HELLP Syndrome Medication

Updated: Jan 08, 2018
  • Author: Huma Khan, MD; Chief Editor: Ronald M Ramus, MD  more...
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Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

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Antihypertensive Agent

Class Summary

These agents reduce blood pressure through various mechanisms.

Labetalol (Trandate)

Combined alpha- and beta-adrenergic blocking agent widely used in treating hypertension during pregnancy. Not associated with mild fetal growth restriction (unlike some other beta-blockers).

Intravenous and oral forms are used as an alternative to hydralazine in severe preeclampsia/eclampsia.

Hydralazine

Decreases systemic resistance through direct vasodilation of arterioles.

Nifedipine (Adalat, Afeditab, Nifediac, Procardia, Procardia XL)

Relaxes coronary smooth muscle and produces coronary vasodilation, which in turn improves myocardial oxygen delivery. Sublingual administration is generally safe, despite theoretical concerns.

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Anticonvulsants

Class Summary

Magnesium can terminate ongoing eclamptic seizures and prevent further seizures.

Magnesium sulfate

Several studies have revealed that it is the drug of choice for treating eclamptic seizures. Successful in controlling seizures in >95% of cases. Agent gives physiologic advantages to fetus by increasing uterine blood flow.

Inhibits the release of acetylcholine at motor endplate. In addition, magnesium has direct effect on skeletal muscle by virtue of competitive antagonistic effects with calcium.

Exclusively by kidneys and has little antihypertensive effect. Effective anticonvulsant and helps prevent recurrent seizures and maintain uterine and fetal blood flow.

Can be administered both IV and IM. Intravenous route is preferred over IM route because administration is controlled more easily and time to therapeutic levels is shorter. Intramuscular administration of magnesium sulfate tends to be more painful and less convenient. If IV access or close patient monitoring is unavailable, this is an effective therapy.

Goals of magnesium therapy are to terminate ongoing seizures and prevent further seizures. Patient should be evaluated qh to assure that deep tendon reflexes are present, respirations are at least 12 breaths per min, and urine output is at least 100 mL during the preceding 4 h.

When using magnesium sulfate IV, close monitoring of patient and fetus is necessary.

Magnesium therapy usually is continued for 12-24 h following delivery and may be stopped when hypertension resolves and patient has shown adequate diuresis.

Renally compromised patients should be monitored with magnesium levels, with aggressive adjustments made to facilitate levels at 6-8 mg/dL. Patients with increased urine output may need maintenance dose increased to 3 g/h to maintain therapeutic levels. Monitor patient for signs of worsening condition and magnesium toxicity.

The Parkland IM protocol is as follows:

Magnesium sulfate 4 g IV over 5 min, plus magnesium sulfate 10 g deep IM (3-in needle) divided in both buttocks and mixed with 1 mL 2% lidocaine. If a seizure persists more than 15 min after above dose, administer an additional 2 g of magnesium sulfate IV over 3-5 min.

Magnesium sulfate 5 g IM q4h, starting 4 h later unless patellar reflexes are absent, respiratory depression occurs, or urine output is < 100 mL in the prior 4 h. Therapeutic levels are 4.8-8.4 mg/dL. With the above protocol, serum magnesium levels usually are 4-7 mg/dL in a patient with an average volume of distribution and normal renal function.

Actual serum magnesium levels are monitored only in patients with symptomatic magnesium toxicity or renal compromise.

Patients may have seizures while receiving magnesium sulfate. If seizure occurs in first 20 min after loading dose, the convulsion usually is short, and no additional treatment is indicated. If seizure occurs >20 min after the loading dose, an additional 2-4 g of magnesium may be administered.

In adults, 60-180 mEq of potassium, 10-30 mEq of magnesium, and 10-40 mM of phosphate per day may be necessary for optimum metabolic response.

Give IV/IM for seizure prophylaxis in preeclampsia. Use IV route for quicker onset of action in true eclampsia.

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Corticosteroids

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Dexamethasone (Baycadron, Maxidex, Ozurdex, Dexamethasone Intensol)

Has many pharmacologic benefits but significant adverse effects. Stabilizes cell and lysosomal membranes, increases surfactant synthesis, increases serum vitamin A concentration, inhibits prostaglandin and proinflammatory cytokines (eg, TNF-alpha, IL-6, IL-2, and IFN-gamma). The inhibition of chemotactic factors and factors that increase capillary permeability inhibits recruitment of inflammatory cells into affected areas. Suppresses lymphocyte proliferation through direct cytolysis and inhibits mitosis. Breaks down granulocyte aggregates, and improves pulmonary microcirculation. Adverse effects are hyperglycemia, hypertension, weight loss, GI bleeding or perforation synthesis, cerebral palsy, adrenal suppression, and death. Most of the adverse effects of corticosteroids are dose-dependent or duration-dependent.

Readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. Lacks salt-retaining property of hydrocortisone.

Patients can be switched from an IV to PO regimen in a 1:1 ratio.

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