Maternal-Fetal Medicine

01 Maternal Physiology & Pregnancy Essentials

Maternal-fetal medicine (MFM), also called perinatology, is the obstetric subspecialty focused on high-risk pregnancy. MFM physicians manage pregnancies complicated by maternal medical disease (diabetes, hypertension, lupus, cardiac disease), obstetric complications (preeclampsia, preterm labor, placental disorders), fetal disorders (growth restriction, anomalies, isoimmunization), and multiple gestations. They also perform invasive fetal diagnostic and therapeutic procedures. Scribes in MFM clinics encounter a mix of consult visits, ultrasound-integrated encounters, antepartum testing visits, and inpatient antepartum/L&D documentation.

Gestational Dating & Trimesters

Every MFM note begins with gestational age, expressed as weeks + days (e.g., "32w4d"). Gestational age (GA) is calculated from the last menstrual period (LMP) and confirmed or revised by first-trimester ultrasound (most accurate dating). The estimated due date (EDD) is 40 weeks from LMP. Pregnancy is divided into the first trimester (0–13w6d), second trimester (14w0d–27w6d), and third trimester (28w0d–delivery). Term is 37–41w6d; early term is 37w0d–38w6d, full term is 39w0d–40w6d, late term is 41w0d–41w6d, post-term is ≥42w0d. Preterm is <37w0d (subdivided into late preterm 34–36w6d, moderate 32–33w6d, very preterm 28–31w6d, and extremely preterm <28w0d).

Gravidity & Parity (GTPAL)

Every obstetric note uses a GTPAL (or GPA) summary. G = gravidity (total pregnancies including current). T = term deliveries (≥37w). P = preterm deliveries (20–36w6d). A = abortions (spontaneous or elective losses <20w, plus ectopics). L = living children. A G3P1011 woman has had 3 pregnancies, 1 term delivery, 0 preterm, 1 loss, and 1 living child.

Maternal Physiologic Changes

Pregnancy produces predictable physiologic changes the scribe will see quoted in notes and vitals. Cardiovascular: plasma volume increases 40–50%, cardiac output rises 30–50%, heart rate increases 10–20 bpm, systemic vascular resistance falls (BP drops in mid-pregnancy, returns to baseline by term). Hematologic: dilutional anemia (Hgb nadir ~10.5 g/dL in the second trimester); procoagulant shift with rising fibrinogen, factors VII, VIII, X, and von Willebrand factor, making pregnancy and the puerperium a high VTE-risk state. Respiratory: tidal volume and minute ventilation rise; compensated respiratory alkalosis is normal (pCO₂ ~30 mm Hg). Renal: GFR rises ~50%, serum creatinine falls (normal pregnancy Cr <0.8 mg/dL; ≥1.0 is abnormal). Endocrine: insulin resistance rises progressively due to placental hormones (hPL, cortisol, progesterone), driving gestational diabetes. Thyroid-binding globulin rises; total T4 rises but free T4 remains normal.

02 Scribe Documentation Framework in MFM

The MFM Consultation Note

MFM encounters are usually consultations from a general OB or primary care provider. The note structure is: reason for consult, pregnancy history (GTPAL, EDD, dating method), current pregnancy course, PMH/PSH, medications, allergies, family history, social history, ROS, vitals, fundal height, fetal heart tones (FHT), ultrasound findings, assessment, and plan. The assessment frames the problem in terms of both maternal risk and fetal risk, and the plan is typically broken into maternal surveillance, fetal surveillance, delivery planning, and patient counseling.

The Antepartum Testing (AFT) Visit

Many MFM visits are "AFT" visits dedicated to fetal surveillance. These are short, focused notes documenting nonstress test (NST) results, biophysical profile (BPP) findings, amniotic fluid assessment, fetal growth (if interval), and Doppler velocimetry when indicated. The note closes with a reactive/nonreactive or reassuring/nonreassuring determination and a plan for timing of delivery.

03 Chronic Medical Conditions in Pregnancy

A large portion of MFM consults are for pregestational (chronic) medical disease. Pregnancy changes the pharmacokinetics, disease activity, and fetal risk profile of nearly every chronic condition.

Pregestational Diabetes (Type 1 & Type 2)

Pregestational DM carries markedly elevated risks of congenital anomalies (cardiac, neural tube, caudal regression), miscarriage, stillbirth, macrosomia, shoulder dystocia, neonatal hypoglycemia, and preeclampsia. Glycemic control before conception is the single strongest determinant of outcome; a first-visit HbA1c <6.5% is the target. Management centers on insulin (oral agents are second-line; metformin and glyburide cross the placenta). Goals: fasting <95, 1-hour postprandial <140, 2-hour <120 mg/dL. Delivery is typically at 39w0d for well-controlled patients and earlier (36–38w) for poorly controlled or vasculopathy. ACOG Practice Bulletin 201 (Pregestational Diabetes) is the standard reference.

Chronic Hypertension

Defined as BP ≥140/90 before pregnancy or before 20w. Chronic HTN doubles the risk of superimposed preeclampsia, abruption, FGR, and preterm birth. The CHAP trial established that treating BP to <140/90 in pregnancy reduces adverse perinatal outcomes without compromising fetal growth. First-line agents: labetalol, nifedipine ER, methyldopa. ACE inhibitors and ARBs are contraindicated (fetal renal agenesis, oligohydramnios).

Lupus & Antiphospholipid Syndrome (APS)

SLE increases risks of preeclampsia, FGR, preterm birth, stillbirth, and neonatal lupus (anti-Ro/SSA antibodies cause congenital heart block). Pregnancy should be planned during a ≥6-month quiescent period. Hydroxychloroquine is continued throughout. APS (positive lupus anticoagulant, anti-cardiolipin, or anti-β2 glycoprotein antibodies with clinical criteria) is treated with prophylactic heparin/LMWH plus low-dose aspirin. Secondary APS with prior thrombosis requires therapeutic anticoagulation.

Other Chronic Conditions

04 Gestational Diabetes Mellitus (GDM)

GDM is glucose intolerance first recognized in pregnancy, driven by placental insulin resistance. It affects roughly 6–10% of US pregnancies. Untreated GDM causes macrosomia, shoulder dystocia, birth trauma, neonatal hypoglycemia, polycythemia, hyperbilirubinemia, and an elevated lifetime risk of type 2 DM for the mother.

Screening & Diagnosis

Universal screening at 24–28 weeks using the two-step approach (preferred in the US): a 50-g 1-hour glucose challenge test (GCT) with a threshold of 130, 135, or 140 mg/dL, followed by a diagnostic 100-g 3-hour oral glucose tolerance test (OGTT) using Carpenter-Coustan criteria if screen-positive. Two or more abnormal values on the 3-hour OGTT confirm GDM.

Classification & Management

White/modified classification: A1GDM — diet-controlled; A2GDM — requires pharmacologic therapy. First-line treatment is insulin (does not cross placenta). Metformin and glyburide are alternatives but cross the placenta. Fetal surveillance is intensified for A2GDM (weekly NSTs or BPPs from 32–34 weeks). Delivery: A1GDM — 39w0d–40w6d; A2GDM well-controlled — 39w0d; A2GDM poorly controlled — 36w0d–39w0d individualized. ACOG Practice Bulletin 190 (Gestational Diabetes) guides thresholds and delivery timing.

05 Hypertensive Disorders of Pregnancy

Hypertensive disorders complicate 10–15% of pregnancies and remain a leading cause of maternal mortality globally. The four categories:

Gestational Hypertension

New-onset BP ≥140/90 on two occasions ≥4 hours apart after 20 weeks, without proteinuria or severe features. Up to half progress to preeclampsia. Treatment: antihypertensives for BP ≥140/90 per CHAP; delivery at 37w0d.

06 Preeclampsia, Eclampsia & HELLP

Preeclampsia is a multisystem disorder of pregnancy characterized by new-onset hypertension and end-organ dysfunction after 20 weeks. Pathophysiology centers on abnormal placentation: shallow trophoblastic invasion of the spiral arteries leads to placental hypoperfusion, release of antiangiogenic factors (sFlt-1, soluble endoglin) that antagonize VEGF and PlGF, and systemic endothelial dysfunction. The clinical manifestations — hypertension, proteinuria, hepatic injury, thrombocytopenia, cerebral edema — are all downstream of that endothelial injury.

Diagnostic Criteria

BP ≥140/90 on two occasions ≥4 hours apart plus one of: proteinuria (≥300 mg/24h, P/Cr ≥0.3, or dipstick 2+), thrombocytopenia (<100k), serum creatinine >1.1 or doubling, transaminases ≥2× upper limit, pulmonary edema, or new-onset cerebral/visual symptoms.

HELLP Syndrome

A severe variant with Hemolysis, Elevated Liver enzymes, and Low Platelets. Tennessee criteria: platelets <100k, AST ≥70, LDH ≥600, peripheral smear with schistocytes or total bilirubin ≥1.2. Mississippi criteria further grade by platelet nadir (Class 1 <50k, Class 2 50–100k, Class 3 100–150k). HELLP can occur without significant hypertension or proteinuria.

Eclampsia

New-onset generalized tonic-clonic seizure in a patient with preeclampsia (or as the presenting feature). Mortality is high; cerebral edema and stroke are the killers. Treatment: magnesium sulfate 4–6 g IV loading + 1–2 g/hr infusion, airway protection, BP control, and delivery.

Management

Definitive treatment is delivery. Timing depends on severity and gestational age:

Seizure prophylaxis with magnesium sulfate for all patients with preeclampsia with severe features and during intrapartum/postpartum (24 hours). Acute severe hypertension (≥160/110 sustained >15 minutes) requires emergent treatment within 30–60 minutes using IV labetalol, IV hydralazine, or PO immediate-release nifedipine. Low-dose aspirin (81–162 mg) starting at 12–16 weeks reduces preeclampsia risk in high-risk patients per USPSTF preeclampsia prevention guidance.

07 Intrahepatic Cholestasis & Hyperemesis Gravidarum

Intrahepatic Cholestasis of Pregnancy (ICP)

A third-trimester hepatic disorder presenting with generalized pruritus (especially palms and soles, worse at night) without a rash. Diagnosis: elevated total serum bile acids (≥10 µmol/L; severe ≥40; very severe ≥100). Transaminases are often mildly elevated. Fetal risks include preterm birth, meconium-stained fluid, and intrauterine fetal demise — risks rise sharply at bile acids ≥100. Treatment: ursodeoxycholic acid (UDCA) 300 mg TID improves pruritus. Delivery timing: 36w0d–37w0d for typical ICP; 34w0d–36w0d for severe (≥100 µmol/L) per SMFM Consult Series 53 on ICP.

Hyperemesis Gravidarum (HG)

Severe nausea and vomiting of pregnancy with weight loss >5% of pre-pregnancy weight, dehydration, and ketosis. Differential includes thyroid storm (beta-hCG cross-stimulates TSH receptor), molar pregnancy, and multiple gestation. Treatment ladder: vitamin B6 (pyridoxine) ± doxylamine → dimenhydrinate/diphenhydramine → metoclopramide/promethazine → ondansetron → IV fluids, thiamine (before dextrose to prevent Wernicke), and methylprednisolone for refractory cases.

08 Placental Disorders

Placenta Previa

The placenta covers or approaches the internal cervical os. Classic presentation: painless, bright-red vaginal bleeding in the second or third trimester. No digital exam — transvaginal ultrasound is the diagnostic modality. Many previas diagnosed at anatomy scan resolve by term due to lower uterine segment development; follow-up scan at 32w. Delivery: scheduled cesarean at 36w0d–37w6d for persistent previa.

Placental Abruption

Premature separation of the normally implanted placenta. Classic triad: abdominal pain, vaginal bleeding (may be concealed), and a tense, tender uterus. Risk factors: hypertension, prior abruption, trauma, cocaine use, PPROM, smoking, advanced maternal age. Ultrasound is insensitive — diagnosis is clinical. Complications: maternal hemorrhage, DIC, fetal distress, stillbirth. Management depends on severity and fetal status: expectant with close monitoring (stable, remote from term) or emergent delivery (unstable or nonreassuring fetal status).

Placenta Accreta Spectrum (PAS)

Abnormal trophoblastic invasion into the uterine wall. Three severities:

Primary risk factors: prior cesarean delivery (risk rises with number of prior CDs) + placenta previa. Scheduled delivery at 34w0d–35w6d in a referral center with multidisciplinary team, cesarean hysterectomy planned, blood products available. ACOG/SMFM Placenta Accreta Spectrum Obstetric Care Consensus.

Vasa Previa

Fetal vessels (unprotected by cord or placenta) traverse the membranes over the cervical os. Rupture at ROM causes rapid fetal exsanguination. Screening transvaginal US with color Doppler in at-risk patients (velamentous cord, succenturiate lobe, low-lying placenta in second trimester). Scheduled cesarean at 34w0d–37w0d before ROM.

09 VTE in Pregnancy

Pregnancy is a hypercoagulable state; VTE risk is 4–5× baseline and highest in the postpartum period. PE remains a leading cause of maternal mortality. DVT in pregnancy preferentially involves the left iliofemoral veins (right iliac artery compresses the left iliac vein).

Diagnosis

Suspected DVT: compression ultrasound. Suspected PE: start with CXR; then CT-PA (preferred in most patients) or V/Q scan (lower maternal breast radiation). D-dimer is unreliable in pregnancy because it rises physiologically. Treatment: LMWH (enoxaparin) is first-line — it does not cross the placenta. Unfractionated heparin for patients with renal failure or when rapid reversibility is needed. Warfarin is contraindicated (teratogenic — warfarin embryopathy) except in mechanical heart valves. DOACs are not used in pregnancy.

Prophylactic dosing (enoxaparin 40 mg SC daily) for patients with prior VTE or high-risk thrombophilia; therapeutic dosing (1 mg/kg BID) for acute VTE. LMWH is held 24 hours before planned delivery/neuraxial anesthesia. Anticoagulation is continued throughout pregnancy and at least 6 weeks postpartum per ACOG Practice Bulletin 196 (Thromboembolism).

10 Fetal Growth Restriction & LGA

Fetal Growth Restriction (FGR / IUGR)

Defined as estimated fetal weight (EFW) or abdominal circumference (AC) <10th percentile for gestational age. Severe FGR is <3rd percentile. FGR is further categorized as early-onset (<32 weeks; usually placental insufficiency; high risk of preeclampsia and stillbirth) and late-onset (≥32 weeks; milder placental dysfunction). Causes: placental insufficiency, maternal vascular disease, infections (CMV, toxoplasmosis), aneuploidy, maternal substance use, multiple gestation.

Surveillance & Doppler

Serial growth every 3–4 weeks. Weekly NSTs and BPPs starting at diagnosis. Umbilical artery Doppler velocimetry is central: normal flow, elevated S/D, absent end-diastolic flow (AEDF), and reversed end-diastolic flow (REDF) represent progressive placental dysfunction. Middle cerebral artery (MCA) Doppler detects fetal brain-sparing (“cephalization”) and fetal anemia (peak systolic velocity). Ductus venosus (DV) Doppler is used in severe early-onset FGR for delivery timing.

Large for Gestational Age (LGA) & Macrosomia

LGA: EFW >90th percentile. Macrosomia: EFW ≥4,000 g (high risk) or ≥4,500 g (extreme, shoulder dystocia risk). Cesarean is offered for EFW ≥5,000 g in non-diabetics or ≥4,500 g in diabetics.

11 Amniotic Fluid Disorders

Amniotic fluid is measured on ultrasound by the amniotic fluid index (AFI) — the sum of the deepest vertical pocket in each of four uterine quadrants — or by the single deepest pocket (SDP / MVP).

Oligohydramnios causes: PPROM, placental insufficiency, post-term pregnancy, fetal renal anomalies (agenesis, posterior urethral valves), maternal ACE inhibitor/NSAID use. Polyhydramnios causes: fetal GI obstruction (esophageal/duodenal atresia), neurologic impairment (impaired swallowing), diabetes, fetal anemia, hydrops, TTTS (recipient twin). Severe polyhydramnios can be managed with amnioreduction for maternal respiratory distress.

12 Multiple Gestation

Multiple gestation is a core MFM domain. Outcomes depend on chorionicity (number of placentas) and amnionicity (number of sacs), which are determined by the timing of embryo splitting and must be assigned in the first trimester.

Twin-Twin Transfusion Syndrome (TTTS)

Unbalanced placental vascular anastomoses in monochorionic twins create a donor–recipient imbalance. Quintero staging:

Stage II+ is treated with fetoscopic laser photocoagulation of the placental anastomoses. SMFM Consult Series on Twin Complications.

Other Monochorionic Complications

TAPS (twin anemia-polycythemia sequence): chronic slow transfusion through small anastomoses, without fluid discordance. Diagnosed by MCA Doppler (donor high PSV, recipient low). sIUGR (selective IUGR): unequal placental sharing; classified by umbilical artery Doppler pattern (Types I, II, III). TRAP sequence: twin reversed arterial perfusion — acardiac twin perfused by the pump twin.

Delivery Timing

13 Cervical Insufficiency, Preterm Labor & PPROM

Cervical Insufficiency & Cerclage

Painless cervical dilation in the second trimester leading to recurrent pregnancy loss or extreme preterm birth. Indications for cerclage: history-indicated (≥1 prior second-trimester loss or preterm birth; placed 12–14w); ultrasound-indicated (short cervix <25 mm before 24w in a patient with prior preterm birth); exam-indicated / “rescue” (dilated cervix on exam in the second trimester without labor). McDonald and Shirodkar are the two common techniques. Cerclage is removed at 36–37w or with labor/PPROM.

Preterm Labor

Regular contractions with cervical change before 37 weeks. Evaluation: speculum exam (rule out PPROM), fetal fibronectin (fFN) in borderline cases, transvaginal cervical length (<20 mm is concerning). Management:

PPROM (Preterm Prelabor Rupture of Membranes)

Rupture of membranes before 37w without labor. Diagnosis: pooling on speculum exam, nitrazine test (pH >6.5, amniotic fluid is alkaline), ferning, and commercial immunoassays (AmniSure, ROM Plus). Management is gestational-age dependent: expectant with latency antibiotics (ampicillin + azithromycin + amoxicillin) and steroids before 34w, delivery at 34w0d if uncomplicated. ACOG Practice Bulletin 217 (Prelabor Rupture of Membranes).

14 Fetal Demise & Recurrent Pregnancy Loss

Intrauterine Fetal Demise (IUFD / Stillbirth)

Fetal death ≥20 weeks. Workup after delivery: fetal autopsy, placental pathology, karyotype/microarray, Kleihauer-Betke (fetomaternal hemorrhage), antiphospholipid antibodies, screening for hereditary thrombophilias (selectively), HbA1c, TSH, and toxicology. Delivery mode is typically induction of labor; dilation and evacuation remains an option in select cases. Counseling on future pregnancy recurrence risk is part of the MFM follow-up.

Recurrent Pregnancy Loss (RPL)

Two or more clinical pregnancy losses. Workup: parental karyotype, antiphospholipid antibody panel (LA, aCL, β2-GPI), uterine imaging (HSG or saline infusion sonography for septum/fibroids/synechiae), TSH, HbA1c. Most RPL is unexplained; reassurance and close early surveillance are the mainstay. Low-dose aspirin + LMWH if APS confirmed.

15 Fetal Anomalies, Isoimmunization & Hydrops

Aneuploidy Screening & Diagnostic Testing

First-trimester screening combines nuchal translucency (NT) ultrasound at 11w0d–13w6d with serum PAPP-A and free β-hCG. Cell-free DNA (cfDNA) / NIPT tests maternal blood for fetal chromosomal aneuploidy (trisomy 21, 18, 13, sex chromosome aneuploidy) from 10w onward with high sensitivity but requires confirmation for positives. Diagnostic testing: chorionic villus sampling (CVS) at 10w0d–13w6d or amniocentesis at ≥15w.

Anatomy Ultrasound

Detailed fetal anatomy scan at 18w0d–22w6d assesses cranium, face, heart, spine, abdomen, kidneys, limbs, and placenta. A detailed survey (SMFM definition) is performed in high-risk pregnancies (diabetes, teratogen exposure, abnormal screening, FGR, multiples).

Fetal Echocardiography

Specialized cardiac imaging at 20–22w for congenital heart disease screening in high-risk pregnancies (pregestational diabetes, maternal CHD, fetus with extracardiac anomaly, family history, NT ≥3.5 mm, monochorionic twins, teratogen exposure). Evaluates four-chamber view, outflow tracts, aortic arch, ductal arch, and atrial/ventricular septa.

Isoimmunization (Rh, Kell, Duffy)

Maternal alloantibodies against fetal red cell antigens cross the placenta and cause fetal hemolysis. Anti-D (Rh) is classic; anti-Kell (Kell kills) is especially severe because it suppresses erythropoiesis in addition to hemolysis. Workup: maternal antibody titer (critical titer ≥1:16 for most antibodies, any titer for Kell), paternal antigen status, fetal genotype (cfDNA or amniocentesis), and serial MCA peak systolic velocity (MCA-PSV) Doppler. MCA-PSV >1.5 multiples of the median (MoM) predicts moderate-severe fetal anemia. Treatment: intrauterine transfusion (IUT) via cordocentesis. Anti-D immunoglobulin (RhoGAM) 300 µg at 28 weeks and within 72 hours of delivery (and after any sensitizing event: bleeding, trauma, amniocentesis) prevents Rh isoimmunization.

Fetal Hydrops

Abnormal fluid accumulation in two or more fetal compartments (ascites, pleural effusion, pericardial effusion, skin edema, polyhydramnios, placentomegaly). Immune hydrops: isoimmunization. Nonimmune hydrops: cardiac anomalies/arrhythmias, chromosomal, infections (parvovirus B19, CMV, toxo, syphilis), TTTS, chylothorax, α-thalassemia major (Bart hydrops), lymphatic anomalies. Workup is exhaustive; treatment is directed at the cause (IUT for parvovirus anemia, digoxin for SVT, laser for TTTS).

16 Congenital Infections (TORCH, GBS, HSV, HIV)

The TORCH acronym catches perinatal infections that cause fetal injury: Toxoplasmosis, Other (syphilis, parvovirus, varicella, Zika, listeria), Rubella, CMV, HSV.

17 Substance Use & Severe Maternal Morbidity

Substance Use in Pregnancy

Universal screening with validated tools (4P's, NIDA, SURP-P). Opioid use disorder is treated with medication-assisted therapy — buprenorphine or methadone (both safer than withdrawal, which increases fetal loss). Neonatal abstinence syndrome (NAS) is anticipated. Alcohol is teratogenic (FASD). Tobacco cessation counseling every visit; nicotine replacement is preferred to continued smoking. Cocaine and methamphetamine increase abruption and preterm birth risk.

Peripartum Cardiomyopathy (PPCM)

New-onset heart failure with LVEF <45% in the last month of pregnancy or within 5 months postpartum, without other identifiable cause. Treatment per standard HFrEF protocols with pregnancy-safe drugs (no ACE/ARB antepartum; safe postpartum if not breastfeeding or with enalapril/captopril). Anticoagulation for LVEF <30% due to LV thrombus risk. Future pregnancies are high-risk, especially if LVEF does not recover.

Amniotic Fluid Embolism (AFE)

Catastrophic syndrome of cardiovascular collapse, hypoxia, and DIC during labor or immediately postpartum. Pathogenesis is an anaphylactoid reaction to fetal antigens. Mortality is high; management is supportive: ACLS, intubation, massive transfusion protocol, fibrinogen repletion.

Severe Maternal Morbidity (SMM)

CDC defines SMM by 21 indicators (ICU admission, massive transfusion, hysterectomy, eclampsia, acute MI, etc.). MFM teams lead SMM case review and quality improvement. Documentation of quantitative blood loss, maternal early warning system (MEWS) triggers, and time-stamped responses is emphasized.

18 MFM Procedures — A to Z

19 Fetal Assessment & Imaging

Nonstress Test (NST)

External fetal monitoring for at least 20 minutes. Reactive NST (≥32w): ≥2 accelerations of ≥15 bpm lasting ≥15 seconds in 20 minutes. Before 32 weeks: ≥2 accelerations of ≥10 bpm for ≥10 seconds. Nonreactive NSTs prompt BPP or further assessment.

Biophysical Profile (BPP)

Doppler Velocimetry

Umbilical artery (UA): S/D ratio, PI, RI. Normal flow → elevated S/D → AEDF → REDF is a progression of placental resistance. Middle cerebral artery (MCA): PSV for fetal anemia; PI for brain-sparing (low PI → cephalization). Ductus venosus (DV): reversed a-wave is an ominous sign in severe early FGR. Uterine artery: bilateral notching in the early second trimester predicts preeclampsia/FGR.

Cervical Length

Transvaginal measurement from internal to external os. A length <25 mm before 24 weeks is short; <15 mm is a threshold for especially high PTB risk. Serial measurements every 2 weeks in high-risk patients.

Imaging Modalities & Labs

Obstetric labs every scribe will document: prenatal panel (CBC, type & screen, rubella, syphilis, HIV, hepatitis B/C, urine culture), aneuploidy screen, 1-hour GCT at 24–28w, repeat CBC and type screen at 28w, GBS culture at 36w, and TSH/HbA1c for chronic conditions. Fetal MRI is used when ultrasound is inconclusive (CNS anomalies, placenta accreta spectrum) per ACR Appropriateness Criteria for obstetric imaging.

20 Medications You Must Know

Antihypertensives

Diabetes

Preeclampsia & Preterm Labor

Anticoagulation

Miscellaneous Pregnancy Medications

• Levothyroxine: Hypothyroidism; increase dose ~30% at pregnancy confirmation.
• Prednisone: Autoimmune disease; minimally crosses placenta (11β-HSD2 inactivation).
• Hydroxychloroquine, azathioprine, certolizumab, tacrolimus: Immunosuppressants compatible with pregnancy.
• Antiretrovirals (HIV): Continue ART throughout; integrase inhibitor-based regimens preferred.
• Ursodeoxycholic acid: ICP treatment.
• Anti-D immunoglobulin (RhoGAM): 300 µg IM at 28w and postpartum (within 72h), after any sensitizing event.
• Penicillin G: Syphilis treatment; desensitize for allergy.
• Azithromycin + ampicillin + amoxicillin: PPROM latency regimen.
• Rh(D)-negative pregnancy kits, tranexamic acid (TXA): Postpartum hemorrhage management.

21 Classification Systems & Criteria

Bishop Score (Cervical Readiness for Induction)

Modified WHO Maternal Cardiovascular Risk (mWHO)

Other Systems Referenced Throughout

Quintero staging for TTTS (Section 12), Carpenter-Coustan and IADPSG for GDM (Section 4), BPP Manning criteria (Section 19), PAS accreta/increta/percreta (Section 8), HELLP Tennessee and Mississippi criteria (Section 6), White classification of diabetes in pregnancy (A1/A2 + pregestational B–T).

22 Obstetric Physical Exam

The MFM physical exam is focused and standardized. Every visit includes:

Fundal Height

From 20 weeks, the fundal height in centimeters from the pubic symphysis should approximate gestational age in weeks (±2 cm). Lag suggests FGR or oligohydramnios; excess suggests LGA, polyhydramnios, or multiples.

Leopold Maneuvers

Four palpations to determine fetal lie, presentation, and position: (1) fundal grip — which pole is in the fundus (head vs breech)? (2) umbilical grip — which side is the back? (3) suprapubic grip — is the presenting part engaged? (4) pelvic grip — attitude of the head.

Cervical Exam

Documented as dilation / effacement / station (e.g., “4/90%/−1”). Station is measured in cm above (−) or below (+) the ischial spines; −5 to +5. Position and consistency complete the Bishop score.

23 Abbreviations Master List

Pregnancy & Anatomy

Diagnoses

Procedures & Testing

Medications

24 Sample HPI Templates

Closing Note

Maternal-fetal medicine sits at the intersection of two patients, two physiologies, and two sets of stakes. Great MFM scribes master both: they chart the mother's blood pressure trend and the fetus's Doppler waveform with equal care. They recognize that a single sentence — “headache”, “decreased fetal movement”, “leaking fluid” — can redirect a visit from a routine growth scan into an emergent admission. Know the numbers, know the thresholds, and when in doubt, write it down. In high-risk obstetrics, the documentation you create becomes the safety net both patients depend on.

25 References & Sources

Clinical Practice Guidelines

Landmark Clinical Trials

Diagram & Figure Sources