Eduovisual
Pregnancy, Childbirth & Puerperium
Pregestational diabetes in pregnancy: management
— Distinct from gestational diabetes (GDM), which is identified at 24–28 weeks via OGTT.
— Any patient with known DM, prior macrosomia (>4000 g), prior unexplained stillbirth, polycystic ovary syndrome, BMI ≥30, age ≥35, family history of DM, or prior GDM.
— High-risk patients should have early screening at the initial visit (HbA1c, fasting glucose, or 75-g OGTT) — if criteria met, label as PGDM, not GDM.
— PGDM carries a markedly higher risk of congenital anomalies (cardiac, neural tube, caudal regression, sacral agenesis) because hyperglycemia during organogenesis (weeks 5–8) is teratogenic. GDM does not, because it begins later.
— PGDM also drives first-trimester miscarriage, diabetic embryopathy, and maternal end-organ progression (retinopathy, nephropathy).
— Target HbA1c <6.5% (ideally <6.0% if achievable without hypoglycemia) before conception.
— Start folic acid 0.4–1 mg daily (some recommend 4 mg given anomaly risk).
— Switch teratogenic meds: stop ACEi/ARB, statins, SGLT2 inhibitors, GLP-1 agonists; transition to insulin-based regimen.
Board pearl: A patient with type 2 DM presenting at 8 weeks with HbA1c 8.2% on metformin and lisinopril → stop lisinopril immediately, transition to insulin, start high-dose folate, and obtain detailed anatomy ultrasound + fetal echo at 20–22 weeks.
— Known type 1 DM, planning pregnancy: focus on preconception A1c, retinal exam, renal function, thyroid screen (autoimmune overlap).
— Established type 2 DM on oral agents presents at 6–10 weeks: must address medication safety and glycemic targets.
— Undiagnosed type 2 DM discovered on early prenatal labs (A1c 7%, fasting glucose 140) — treat as PGDM, not GDM.
— Duration of diabetes, prior DKA episodes, hypoglycemia awareness (critical — pregnancy blunts counterregulatory response).
— Current regimen: insulin type/doses, pump use, CGM use, oral agents.
— End-organ assessment baseline: vision changes (retinopathy), foaming urine or known albuminuria (nephropathy), orthostasis or gastroparesis symptoms (autonomic neuropathy), prior CV disease.
— Obstetric history: prior macrosomia, shoulder dystocia, stillbirth, preeclampsia, anomalies, NICU admissions.
— Medication review for teratogens: ACEi/ARB, statins, SGLT2i, GLP-1 RAs, certain antihypertensives.
— Polyuria/polydipsia beyond physiologic pregnancy changes, recurrent vaginal candidiasis, blurred vision, weight loss despite gravid state.
— Nausea/vomiting + abdominal pain + tachypnea in a type 1 → consider euglycemic DKA, which can occur at lower glucose levels (<200) in pregnancy due to relative insulin resistance and ketogenesis.
— Adherence patterns, food security, glucose monitoring access, work schedule (shift work disrupts dosing), prior diabetes education.
Key distinction: PGDM vs GDM by timing of A1c elevation — A1c ≥6.5% at the first prenatal visit means PGDM (preexisting), even if never previously diagnosed. This redirects management toward anomaly screening and tighter early control, not just third-trimester surveillance.
Step 3 management: At the intake visit, order baseline A1c, urine albumin-to-creatinine ratio, serum creatinine, TSH (if type 1), and refer to ophthalmology for dilated retinal exam in the first trimester.
— BMI and blood pressure at every visit; hypertension is common in PGDM and synergizes with preeclampsia risk.
— Skin: acanthosis nigricans (insulin resistance marker), injection-site lipohypertrophy (rotation issues → erratic absorption), candidal intertrigo.
— Thyroid palpation in type 1 (autoimmune thyroid coexists).
— Baseline auscultation; long-standing DM with CV risk factors may warrant baseline EKG, especially if age ≥35, hypertension, or smoking history.
— Check peripheral pulses and capillary refill — vascular disease worsens placental perfusion.
— Monofilament and vibration testing for peripheral neuropathy at baseline.
— Ask about hypoglycemia unawareness — a key safety issue intrapartum.
— Fundal height: discordance suggests macrosomia (LGA) or, paradoxically, growth restriction in patients with vasculopathy/nephropathy (uteroplacental insufficiency).
— Polyhydramnios is common with hyperglycemia (fetal polyuria from osmotic diuresis).
— Fetal movement counts starting ~28 weeks.
— Tachycardia + tachypnea in a type 1 mother → screen for euglycemic DKA with a venous gas, anion gap, beta-hydroxybutyrate, even if glucose is only 180–220.
— BP ≥140/90 with proteinuria after 20 weeks → preeclampsia (4× more common in PGDM).
Board pearl: Symmetric IUGR + oligohydramnios in a long-standing type 1 diabetic with creatinine 1.4 reflects diabetic vasculopathy/nephropathy limiting placental flow — opposite of the classic macrosomia/polyhydramnios picture. These pregnancies often require earlier delivery for fetal indications.
— HbA1c — confirms diagnosis if ≥6.5% and trends glycemic control; recheck every 4–8 weeks (red blood cell turnover in pregnancy lowers A1c ~0.5%, so a "normal" value can be misleading later).
— Fasting and random glucose to anchor the regimen.
— Urine albumin-to-creatinine ratio (UACR) and serum creatinine — baseline nephropathy assessment; >300 mg/g defines overt diabetic nephropathy and predicts preeclampsia and preterm birth.
— TSH (especially type 1, due to autoimmune thyroid overlap).
— Lipid panel (informational, not for statin initiation — statins held in pregnancy).
— EKG if long-duration DM, age ≥35, hypertension, or symptoms.
— First-trimester aneuploidy screen offered as for any pregnancy.
— Detailed anatomy ultrasound at 18–22 weeks with attention to neural tube, sacrum, and cardiac outflow tracts.
— Fetal echocardiogram at 20–24 weeks — standard in PGDM because of the 5× increased risk of congenital heart disease.
— Capillary glucose fasting + 1-hour postprandial (preferred) or 2-hour postprandial after each meal, plus bedtime — minimum 4–7 checks/day.
— CGM is preferred where available; type 1 patients especially benefit.
Step 3 management: When a previously undiagnosed patient is identified at 9 weeks with A1c 7.4%, your initial orders are: HbA1c, UACR, creatinine, TSH, EKG, ophthalmology referral, fetal anatomy + echo scheduled, and folic acid 4 mg daily. Do not wait for the 24–28 week OGTT — she has PGDM.
— Fasting <95 mg/dL
— 1-hour postprandial <140 mg/dL
— 2-hour postprandial <120 mg/dL
— Avoid glucose <70 (hypoglycemia risk, especially type 1 with blunted awareness in pregnancy).
— <6.0–6.5% in pregnancy when achievable without hypoglycemia; <7% is acceptable if hypoglycemia is limiting.
— Trend every 4–8 weeks; values fall physiologically due to increased RBC turnover.
— Strongly preferred in type 1; reduces macrosomia, LGA, NICU admission, and neonatal hypoglycemia (CONCEPTT trial).
— Time in range (63–140 mg/dL) goal ≥70%, time below range <4%, time above range <25%.
— Urine or blood ketones with illness, vomiting, or persistent glucose >200 — especially in type 1; threshold for DKA in pregnancy is lower.
— Detailed anatomy + fetal echo at 18–24 weeks.
— Growth ultrasounds every 4 weeks from 28 weeks onward (to detect macrosomia or IUGR).
— Antenatal testing (NST/BPP) starting 32 weeks, often twice weekly, given stillbirth risk; earlier if vasculopathy, poor control, hypertension, or IUGR.
— Repeat UACR, BP at every visit; preeclampsia labs (CBC, LFTs, creatinine, urine protein) with any concerning sign.
— Repeat retinal exam each trimester if retinopathy present.
CCS pearl: On the CCS-style case, set "advance clock" intervals matching the schedule above — recheck A1c at 4–6 weeks, growth scan at 28/32/36 weeks, and don't forget twice-weekly NSTs starting at 32 weeks. Missing antenatal testing is a high-yield CCS scoring penalty for PGDM.
— Type of diabetes (1 vs 2 — different insulin physiology and DKA risk).
— Duration and end-organ disease (White classification still appears on exams: classes B–F/R/H reflect duration, vascular, renal, retinal, and cardiac involvement).
— Glycemic control at entry (A1c <6.5% vs >8% drives anomaly risk discussion).
— Comorbid hypertension, obesity, prior obstetric complications.
— A1c <6.5%: background risk (~2–3%).
— A1c 7–9%: ~5–10% risk.
— A1c >10%: up to 20–25% risk of major anomalies — this is the counseling point at preconception.
— Nephropathy (UACR >300 or Cr >1.4) → high risk of preeclampsia (40–50%), preterm birth, IUGR.
— Proliferative retinopathy → treat with laser before pregnancy or in early pregnancy.
— CAD → high maternal mortality; consider preconception cardiology evaluation.
— 1. Glycemic control with insulin (transition off most orals/non-insulin injectables).
— 2. Anomaly screening (anatomy US + fetal echo).
— 3. Preeclampsia prevention — low-dose aspirin 81–162 mg starting 12–16 weeks in all PGDM patients (USPSTF/ACOG).
— 4. Surveillance (growth, NSTs, retinal, renal).
— 5. Timed delivery based on control and complications.
— Discuss anomaly risk in concrete numerical terms.
— Address hypoglycemia plan, including glucagon at home.
— Discuss likelihood of cesarean (higher in PGDM) and NICU admission.
Board pearl: Every PGDM pregnancy should receive low-dose aspirin starting at 12–16 weeks to reduce preeclampsia — this is a frequently-missed standing order on exams.
— Total daily dose (TDD) ≈ 0.7–1.0 units/kg/day by trimester:
— 1st trimester: 0.7 U/kg
— 2nd trimester: 0.8 U/kg
— 3rd trimester: 0.9–1.0 U/kg (insulin resistance peaks).
— Split 50% basal / 50% bolus, then divide bolus across meals.
— Basal: NPH (twice daily) or detemir or glargine U-100 — all have safety data.
— Bolus (prandial): aspart or lispro — preferred over regular due to better postprandial control and lower late hypoglycemia.
— Avoid degludec and glulisine unless already established (limited pregnancy data, though increasingly used).
— Maintain pump if previously well-controlled; otherwise multiple daily injections.
— First-trimester insulin needs often fall (nausea, increased insulin sensitivity, increased fetal glucose draw) → hypoglycemia risk peaks at 8–16 weeks.
— Needs rise steeply after ~18–20 weeks, often doubling by term.
— A sudden drop in insulin requirement in the third trimester can signal placental insufficiency.
— Metformin crosses the placenta; not first-line, but acceptable adjunct if patient declines insulin or as continuation in type 2 with mild disease — counsel on long-term offspring data uncertainty.
— Glyburide is no longer recommended (worse neonatal outcomes vs insulin).
— Stop SGLT2i, GLP-1 RA, DPP-4i preconception or at first visit.
— Glucagon kit at home for type 1; family trained.
— Treat lows with 15 g fast carbs, recheck in 15 min.
Step 3 management: A type 1 patient at 30 weeks with TDD 60 U pre-pregnancy now needs ~90–100 U/day; titrate basal by fasting glucose, bolus by postprandials, weekly.
— Can be euglycemic (glucose <200) due to enhanced ketogenesis and fetal glucose siphon.
— Fetal mortality 10–25%; non-reassuring tracings often resolve with maternal correction, not delivery.
— Management: IV fluids (NS then ½NS), insulin drip 0.1 U/kg/hr, replace potassium aggressively (often needs replacement before insulin if K <3.3), dextrose-containing fluids when glucose <200, treat precipitant (infection, missed dose, betamethasone, beta-agonists).
— Do not deliver for fetal distress until maternal status corrected unless persistently non-reassuring.
— Given for anticipated preterm delivery <34 weeks.
— Cause significant hyperglycemia for 3–5 days — anticipate insulin uptitration 20–40% and frequent glucose checks; consider inpatient insulin drip if needed.
— Well-controlled, uncomplicated PGDM: 39 0/7–39 6/7 weeks.
— Poorly controlled or vasculopathy/nephropathy/IUGR/preeclampsia: 36 0/7–38 6/7, individualized.
— Estimated fetal weight ≥4500 g → offer scheduled cesarean to reduce shoulder dystocia/brachial plexus injury.
— Target maternal glucose 70–110 mg/dL in labor to minimize neonatal hypoglycemia.
— Type 1: insulin drip + D5 infusion, glucose checks every 1–2 hours.
— Type 2: often needs little/no insulin in labor.
— Hold long-acting insulin morning of induction or scheduled C-section; resume ~50% of pre-pregnancy dose postpartum (insulin resistance drops abruptly with placental delivery).
CCS pearl: On a CCS DKA case in pregnancy, order continuous fetal monitoring and maternal ICU-level care simultaneously — fix the mother, the fetus follows.
— Defined by baseline UACR >300 mg/g or creatinine elevation.
— Pregnancy can transiently worsen proteinuria; stable creatinine usually returns to baseline postpartum unless Cr >1.4 pre-pregnancy (then irreversible decline possible).
— Risks: preeclampsia (40–50%), IUGR, preterm birth (often <34 weeks), stillbirth.
— Management: aspirin 81–162 mg, tight BP control, avoid ACEi/ARB in pregnancy (substitute labetalol, nifedipine, methyldopa); resume ACEi/ARB postpartum (compatible with breastfeeding).
— Target BP <140/90 (some target <135/85). Use labetalol, nifedipine ER, methyldopa.
— Avoid atenolol (IUGR), thiazides (controversial in pregnancy), and ACEi/ARB (teratogenic — fetal renal dysgenesis, oligohydramnios).
— Long-standing type 1 with CAD or cardiomyopathy: high maternal mortality (especially with ischemic disease, EF <40%).
— Consider preconception cardiology consultation; some patients should be counseled against pregnancy.
— Watch for HELLP overlap with preeclampsia; LFTs at each visit if nephropathy or hypertension.
— Type 1 has autoimmune thyroid in ~25%; screen TSH each trimester. Treat hypothyroidism aggressively — fetal neurodevelopment depends on maternal thyroxine in early pregnancy.
— Compounds anomaly, preeclampsia, stillbirth, and cesarean risks; lowers threshold for earlier antenatal testing.
Key distinction: Worsening proteinuria alone in a known nephropathy patient is expected and not, by itself, diagnostic of superimposed preeclampsia — look for new hypertension, end-organ signs (LFT elevation, thrombocytopenia, headache, RUQ pain), or doubling of baseline proteinuria to make that call.
— Achieve A1c <6.5% (ideally <6.0%) before conception → reduces anomaly rate to near baseline.
— Folic acid 0.4–1 mg daily (4 mg often recommended given anomaly risk and obesity).
— Switch from teratogens: stop ACEi/ARB, statins, SGLT2i, GLP-1 RAs.
— Establish effective contraception until A1c at goal — LARC (IUD, implant) preferred in patients with DM (no glycemic impact, high efficacy).
— Baseline retinal, renal, cardiac, thyroid evaluation.
— Address transition of care from pediatric to adult endocrine and obstetric services.
— High rates of insulin omission, eating disorders ("diabulimia"), and contraceptive gaps.
— Confidential preconception counseling at every visit once reproductively capable.
— Insulin requirements drop ~50% immediately after placental delivery; restart half of pre-pregnancy dose and titrate.
— Encourage breastfeeding — reduces type 2 progression in mother and obesity/DM risk in child; monitor for hypoglycemia in nursing mothers.
— Resume ACEi/ARB, metformin postpartum (both compatible with breastfeeding). Statins are generally held during lactation (limited data); restart after weaning unless high cardiovascular risk.
— Contraception counseling before discharge — LARC ideal; avoid combined estrogen if vascular disease, severe nephropathy, or uncontrolled hypertension.
— Wait until A1c at goal again before next conception.
— Discuss interpregnancy weight management (especially type 2).
Board pearl: A patient with PGDM and BMI 38 asks about contraception postpartum — best choices are levonorgestrel IUD or etonogestrel implant; avoid combined OCPs because of vascular risk in PGDM.
— Preeclampsia (4× baseline risk; up to 40–50% with nephropathy).
— Progression of retinopathy (especially proliferative — risk of vitreous hemorrhage).
— Nephropathy progression (transient or permanent, depending on baseline).
— DKA (lower threshold; can be euglycemic; high fetal mortality).
— Hypoglycemia (especially type 1, especially early pregnancy and intrapartum).
— Infection: UTI, pyelonephritis, wound infection postpartum.
— Cesarean delivery (markedly increased).
— Cardiovascular events in patients with established CAD.
— Congenital anomalies: cardiac (TGA, VSD, hypoplastic left heart), neural tube defects, caudal regression/sacral agenesis (classic association), renal, GI.
— Macrosomia / LGA → shoulder dystocia, brachial plexus injury (Erb-Duchenne), clavicle fracture, birth asphyxia.
— IUGR in vasculopathic mothers.
— Polyhydramnios → preterm labor, PPROM, cord prolapse.
— Stillbirth (3–5× baseline; clusters in 3rd trimester with poor control).
— Preterm birth (often iatrogenic for preeclampsia/IUGR).
— Neonatal hypoglycemia (fetal hyperinsulinemia persists after cord clamp).
— Respiratory distress syndrome (insulin delays surfactant; greater risk at any gestational age).
— Neonatal hypocalcemia, hypomagnesemia, polycythemia, hyperbilirubinemia, hypertrophic cardiomyopathy (typically reversible).
— Childhood obesity, metabolic syndrome, type 2 DM (Pedersen/Barker hypotheses).
Board pearl: Newborn of PGDM mother who develops respiratory distress and tachypnea at hour 2: differential includes transient tachypnea, RDS (delayed surfactant), and hypertrophic cardiomyopathy — get an echocardiogram and glucose immediately.
— Maternal-fetal medicine (MFM), endocrinology, nutrition/diabetes educator, ophthalmology, nephrology if Cr elevated, cardiology if longstanding/CAD, anesthesia consult in third trimester.
— A1c not improving despite intensified regimen → endocrine referral and consider hospitalization for insulin titration.
— New proteinuria or BP elevation → MFM, possibly admit for preeclampsia workup.
— Worsening retinopathy → urgent ophthalmology for possible laser.
— DKA (ICU or stepdown).
— Severe hyperglycemia with persistent vomiting or inability to maintain control at home.
— Recurrent severe hypoglycemia with loss of awareness.
— Preeclampsia with severe features (delivery planning, magnesium, antihypertensives).
— Non-reassuring fetal testing, IUGR with abnormal Dopplers, oligohydramnios.
— Preterm labor or PPROM — manage hyperglycemia from betamethasone with insulin drip.
— DKA with hemodynamic instability, severe acidosis (pH <7.1), altered mental status, K <3.0 or >6.0, or non-reassuring fetal status during DKA.
— Severe preeclampsia with end-organ failure, pulmonary edema, eclampsia.
— Cardiac decompensation in pregestational CAD/cardiomyopathy.
— Early consult if obesity, prior difficult intubation, autonomic neuropathy (cardiovascular instability), or cardiac disease.
— Early epidural in labor minimizes catecholamine surge and hyperglycemia.
CCS pearl: On a DKA case at 28 weeks, admit to ICU, start insulin drip + IV fluids + potassium, place on continuous fetal monitoring if ≥viability, consult MFM and endocrinology, and delay delivery unless fetal status remains non-reassuring after maternal correction.
— Identified at 24–28 weeks by 1-step (75-g OGTT) or 2-step (50-g screen then 100-g OGTT) testing.
— Distinguishing feature: normal early-pregnancy glycemia (no first-trimester A1c ≥6.5%); typically resolves postpartum.
— Lower anomaly risk because hyperglycemia begins after organogenesis.
— After betamethasone for fetal lung maturity, glucose rises sharply for 3–5 days even in normoglycemic women.
— Distinguish from new diabetes by demonstrating return to normal after steroid washout.
— Rare; consider with refractory hyperglycemia + classic features (moon facies, striae, acromegalic features).
— Family history of mild, autosomal dominant DM with onset <25 yo, lean, no autoimmunity.
— MODY-2 (GCK): mild fasting hyperglycemia; treatment in pregnancy depends on fetal genotype — if fetus inherits the variant, tight maternal control can cause IUGR.
— MODY-3 (HNF1A): responds to sulfonylureas outside pregnancy; in pregnancy, use insulin.
— Slowly progressive autoimmune diabetes in adults often misdiagnosed as type 2. Suspect when "type 2" patients become insulin-requiring quickly and have GAD antibodies.
— Type 3c DM from chronic pancreatitis, cystic fibrosis–related diabetes — manage as type 1 physiologically.
— Thyroid dysfunction, atypical antipsychotics, tacrolimus (post-transplant pregnancies).
Key distinction: A1c ≥6.5% at the first prenatal visit defines PGDM, not GDM — this is the single most testable diagnostic boundary.
— Both cause vomiting and ketosis; hyperemesis is starvation ketosis with normal glucose and no anion gap acidosis, whereas DKA has anion gap acidosis, elevated beta-hydroxybutyrate, often hyperglycemia (but may be euglycemic).
— Both have proteinuria; preeclampsia adds new hypertension after 20 weeks, thrombocytopenia, LFT elevation, elevated creatinine relative to baseline, severe features (headache, vision changes, RUQ pain).
— Diabetic nephropathy alone: proteinuria gradually worsens without these systemic features.
— Fundal height >gestational age can reflect either; ultrasound differentiates EFW from AFI.
— RDS: ground-glass on CXR, surfactant deficiency, especially in poorly controlled PGDM.
— TTN: wet lungs, fluid in fissures, resolves <72 h.
— Hypertrophic cardiomyopathy: septal hypertrophy on echo, can cause LVOT obstruction — usually resolves over weeks.
— Sepsis, adrenal insufficiency, insulinoma, dumping syndrome post-bariatric surgery — consider when hypoglycemia patterns don't fit insulin regimen.
— Both present with fatigue, palpitations, weight changes — check TSH.
— Type 1 patient on pump with sudden hyperglycemia — consider cannula occlusion before adjusting basal rate; instruct to give correction by syringe/pen and change site.
Board pearl: A type 1 pump user at 32 weeks with nausea, glucose 240, and anion gap 18 — stop the pump, give SC rapid insulin, fluids, admit for DKA workup, and replace the infusion set.
— Reduce insulin to ~50% of pre-pregnancy dose at delivery; type 2 may need none briefly.
— Type 2 PGDM: resume metformin, can resume ACEi/ARB (lisinopril, enalapril compatible with breastfeeding), restart antihypertensives as needed.
— Stop pregnancy-specific aspirin unless other indication.
— Hold statins during breastfeeding (limited data); resume after weaning if indicated by ASCVD risk.
— Encourage breastfeeding — reduces maternal type 2 progression and offspring metabolic risk; monitor for nursing-related hypoglycemia.
— Contraception before discharge — LARC (IUD or implant) preferred; avoid combined estrogen contraceptives in patients with vascular disease, nephropathy (UACR >300), uncontrolled HTN, or DM duration >20 years.
— Postpartum visit with comprehensive review: BP, glucose, weight, mood (PPD screen), contraception adherence, infant feeding.
— Reassess A1c at 6–12 weeks.
— Reaffirm endocrinology follow-up.
— Annual dilated retinal exam, urine ACR, lipid panel, foot exam.
— Aspirin 81 mg if ASCVD risk warrants (not routine in young patients without other risk factors).
— Statin when not breastfeeding, per ASCVD risk and ADA criteria.
— ACEi/ARB if albuminuria or hypertension; ensure effective contraception while on these agents.
— Weight management, structured exercise, smoking cessation.
— Pneumococcal, influenza, COVID, Tdap vaccinations on schedule.
Step 3 management: At the 6-week postpartum visit for a type 2 PGDM patient, restart metformin and lisinopril, place levonorgestrel IUD, schedule endocrinology in 4 weeks for A1c-guided regimen adjustment, and refer to ophthalmology and nephrology annually.
— Every 1–2 weeks until 28 weeks, then weekly through delivery. More frequent if poor control, hypertension, or complications.
— Bring logs/CGM downloads to every visit; titrate insulin weekly or more often in late pregnancy.
— A1c every 4–8 weeks.
— UACR and creatinine each trimester (more often if nephropathy).
— TSH each trimester in type 1 or if hypothyroid.
— Preeclampsia labs (CBC, LFTs, Cr, urine protein) with any concerning sign and routinely after 28 weeks in high-risk patients.
— Anatomy scan 18–22 weeks; fetal echo 20–24 weeks.
— Growth ultrasound at 28, 32, 36 weeks (or every 4 weeks).
— NSTs twice weekly starting 32 weeks, often earlier with vasculopathy or poor control.
— Ophthalmology each trimester if any retinopathy.
— Endocrinology/diabetes educator monthly or as needed.
— MFM consult or co-management throughout.
— Anesthesia consult in 3rd trimester.
— Hypoglycemia recognition and treatment; glucagon training for family.
— Sick-day rules: never omit basal insulin, check ketones, hydrate, contact team for glucose >250 with ketones or persistent vomiting.
— Kick counts from ~28 weeks.
— Signs of preeclampsia, preterm labor, decreased fetal movement → when to call.
— Breastfeeding plan and postpartum insulin reduction expectations.
— Future contraception and interpregnancy interval.
— Screen for depression and diabetes distress at intake, each trimester, and 6 weeks postpartum (EPDS or PHQ-9).
Board pearl: Sudden, marked drop in insulin requirement in the third trimester is a red flag for placental insufficiency — escalate fetal surveillance immediately.
— Discontinuing ACEi/ARB, statins, SGLT2i, GLP-1 RAs at conception/positive pregnancy test requires explicit discussion of teratogenic risks and documented patient understanding — high-risk transition point for medication errors.
— Counsel that metformin crosses the placenta with uncertain long-term offspring data; document shared decision-making if continued.
— Patient may refuse insulin, antenatal testing, or scheduled cesarean for macrosomia. Respect autonomy after providing thorough counseling; document the conversation, alternatives offered, and risks understood. Continue care without coercion.
— A patient with A1c 11% and unintended pregnancy raises ethical questions but is never grounds to delay or restrict care. Frame contraception conversations as harm reduction, not judgment, and assure confidentiality especially in adolescents.
— Hospital handoffs: intrapartum insulin drip orders, postpartum dose reduction, and inpatient-to-outpatient handoff (resumption of home regimen, ACEi/ARB, metformin) are common error points. Use medication reconciliation at every transition.
— Outpatient handoff postpartum: explicit endocrinology and primary care follow-up appointments scheduled before discharge, not "as needed."
— Reassure patients that metformin, insulin, labetalol, nifedipine, ACEi/ARB are compatible; counsel against SGLT2i, GLP-1 RAs while breastfeeding (limited data).
— No mandatory reporting for diabetes-related issues per se, but screen for intimate partner violence, food insecurity, and insurance gaps that prevent insulin/CGM access — these are medical safety issues.
Step 3 management: Before discharge of any postpartum PGDM patient, reconcile medications, schedule endocrine follow-up within 4–6 weeks, document contraception, and confirm CGM/insulin coverage with social work or pharmacy — missed handoffs are a sentinel event in this population.
— Caudal regression syndrome / sacral agenesis — pathognomonic association with PGDM.
— Cardiac: transposition of the great arteries, VSD, hypoplastic left heart, truncus arteriosus.
— Neural tube defects (anencephaly, spina bifida).
— Small left colon syndrome.
— Renal agenesis, situs inversus.
— A1c <6.5% preconception goal; <6.0% if no hypoglycemia.
— Fasting <95, 1-hr PP <140, 2-hr PP <120 mg/dL pregnancy targets.
— Aspirin 81 mg starting 12–16 weeks for preeclampsia prevention.
— Folate 4 mg daily preconception in PGDM (some guidelines).
— Insulin TDD: 0.7 → 0.8 → 0.9–1.0 U/kg by trimester.
— Delivery 39 weeks if well-controlled; 36–38 weeks if complicated.
— EFW ≥4500 g → offer scheduled cesarean.
— NSTs twice weekly from 32 weeks.
— Postpartum insulin: 50% pre-pregnancy dose.
— ACEi/ARB (renal dysgenesis, oligohydramnios).
— Statins (held in pregnancy and during breastfeeding).
— SGLT2 inhibitors, GLP-1 receptor agonists, DPP-4 inhibitors.
— Warfarin (replace with LMWH).
— CONCEPTT trial: CGM in pregnant type 1 women → better neonatal outcomes.
— White classification: still appears on exams.
— MODY-2 GCK: manage based on fetal genotype.
— Newborn of diabetic mother: check glucose, calcium, magnesium, hematocrit, bilirubin; consider echo for septal hypertrophy.
Board pearl: A 2-day-old infant of a poorly controlled diabetic mother develops a systolic murmur and respiratory distress — think hypertrophic cardiomyopathy (transient septal hypertrophy from fetal hyperinsulinemia) and order an echocardiogram.
— Recognize as PGDM (not GDM). Answer: stop ACEi/ARB and statin, start folic acid, start insulin, schedule anatomy ultrasound and fetal echo, begin low-dose aspirin at 12 weeks.
— DKA in pregnancy. Answer: IV fluids, insulin drip, potassium replacement (before insulin if K <3.3), continuous fetal monitoring, ICU admission, do not deliver for fetal distress until maternal status corrected.
— Answer: offer scheduled cesarean delivery at 39 weeks to reduce shoulder dystocia/brachial plexus injury.
— Answer: echocardiogram to evaluate for transient hypertrophic cardiomyopathy/LVOT obstruction; also check glucose, calcium.
— Answer: red flag for placental insufficiency; escalate fetal surveillance, consider delivery.
— Answer: insulin needs fell dramatically — reduce basal/bolus to ~50% of pre-pregnancy dose.
— Answer: stop lisinopril, atorvastatin, empagliflozin; continue metformin or transition to insulin; achieve A1c <6.5% before conception; start folate.
— Answer: chronic diabetic nephropathy; baseline labs, aspirin at 12 weeks, switch antihypertensive to labetalol or nifedipine, MFM co-management.
— Answer: confidential contraception (LARC preferred), preconception counseling, ongoing endocrine care.
Key distinction: When the stem gives first-trimester glucose/A1c data — it's PGDM logic, not GDM logic.
Pregestational diabetes in pregnancy is a high-risk condition where preconception A1c optimization, transition off teratogens, insulin-based glycemic control to pregnancy-specific targets, aspirin prophylaxis, anomaly and fetal echo screening, intensified antenatal surveillance, and timed delivery collectively reduce maternal-fetal morbidity that is otherwise dramatically elevated above background.
Board pearl: The single most powerful intervention for PGDM is preconception A1c optimization — driving anomaly risk from 20–25% (A1c >10%) down toward population baseline (~2–3%) when A1c <6.5%. Every encounter with a reproductive-age woman with diabetes is a preconception care opportunity, and recognizing A1c ≥6.5% at the first prenatal visit as PGDM (not GDM) is the diagnostic pivot that drives all subsequent management decisions on Step 3.