preeclampsia (sp)

I had it at 30 weeks and had to deliver asap.  He wants to see you every week to keep track of your vitals and protein levels.  If they get too high, you'll have to deliver.

I'm sorry. I don't know much about pre-e. If you have questions, you should call and talk to your doctor or his nurse. They can give you more info.

I was borderline for my last and I am heading in that direction again.  I hate to say this, but we all know it is true - the worst thing for you to do about it is to freak out!  Stress is bad for the body and one of the biggest issues is high blood pressure.  Some markers are headaches, high blood pressure, swelling and protein in your urine.  The reason they will often induce is that if preeclampsia turns into eclampsia you could have seizures, which will reduce oxygen to the fetus.  Don't freak out!  Eclampsia (seizures) happens in less than 1% of women.  Until your doc can see you, WebMD has excellent resources of information if you want to read more.  There are treatments, medication they can give you to keep this under control.  However, and I can't stress this enough to all pregnant women, DO NOT leave his office again with questions.  Write everything you can think of now, and bring them with you - talk to your SO about their questions and do not let the doc leave that room until you feel everything has been answered.  A lot of dr's assume we know a lot and don't know what we don't know.  ASK.  Ask about treatment options, ask about signs to look for that it is getting worse, ask about what you can do (rest, etc.) to keep it from getting worse.  For them, this is an everyday thing and I think they forget how new and different this is for you.  Let them know if you are concerned - they need to know that so they can keep you calm.  Good luck - preeclampsia doesn't always result in inductions - I don't know what your other risk factors are.  But, deep breaths....take it easy....

Thank you

I've had it with all 3, and diagnosed way earlier than yourself! What were the symptoms that led him to his diagnosis?

You and the baby can die or have a stroke when blood pressure rises too high.

I had it with all three. Only my first was born early, though I was always induced. They will watch your blood pressure. The will check your urine at each appointment for protein. They will give you warning signs to watch for, upper right quadrant pain, headache and swelling. You will be induced if you have certain symptoms. They watch so close, because if you get worse and get eclampsia or HELLP you can end up with a stroke or other problems. Please know that if you do need to go early, you do NOT need a c section. (Unless you want one... I can see how that might be.) Ask about BP meds. They are the reason I made it to 37 with my last child. I could not be on them with my first because she was not growing. Ask questions! ask how often the will be testing your platelet count and liver enzymes, how often you will have an ultra sound to monitor growth (bio physical profile) Ask what other tests they will be doing. Rest. Try not to worry. I have 3 healthy kids and I spent between 6 and 20 weeks on bed rest.

Go to the health food store and pick up some magnesium supplements (chelated, capsules) and start taking at least 200mg 3x day with food.  Pre-eclampsia is a magnesium deficiency disorder.  Also, pick up some epsom salts (magnesium sulfate) and put them it in your bath to soak in or in a foot bath.  

http://www.mgwater.com/Seelig/Magnesium-Deficiency-in-the-Pathogenesis-of-Disease/chapter2.shtml

2.3.2. Preeclampsia and Eclampsia: Magnesium Levels and Treatment

The use of magnesium salts parenterally for control of manifestations of acute eclampsia long antedated the demonstration that serum levels of magnesium tend to be lower in women with toxemic pregnancies (especially early in the course of pregnancy) than they are during normal pregnancies. Less reliable as an index of magnesium deficiency of toxemic pregnancy is the serum level toward the end of gestation, when renal damage can interfere with magnesium excretion, as it does in patients with nephritis. The first published reports of the anticonvulsant properties of magnesium sulfate in eclampsia appeared in Europe (Einar, 1907; Kaas, 1917). It became a favored treatment of convulsions of pregnancy in the United States from the time Lazard (1925) and McNeile and Vruwink (1926) recommended its use intravenously, Dorsett (1926) described its use intramuscularly, and Alton and Lincoln (1925) reported its use intrathecally. Hirschfelder (1934) first reported a markedly low serum magnesium level (0.8 mEq/liter) in a 47-year-old patient with eclampsia, who then responded favorably to high dosage oral magnesium sulfate therapy. Among eight eclamptic women, Haury and Cantarow (1942) reported three with serum magnesium levels of 0.8-1.0 mEq/liter and three with levels of 2.7-3.2 mEq/liter. Their stages of pregnancy were not given. Achariet al. (1961) reported that 21 eclamptic women had a mean serum magnesium level of 0.83 mEq/liter (range = 0.25-1.84). Eclamptic women frequently have higher plasma or serum magnesium levels toward the end of pregnancy than do normal pregnant women at term (Pritchard, 1955; Hall, 1957; Kontopoulos et al. 1976/1979), but such normal or even elevated levels are not considered a contraindication to the use of large doses of magnesium salts, which are administered parenterally for their pharmacodynamic neurosedative, antihypertensive effects and not to correct a deficiency. As much as 200 mg of magnesium an hour, given intravenously as the sulfate, was recommended in the early studies (Lazard, 1925, 1933; McNeile, 1934; Winkler et al., 1942). This route is recommended by many either as the sole approach (Zuspan and Ward, 1964, 1965; Zuspan, 1966, 1969; Harbert et al., 1968; Hutchinson et al., 1963), or in combination with intramuscular injections (Pritchard, 1955; Flowers et al. 1962; Flowers, 1965, 1975; Kontopoulos et al., 1976/1980, Weaver, 1976/1980; Flowers et al., 1962, Fig. 2-3). Pritchard (1955) observed that administration of large doses of epsom salts orally exerted no effect on the plasma magnesium levels. Since only 5% of the administered dose appeared in the urine, the possibility that only a small percentage of the administered dose was absorbed was considered. However, even after administration of 150 g of magnesium sulfate intramuscularly over a five-day period, he found that the plasma levels were maintained between 3.5 and 7 mEq/liter. When treatment was initiated with 4 g of MgSO 4 intravenously, there was an initial peak, followed by a prompt rapid fall and then a gradual decline. He found that the cerebrospinal fluid magnesium levels did not reflect the high plasma levels induced by therapy. Flowers (1965) found it necessary to use a mean of 70 g of magnesium sulfate over a three-thy period to control eclampsia. Similarly, Harbert et al. (1968) found it necessary to use 40-60 g of magnesium sulfate per 24 hours to maintain neurosedative serum levels of magnesium of 6-8 mEq/liter. Perhaps the failure to develop hypermagnesemia more frequently toward the end of an eclamptic pregnancy and the difficulty in maintaining pharmacologic blood levels may reflect not only repletion of maternal stores but high fetal requirements, which might not have been supplied during the abnormal pregnancy.

2.3.2.1. Possible Contribution of Magnesium Deficiency to Eclamptic Pregnancy

Hall (1957), because of the experimental and clinical evidence that magnesium deficiency is associated with neuromuscular irritability and convulsions, and because of the long-recognized efficacy of magnesium in the management of preeclampsia and eclampsia, considered the possibility that magnesium deficiency might contribute to toxemia of pregnancy. He found that the mean of plasma magnesium levels had been somewhat lower among toxemic than among normal pregnant women from the 12th through the 25th week. He charted a tendency of the magnesium levels to rise slightly toward the end of pregnancy in toxemic women (Fig. 2-2, Hall, 1957), a finding that might be related to increasing renal damage in that group. The percentage variations from the normal nonpregnant levels were as great as 50%-90% below the mean at different times during pregnancy. However, since the differences between the levels in the normal and toxemic pregnant women were not statistically significant, Hall questioned whether the low magnesium levels contributed to the symptoms of toxemia. Two years earlier a preeclamptic woman with pseudohypoparathyroidism (serum calcium of 4-6 mg percent and lack of response to PTH), and hypomagnesemia (1.1 mEq/liter) associated with mental aberrations, had been reported from the same medical center (Suter and Klingman, 1955). The possibility was considered that lowered serum magnesium levels during pregnancy might predispose to seizures during pregnancy in susceptible women, such as those with a tendency toward epilepsy (Suter and Klingman, 1957). Flowers et al. (1965) suggested that depletion of tissue stores of magnesium might explain eclamptic patients' tolerance and requirement for such large doses of magnesium. McGanity (1965) proposed that dietary magnesium deficiency might be etiologic in preeclampsia.

In France, where latent tetany had long been recognized as a manifestation of subacute magnesium deficiency (Durlach and LeBrun, 1959; 1960; Durlach, l969a) uterine cramps and abnormal contractility during pregnancy have been shown to be responsive to treatment with magnesium, and have been proposed as a manifestation of its deficiency (Dumont, 1965; Muller, 1968; Muller et al., 1971/l973).It was observed that patients with this complaint frequently also exhibited latent tetany and often had marginal hypomagnesemia (1.5 mEq/liter or lower levels), with and without hypocalcemia (Dumont, 1965). Uterine hypercontractility has been added to the signs of toxemia of pregnancy and has also responded to intravenous magnesium therapy (Hutchinson et al., 1963; Cobo, 1964).

The efficacy of pharmacologic doses of magnesium in the treatment of manifestations of toxemias of pregnancy has led to consideration of magnesium as a drug, in that condition, far more commonly than consideration of the fact that it is a nutrient, the supply of which must be increased substantially during gestation. Two years before hypomagnesemia was first reported in an eclamptic woman (Hirschfelder, 1934), magnesium deficiency was associated with abnormalities of pregnancy and during early lactation in cows (Sjollema, 1932). Neuromuscular manifestations in pregnant and lactating herbivores included tetany and convulsions; cardiovascular lesions were found at autopsy (Sjollema, 1932; Rook and Storry, 1962; Storry and Rook, 1962; Rook, 1963; Herd, 1966a,b; Hjerpe, 1971). Magnesium deficiency has been accepted as contributory to toxemia of pregnancy in grazing animals, and magnesium recognized as protective.

The possibility is increasingly being considered that magnesium deficiency can also contribute to major and lesser manifestations of toxemias of pregnancy (Dumont, 1965; McGanity, 1965; Lim et al., 1969b; Muller, 1968; Muller et al., 1971/1973; Hurley, 1971; Seelig, 1971; Seelig and Bunce, 1972; Kontopoulos et al., 1976/1980; Weaver, 1976/1980). There is evidence that the magnesium intake during pregnancy is likely to be suboptimal (Review: Seelig, 1971). That it might be sufficiently low to contribute to early and late abnormalities of pregnancy is suggested by the survey that showed magnesium intakes during pregnancy that are low (N. Johnson and Philipps, 1976/1980), even by standards for nonpregnant women (Seelig, 1964). The women with the lowest magnesium intakes gave birth to low-birth- weight infants, a finding that suggests intrauterine growth retardation. Mahran and Hanna (1968) expressed concern about the magnesium deficit, early in gestation, that might be caused by hyperemesis gravidarum. When one considers how frequently lesser degrees of nausea and vomiting (i.e., "morning sickness") interfere with proper nutrition in the first trimester, and one recalls the evidence that hypomagnesemia is encountered at that time (de Jorgeet al., 1965a,b) and shortly thereafter (Hall, 1957), the possibility of early magnesium deficiency being etiologic in abnormalities of pregnancy, placental abnormalities, intrauterine malnutrition, and fetal abnormalities should be seriously entertained. That hyperemesis can precipitate acute hypomagnesemia later in pregnancy was demonstrated in a report by R. Fraser and Plink (1951) of a 33-year-old woman who developed hypochloremic, hypokalemic alkalosis in association with hypomagnesemia a few days before delivery of her eighth child. It should be noted that so young a woman, completing her eighth pregnancy, would be expected to be magnesium depleted.

Just extra monitoring to make sure you and the baby are safe.  Good luck!

Yep what she said. I had it with all of mine and the only one I had to get indices before 35 weeks is my youngest.

Quoting jillbailey26:

I had it at 30 weeks and had to deliver asap.  He wants to see you every week to keep track of your vitals and protein levels.  If they get too high, you'll have to deliver.