gain during pregnancy. Prepregnancy weight-for-height value is expressed as body mass index (BMI). BMI is defined as weight in kilograms divided by the square of height in meters. In 1959, the Metropolitan Life Insurance Company defined its weight-for-height standards by BMI. These standards are in common use today. Underweight is defined as a BMI of less than 19.8. Normal weight is defined as a BMI of 19.8-26, which corresponds to between 25% and 75% of the expected weight-for-height value. Overweight is defined as a BMI of 26-29. Lastly, obesity is defined as a BMI that exceeds 29. Birth weight is affected by prepregnancy BMI independent of actual weight gain during pregnancy. Women who are underweight are at increased risk for low birth weight babies; women who are overweight or obese are at increased risk for macrosomic infants. Macrosomia is variably defined as weight exceeding 4000 g, 4500 g, or the 90th percentile. Macrosomic infants are at increased risk for shoulder dystocia and brachial plexus injuries. Morbid obesity is defined by a BMI exceeding 35. Morbidly obese patients are at increased risk for preeclampsia, nonreassuring fetal heart tracings, meconium aspiration, late intrauterine fetal death, and early neonatal death (Cedergren, 2004). Of course, birth weight is also affected by weight gain during pregnancy. Although weight should be gained throughout pregnancy, it is most critical in the second trimester. Even if overall weight gain is poor, birth weight is usually acceptable with appropriate second-trimester weight gain. The following table relates low birth weight to both prepregnancy weight and pregnancy weight gain. Rates of Low Birth Weight (<2500 g) by Weight and Weight Gain Pregnancy Weight Gain, lb______________Prepregnancy Weight, lb ______________________________<110__110-129__130-149__>150 <16____________________________30%___ 20%____15%_____7-8% 25-35__________________________7-8%___6-7%___4-5%_____3-4% >35____________________________5-6%___3-4%___3-4%_____3-4% In 1990, the Institute of Medicine issued recommendations for weight gain during pregnancy (Institute of Medicine, 1990). These recommendations are based on prepregnancy BMI. Women who are underweight are advised to gain a total of 12.5-18 kg (28-40 lb). This translates to 0.5 kg/wk in the second and third trimesters. Women of normal weight are advised to gain a total of 11.5-16 kg (25-35 lb), or 0.4 kg/wk, in the second and third trimesters. Women who are overweight or obese should limit their weight gain to 7-11.5 kg (15-25 lb), or 0.3 kg/wk, in the second and third trimesters. Dieting during pregnancy is never recommended, even for patients who are morbidly obese. Severe restriction of energy (caloric) intake is associated with a 250-g decrease in average birth weight. Because of the expansion of maternal blood volume and construction of fetal and placental tissues, some weight gain is essential for a healthy pregnancy. Weight gain within these parameters is associated with a lower rate of cesarean delivery, fewer infants with growth restriction or macrosomia, and a decreased incidence of postpartum obesity. Nevertheless, only 30-40% of pregnant women achieve appropriate weight gain (Hickey, 2000). Further evaluation is needed if weight gain is persistently slow or does not equal 10 lb by mid pregnancy. DIET IN PREGNANCY The demands of pregnancy necessitate additional dietary requirements. Obviously, additional energy (caloric) intake is required to support recommended weight gain. Because energy requirements in pregnancy are increased by 17% over the nonpregnant state, a woman of normal weight should consume an additional 126 kJ/d (300 kcal/d); however, this energy should be of high nutrient density. Nutrient density reflects the amount of protein, vitamins, and minerals per 418 kJ (100 kcal) of food. Protein should comprise 20% of a normal pregnancy diet. The recommended daily allowance (RDA) in pregnancy is 60 g. Fortunately, most American diets already contain more than enough protein. Pregnant women should be aware that many animal sources of protein are very high in fat and might contribute to excessive weight gain; therefore, animal proteins should be taken sparingly. Fat should only comprise 30% of a normal pregnancy diet. Carbohydrates should comprise the remaining 50%. A sample diet for normal pregnancy is based on the food pyramid and should include 6-11 servings of grains; 3-5 servings of vegetables; 2-4 servings of fruit; 3-4 servings of dairy; 2-3 servings of meats, beans, or nuts; and 1 serving of sweets. Total energy intake should vary by BMI, but the average recommendation is 10,460 kJ/d (2500 kcal/d). [Ссылки доступны только зарегистрированным пользователям ]
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#70
25.07.2006, 18:08
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Здравствуйте! А вы не знаете, в интернете есть полный текст учебника в свободном(бесплатном доступе)? и на всякий случай: где можно, заказывать подобные книги через интернет?
тоже хочется быть умным и хорошим врачем..
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#71
25.07.2006, 18:11
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Williams Obstetrics > Section III. Antepartum >
Chapter 8. Prenatal Care Nutrition Meaningful studies of nutrition in human pregnancy are exceedingly difficult to design. For ethical reasons, experimental dietary deficiency must not be produced deliberately. In those instances in which severe nutritional deficiencies have been induced as a consequence of social, economic, or political disaster, coincidental events often have created many variables, the effects of which are not amenable to quantification. Some past experiences suggest, however, that in otherwise healthy women a state of near starvation is required to establish clear differences in pregnancy outcome. During the severe European winter of 1944–1945, nutritional deprivation of known intensity prevailed in a well-circumscribed area of the Netherlands occupied by the German military (Stein and associates, 1972). At the lowest point during the Hunger Winter, rations reached 450 kcal/day, with generalized rather than selective malnutrition. Smith (1947) analyzed the outcomes of pregnancies that were in progress during this 6-month famine. Median infant birthweights decreased about 250 g and rose again after food became available. This indicated that birthweight can be influenced significantly by starvation during later pregnancy. The perinatal mortality rate, however, was not altered, nor was the incidence of malformations significantly increased. Interestingly, the frequency of pregnancy "toxemia" was found to decline. Evidence of impaired brain development has been obtained in some animal fetuses whose mothers had been subjected to intense dietary deprivation. Subsequent intellectual development was studied by Stein and associates (1972) in young Dutch adults whose mothers had been starved during pregnancy. The comprehensive study was made possible because all males at age 19 underwent compulsory examination for military service. It was concluded that severe dietary deprivation during pregnancy caused no detectable effects on subsequent mental performance. Conversely, there is evidence that maternal weight gain during pregnancy influences birthweight. This was studied by Martin and colleagues (2002b) who used birth certificate data for 2001. As shown in Figure 8–7, nearly two thirds of pregnant women gained 26 lb or more. The median weight gain was 30.5 lb. Maternal weight gain had a positive correlation with birthweight, and women with the greatest risk—14 percent—for delivering an infant weighing less than 2500 g were those with weight gains less than 16 lb. This incidence was 20 percent in African-American women who gained 15 lb or less. Cohen and associates (2001) studied more than 4000 pregnant women and concluded that ethnic differences in pregnancy outcomes were not explained by nutritional variations. Recommendations for Weight Gain For the first half of the 20th century, it was recommended that weight gain during pregnancy be limited to less than 20 lb (9.1 kg). It was believed that such restriction would prevent pregnancy hypertensive disorders and fetal macrosomia resulting in operative deliveries. By the 1970s, however, women were encouraged to gain at least 25 lb (11.4 kg) to prevent preterm birth and fetal growth restriction, a recommendation that subsequent research continues to support (Ehrenberg and associates, 2003). In 1990, the Institute of Medicine recommended a weight gain of 25 to 35 lb (11.5 to 16 kg) for women with a normal prepregnancy body mass index (BMI). This index is easily calculated using the chart shown in Figure 43–1. Weight gains recommended by the Institute of Medicine (1990) according to prepregnant BMI categories are shown in Table 8–6. The American Academy of Pediatrics and the American College of Obstetricians and Gynecologists (2002) have endorsed these guidelines. Of note, in 2001, almost 1 in 3 women had weight gains outside the Institute of Medicine guidelines (Martin and colleagues, 2002b). Feig and Naylor (1998) from Canada have challenged recommendations for liberal weight gain in industrial nations. They concluded that these recommendations encourage women to overeat during pregnancy without addressing other causes of low-birthweight infants such as adolescent pregnancy, drug abuse, and heavy smoking. They endorsed the recommendation by the Committee on Medical Aspects of Food Policy (1991) in the United Kingdom that a pregnant woman with a normal BMI should gain 15 to 25 lb during pregnancy. Disadvantages of excessive maternal weight gain and fetal macrosomia must be considered. Thorsdottir and associates (2002) analyzed pregnancy outcome in relation to weight gain in 615 healthy women with a normal BMI before pregnancy. The frequency of antepartum and intrapartum complications, including fetal macrosomia, was highest among women who gained more than 44 lb (20 kg) during pregnancy. Conversely, these complications were lowest among those whose weight gain was within the range recommended by the Institute of Medicine. Similarly, Rhodes and co-workers (2003) found in their analysis of 1999–2000 United States birth certificate data that excessive weight gain—defined as more than 40 lb—correlated closely with fetal macrosomia. Weight Retention After Pregnancy Not all the weight put on during pregnancy is lost during and immediately after parturition (Hytten, 1991). The average-sized normal woman who gains 28 lb (12.5 kg) in pregnancy is about 9 lb (4.4 kg) above her prepregnant weight when discharged postpartum. Schauberger and co-workers (1992) studied prenatal and postpartum weights in 795 women delivered in Wisconsin. Their average weight gain was 28.6 ± 10.6 lb (13.0 ± 4.8 kg). As shown in Figure 8–8, the majority of maternal weight loss was at delivery—about 12 lb (5.5 kg)—and in the ensuing 2 weeks thereafter—about 9 lb (4 kg). An additional 5.5 lb (2.5 kg) was lost between 2 weeks and 6 months postpartum. The average total weight loss resulted in an average retained weight of 3 ± 10.5 lb (1.4 ± 4.8 kg) due to pregnancy. Overall, the more weight gained during pregnancy, the more that was lost postpartum. Parous women retained more of their pregnancy weight, and this is linked to long-term obesity (see Chap. 43, Long-Term Consequences). The effect of breast feeding on maternal weight loss was negligible. Summary of Weight Gain Perhaps the most remarkable finding about weight gain in pregnancy is that a wide range is compatible with good clinical outcomes. Moreover, departures from "normal" are nonspecific for any outcome in a given individual. Recommended Dietary Allowances Periodically, the Food and Nutrition Board of the Institute of Medicine recommends dietary allowances for women, including those who are pregnant or lactating. Its latest recommendations (2004) are summarized in Table 8–7. Certain prenatal vitamin–mineral supplements may lead to intakes well in excess of the recommended allowances. Moreover, the use of excessive supplements—for example, 10 times the recommended daily allowances—which often are self-prescribed, has led to concern about nutrient toxicities during pregnancy. Nutrients that can potentially exert toxic effects include iron, zinc, selenium, and vitamins A, B6, C, and D. Vitamin and mineral intake more than twice the recommended daily dietary allowance shown in Table 8–7 should be avoided during pregnancy (American Academy of Pediatrics and the American College of Obstetricians and Gynecologists, 2002).
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#72
25.07.2006, 18:20
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Цитата:
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#73
25.07.2006, 18:35
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Цитата:
Шучу. Практика показывает, что кому не помогло, тому и не поможет, у остальных вильямс есть (и даже эндокринология  )
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#74
25.07.2006, 18:43
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Williams Obstetrics > Section VII. Obstetrical Complications >
Chapter 34. Hypertensive Disorders in Pregnancy Terminology and Classification The term gestational hypertension is used now to describe any form of new-onset pregnancy-related hypertension. It was adopted by the Working Group of the NHBPEP (2000), which proposed a classification system based on clinical simplicity to guide management. The term was chosen to emphasize the cause-and-effect connection between pregnancy and its unique form of hypertension—preeclampsia and eclampsia. It is also meant to be a working term that is purposefully vague, but it should convey that the development of hypertension in a previously normotensive pregnant woman should and must be considered potentially dangerous to both herself and her fetus. In the past several editions of Williams Obstetrics, the term pregnancy-induced hypertension was used. It was popularized by Dr. Jack Pritchard to convey the same principles, and it still is used by some interchangeably with gestational hypertension. The classification of hypertensive disorders complicating pregnancy by the Working Group of the NHBPEP (2000) includes five types of hypertensive disease: 1)Gestational hypertension (formerly pregnancy-induced hypertension that included transient hypertension). 2)Preeclampsia. 3)Eclampsia. 4)Preeclampsia superimposed on chronic hypertension. 5)Chronic hypertension. Diagnosis Hypertension is diagnosed when the resting blood pressure is 140/90 mm Hg or greater; Korotkoff phase V is used to define diastolic pressure. In the past, it had been recommended that an incremental increase of 30 mm Hg systolic or 15 mm Hg diastolic pressure be used as diagnostic criteria, even when absolute values were below 140/90 mm Hg. These criteria are no longer recommended because evidence shows that these women are not likely to suffer increased adverse pregnancy outcomes (Levine and co-workers, 2000; North and colleagues, 1999). That said, women who have a rise of 30 mm Hg systolic or 15 mm Hg diastolic warrant close observation. Edema has been abandoned as a diagnostic criterion because it occurs in too many normal pregnant women to be discriminant. Gestational Hypertension The diagnosis of gestational hypertension is made in women whose blood pressure reaches 140/90 mm Hg or greater for the first time during pregnancy but in whom proteinuria is not identified. Gestational hypertension is also called transient hypertension if preeclampsia does not develop and the blood pressure has returned to normal by 12 weeks' postpartum. In this classification, the final diagnosis that the woman does not have gestational hypertension is not made until several weeks after delivery. Thus, gestational hypertension is a diagnosis of exclusion. Importantly, some women with gestational hypertension may later develop other findings of preeclampsia, for example, symptoms such as headaches or epigastric pain, proteinuria, or thrombocytopenia, all of which influence management. When blood pressure rises appreciably during the latter half of pregnancy, it is dangerous, especially to the fetus, not to act simply because proteinuria has not yet developed. As Chesley (1985) emphasized, 10 percent of eclamptic seizures develop before overt proteinuria is identified. Thus, it is clear that when blood pressure begins to rise, both mother and fetus are at increased risk. Proteinuria is a sign of worsening hypertensive disease, specifically preeclampsia. Overt and persistent proteinuria further increases maternal and fetal risks. Preeclampsia This condition is best described as a pregnancy-specific syndrome of reduced organ perfusion secondary to vasospasm and endothelial activation. Proteinuria is an important sign of preeclampsia, and Chesley (1985) rightfully concluded that the diagnosis is questionable in its absence. Significant proteinuria is defined by 24-hour urinary protein exceeding 300 mg per 24 hours, or persistent 30 mg/dL (1+ dipstick) in random urine samples. The degree of proteinuria may fluctuate widely over any 24-hour period, even in severe cases. Therefore, a single random sample may fail to demonstrate significant proteinuria. In their extensive study of renal biopsy specimens obtained from hypertensive pregnant women, McCartney and co-workers (1971) invariably found proteinuria when the glomerular lesion considered to be characteristic of preeclampsia was evident. Importantly, both proteinuria and alterations of glomerular histology develop late in the course. It is apparent that preeclampsia becomes evident clinically only near the end of a covert pathophysiological process that may begin as early as implantation. Thus, the minimum criteria for the diagnosis of preeclampsia are hypertension plus minimal proteinuria. The more severe the hypertension or proteinuria, the more certain is the diagnosis of preeclampsia (see Table 34–1). Similarly, abnormal laboratory findings in tests of renal, hepatic, and hematological function increase the certainty of preeclampsia. In addition, persistent premonitory symptoms of eclampsia, such as headache and epigastric pain, also increase the certainty. The combination of proteinuria and hypertension during pregnancy markedly increases the risk of perinatal mortality and morbidity (Ferrazzani and associates, 1990). A widely quoted study by Friedman and Neff (1976) of more than 38,000 pregnancies was completed over three decades ago. It showed that diastolic hypertension of 95 mm Hg or greater was associated with a threefold increase in the fetal death rate. Worsening hypertension, especially if accompanied by proteinuria, was more ominous, but proteinuria without hypertension was rather benign. In a recent study, however, Newman and co-workers (2003) reported that worsening proteinuria resulted in increasing preterm delivery, but that neonatal survival was not significantly altered. In contrast, following their analysis of more than 9000 nulliparous women ascertained from the Collaborative Perinatal Project, a large cohort study conducted between 1959 and 1965, Zhang and co-workers (2001) concluded that neither blood pressure severity nor proteinuria were sensitive predictors of adverse outcome. Epigastric or right upper quadrant pain is thought to result from hepatocellular necrosis, ischemia, and edema that stretches the Glisson capsule. This characteristic pain is frequently accompanied by elevated serum hepatic transaminase levels and usually is a sign to terminate the pregnancy. The pain presages hepatic infarction and hemorrhage or catastrophic rupture of a subcapsular hematoma. Fortunately, hepatic rupture is rare. Thrombocytopenia is characteristic of worsening preeclampsia, and it probably is caused by platelet activation and aggregation as well as microangiopathic hemolysis induced by severe vasospasm. Evidence of gross hemolysis such as hemoglobinemia, hemoglobinuria, or hyperbilirubinemia is indicative of severe disease. Other factors indicative of severe hypertension include cardiac dysfunction with pulmonary edema as well as obvious fetal growth restriction. Although hypertension is a requisite to diagnosing preeclampsia, absolute blood pressure alone is not always a dependable indicator of its severity. For example, young adolescent women may have 3+ proteinuria and convulsions with a blood pressure of 135/85 mm Hg, whereas most women with blood pressures as high as 180/120 mm Hg do not have seizures. A rapid increase in blood pressure followed by convulsions is usually preceded by an unrelenting severe headache or visual disturbances. For this reason, these symptoms are considered ominous.
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#75
25.07.2006, 18:44
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Eclampsia
The onset of convulsions in a woman with preeclampsia that cannot be attributed to other causes is termed eclampsia. The seizures are generalized and may appear before, during, or after labor. In older studies, in about 10 percent of eclamptic women, especially nulliparas, seizures did not develop until after 48 hours postpartum (Brown and colleagues, 1987; Lubarsky and associates, 1994). As prenatal care improved, many antepartum and intrapartum cases are now prevented, and a more recent study reported that a fourth of eclamptic seizures developed beyond 48 hours postpartum (Chames and co-workers, 2002). Preeclampsia Superimposed on Chronic Hypertension All chronic hypertensive disorders, regardless of their cause, predispose to development of superimposed preeclampsia and eclampsia. These disorders can create difficult problems with diagnosis and management in women who are not seen until after midpregnancy. The diagnosis of chronic underlying hypertension is made when: Hypertension (140/90 mm Hg or greater) is documented antecedent to pregnancy. Hypertension (140/90 mm Hg or greater) is detected before 20 weeks, unless there is gestational trophoblastic disease. Hypertension persists long after delivery. Additional historical factors that help support the diagnosis are multiparity and hypertension complicating a previous pregnancy other than the first. There frequently is also a family history of essential hypertension. The diagnosis of chronic hypertension may be difficult to make if the woman is not seen until the latter half of pregnancy, because blood pressure decreases during the second and early third trimesters in both normotensive and chronically hypertensive women (see Chap. 45, Diagnosis). Thus, a woman with chronic vascular disease, who is seen for the first time at 20 weeks, frequently has blood pressure within the normal accepted range. During the third trimester, however, if blood pressure returns to its former hypertensive level, it presents a diagnostic problem as to whether the hypertension is chronic or induced by pregnancy. In these situations, a search for evidence of end-organ damage from chronic hypertension may help elucidate the underlying cause of hypertension. Examples include left ventricular hypertrophy or retinal changes such as arteriolar narrowing, exudates, or cotton-wool spots. Some of the many causes of underlying hypertension that are encountered during pregnancy are listed in Table 34–3. Essential or familial hypertension is the cause of underlying vascular disease in more than 90 percent of pregnant women. Obesity and diabetes are other common causes. In some women, hypertension develops as a consequence of underlying renal parenchymal disease. Although earlier studies of renal biopsies identified abnormalities, especially in multiparas, Fisher and co-workers (1969) did not confirm a high prevalence of chronic glomerulonephritis. Depending on its duration, chronic hypertension can lead to ventricular hypertrophy and cardiac decompensation, cerebrovascular accidents, or renal damage. These complications are more likely during pregnancy if there is superimposed preeclampsia, which develops in up to 25 percent of these women (Sibai and colleagues, 1998). The risk of placental abruption is also increased substantively if there is superimposed preeclampsia (see Chap. 35, Etiology). Moreover, the fetuses of women with chronic hypertension are at appreciable risks for growth restriction, preterm delivery, and death. In some women with chronic hypertension, blood pressure increases to abnormal levels, typically after 24 weeks. If accompanied by proteinuria, then superimposed preeclampsia is diagnosed. Often, superimposed preeclampsia develops earlier in pregnancy than "pure" preeclampsia, and it tends to be more severe and often accompanied by fetal growth restriction. Indicators of severity shown in Table 34–2 are also used to further characterize superimposed preeclampsia. Incidence and Risk Factors Gestational hypertension more often affects nulliparous women. Because of the increasing incidence of chronic hypertension with advancing age, older women are at greater risk for superimposed preeclampsia. Thus, women at either end of reproductive age are considered to be more susceptible (see Chap. 7, Maternal Age). The incidence of preeclampsia is commonly cited to be about 5 percent, although rather wide variations are reported. The incidence is markedly influenced by parity; it is related to race and ethnicity—and thus to genetic predisposition, and environmental factors likely also play a role. For example, Palmer and associates (1999) reported that living at high altitude in Colorado increased the incidence of preeclampsia. Some investigators have concluded that socioeconomically advantaged women have a lesser incidence of preeclampsia, however, Lawlor and colleagues (2005) did not observe this in an Aberdeen cohort of 3485 women. The incidence of hypertensive disorders in healthy nulliparous women was carefully studied in a trial of dietary calcium supplementation (Hauth and colleagues, 2000). Of 4302 nulliparous women delivered at or beyond 20 weeks, a fourth developed a pregnancy-related hypertensive disorder. When all nulliparas were considered, preeclampsia was diagnosed in 7.6 percent and severe disease developed in 3.3 percent. By contrast, Vatten and Skjærven (2004) reported an incidence of preeclampsia of 2.6 percent in more than 1.6 million Norwegian nulliparas. Other risk factors associated with preeclampsia include chronic hypertension as discussed, multifetal gestation, maternal age over 35 years, obesity, and African-American ethnicity (Conde-Agudelo and Belizan, 2000; Sibai and colleagues, 1997; Walker, 2000). The relationship between maternal weight and the risk of preeclampsia is progressive. It increases from 4.3 percent for women with a body mass index less than 19.8 kg/m2 to 13.3 percent in those with a body mass index greater than 35 kg/m2. In women with twin gestations compared with those with singletons, the incidence of gestational hypertension (13 versus 6 percent) and the incidence of preeclampsia (13 versus 5 percent) are both significantly increased (Sibai and co-workers, 2000). The incidence is unrelated to zygosity (Maxwell and associates, 2001). Although smoking during pregnancy causes a variety of adverse pregnancy outcomes, ironically, smoking has consistently been associated with a reduced risk of hypertension during pregnancy (Bainbridge and associates, 2005; Zhang and colleagues, 1999). Placenta previa has also been reported to reduce the risk of hypertensive disorders in pregnancy (Ananth and colleagues, 1997). Eclampsia This condition is somewhat preventable, and its incidence has decreased in the United States because most women now receive adequate prenatal care. For example, in the 15th edition of Williams Obstetrics (1976), for the prior 25-year period, the incidence of eclampsia at Parkland Hospital was 1 in 700 deliveries. For the 4-year period from 1983 to 1986, it decreased to 1 in 1150 deliveries, and for the 3-year period ending in 1999, it was approximately 1 in 1750 deliveries (Alexander and associates, 2004). In the National Vital Statistics Report, Ventura and colleagues (2000) estimated that the incidence of eclampsia in the United States in 1998 was about 1 in 3250. In the United Kingdom in 1992, Douglas and Redman (1994) reported that the incidence of eclampsia was 1 in 2000.
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Линейный вид
