Section 1
Medication Safety in Pregnancy
Guiding principle: Uncontrolled disease is almost always more dangerous than the medication used to treat it. Neither necessary medications nor diagnostic imaging should be withheld from a pregnant woman because of fetal concerns.
No medications match your search.
✅
Tier 1 — Safe to Use
Extensive human data; no known teratogenicity; standard of care in pregnancy.
Bronchodilators
Albuterol (SABA)
Preferred rescue inhaler; extensive safety data.
[1][2]
Levalbuterol
Less data than albuterol but considered safe.
[1]
Ipratropium
No known teratogenicity.
[1]
Inhaled Corticosteroids
Budesonide
Most pregnancy safety data of any ICS — preferred agent.
[1][2]
Other ICS
Fluticasone, beclomethasone, mometasone
No data suggesting harm; do not switch a well-controlled patient.
[1][2]
LABA / ICS-LABA
Formoterol, Salmeterol, ICS-LABA combos
Safe; do not de-escalate during pregnancy.
[1][2]
Mast Cell Stabilizer
Cromolyn
Excellent safety profile.
[2]
Anticoagulants
LMWH
Enoxaparin, dalteparin
Preferred anticoagulant — does not cross the placenta.
[3][4]
Unfractionated Heparin (UFH)
Does not cross placenta; risk of HIT and osteoporosis with prolonged use.
[3][4]
Antibiotics
Beta-lactams
Penicillins, cephalosporins, carbapenems
No teratogenicity.
[5]
Azithromycin
Preferred macrolide in pregnancy.
[5]
Clindamycin
No increased risk of birth defects.
[5]
Anti-TB (First-line)
Isoniazid
Not teratogenic; monitor LFTs monthly (increased hepatotoxicity risk in pregnancy).
[5][6]
Rifampin
Not teratogenic in humans.
[5][6]
Ethambutol
No evidence of teratogenicity in humans.
[5][6]
Antifungals
Amphotericin B
Including liposomal formulation
Treatment of choice for invasive fungal infections in pregnancy.
[7][8]
Topical antifungals
Minimal systemic absorption.
[7]
Antihypertensives
Labetalol
First-line antihypertensive in pregnancy.
[9]
Nifedipine ER
First-line antihypertensive in pregnancy.
[9]
Alpha-methyldopa
Long track record of safety.
[9]
Hydralazine
Safe.
[9]
Metoprolol
Safe.
[9]
Vasopressors
Norepinephrine
Preferred vasopressor in pregnancy; monitor fetal status.
[10][11]
Phenylephrine
Commonly used in obstetric anesthesia.
[10]
Sedation / Analgesia
Propofol
Preferred sedative; caution near delivery (neonatal depression).
[10]
Acetaminophen
Safe in all trimesters.
Cardiac / GI / Supportive
Digoxin
Safe; may cause low birth weight.
[9]
Proton pump inhibitors
Safe in all trimesters.
Ondansetron
Widely used; limited 1st trimester data.
Insulin
Preferred agent for glycemic control.
Magnesium sulfate
Used for preeclampsia and tocolysis.
Corticosteroids (Fetal Lung Maturity)
Betamethasone / Dexamethasone
Standard of care at 24 0/7 – 33 6/7 weeks.
NMBAs
Cisatracurium
Does not cross placenta — preferred paralytic.
Succinylcholine
Minimal clinical effects on neonate.
⚠️
Tier 2 — Mild Concern: Use with Awareness
Limited data or minor theoretical concerns; generally safe when clinically indicated.
Asthma
Montelukast (LTRA)
Animal data reassuring; continue if well-controlled pre-pregnancy.
[1][2]
Theophylline
Requires monitoring (target 5–12 mcg/mL); narrow therapeutic index.
[1][2]
Systemic corticosteroids
Prednisone, methylprednisolone
Use for exacerbations; possible association with preeclampsia/prematurity (may be confounded by disease severity).
[1][2]
Pulmonary Hypertension
Epoprostenol (IV)
Benefit outweighs risk; most studied prostacyclin in pregnancy.
[3][4][5]
Treprostinil
IV / SC / inhaled
Benefit outweighs risk.
[3][4]
Iloprost (inhaled)
Benefit outweighs risk.
[3][4]
Sildenafil / Tadalafil
Benefit outweighs risk.
[3][4]
CCBs
Vasodilator-responsive PAH
May continue.
[3]
Sedation
Dexmedetomidine
No significant adverse fetal events in available data.
[6]
Opioids
Fentanyl, morphine
Caution near delivery (neonatal respiratory depression); prolonged use may cause neonatal abstinence syndrome.
[6]
Antibiotics
Vancomycin
Limited 1st trimester data; no neonatal renal or ototoxicity reported.
[7]
Linezolid
Not teratogenic in animals; limited human data.
[7]
Antihypertensives
Amlodipine
Second-line; less data than labetalol or nifedipine.
[3]
Furosemide / Diuretics
Monitor for volume depletion and oligohydramnios.
[3]
NMBAs
Rocuronium
Acceptable for RSI; crosses placenta but no adverse fetal events reported.
Anti-TB
Pyrazinamide
WHO recommends routine use; US guidelines suggest case-by-case risk-benefit assessment.
[7][8]
🟠
Tier 3 — Moderate Concern
Meaningful risk signals or very sparse data. Use only when no safer alternative exists.
Asthma Biologics
Omalizumab
Registry data show no increased risk of major malformations; weigh against risk of uncontrolled asthma.
Registry data only
[1]
Mepolizumab, dupilumab, other biologics
Very limited pregnancy data; case-by-case basis.
Very sparse data
[1]
Sedation
Midazolam / Benzodiazepines
Conflicting data on teratogenicity; neonatal depression near delivery.
Conflicting teratogenicity data
[2]
Ketamine
Less favorable safety profile than propofol or dexmedetomidine.
Vasopressors
Vasopressin
Theoretical interaction with oxytocin receptors; limited data.
Theoretical risk
[2]
Epinephrine
May reduce placental blood flow; use when clearly indicated.
Antibiotics
Fluoroquinolones
Arthropathy in immature animal models; human studies generally reassuring. Reserve for serious infections with no safer alternative.
Reserve for serious infections only
[3]
Aminoglycosides
Gentamicin, tobramycin
Theoretical risk of fetal renal and 8th nerve damage.
[3]
TMP-SMX
Folate antagonist; avoid in 1st trimester if possible.
Antifungals
Fluconazole (≤150 mg single dose)
Debated; teratogenic at doses ≥400 mg. Low single doses remain controversial.
Dose-dependent risk
[4][5]
Anticoagulants
Warfarin (2nd/3rd trimester only)
May be used for mechanical valves with careful risk-benefit discussion; switch to heparin by 36 weeks.
Requires MFM consultation
[6][7]
Anti-TB
Bedaquiline
Limited data; increased frequency of low birth weight reported.
Sparse data, growth concerns
[3]
🚫
Tier 4 — Contraindicated
Known teratogenicity, fetal toxicity, or strong contraindication. Avoid in pregnancy.
Pulmonary HTN — Endothelin Receptor Antagonists
Bosentan
Teratogenic (mandibular/cardiac defects); reduces efficacy of hormonal contraceptives.
Teratogenic
[1][2][3]
Ambrisentan
Teratogenic
[1][2][3]
Macitentan
Teratogenic
[1][2][3]
Riociguat
Teratogenic
[1][2][3]
Anticoagulants
Warfarin (1st trimester)
Embryopathy risk (weeks 6–12).
Embryopathy
[4][5]
DOACs
Apixaban, rivaroxaban, edoxaban
Cross placenta; insufficient safety data; excluded from pregnancy trials.
Crosses placenta, no safety data
[5][6]
Antihypertensives
ACE Inhibitors
Teratogenic: oligohydramnios, renal and skeletal malformations.
Teratogenic
[1]
ARBs
Same teratogenic risks as ACE inhibitors.
Teratogenic
[1]
Sacubitril/valsartan (ARNI)
Contains ARB component.
Contains ARB
[1]
Spironolactone / Eplerenone
Antiandrogenic effects on fetus.
Antiandrogenic
[1]
SGLT2 inhibitors
Renal changes in animal studies; no human pregnancy data.
No human data, animal signal
[1]
Atenolol
Associated with intrauterine growth restriction.
IUGR risk
[1]
Ivabradine
Contraindicated.
Contraindicated
[1]
Analgesics
NSAIDs after 20 weeks
Ibuprofen, ketorolac
Risk of premature ductus arteriosus closure and oligohydramnios.
Premature DA closure
Antibiotics
Clarithromycin
Increased risk of birth defects in animal studies; possible spontaneous abortion.
Teratogenic signal
[7]
Doxycycline / Tetracyclines
Hepatotoxicity; staining of fetal teeth and bones.
Fetal bone/tooth staining
[7]
Telavancin (1st trimester)
Limb malformations in animal studies.
Animal malformation data
[7]
Antifungals
Fluconazole (high dose / prolonged)
Teratogenic in 1st trimester at ≥400 mg.
Teratogenic at high dose
[8][9]
Voriconazole
Fetal abnormalities in animal models — contraindicated.
Contraindicated
[8][9]
Echinocandins
Caspofungin, micafungin, anidulafungin
Teratogenic in animal studies; no human data.
Teratogenic animal data
[8][9]
Flucytosine
Teratogenic (converted to 5-FU) — contraindicated.
Contraindicated — metabolized to 5-FU
[8][9]
Anti-TB
Streptomycin
~10% risk of fetal ototoxicity.
~10% ototoxicity risk
[7]
Kanamycin
~2% risk of fetal ototoxicity.
~2% ototoxicity risk
[7]
Section 2
Lab Values: Pregnant vs. Non-Pregnant
Arterial Blood Gas (ABG)
| Parameter | Non-Pregnant | Pregnant (3rd Trimester) | Change | Clinical Pearl |
|---|---|---|---|---|
| pH | 7.35–7.45 | 7.40–7.47 | ↑ | Compensated respiratory alkalosis is normal in pregnancy |
| PaCO₂ (mm Hg) | 35–45 | 28–32 | ↓↓ | A "normal" PaCO₂ of 40 mm Hg in pregnancy signals impending respiratory failure |
| PaO₂ (mm Hg) | 90–100 | 100–107 (↓ slightly toward term) | ↑ early | Even mild PaO₂ reduction may signify pathology |
| HCO₃⁻ (mEq/L) | 22–26 | 18–21 | ↓ | Renal compensation for chronic respiratory alkalosis; reduced buffering capacity |
| Base Excess (mEq/L) | −2 to +2 | −3 to −4 | ↓ | Reflects compensatory metabolic adjustment |
| A-a Gradient (mm Hg) | 5–15 | 5–15 (unchanged) | → | No significant change despite other ABG shifts |
| P₅₀ (mm Hg) | 27 | 30 (maternal); fetal P₅₀ = 19 | ↑ maternal | Right-shifted maternal OxyHb curve; higher PaO₂ needed for same SpO₂. Fetal curve is left-shifted (facilitates O₂ transfer) |
Venous Blood Gas (VBG)
| Parameter | Non-Pregnant (Peripheral VBG) | Pregnant (Estimated VBG) | Change | Clinical Pearl |
|---|---|---|---|---|
| pH | 7.30–7.43 | 7.35–7.42 | ↑ slight | VBG pH is ~0.03–0.05 lower than arterial; in pregnancy, still reflects compensated respiratory alkalosis |
| PvCO₂ (mm Hg) | 38–58 | 33–37 (estimated) | ↓↓ | VBG pCO₂ is ~5–6 mm Hg higher than arterial; a VBG pCO₂ of 45 mm Hg in pregnancy signals impending respiratory failure |
| PvO₂ (mm Hg) | 19–65 | Not clinically useful | — | VBG pO₂ does NOT reliably reflect arterial oxygenation; use SpO₂ or ABG |
| HCO₃⁻ (mEq/L) | 22–30 | 19–23 | ↓ | ~1 mEq/L higher than arterial; still reflects reduced buffering capacity in pregnancy |
| Base Excess (mEq/L) | −1.9 to +4.5 | −3 to −2 | ↓ slight | Similar to arterial trend |
| Lactate (mmol/L) | 0.4–2.2 | 0.4–2.2 (↑ in labor) | → (↑ labor) | VBG lactate correlates well with arterial; rises during active labor — not pathologic in that context |
| SvO₂ / peripheral (%) | 23–93% (wide range) | Not clinically useful | — | Peripheral venous O₂ sat varies widely by site; not a substitute for SpO₂ |
Comprehensive Metabolic Panel (CMP) — Electrolytes
| Parameter | Non-Pregnant | Pregnant (3rd Trimester) | Change | Clinical Pearl |
|---|---|---|---|---|
| Sodium (mEq/L) | 136–145 | 130–140 (↓ 3–6 mEq/L) | ↓ | Reset osmostat; lower ADH threshold. Do not correct mild hyponatremia in pregnancy |
| Potassium (mEq/L) | 3.5–5.0 | 3.2–4.7 (↓ ~0.3 mEq/L) | ↓ mild | Progesterone counteracts aldosterone-driven K⁺ wasting; increased predilection for rhabdomyolysis with hypokalemia |
| Chloride (mEq/L) | 98–106 | 97–105 | ↓ mild | Follows sodium trend |
| CO₂/Bicarbonate (mEq/L) | 22–26 | 18–21 | ↓ | Renal compensation for respiratory alkalosis; reduced buffering capacity |
| Calcium, total (mg/dL) | 8.5–10.5 | 8.0–9.5 | ↓ | Dilutional + reduced albumin; ionized Ca²⁺ generally unchanged — use ionized measurement |
| Magnesium (mg/dL) | 1.7–2.2 | 1.5–2.0 | ↓ mild | Mild decrease common; important to monitor closely if patient is on MgSO₄ |
| Phosphate (mg/dL) | 2.5–4.5 | 2.5–4.5 (unchanged) | → | Generally stable throughout pregnancy |
| Plasma Osmolality (mOsm/kg) | 275–295 | 270–285 (↓ 5–10 mOsm/kg) | ↓ | Reset osmostat; lower thirst and ADH thresholds — physiologic, do not over-interpret |
CMP — Renal Function
| Parameter | Non-Pregnant | Pregnant (3rd Trimester) | Change | Clinical Pearl |
|---|---|---|---|---|
| BUN (mg/dL) | 7–20 | 5–12 | ↓ | GFR increases 40–50% → increased urea clearance |
| Creatinine (mg/dL) | 0.6–1.2 | 0.4–0.8 | ↓↓ (~25%) | A "normal" Cr of 1.0 mg/dL in pregnancy may indicate renal impairment. Cr >0.8 warrants attention |
| eGFR | ~90–120 mL/min | ~120–180 mL/min | ↑↑ (40–50%) | Standard CKD-EPI formulas not validated in pregnancy; use creatinine clearance if precise measurement needed |
| Uric Acid (mg/dL) | 2.5–6.0 | 2.0–5.0 (T1/T2); rises toward term | ↓ then ↑ | Falls early due to increased GFR; rises in 3rd trimester. Elevated uric acid associated with preeclampsia |
CMP — Glucose
| Parameter | Non-Pregnant | Pregnant (3rd Trimester) | Change | Clinical Pearl |
|---|---|---|---|---|
| Fasting Glucose (mg/dL) | 70–100 | 60–90 | ↓ | Fetal glucose consumption + increased insulin production; accelerated starvation physiology |
| Random Glucose (mg/dL) | 70–140 | May be higher postprandially | ↑ postprandial | Insulin resistance increases in 2nd/3rd trimester (human placental lactogen effect) |
CMP — Hepatic Function
| Parameter | Non-Pregnant | Pregnant (3rd Trimester) | Change | Clinical Pearl |
|---|---|---|---|---|
| ALT (IU/L) | 0–35 | 6–32 (unchanged) | → | Any elevation should be evaluated — ALT does NOT rise in normal pregnancy |
| AST (IU/L) | 0–40 | 10–30 (unchanged) | → | Same as ALT; elevation suggests pathology (HELLP, AFLP, viral hepatitis) |
| Alkaline Phosphatase (IU/L) | 30–150 | T1: 32–100 / T2: 43–135 / T3: 133–418 | ↑↑↑ | Placental origin; fractionation confirms source. ALP is not a useful liver marker in pregnancy |
| GGT (IU/L) | 7–33 | 3–43 (unchanged to ↓) | → to ↓ | Decreases in 2nd/3rd trimester; useful to differentiate hepatic vs. placental ALP elevation |
| Total Bilirubin (mg/dL) | 0.1–1.2 | 0.1–0.8 | ↓ | Lower due to hemodilution; any elevation warrants workup |
| Albumin (g/dL) | 3.5–4.6 | 2.8–3.7 | ↓↓ | Hemodilution; affects total calcium interpretation and drug binding — use ionized Ca²⁺ |
| Total Protein (g/dL) | 6.0–8.3 | 5.5–7.5 | ↓ | Hemodilution; decreases progressively through gestation |
Hematologic & Coagulation
| Parameter | Non-Pregnant | Pregnant (3rd Trimester) | Change | Clinical Pearl |
|---|---|---|---|---|
| Hemoglobin (g/dL) | 12.0–16.0 | 10.0–14.0 | ↓ | Dilutional anemia: plasma volume ↑ ~50%, RBC mass ↑ ~25% |
| Hematocrit (%) | 36–46 | 31–41 | ↓ | Same mechanism as Hgb reduction |
| WBC (×10⁹/L) | 4.5–11.0 | 6.0–16.0 (up to 30 in labor) | ↑ | Predominantly neutrophilia; do not reflexively attribute elevated WBC to infection |
| Platelets (×10⁹/L) | 150–400 | 130–400 | ↓ mild | Gestational thrombocytopenia (dilutional); count <100 warrants workup |
| Fibrinogen (mg/dL) | 200–400 | 300–600+ | ↑↑ | Reflects hypercoagulable state of pregnancy |
| D-dimer (μg/mL FEU) | <0.50 | T1: 0.95 / T2: 1.29 / T3: 1.70 | ↑↑↑ | Standard non-pregnant cutoff is unreliable; use trimester-specific thresholds |
| PT (seconds) | 11–13.5 | 9.5–12.5 | ↓ | Shortened due to elevated clotting factors |
| aPTT (seconds) | 25–35 | 23–33 | ↓ | Same mechanism as PT shortening |
Other Pulmonary-Relevant Labs
| Parameter | Non-Pregnant | Pregnant | Change | Clinical Pearl |
|---|---|---|---|---|
| BNP (pg/mL) | <100 | Generally <100 (mildly elevated) | → / ↑ | Elevated BNP + PE should raise concern for RV strain |
| NT-proBNP (pg/mL) | <125 | Can be mildly elevated | → / ↑ | No validated pregnancy-specific cutoffs; interpret with caution |
| Procalcitonin (ng/mL) | <0.10 | Generally unchanged | → | Remains useful for bacterial infection assessment in pregnancy |
| Lactate (mmol/L) | 0.5–2.0 | 0.5–2.0 (↑ in active labor) | → (↑ labor) | Rises during active labor; not pathologic in that context |
| Serum Bicarbonate (mEq/L) | 22–26 | 18–21 | ↓ ~25% | Reduced buffering capacity → faster onset of DKA and starvation ketoacidosis |
| Plasma Ketones (mmol/L) | ~0.13 | ~0.43 | ↑↑ | Starvation ketoacidosis can occur after just 16 hours of fasting in 2nd/3rd trimester |
Section 3
PFT Physiology in Pregnancy
Key Takeaway: The hallmark of pregnancy PFT physiology is a reduced FRC with preserved spirometry (FEV₁, FVC). The decreased FRC combined with increased O₂ consumption creates a critically reduced oxygen reserve — explaining the rapid desaturation seen with apnea or hypoventilation in pregnant patients.
| Parameter | Non-Pregnant | Pregnant (3rd Trimester) | Change | Mechanism |
|---|---|---|---|---|
| Tidal Volume (mL) | ~500 | ~700 (↑ 30–40%) | ↑↑ | Progesterone-driven increase in ventilatory drive |
| Minute Ventilation (L/min) | ~6–8 | ~9–11 (↑ 30–50%) | ↑↑ | Driven by increased tidal volume; respiratory rate unchanged |
| Respiratory Rate | 12–20 | 12–20 (unchanged) | → | Increased minute ventilation is entirely from increased TV |
| FRC (mL) | ~2400 | ~1800–2000 (↓ 10–25%) | ↓↓ | Diaphragm elevation by gravid uterus |
| ERV (mL) | ~1200 | ~800 (↓ 15–20%) | ↓ | Component of FRC reduction |
| RV (mL) | ~1200 | ~1000 (↓ 5–15%) | ↓ mild | Component of FRC reduction |
| IC (mL) | ~2500 | ~2800–3000 (↑ 15–20%) | ↑ | Compensatory increase via increased tidal volume and IRV |
| TLC (mL) | ~5900 | ~5600–5700 (↓ 0–5%) | ↓ minimal | IC increase partially offsets FRC decrease |
| VC (mL) | ~3500 | ~3500 (unchanged) | → | Preserved despite mechanical changes |
| FEV₁ | Normal | Unchanged | → | No airflow obstruction from pregnancy itself |
| FVC | Normal | Unchanged | → | No true restriction despite reduced FRC |
| FEV₁/FVC | Normal | Unchanged | → | Ratio preserved |
| DLCO | Normal | Normal to mildly ↑ | → / ↑ | Increased cardiac output and pulmonary blood flow |
| O₂ Consumption (mL/min) | ~250 | ~300–330 (↑ 20–33%) | ↑↑ | Combined fetal and maternal metabolic demands |
Section 4
Ventilator Goals in Pregnancy
| Parameter | Non-Pregnant (Standard ARDS) | Pregnant | Rationale |
|---|---|---|---|
| Tidal Volume | 6–8 mL/kg IBW | 6–8 mL/kg IBW Use pre-pregnancy weight | Lung-protective ventilation applies equally |
| Plateau Pressure | ≤30 cm H₂O | ≤30 cm H₂O | Same barotrauma prevention goals |
| Driving Pressure | ≤15 cm H₂O | ≤15 cm H₂O | Same as non-pregnant |
| PEEP | Titrate per FiO₂/PEEP table | Cautious titration | Excessive PEEP may reduce venous return (already compromised by IVC compression) |
| PaCO₂ Target | 35–45 mm Hg | 28–32 mm Hg | Must maintain maternal respiratory alkalosis for fetal CO₂ clearance |
| pH Target | 7.35–7.45 | 7.40–7.47 | Avoid maternal acidosis (fetal acidosis risk) |
| SpO₂ Target | ≥88–92% (ARDS) | ≥92–95% | Higher target needed due to right-shifted maternal OxyHb curve; fetal oxygenation depends on maternal PaO₂ |
| PaO₂ Target | ≥55–80 mm Hg | ≥70 mm Hg | Fetal well-being requires higher maternal PaO₂ |
| Permissive Hypercapnia | Accepted in ARDS | Avoid if possible | Elevated maternal PaCO₂ reduces fetal CO₂ gradient → fetal acidosis |
| FiO₂ | Lowest to maintain SpO₂ | Lowest to maintain SpO₂ ≥92% | Hyperoxygenation may reduce fetal cardiac output |
| Positioning | Prone for severe ARDS | Semi-prone or lateral Feasible up to ~30 wks; modified prone with abdominal support later | Left lateral tilt ≥15° to relieve aortocaval compression |
Critical Pearls
PaCO₂ of 40 mm Hg is NOT normal in pregnancy. In a pregnant patient, a PaCO₂ at the low end of the non-pregnant normal range signals impending respiratory failure and should prompt urgent reassessment.
Permissive hypercapnia is poorly tolerated. Unlike standard ARDS management, elevated maternal CO₂ impairs the transplacental CO₂ gradient and risks fetal acidosis. Target pregnant-normal PaCO₂ (28–32 mm Hg) on the ventilator.
Rapid desaturation risk. The reduced FRC and increased O₂ consumption mean pregnant patients desaturate extremely rapidly after apnea. Preoxygenation before intubation is essential. The failed intubation rate in obstetrics is approximately 1 in 224 — roughly 8× higher than in the general population.
Universal Clinical Reminders
⚖️Uncontrolled disease is almost always more dangerous than the medication used to treat it.
🏥Neither necessary medications nor diagnostic imaging should be withheld from a pregnant woman because of fetal concerns.
💉Pregnancy alters pharmacokinetics (increased GFR, plasma volume, cardiac output; decreased gastric emptying) — dose adjustments may be needed.
👥Always consult pharmacy and maternal-fetal medicine when managing critically ill pregnant patients.
References
- [1]Sigelko AD, Strek ME, Wolfe KS. Asthma in Pregnancy. Obstet Gynecol. 2025;146(1):39-58. PubMed
- [2]NAEPP Expert Panel Report. Managing Asthma During Pregnancy: 2004 Update. J Allergy Clin Immunol. 2005;115(1):34-46. PubMed
- [3]Greer IA. Pregnancy Complicated by Venous Thrombosis. N Engl J Med. 2015;373(6):540-7. NEJM
- [4]ACOG Practice Bulletin No. 196: Thromboembolism in Pregnancy. Obstet Gynecol. 2018;132(1):e1-e17. DOI
- [5]Benson C, Brooks J, Dhanireddy S, et al. Guidelines for OI Prevention and Treatment in Adults with HIV. IDSA/OARAC 2025. PDF
- [6]Nahid P, Dorman SE, Alipanah N, et al. ATS/CDC/IDSA Guidelines: Treatment of Drug-Susceptible Tuberculosis. Clin Infect Dis. 2016;63(7):e147-e195. PMC
- [7]Gaultier S, Tazi A, Charre C, et al. Infectious Diseases in Pregnant Women With Haematological Malignancies. Lancet Haematol. 2025;12(10):e836-e849. PubMed
- [8]Pappas PG, Kauffman CA, Andes DR, et al. IDSA Guideline for Management of Candidiasis: 2016 Update. Clin Infect Dis. 2016;62(4):e1-50. PMC
- [9]Halpern DG, Weinberg CR, Pinnelas R, et al. Medication for Cardiovascular Disease During Pregnancy. J Am Coll Cardiol. 2019;73(4):457-476. PubMed
- [10]Gewarges M, Cao A, Alexopoulos K, et al. Management of the Critically Ill Cardiac Patient During Pregnancy. JACC Adv. 2025;4(10):102037. PubMed
- [11]Shields AD, Plante LA, Pacheco LD, Louis JM. SMFM Consult Series #67: Maternal Sepsis. Am J Obstet Gynecol. 2023;229(3):B2-B19. ScienceDirect