Preterm Labor

Preterm Labor

Premature delivery complicates 8 to 10% of all births in the United States, and prematurity continues to be the single greatest cause of neonatal morbidity and mortality.

A wide variety of treatments for the inhibition of labor have been advocated, including bedrest, beta-agonist agents such as terbutaline and ritodrine, magnesium sulfate (MgSO4 ), prostaglandin inhibitors, and calcium-channel blockers.

Currently, the cornerstones of pharmacologic management of preterm labor are the use of beta-adrenergic receptor agonists and MgSO4.

DIAGNOSIS

Presumptive diagnosis of premature labor may be made in the woman who

is between 20 and 37 weeks' gestation
in the presence of regular uterine contractions
occurring at intervals of 5 to 8 minutes or less
that are accompanied by one or more of the following:

progressive cervical effacement and dilation
cervical dilation of >=2 cm, or
cervical effacement of 75 to 80% or more.

Because rupture of the membranes frequently means that delivery is imminent, uterine contractions accompanied by membrane rupture may also be used to establish the diagnosis. External monitoring devices, when available, are helpful by providing objective evidence of the character of uterine contractions as well as the condition of the fetus. Extended observation is undesirable because the effectiveness of tocolytic therapy diminishes as labor advances.

MANAGEMENT

obstetric consultation should be obtained

transferred immediately to labor and delivery for monitoring and determination of fetal maturity.

When appropriate obstetric facilities are not available, attempt to arrest labor in the ED

Agents Used for the Emergency Management of Preterm Labor
Ritodrine
Dose	50 to 100 mug/min IV infusion
	Increase 50 mug/min q 10 to 20 min
Endpoint	Cessation of uterine contrations
	Intolerable maternal side effects
	Maximum dose 350 mug/min
Terbutaline
Dose	0.25 mg SQ, may repeat q 20 to 60 min
	or
	2.5 to 5 mug/min IV infusion,
	Increase 2.5 to 5 mug/min q 20 min
Endpoint	Cessation of uterine contractions
	Intolerable maternal side effects
	Maximum dose 25 mug/min
Magnesium sulfate
Dose	4 to 6 g IV over 20 min upto 2 to 4 g/hr IV infusion
Endpoint	Cessation of uterine contractions
	Signs of magnesium toxicity (e.g., depressed respirations, hypotension, somnolence)

Tocolytic Therapy

Basic maneuvers to improve uterine and fetal status should be initiated before instituting pharmacologic tocolytic therapy when either preterm labor or fetal distress is suspected.

Because uterine hypoxia may induce uterine contractions, improve uterine perfusion

supplemental O2

IV infusion of 500 mL of crystalloid

assumption of the left lateral decubitus position

Because uterine, cervical, or urinary tract infections account for 30 to 40% of cases of preterm labor, a specific cause should be sought and treated as appropriate.

If contractions persist and cervical changes are documented despite these basic interventions, pharmacologic tocolytic therapy with either the selective beta2 -adrenergic agents or MgSO4 may be indicated.

Relative contraindications to tocolytic therapy include

uncorrected fetal distress or fetal death

chorioamnionitis

ruptured or bulging membranes

obstetric complications requiring early delivery

severe pregnancy-induced hypertension

maternal hemorrhage

polyhydramnios.

beta 2 -Receptor agonists.

selective beta2 -adrenergic agents

ritodrine (Yutopar)

the only agent approved for tocolysis in the United States

IV infusion

If labor arrested, continued for at least 12 hours after contractions cease

repeated if further episodes

terbutaline (Brethine, Bricanyl)

not approved by the U.S. FDA for use as a tocolytic

terbutaline may be given subcutaneously or by IV infusion

both have beta1 -activity, responsible for their side effects. used cautiously in patients with

cardiovascular disease

hypertension

hyperthyroidism

diabetes

bronchospastic disease concurrently on sympathomimetic bronchodilator agents.

Maternal cardiovascular effects include

dose-related increase in heart rate

increase in systolic pressure

decrease in diastolic blood pressure

Pulmonary edema

chest pain, shortness of breath, tremor, nausea and vomiting, headache, or erythema

Fetal

heart rate increases slightly

Side effects are usually self-limited and resolve with dosage reduction or discontinuation of the drug. Treatment of the majority of side effects is supportive; severe cardiovascular effects may be treated with beta-blocking agents.

Magnesium sulfate

not approved in the United States for use as a tocolytic agent.

many perinatal centers prefer MgSO4 over the beta-mimetic agents

comparable efficacy

low incidence of intolerable side effects.

effect is not fully understood

4 to 6 g of MgSO4 IV over 20 to 30 minutes

maintenance IV infusion beginning at 2 g/hour

titrated to the cessation of uterine contractions or clinical evidence of magnesium toxicity

SIDE EFFECTS.

sweating, warmth, and flushing

rapid parenteral administration may cause transient nausea, vomiting, headache, or palpitations

Infrequently, pulmonary edema or chest pain : stop the drug

The first sign of magnesium toxicity, decrease of the patellar reflex, typically occurs as serum magnesium levels exceed 4 mEq/L, with loss of the reflex as levels approach 10 mEq/L.

major side effect: impairment of the muscles of respiration with subsequent respiratory arrest

usually not seen until the serum magnesium level exceeds 10 mEq/L.

Because magnesium is almost totally excreted by the kidney, magnesium is contraindicated in the presence of renal failure, and urinary output and renal function should be monitored throughout therapy.

If respiratory depression develops, 10 mL of a 10% solution of calcium gluconate or calcium chloride injected over 3 minutes is an effective antidote.

For severe respiratory depression and arrest, prompt endotracheal intubation may be lifesaving. MgSO4 should be used with caution in patients with impaired renal function or heart disease and is contraindicated in patients with myasthenia gravis.