What it is:The art of treating a person who happens to be growing another person at the same time. Almost every drug decision in pregnancy is a two-patient calculation, and almost every drug decision in lactation is a one-and-a-half-patient calculation (the infant gets a fraction, not the full dose).
The core problem:Pregnancy rewires absorption, volume of distribution, protein binding, and clearance, so "normal" adult dosing can under- or overshoot. Meanwhile the placenta isn't a wall, it's a filter that lets most small, lipophilic drugs through. The question is never "does it cross," it's "how much, and when does that exposure matter."
What you do about it:Pick agents with the strongest safety data, dose at the low end, cut anything nonessential, and think hard about timing. The same drug can be fine in the third trimester and devastating in week 6.
The organizing idea for this whole chapter: the untreated disease is usually more dangerous to the fetus than the medication is.Uncontrolled asthma, epilepsy, HIV, depression, or hypertension all cause worse outcomes than the drugs used to treat them. Don't let "it's pregnancy" become a reason to withhold necessary therapy. It's a reason to choose the best-studied option and use the lowest effective dose, not a reason to do nothing.
Pregnancy runs about 280 daysfrom the first day of the last menstrual period, split into three trimesters of three calendar months each. Hypertensive disorders of pregnancy (HDP) get their own four-way classification, and mixing these up is a classic exam trap because the management differs for each.
| Category | Definition | Notes |
|---|---|---|
| Chronic HTN | Preexisting HTN, or new HTN found before 20 weeks gestation | Affects up to 8–10% of pregnancies |
| Gestational HTN | New SBP >140 or DBP >90 after 20 weeks, withoutproteinuria or end-organ dysfunction | 15–45% progress to preeclampsia |
| Preeclampsia | New HTN withproteinuria or end-organ dysfunction after 20 weeks | Can be the first sign of any HDP, not just a progression |
| Chronic HTN + superimposed preeclampsia | Worsening HTN plus new-onset proteinuria after 20 weeks, in someone who already had chronic HTN | Higher risk than either condition alone |
Proteinuria is no longer required to diagnose preeclampsia.The old teaching (HTN + proteinuria + edema) is outdated. New-onset HTN after 20 weeks plus anyevidence of end-organ dysfunction (thrombocytopenia, renal insufficiency, impaired liver function, pulmonary edema, new headache or visual symptoms) is enough, even with a clean urine dip. Dependent edema was dropped as a defining feature entirely, since most pregnant patients swell to some degree.
Diagnostic BP thresholds:HTN in pregnancy = SBP ≥140 mm Hg or DBP ≥90 mm Hg on two measurements at least 4 hours apart. Severe HTN = SBP >160 or DBP >110 on two measurements at least 15 minutes apart, and it gets treated urgently regardless of what category it falls under.
Read this section before anything else in the chapter. Every dosing quirk downstream traces back to one of these four changes.
| System | Change | Clinical consequence |
|---|---|---|
| Absorption | Delayed gastric emptying, vomiting, ↑ gastric pH | Altered absorption of weak acids and bases; erratic oral dosing when nauseated |
| Distribution | Plasma volume ↑50%, body fat ↑, albumin ↓ | ↑ Vd for fat-soluble drugs; ↑ Vd for highly protein-bound drugs (but often little net serum change, since free drug clears faster too) |
| Elimination - renal | Cardiac output ↑30–50%, GFR ↑50–80% | Lower plasma concentration of renally cleared drugs; may need higher or more frequent dosing |
| Elimination - hepatic | ↑ Hepatic perfusion; estrogen/progesterone alter enzyme activity | Faster clearance of some drugs, accumulation of others - unpredictable without drug-specific data |
Transfer depends mostly on molecular weight. Drugs under 500 Da cross readily. Those 600–1000 Da cross more slowly. Those over 1000 Da, like insulin and heparin, don't cross in meaningful amounts.Lipophilic drugs (opioids, many antibiotics) cross more easily than water-soluble ones, and some protein-bound drugs actually reach higherconcentrations in the fetal compartment than in the pregnant patient's own plasma.
Insulin and heparin (and LMWH) are first-line in pregnancy for diabetes and VTE because they're too big to cross the placenta, not just because someone decided they were "safer." That's a pharmacokinetic fact, not a policy choice, and it explains why you'll see both drugs reappear throughout this chapter as the default answer whenever a chronic disease needs treatment.
Baseline congenital malformation risk in the general population is 3–5%, and less than 1% of all birth defectsare caused by medication exposure. What that 1% looks like depends entirely on whenexposure happens.
Non-drug exposures matter too and often get underweighted in the literature: tobacco, alcohol, recreational substances, environmental exposures, and uncontrolled maternal disease all independently worsen outcomes.
Four principles drive every prescribing decision in this chapter: (1)choose agents with the strongest safety data, (2)dose at the low end of the effective range, (3)eliminate anything nonessential and discourage self-medication, and (4)avoid medications known to be harmful outright.
| Complaint | Approach |
|---|---|
| Constipation | Fiber, fluids, and exercise first. If needed: supplemental fiber, stool softener, or intermittent PEG/lactulose/sorbitol. Senna and bisacodyl occasionally. Avoid castor oil and mineral oil; avoid magnesium/sodium salt-based laxatives regularly (electrolyte imbalance). |
| GERD | Lifestyle first (small frequent meals, avoid alcohol/tobacco/caffeine, avoid food before bed, elevate head of bed). Then aluminum/calcium/magnesium antacids, sucralfate, or H2 blockers (cimetidine). PPI if H2 blocker response is inadequate. Avoid sodium bicarbonate and magnesium trisilicate. |
| Hemorrhoids | High fiber, adequate fluids, sitz baths. Add laxatives/stool softeners if inadequate. Topical anesthetics, protectants, and astringents for irritation; topical hydrocortisone for inflammation/pruritus. |
| Nausea/vomiting | Nonpharm same as GERD, plus acupressure and trigger avoidance. Pharm ladder below. |
First line (ACOG):pyridoxine alone or combined with doxylamine. Second line:dimenhydrinate, diphenhydramine, prochlorperazine, promethazine. Third line:metoclopramide, ondansetron, trimethobenzamide.
Metoclopramide and phenothiazines(prochlorperazine, promethazine) can cause sedation and extrapyramidal effects. Ondansetroncarries an association with oral clefts. None of these are absolute contraindications, but they're why pyridoxine/doxylamine gets tried first rather than reaching straight for the most effective antiemetic.
Hyperemesis gravidarum(severe N/V with >5% prepregnancy weight loss, dehydration, and ketonuria) can respond to corticosteroids, but hold them until after 10 weeksgestation because of an associated oral cleft risk earlier in pregnancy.
Every pregnant patient without preexisting T1DM or T2DM gets screened for gestational diabetes mellitus (GDM), typically around 24–28 weeks gestation. Patients at high risk get screened earlier, at the first prenatal visit.
Early in pregnancy, placental hormones promote lipogenesis and pancreatic beta-cell proliferation, building up insulin-secreting capacity. As pregnancy progresses, those same placental hormones (notably human placental lactogen/hCS) flip toward increasing maternal lipolysis and insulin resistance while inhibiting glycogenesis. That's not a bug, it's the placenta deliberately keeping more glucose circulating for the fetus by making the mother's own tissues less responsive to insulin. The pancreas compensates by secreting more insulin. GDM is what happens when beta-cell compensation can't keep upwith the resistance the placenta is generating.
The same placental hormone driving the insulin resistance is exactly why insulin doesn't cross the placentaand remains first-line: it treats the mother's glucose without adding fetal exposure. Glyburide and metformin are alternatives, but with less long-term safety data and, per the handbook, they may not control glucose as effectively as insulin.
| One-Step Method | Two-Step Method |
|---|---|
| 75-g OGTT, fasting overnight ≥8h. Plasma glucose at fasting, 1h, 2h. Any onevalue meeting/exceeding fasting 92, 1h 180, or 2h 153 mg/dL confirms GDM. | Step 1:50-g nonfasting load, glucose at 1h. If ≥140 mg/dL, proceed to step 2. Step 2:100-g OGTT, glucose at fasting/1h/2h/3h. At least twovalues meeting/exceeding fasting 95, 1h 180, 2h 155, or 3h 140 mg/dL confirms GDM. |
Some providers use a lower step-1 threshold of 130–135 mg/dL; the American Diabetes Association recommends 140 mg/dL.
First line:exercise, dietary modification, caloric restriction if obese, and daily self-monitoring of blood glucose. If lifestyle measures don't achieve control, start medication when fasting glucose consistently >95 mg/dL, 1-hour postprandial consistently >140 mg/dL, or 2-hour postprandial consistently >120 mg/dL. Insulin is first-line pharmacotherapy; glyburide and metformin are alternatives.
Screen everyone diagnosed with GDM with a 2-hour OGTT at 4–12 weeks postpartumto catch preexisting type 2 diabetes that pregnancy unmasked.
HDP complicates up to 10% of pregnanciesand is a leading cause of maternal and fetal morbidity and mortality worldwide. Preeclampsia specifically affects 2–8%of pregnancies globally and accounts for an estimated 16.1% of maternal deathsin developing countries.
Preexisting hypertensive disorder, diabetes (any type), chronic kidney disease, obesity, maternal age >35, genetic predisposition, family history, nulliparity, multifetal pregnancy, and IVF conception.
Stage I (first/second trimester):shallow trophoblast invasion causes poor spiral artery remodeling, so the arteries stay constricted instead of becoming the low-resistance, high-flow vessels normal pregnancy requires. That produces reduced placental perfusion.
Stage II (third trimester):the underperfused placenta releases factors that cause systemic endothelial disruption, vasospasm, and coagulation abnormalities. That single mechanism explains the entire clinical picture: vasospasm→ hypertension, cerebral vasospasm (headache, hyperreflexia, seizures), retinal arteriolar spasm (visual changes, scotoma); glomerular endotheliosis→ proteinuria, ↑ SCr and uric acid, oliguria; hepatic ischemia→ elevated liver enzymes, RUQ pain, nausea; coagulation abnormalities→ HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets).
BP >160/110 mm Hg · platelets <100,000/mm³ · impaired liver function · SCr >1.1 mg/dL and rising · pulmonary edema · new visual disturbance or RUQ pain. Any one of these reclassifies the patient and accelerates the delivery timeline.
For patients at risk, low-dose aspirin (81–162 mg/day)starting weeks 12–28 of gestation reduces preeclampsia risk, and also lowers preterm birth, intrauterine growth restriction, and perinatal mortality. Nonpharmacologic measures - stress reduction and light exercise or activity restriction - matter too: exercise more than 50 minutes 3 days a week can reduce HTN incidence roughly threefold compared to a sedentary pregnancy. Calcium supplementation (1.5–2 g elemental calcium) is another studied option; vitamins C and E have not shown effectiveness. A history of preeclampsia raises recurrence risk in a future pregnancy roughly 10–15-fold, which is worth flagging at every subsequent pregnancy intake.
Pharmacologic therapy starts once BP is persistently ≥160/110 mm Hg. When treating, the target is SBP 120–160 and DBP 80–105 mm Hg, not a normal nonpregnant target. If there's no end-organ damage and SBP stays below 160 with DBP below 105, guidelines don't recommend starting pharmacologic therapy at all - overshooting the BP reduction can compromise uteroplacental flow.
| Drug | Dose | Notes |
|---|---|---|
| Acute, severe HTN (SBP>160 or DBP>110) - reduce over hours, not minutes | ||
| Labetalol | IV, dosed to response | Avoid in asthma or bradycardia (nonselective β-blockade) |
| Hydralazine | 5 mg IV or 10 mg IM, repeat 5–10 mg q20–30min, max 20 mg IV / 30 mg IM | Direct vasodilator; can cause rebound tachycardia and hypotension |
| Nifedipine (immediate-release, oral) | Per protocol | Expect flushing, peripheral edema, reflex tachycardia, headache |
| Chronic oral maintenance | ||
| Labetalol | 200–1200 mg/day in 2–3 divided doses | First-line chronic agent alongside nifedipine |
| Nifedipine (extended-release) | 30–120 mg/day | Twice-daily dosing is a practical limitation |
| Methyldopa | 250–800 mg PO q8h | Reduces SVR; expect headache, flushing, tachycardia. Second/third line |
| Hydrochlorothiazide | - | Second or third line |
Atenolol, ACE inhibitors, ARBs, renin inhibitors, and mineralocorticoid receptor antagonists are not recommended in pregnancy.Clonidine and prazosin are generally reserved for patients closely followed by a specialist. This is a favorite place for exam writers to hide a "which of these is contraindicated" question - if you see an ACEi/ARB as an answer choice for a pregnant patient, it's wrong.
Eclampsia = preeclampsia + new-onset generalized tonic-clonic seizures(or coma) in a patient without a preexisting seizure disorder. It's a medical emergency. Epidemiologically it occurs in roughly 1.5–10 per 10,000 deliveries.
Magnesium sulfate is a seizure prophylaxis/treatment drug, not an antihypertensive.It's given for eclampsia and severe preeclampsia (or after a cesarean delivery done for preeclampsia) specifically to decrease progression to eclampsia and to treat eclamptic seizures once they start. Blood pressure gets managed separately with labetalol/nifedipine/hydralazine.
Loading dose 4–6 g IV, followed by a maintenance infusion in the 1–3 g/hour rangeper institutional protocol, started during active labor and continued 12–24 hours postpartum. Benzodiazepines or phenytoin are alternatives if magnesium is contraindicated.
Why it works:magnesium potentiates the effect of beta blockers, increases the potency and duration of nondepolarizing muscle relaxants, decreases platelet activity, lowers plasma endothelin-1 (protecting vascular endothelium), and causes cerebral arterial vasodilation that can relieve cerebral ischemia.
Expected/adverse effects:feeling of warmth, flushing, metallic taste, diaphoresis, nausea, loss of deep tendon reflexes, somnolence, decreased fetal heart rate variability, and at higher levels, respiratory depression.
Track level of consciousness, respiratory rate, deep tendon reflexes, blood pressure, and urine outputthroughout the infusion. Calcium gluconate is the antidoteand should be readily available at the bedside any time magnesium is running.
Severe preeclampsia:deliver after 34 weeks, or earlier if maternal or fetal status deteriorates. Mild preeclampsia:expectant management until 37 weeks with close monitoring is reasonable. Eclampsia:deliver after maternal stabilization regardless of gestational age. The definitive treatment for preeclampsia and eclampsia is delivery of the placenta- every drug in this section is buying time or protecting the mother/fetus until that happens.
Antenatal corticosteroids(fetal lung maturation) are given for anticipated preterm delivery between 24 and 34 weeks: betamethasone 12 mg IM q24h × 2 doses, or dexamethasone 6 mg IM q12h × 4 doses. Benefit is believed to begin within 24 hours of the first dose.
Postpartum:continue monitoring at least 72 hours after delivery, maintain magnesium 24 hours postpartum, continue antihypertensives as needed, and watch for HELLP syndrome, pulmonary edema, and renal failure - severe preeclampsia doesn't resolve the instant the placenta is out.
The theme across every condition below: optimize before conception when possible, and don't withhold necessary treatment just because the patient is pregnant.
Diagnosis and staging are the same as in nonpregnant patients, just with more frequent follow-up. The risk of medication to the fetus is lower than the risk of untreated asthma.
Asthma:continue inhaled corticosteroids for anyone planning pregnancy or already pregnant (they reduce exacerbation risk); step-down therapy is a low priority until postpartum. Every pregnant asthma patient should have access to a short-acting beta agonist, albuterol preferred. Long-acting beta agonists are safe. Cromolyn, leukotriene receptor antagonists, and theophylline are alternatives but not preferred. Systemic corticosteroids for the most severe disease.
Allergic rhinitis:first line is intranasal corticosteroids (beclomethasone and budesonide have the most use), nasal cromolyn, or first-generation antihistamines (chlorpheniramine, diphenhydramine, hydroxyzine). Intranasal steroids are the most effective option with low systemic risk. Loratadine and cetirizine don't appear to increase fetal risk but are less extensively studied. Immunotherapy isn't contraindicated, but don't start it fresh during pregnancy because of anaphylaxis risk.
Major malformations are 2–3 times more likelyin children born to patients taking antiseizure medications (ASMs) than those who aren't - but the risk of untreatedepilepsy to the fetus is still considered greater than the ASM risk.
Monotherapy is recommended.When possible, avoid valproic acid, phenytoin, carbamazepine, phenobarbital, and polytherapy during the first trimester; if any of these must be used, use the lowest effective dose. Topiramate and zonisamide have been associated with lower birth weight and length.
Pharmacologic therapy should be optimized beforeconception, and if medication withdrawal is planned, it should be fully completed before conception, not during. Supplement folic acid 0.4–4 mg dailystarting before pregnancy and continuing through at least the first trimester (preferably the whole pregnancy) for anyone on ASMs.
Start antiretroviral therapy (ART) as soon as pregnancy is confirmed in anyone newly diagnosed or ART-naive - earlier viral suppression means lower risk of perinatal transmission.Regimens are chosen from those recommended for nonpregnant adults, with attention to each drug's teratogenic profile. Patients already on ART and virally suppressed should continue their existing regimen.
HIV RNA >1000 copies/mL approaching delivery → schedule cesarean at 38 weeksto cut perinatal transmission risk. At or below that threshold, cesarean isn't necessary for this reason. If the viral load is above 1000, unknown, or unfavorable, give IV zidovudine: 1-hour loading dose of 2 mg/kg, then a continuous infusion of 1 mg/kg/hour for 2 hours if cesarean, with a minimum of 3 hours total. Patients at or below 1000 copies/mL near delivery don't need IV zidovudine, just continued ART.
Depressive symptoms are often overlooked in pregnancy because they overlap with normal pregnancy symptoms (fatigue, appetite change, sleep disruption). Screen prenatally and postpartum, every time.Use the lowest effective dose for the shortest necessary duration, and prefer monotherapy over polytherapy even if that means a higher single-drug dose.
SSRIs are not considered major teratogens, with one notable exception: paroxetine has been associated with cardiovascular malformations.SNRIs are less well characterized. Using SSRIs/SNRIs late in pregnancy is associated with persistent pulmonary hypertension of the newborn and poor neonatal adaptation syndrome (usually mild and self-limited). Second-generation antipsychotics are an option for treatment-resistant depression but carry weight gain, gestational diabetes, and metabolic syndrome risk, all of which independently worsen obstetric outcomes. TCAs aren't major teratogens either, but late-pregnancy use has been linked to neonatal withdrawal syndrome. For anxiety symptoms, buspironeis an option since benzodiazepines aren't recommended.
Gestational transient thyrotoxicosis can occur, but usually doesn't need antithyroid medication.
Hypothyroidism:initiate levothyroxine 0.1 mg/day. Patients already on replacement before pregnancy often need a dose increase during pregnancy. Monitor TSH every 4–6 weeks to guide titration.
Hyperthyroidism:thioamides (methimazole, propylthiouracil). Goal is free T4 near the upper limit of normal, not a fully "normal" mid-range value.
LMWH is preferred over unfractionated heparin or warfarinfor treating and preventing acute VTE in pregnancy. Continue throughout pregnancy and for 6 weeks postpartum, with total duration never less than 3 months. Fondaparinux is an option if heparin can't be used. Dabigatran, rivaroxaban, and apixaban are not recommendeddue to limited pregnancy data.
Avoid warfarin in pregnancy - it can cause fetal bleeding, nasal hypoplasia, stippled epiphyses, and CNS anomalies (warfarin embryopathy). This connects directly back to the placental transfer rule: warfarin is small and crosses easily, unlike heparin/LMWH.
For patients at intermediate or high risk of recurrent VTE, use antepartum LMWH or heparin plus 6 weeks of postpartum LMWH or warfarin (warfarin is fine postpartum since it isn't breastfed/placentally transferred the same way and isn't crossing into a fetus). Prosthetic heart valves, thrombophilias, and very-high-risk patients need guideline-directed, individualized management.
Nonpharmacologic measures (relaxation, stress management, biofeedback) are first line for both tension and migraine headaches.
Tension headache:acetaminophen is the treatment of choice. NSAIDs and aspirin are not recommended, and are contraindicated after 20 weeksbecause of prostaglandin inhibition. Antiemetics can help if there's associated nausea. Opioids are rarely used.
Migraine:acetaminophen plus antiemetics (promethazine, prochlorperazine, metoclopramide) are common first steps. Opioids can worsen nausea and, with long-term use, cause neonatal withdrawal. For nonresponsive migraines, triptans (sumatriptan)can be used. Ergotamine and dihydroergotamine are contraindicated.
For frequent, severe migraines needing prevention, propranolol at the lowest effective doseis an option, with amitriptyline or nortriptyline (10–25 mg daily) as alternatives.
E. coliis the principal pathogen. Untreated bacteriuria (even asymptomatic) raises the risk of pyelonephritis, preterm birth, and low birth weight, which is why asymptomatic bacteriuria gets treated in pregnancythe same way symptomatic cystitis does - typically a 3–7 day course.
First-choice agents are beta-lactams(penicillins, cephalosporins) and nitrofurantoin. E. coliresistance to ampicillin/amoxicillin is increasingly problematic.
Nitrofurantoin:not active against Proteus, and avoid after week 37 in patients with G6PD deficiency (risk of neonatal hemolytic anemia). Sulfa drugs:avoid in the last weeks of gestation (kernicterus risk in the newborn). Trimethoprim:relatively contraindicated in the first trimester (folate antagonist, cardiovascular malformation association); regional TMP-SMX resistance further limits its use. Fluoroquinolones and tetracyclines are contraindicatedthroughout.
Pyelonephritisis treated inpatient with parenteral broad-spectrum beta-lactams (cefazolin, ceftriaxone, cefuroxime, or ampicillin plus gentamicin). Switch to oral once afebrile for 48 hours, but avoid nitrofurantoin, fosfomycin, and fluoroquinolones for that oral step. Total antibiotic duration is 7–14 days.
Screen at the first prenatal visit, with repeat testing for some infections later in pregnancy.
| STI | Recommended therapy |
|---|---|
| Bacterial vaginosis(not actually an STI) | Metronidazole 500 mg PO BID × 7 days, or metronidazole 0.75% gel intravaginally daily × 5 days, or clindamycin (cream, oral, or ovules) |
| Chlamydia | Azithromycin 1 g PO × 1 (alt: amoxicillin 500 mg TID × 7 days) |
| Genital herpes | Acyclovir 400 mg PO TID or valacyclovir 500 mg PO BID |
| Gonorrhea | Ceftriaxone 500 mg IM × 1; treat for chlamydia too unless excluded |
| Syphilis(primary/secondary/early latent) | Benzathine penicillin G 2.4 million units IM × 1 (± 2nd dose 1 week later) |
| Syphilis(tertiary/late latent) | Benzathine penicillin G 2.4 million units IM weekly × 3 doses |
| Neurosyphilis | Aqueous crystalline penicillin G 3–4 million units IV q4h (or 18–24 million units/day continuous) × 10–14 days |
| Trichomoniasis | Metronidazole 500 mg PO BID × 7 days |
Why each of these matters beyond the maternal infection:untreated chlamydiacan transmit at birth and cause neonatal conjunctivitis and a subacute, afebrile pneumonia. Gonorrheacan cause neonatal rhinitis, vaginitis, urethritis, ophthalmia neonatorum, and sepsis starting 2–5 days after birth, including blindness - which is why every neonate gets ocular erythromycin ointment prophylaxis within 24 hours of deliveryregardless of maternal screening status. Syphilistreatment with penicillin both prevents transmission and treats an already-infected fetus; penicillin allergy requires desensitization, since there's no proven alternative. BV, though not an STI, is a risk factor for PROM, preterm labor/birth, intra-amniotic infection, and postpartum endometritis if untreated. Trichomoniasisraises risk of PROM, preterm delivery, and low birth weight, and treatment may prevent neonatal respiratory or genital infection. Genital herpestreatment's real goal is preventing neonatal transmission during birth; both acyclovir and valacyclovir need more frequent dosing in pregnancy because renal elimination is increased.
Preterm labor= labor before 37 weeks with cervical dilation/effacement changes plus regular contractions, or an initial presentation of regular contractions with cervical dilation ≥2 cm.
Tocolytics don't fix preterm labor, they buy time: for antenatal steroids to finish working, for transport to a facility equipped for high-risk delivery, or to ride out a self-limited trigger. They're started once there are regular contractions with cervical change, and generally not used before viability or beyond 34 weeks. Notably, prolonging pregnancy with tocolytics hasn't been shown to meaningfully reduce rates of respiratory distress syndrome, neonatal death, or birth before 37 weeks - the benefit is entirely about buying the specific window of time above.
| Class / Drug | Dose | Watch for |
|---|---|---|
| Terbutaline(β-agonist) | 250 mcg SC, may repeat in 15–30 min, max 500 mcg/4h | Black boxno oral dosing or prolonged parenteral use (>48–72h) - maternal cardiotoxicity and death risk |
| Magnesium sulfate | Per protocol | Here used mainly for fetal neuroprotection, reducing cerebral palsy risk - a different indication than the eclampsia use above |
| Nifedipine(CCB) | Per protocol | Fewer maternal adverse effects than magnesium/β-agonists; reduces risk of delivery within 7 days vs β-agonist. Dizziness, flushing, hypotension |
| Indomethacin(NSAID) | 50–100 mg PO/PR, then 25–50 mg PO q6h × 48h | Preferred agent if already on magnesium. Risk of premature ductus arteriosus constriction |
Universal vaginal/rectal culture screening at 36–38 weeks. Treat if culture-positive, or if there's a prior infant with invasive GBS disease, or GBS bacteriuria this pregnancy. Penicillin G IV every 4 hours until deliveryis first-line; alternatives are ampicillin IV q4h, cefazolin q8h, clindamycin IV q8h, or erythromycin q6h. If penicillin-allergic andsensitivity testing shows resistance to clindamycin and erythromycin, use vancomycin IV q8h until delivery.
Prostaglandin E2 analogs(dinoprostone: Prepidil gel, Cervidil vaginal insert) are common for cervical ripening; fetal heart rate monitoring is required with Cervidil and for 15 minutes after removal. Misoprostol(PGE1) is effective and inexpensive, given intravaginally, orally, sublingually, or buccally, but is associated with uterine hyperstimulation, meconium-stained fluid, and uterine rupture. Oxytocinis the most commonly used agent for labor induction after ripening.
Analgesia:nonpharm options (massage, water immersion, acupressure, breathing/visualization techniques, partner support) are associated with more vaginal deliveries and less epidural use. IV/IM opioids (fentanyl, morphine, butorphanol) are common but less effective than epidural analgesia. Epidural analgesia(opioid ± anesthetic like fentanyl/bupivacaine via catheter) gives the best pain control but is associated with longer labor stages, more instrumental deliveries, and maternal fever compared to parenteral narcotics; complications include hypotension, itching, and urinary retention. Patient-controlled epidural dosing reduces total local anesthetic exposure.
PPH is an obstetric emergency and a major cause of maternal morbidity and mortality worldwide. Management is stepwise, starting with excluding retained products of conception. Oxytocinreduces blood loss, PPH incidence, and shortens the third stage of labor. Other agents used in escalation: methylergonovine, carboprost, and tranexamic acid.
Prolactin secretion begins around week 5 of pregnancy, but high estrogen and progesterone levels actively suppress its lactogenic effect throughout pregnancy. After delivery, E and P crash sharply, releasing that brake, and prolactin starts driving milk production. From that point, prolactin secretion becomes pulsatile and suckling-driven, returning to baseline between feeds. If nursing stops, the mammary gland loses its ability to produce milk within about a week; with continued stimulation, lactation can persist for years.
| Prolactin reference range | Level |
|---|---|
| Not pregnant or breastfeeding | <25 ng/mL |
| Pregnant or breastfeeding | 80–400 ng/mL |
Control is mostly inhibitory via dopamine(prolactin is the one anterior pituitary hormone without its own dedicated releasing factor). TRH and VIP can stimulate release. This is why dopamine antagonists(many antipsychotics) cause hyperprolactinemia as a side effect, and why dopamine agonistslike bromocriptine suppress lactation (historically used for postpartum lactation suppression, though that's fallen out of favor).
Transfer happens by passive diffusion of the nonionized, non-protein-bound fractionof a drug. Higher molecular weight, lower lipid solubility, and higher protein binding all mean less transfer into milk. The higher the maternal serum concentration, the higher the milk concentration. Longer half-life drugs maintain higher milk levels for longer. Timing and frequency of feeds, and how much milk the infant actually takes, also affect real-world exposure.
When two options are otherwise similar, pick the one with a shorter half-life, higher protein binding, lower bioavailability, and lower lipid solubility- that combination minimizes what actually reaches the infant. And remember most medications arecompatible with breastfeeding; reflexively telling a patient to "pump and dump" is often unnecessary and discourages continued breastfeeding for no real benefit.
Galactogogues(metoclopramide, domperidone) aren't recommended first-line for low milk supply - the evidence is inconclusive and both carry adverse effect potential. Try nonpharmacologic measures, especially working with a lactation consultant, first.
Penicillin-resistant Staphylococcus aureusis the most common cause. Treat with a penicillinase-resistant penicillin or a first-generation cephalosporin. Heat, direct massage, and NSAIDs help with pain.
VTE risk spikes sharply right after delivery because of the same abrupt estrogen/progesterone shift that turns on lactation. Baseline VTE risk is about 1–5 per 10,000 woman-years; on a combined oral contraceptive it's 3–9; in pregnancy it climbs to roughly 5–20; and in the immediate postpartum period it's the highest of all.
Contraindicated in the first 21 days postpartum(VTE risk). Use caution from day 21–42, especially with additional VTE risk factors like hypertension or diabetes. Risk normalizes by day 42.There's also a theoretical, weakly supported concern that early estrogen exposure could blunt milk supply, which is part of why some guidelines suggest waiting even longer before starting estrogen-containing methods.
Lactational amenorrhea method:high prolactin from frequent suckling suppresses ovulation, similarly to how exogenous estrogen/progestin does. It's not reliable contraception unless the patient is exclusively breastfeeding for every infant feed; reliability drops once solid foods are introduced or exclusivity breaks.
Affects up to 13%of postpartum patients, with nearly 5%experiencing major depression. Nonpharmacologic treatment includes interpersonal psychotherapy, CBT, and group/family therapy. Sertraline, paroxetine, fluoxetine, and nortriptylineare the most studied agents in the postpartum period - when choosing, favor the option with lower transfer into breast milk for a given patient's situation.
| Parameter | When | Watching for |
|---|---|---|
| Blood pressure | Every prenatal visit; more often once any HDP is suspected | Progression to preeclampsia or severe features |
| Urine protein (dip or PCR) | New HTN or preeclampsia symptoms | Renal involvement - though not required for diagnosis |
| Platelets, LFTs, SCr | Any suspicion of severe features | HELLP syndrome, severe preeclampsia |
| SMBG (fasting/postprandial) | Daily once GDM diagnosed | Glycemic control; need to escalate to medication |
| TSH | Every 4–6 weeks in treated hypothyroidism | Dose titration for levothyroxine |
| Magnesium therapy: LOC, RR, DTRs, BP, urine output | Continuously during infusion | Magnesium toxicity, respiratory depression |
| Fetal heart rate | During magnesium, oxytocin, or Cervidil use | Fetal distress, uterine hyperstimulation |
| HIV viral load | Approaching delivery (~36 weeks) | Determines mode of delivery (1000 copies/mL cutoff) and need for IV zidovudine |
| Postpartum monitoring window | ≥72 hours after delivery for severe preeclampsia/eclampsia | HELLP, pulmonary edema, renal failure |
| Depression screening | Prenatally and postpartum | Antenatal depression and postpartum depression, both underrecognized |