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MS WordPerinatologist Corner - C.E.U/C.M.E. Modules
Hypertension in Pregnancy
Sponsored by The Indian Health Service Clinical Support Center
Part 1: Mild Pre-Eclampsia
5. Read the material on management
Antenatal management
As noted above, preeclampsia will not resolve while the placenta still functions, and delivery remains the only "cure". The decision to deliver a woman with preeclampsia however depends on a balance of both the maternal and fetal risks. Continued observation is appropriate for the woman remote from term as long as her disease remains mild. This requires frequent periodic evaluation, usually twice weekly, and the woman may be managed at home if logistically feasible.
Bedrest
There is not consistent Level I data to support the use of bedrest to improve the maternal or fetal outcomes in pre-eclampsia.
Bed Rest for pregnancy related hypertension: Evidence is Weak
Authors' conclusions: Few randomised trials have evaluated rest for women with hypertension during pregnancy, and important information on side-effects and cost implication is missing from available trials. Although one small trial suggests that some bed rest may be associated with reduced risk of severe hypertension and preterm birth, these findings need to be confirmed in larger trials. At present, there is insufficient evidence to provide clear guidance for clinical practice. Therefore, bed rest should not be recommended routinely for hypertension in pregnancy, especially since more women appear to prefer unrestricted activity, if the choice were given.
Meher S, Abalos E, Carroli G. Bed rest with or without hospitalisation for hypertension during pregnancy.
The Cochrane Database of Systematic Reviews 2005, Issue 4. Art. No.: CD003514.pub2. DOI: 10.1002/14651858.CD003514.pub2
Sodium
Sodium restriction is futile as this mechanism is not operant in this disease the way it is in essential hypertension. The physiology of pregnancy is set up to raise cardiac output to meet the demands of the fetoplacental unit. This is accomplished by expanding stroke volume (preload) through retention of sodium and water, and this potent pregnancy-specific physiology cannot be readily reversed.
Pharmacotherapy
Pharmacotherapy also has very little place in the management of this disorder. "Prophylactic" anticonvulsant therapy or maternal sedation with phenobarbital is of unproven benefit and may have adverse fetal effects. It is probably inappropriate to try to lower the elevated BP with oral anti-hypertensive therapy. Again, this is not the same disease that your non-pregnant hypertensive patients have! If the pressure is >160/110, the patient needs to be delivered. If the pressure remains in the non-severe range, and all else is stable, reduction of perfusion pressure will only have adverse effects on the already compromised uteroplacental perfusion. This concept is somewhat different for women with chronic hypertension, as will be discussed below.
Clinic follow-up
In addition to frequent evaluation of maternal blood pressure, weight, serial reflexes, and symptoms, an initial baseline laboratory assessment including CBC (hemoconcentration?), platelet count (thrombocytopenia?), creatinine (normal renal function?), and liver enzymes (signs of early hepatic involvement?) is useful. This panel may be repeated weekly, but as noted above, the diagnosis of preeclampsia is largely clinical, and patients who are developing severe preeclampsia will usually manifest it by the development of symptoms, not early changes in biochemical parameters.
Antenatal fetal surveillance
Recommendations for fetal surveillance depend on the severity of the disease and are largely formulated on the basis of "expert opinion" rather than the results of randomized trials. For women with mild preeclampsia, a baseline ultrasound for fetal growth and amniotic fluid index (AFI) should be obtained at diagnosis. Non-stress testing should be initiated and repeated on a weekly basis, but if fetal growth restriction or oligohydramnios are diagnosed (more common in women with chronic hypertensive, not "pure" preeclampsia), testing should be carried out twice weekly, or more frequently depending on fetal status. Testing should be repeated at any time there is an abrupt change in maternal condition. Placental abruption always remains a threat to the fetus of the hypertensive woman.
Where to deliver?
The management of a woman with preeclampsia is best accomplished in a referral setting or in consultation with an obstetrician--gynecologist with training, experience, and demonstrated competence in the management of high-risk pregnancies. Invasive hemodynamic monitoring should be considered in preeclamptic women with severe cardiac disease, renal disease, refractory hypertension, pulmonary edema, or unexplained oliguria.
Intrapartum management
There is probably no benefit in delaying delivery once the patient has reached term. With the introduction of the current prostaglandin preparations, the "unripe" cervix is usually no longer a major obstacle to promptly establishing labor. Any deterioration of maternal or fetal condition with the development of severe preeclampsia prior to term is an indication for prompt delivery.
Mode of delivery
There is no demonstrated benefit to cesarean delivery for other than the usual obstetric indications. Rushing to operation in the unstable severe preeclamptic may be hazardous. Induction of labor is safe with either oxytocin or prostaglandins. If analgesia/anesthesia is required, regional or neuraxial analgesia/anesthesia should be used because it is efficacious and safe for intrapartum management of women with severe preeclampsia in the absence of coagulopathy.
Magnesium sulfate
Magnesium sulfate (MgSO4) is the mainstay of intrapartum therapy in the United States for both mild and severe preeclampsia. There is not enough Level I evidence to establish the benefits and hazards of anticonvulsants for women with pre-eclampsia. If an anticonvulsant is used, magnesium sulphate appears to be the best choice. (Duley: Cochrane Library) Outside the United States, MgSO4 is only used for severe, not mild, preeclampsia, because it has been demonstrated that over 500 mild preeclamptic women have to be treated to prevent one seizure. (One in 30 severe preeclamptic women may seize if untreated.) Nevertheless, because of its ancillary salubrious effects on the disease process, it remains the drug of choice for all patients with the disease in this country.
It is primarily used for the prevention of seizures, but has many other advantages and is key for stabilizing the patient. Contrary to traditional teaching, MgSO4 is a vasodilator, and, because it is a calcium-channel blocker, it is able to reverse vasospasm, lower blood pressure, and enhance perfusion. In addition to lowering the seizure threshold through its interference with the function of the excitatory neuronal NMDA (N-methyl d-aspartate) receptors, it is also an especially effective cerebral vasodilator and will help reverse the hypoxic-ischemic process that sets up the seizure focus. Other anticonvulsants, such as phenytoin have been used for seizure prevention, but they do not have the other beneficial effects of magnesium, and the data clearly show an advantage to the use of the latter.
Intravenous administration of MgSO4
- Magnesium sulfate is usually administered intravenously. A loading dose of 4-6 g diluted in 100 mL D5W is given over 15 minutes, and is followed immediately by a maintenance drip of 1-3 g per hour. Urine output, deep tendon reflexes, respirations and O2 saturation are probably better parameters to follow than serum magnesium levels.
- Magnesium is a simple cation and is almost completely eliminated by the kidneys in about 15 minutes in women with normal urine output, so the maintenance drip needs to be started immediately after the loading dose in order to achieve the therapeutic effect. Likewise, women with an elevated creatinine (normal in pregnancy is 0.4-0.6 mg/dL, secondary to enhanced glomerular filtration), or poor output, need more vigilance, and utilization of the lower end maintenance rate. Because it is a calcium channel blocker, MgSO4 will also have effects on skeletal muscle, particularly the accessory respiratory musculature, and O2 saturation monitoring is very helpful. This is especially true if renal function is compromised.
Intramuscular administration of MgSO4
- MgSO4 may also be given intramuscularly (at a dose of 10 g mixed with 10 mL of 1% lidocaine and divided between the buttocks) if IV access is logistically problematic, but it is painful and levels may be somewhat unpredictable.
- Despite popular wisdom, the evidence demonstrates that the length of labor
is not different between preeclamptic women "on mag" and parturients being induced
for other reasons, however, labor may be more difficult to initiate, and postpartum
hemorrhage is definitely increased, because magnesium also blocks calcium entry
into uterine smooth muscle.
Postpartum management
Be prepared for postpartum hemorrhage, and remember that ergot preparations, such as methergine, are potent vasoconstrictors, and are contraindicated in preeclamptic women. Oxytocin should be used initially for uterine atony. Rectal misoprostol, a prostaglandin, may be very effective, but has been insufficiently studied to be able to recommend it as a first-line agent at this time., There is little evidence about the optimum length of time MgSO4 should be continued postpartum, but 12-24 hours is usually sufficient, depending on the severity of the disease process. Remember that in as many as 2-4% of women, eclampsia may occur for the first time in the 48 hours following delivery. Watch urine output carefully as postpartum diuresis may be delayed for several days, and magnesium toxicity may develop if the dose is not adjusted appropriately.
Fluid balance
Fluid balance is one of the most critical aspects of the care of the severe preeclamptic woman, because of the fluid compartment shifts so common to this disease. Starling's law of the capillary is helpful to remember here: the low oncotic pressure (secondary to heavy proteinuria), and the high hydrostatic pressure (secondary to hypertension), typical of this disease, favor movement of fluid out of the intravascular space, and into the interstitial space. On admission patients are thus typically intravascular volume depleted and hemoconcentrated with poor urine output and exaggerated vasospasm.
Initial hydration
Initial rapid hydration with 1-2 L of crystalloid is usually helpful to reverse those effects and, often of itself, will foster lowering of the blood pressure. However, fluid will continue to leak into the interstitium and predispose the patient to cerebral or pulmonary edema, so cautious fluid administration is in order, usually 100 mL/hour total fluids, enough to maintain urine output at or slightly above 30 mL/hour. Administration of dextrose in water will only increase "third-spacing" and Ringers or saline should be the solution of choice. Administration of colloids would seem to be a logical solution in this setting, but they have not been shown to be superior to crystalloid and are significantly more costly.
On-going fluid monitoring
"Compulsive" I&O's are critical! Adequate hydration is especially important prior to administration of parenteral anti-hypertensive agents or regional anesthesia because a sudden drop in vascular resistance without volume expansion is very likely to provoke placental hypoperfusion and resultant fetal distress.
Parenteral anti-hypertensive agents
Parenteral anti-hypertensive agents are required in very few women if hydration and magnesium sulfate have been administered to treat the pathophysiology detailed above. For those women whose blood pressure has not been lowered below 160/110 by those measures, hydralazine or labetalol may be considered.
- Hydralazine is a direct arteriolar vasodilator and is the classic drug for this indication. It is administered in 5 mg IV boluses 20 minutes apart, or in a drip of 25 mg in 250 mL of saline on a pump at 15 mL/hr (0.025 mg/min), increased by 15 mL/h q20 min as needed. The goal is to lower the diastolic pressure to 95-100 mm Hg, not make the patient normotensive. Fetal distress is commonly produced by underestimating the cumulative effect of this drug.
- Labetalol is a beta-1 blocker (lowers heart rate and inotropy), a beta-2 agonist (vasodilates), and an alpha-1-antagonist (reverses vasoconstriction). It is not associated with the abrupt drop in pressure commonly seen with hydralazine. Begin with an IV bolus of 10 mg and double the dose (20 mg, 40 mg) every 5-10 minutes until the diastolic comes into the 95-100 range. Continue 40 mg doses until either 200 mg has produced no effect or 300 mg has been given total in 24 hours. About two thirds of patients will respond to this agent. Adding a small dose of hydralazine for those women to whom you have already administered labetalol without the desired effect, will often be effective. Postpartum any agent is usually acceptable.
- Other agents. Angiotensin converting enzyme inhibitors probably work best for the pathophysiology of the disease, but are relatively contraindicated in breastfeeding mothers. Nifedipine 10 mg orally q4-6 h prn diastolic BP>110 is also usually very effective, but remember, combining it with MgSO4, another calcium channel blocker, may potentiate the effects of the latter.
Long-term prognosis
The long-term prognosis for women who have experienced preeclampsia is somewhat population dependent. For Caucasian women, a 10% recurrence of the disease in the next pregnancy is possible, and the incidence of chronic hypertension later in pregnancy is also about 10%, no different than that of the general population. These numbers are doubled for African-American women however. The data specifically available for Native American women show 12.6% in the Navajo though other hypertensive disorders have been increasing recently in Native Americans. Women with early onset preeclampsia (late second or early third trimester occurrence) may have up to a 40% recurrence rate in a subsequent pregnancy. Multiparous women and women who have experienced recurrent preeclampsia have a much higher incidence of eventual chronic hypertension.
Is preeclampsia preventable?
To date the answer is no.
Large randomized trials of both low dose aspirin supplementation and calcium
supplementation have shown no benefit. Negative results for fish oil supplementation
have likewise been the result in three smaller trials. Antioxidants (vitamins
C and E) have shown an effect in one trial, but this awaits confirmation. Smoking
actually reduces the incidence of the disorder, but has obvious other negative
general and fetal health aspects. A high protein diet has not been shown to be
of benefit.
These results are probably to be expected. A disease with this complex a pathophysiology,
that may commence at the time of conception, and which may have a genetic component,
would not be expected to respond to a single simple intervention late in gestation.
