Pregnancy Complications

Why they matter

• Hypertensive disorders of pregnancy are among the leading causes of maternal death and severe maternal morbidity in the United States, and are a leading indication for iatrogenic preterm birth. They complicate a substantial minority of pregnancies — on the order of one in ten — with preeclampsia itself affecting roughly 3–5%.
• Antepartum hemorrhage is a leading cause of obstetric hemorrhage: abruption complicates about 1% of pregnancies, previa roughly 1 in 200 deliveries at term. Both drive transfusion, emergent cesarean, and hysterectomy.
• Timing is the whole disease. By definition, preeclampsia and gestational hypertension require new hypertension after 20 weeks; hypertension before 20 weeks is chronic hypertension. Painless bleeding is previa until proven otherwise; painful bleeding with a tender, tetanic uterus is abruption.

Who gets them

• Preeclampsia favors extremes of the risk spectrum: nulliparas, women over 35, multifetal gestation, chronic hypertension, pregestational diabetes, chronic kidney disease, antiphospholipid syndrome, obesity, and prior preeclampsia. Black women in the US carry disproportionately higher rates of preeclampsia-related morbidity and mortality.
• Previa clusters with prior cesarean delivery and prior uterine instrumentation; abruption clusters with hypertension, trauma, smoking, and cocaine.

• Non-modifiable: nulliparity, prior preeclampsia (the single strongest historical predictor), age >35, multifetal gestation, pregestational diabetes, chronic hypertension, chronic kidney disease, antiphospholipid syndrome and other thrombophilias, SLE, family history, molar pregnancy (preeclampsia before 20 weeks = think hydatidiform mole).
• Modifiable/partly modifiable: obesity, poorly controlled chronic hypertension, IVF/donor-oocyte conception, long interpregnancy interval, and absence of aspirin prophylaxis in a high-risk patient. USPSTF and ACOG both recommend low-dose aspirin for patients with high-risk features.

Mechanism 2 — decidual vessel rupture and shear (abruption)

• Modifiable: cocaine and amphetamine use (vasospasm), cigarette smoking, blunt abdominal trauma including motor vehicle collision and intimate partner violence.
• Non-modifiable: prior abruption (high recurrence), preeclampsia/chronic hypertension, thrombophilia, polyhydramnios or multiple gestation with rapid uterine decompression, preterm premature rupture of membranes, chorioamnionitis, advanced maternal age.

• Non-modifiable/iatrogenic: prior cesarean delivery (risk rises with each), prior previa, prior curettage or myomectomy, multiparity, advanced maternal age, ART, multiple gestation. Previa plus prior cesarean is the classic setup for placenta accreta spectrum.
• Modifiable: smoking (relative placental hypoxia enlarges placental surface area).

Preeclampsia — a two-stage placental-to-maternal disease

• Stage 1 (placental): cytotrophoblasts fail to remodel maternal spiral arteries into low-resistance conduits. The vessels stay muscular and responsive to vasoconstrictors, so intervillous perfusion is intermittent and the placenta becomes ischemic and oxidatively stressed.
• Stage 2 (maternal): the ischemic placenta sheds antiangiogenic factors — soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin — into maternal blood. sFlt-1 is a decoy receptor that scavenges VEGF and placental growth factor (PlGF); endoglin blocks TGF-β signaling. Both are required for endothelial nitric oxide production and fenestrated endothelial maintenance.
• The result is systemic endothelial dysfunction, and every clinical finding follows from it:
• Loss of NO-mediated vasodilation and increased sensitivity to angiotensin II → hypertension.
• Glomerular endotheliosis with podocyte injury → proteinuria and rising creatinine.
• Increased capillary permeability with low oncotic pressure → nondependent edema, facial/hand swelling, pulmonary edema.
• Hepatic sinusoidal fibrin deposition and periportal necrosis stretching Glisson capsule → RUQ pain and transaminitis.
• Endothelial injury with platelet consumption and fibrin strands shearing red cells → thrombocytopenia and microangiopathic hemolysis (HELLP).
• Loss of cerebral autoregulation with hyperperfusion and vasogenic edema (posterior circulation) → headache, scotomata, and eclamptic seizure; imaging correlate is PRES.
• Uteroplacental underperfusion simultaneously produces fetal growth restriction, oligohydramnios, and abnormal umbilical artery Dopplers.

• Persistent occipital or frontal headache unrelieved by acetaminophen: cerebral vasogenic edema; a severe feature by itself.
• Scotomata, photopsia, blurred vision: occipital cortex and retinal arteriolar spasm.
• RUQ or epigastric pain: hepatic capsular stretch — the pain that precedes hepatic subcapsular hematoma.
• Dyspnea and crackles: pulmonary edema from capillary leak plus low oncotic pressure.
• Brisk, sustained clonus and hyperreflexia: cortical irritability heralding seizure.
• Rapid-onset facial and hand edema, oliguria, weight gain: capillary leak and glomerular injury. Dependent leg edema alone is normal in pregnancy.

Third-trimester bleeding — differentiate by pain and tone

• Abruption: painful dark bleeding, tender rigid uterus, high-frequency low-amplitude contractions, category II/III tracing with late decelerations or bradycardia; may present as concealed hemorrhage with maternal shock and a benign-looking perineum.
• Previa: painless, bright red bleeding, soft nontender uterus, often after intercourse or a digital exam, with a reassuring fetal tracing and frequently a malpresentation or high, unengaged head.
• Vasa previa: painless bleeding immediately at rupture of membranes with abrupt fetal bradycardia or a sinusoidal tracing — fetal, not maternal, blood loss.
• Uterine rupture: loss of station, abnormal contour, sudden pain in a patient with a prior uterine scar.

• Proteinuria: ≥300 mg per 24-hour collection, urine protein/creatinine ratio ≥0.3, or dipstick 2+ only when quantitative testing is unavailable.
• Severe features (proteinuria not required): platelets <100,000/µL; serum creatinine >1.1 mg/dL or doubling of baseline; transaminases at least twice the upper limit of normal; pulmonary edema; new-onset headache unresponsive to medication and not otherwise explained; visual disturbances. Note that the degree of proteinuria and fetal growth restriction are no longer severe features.

Bleeding evaluation

• Transabdominal then transvaginal ultrasound for placental location. Never perform a digital cervical exam until previa is excluded — this is the single most tested next-step error. Transvaginal ultrasound is safe and is the confirmatory study for previa.
• Abruption is a clinical diagnosis. Ultrasound is insensitive; a visible retroplacental clot supports but its absence never excludes abruption. Fibrinogen is the best marker of severity and of evolving DIC — a falling or low fibrinogen in a bleeding gravida is ominous. Obtain type and crossmatch, coagulation studies, and continuous fetal monitoring; Kleihauer-Betke quantifies fetomaternal hemorrhage in Rh-negative patients.

• IV labetalol (beta blocker with alpha activity), IV hydralazine (direct arteriolar dilator), or immediate-release oral nifedipine (dihydropyridine calcium channel blocker) — all three are first-line and interchangeable.
• Avoid overshooting; the goal is a safe range, not normotension, because uteroplacental perfusion is pressure-dependent.

Seizure prophylaxis and treatment

• Magnesium sulfate is first-line for preeclampsia with severe features and for eclampsia — typically a 4–6 g IV load over 20–30 minutes followed by 1–2 g/hr infusion, continued 24 hours postpartum. It is superior to phenytoin and diazepam for eclampsia. Monitor deep tendon reflexes, respiratory rate, and urine output; reduce dosing in renal impairment. Calcium gluconate is the antidote.
• For a seizure: protect the airway, left lateral decubitus, oxygen — then magnesium. The seizure itself is not an indication for emergent cesarean; stabilize the mother first, since fetal bradycardia usually resolves as the seizure ends.

Bleeding

• Abruption: two large-bore IVs, crossmatched blood, fibrinogen/cryoprecipitate for DIC, anti-D immune globulin if Rh-negative, and prompt delivery — cesarean for nonreassuring tracing or instability.
• Previa: pelvic rest, no digital exam, and scheduled cesarean in the late preterm/early term window; earlier for recurrent bleeding. Suspected accreta spectrum warrants delivery at a center capable of cesarean hysterectomy.

Maternal emergencies (act immediately)

• Eclampsia: cerebral vasogenic edema from failed autoregulation. Signaled by escalating headache, visual change, and sustained clonus. Magnesium, not an antiepileptic, is the answer.
• Hemorrhagic stroke: the leading cause of death in severe preeclampsia; driven by systolic pressure. This is why severe-range systolic hypertension is treated within an hour.
• HELLP with hepatic subcapsular hematoma rupture: sudden severe RUQ or shoulder pain with hypotension and falling hematocrit. Surgical/interventional emergency.
• DIC: most classically from abruption via decidual tissue factor; signaled by falling fibrinogen, prolonged PT/aPTT, and oozing from IV sites.
• Pulmonary edema: capillary leak plus iatrogenic fluid overload — a major reason to restrict IV fluids in preeclampsia.
• Massive obstetric hemorrhage with hypovolemic shock: from previa, accreta spectrum, concealed abruption, or postpartum atony (a Couvelaire uterus contracts poorly). Sheehan syndrome — failure of lactation, amenorrhea — is the delayed sequela.

Fetal/neonatal

• Fetal growth restriction, oligohydramnios, and abnormal umbilical artery Dopplers from chronic uteroplacental underperfusion.
• Preterm birth and its morbidities, largely iatrogenic and indicated.
• Stillbirth, the feared endpoint of abruption and of cholestasis; fetal exsanguination in ruptured vasa previa.
• Neonatal hypoglycemia, macrosomia, shoulder dystocia, and hyperbilirubinemia in poorly controlled gestational diabetes (fetal hyperinsulinemia).

Treatment-related

• Magnesium toxicity: progressive loss of deep tendon reflexes first, then respiratory depression, then cardiac arrest — accumulates in renal impairment. Stop the infusion and give calcium gluconate.
• Maternal hypotension with fetal bradycardia from aggressive antihypertensive titration, particularly hydralazine.
• Neonatal bradycardia and hypoglycemia after maternal labetalol.
• Cesarean hysterectomy, urologic injury, and massive transfusion in accreta spectrum.

• Proteinuria is not required. New hypertension after 20 weeks plus thrombocytopenia <100,000/µL, creatinine >1.1 mg/dL, transaminases twice normal, pulmonary edema, refractory headache, or visual symptoms diagnoses preeclampsia with severe features (ACOG). The old "BP + protein" dyad is the classic distractor.
• Painless bright red bleeding = previa; painful bleeding with a rigid tender uterus = abruption. Best next step in painless third-trimester bleeding is ultrasound before any digital cervical exam. The digital exam is the wrong answer every time.
• Abruption is a clinical diagnosis. A negative ultrasound does not exclude it, and concealed hemorrhage means the patient can be in shock with almost no visible blood. Abruption is the classic obstetric cause of DIC — watch the fibrinogen.
• Magnesium sulfate prevents and treats eclamptic seizures; it is not an antihypertensive. Blood pressure still needs labetalol, hydralazine, or nifedipine. Reflex loss precedes respiratory depression; the antidote is calcium gluconate.
• Delivery is the only cure — 37 weeks without severe features, 34 weeks with severe features (ACOG). But an eclamptic seizure alone is not an indication for emergent cesarean: stabilize the mother, and the transient fetal bradycardia usually recovers.
• Preeclampsia before 20 weeks means think molar pregnancy; preeclampsia and eclampsia can also first appear postpartum, up to about 6 weeks after delivery.
• ACE inhibitors and ARBs are contraindicated throughout pregnancy (fetal renal dysgenesis, oligohydramnios, skull hypoplasia). Captopril's short half-life makes it convenient for titration outside pregnancy — it does not make it safe in pregnancy. Also avoid methylergonovine in a hypertensive patient.
• Previa + prior cesarean = suspect placenta accreta spectrum, and plan delivery where cesarean hysterectomy is available. The mimic to know is vasa previa: painless bleeding at rupture of membranes with a sinusoidal tracing or abrupt fetal bradycardia — fetal blood, not maternal.
• Low-dose aspirin from 12–28 weeks in high-risk patients is the preventive intervention USPSTF and ACOG endorse.

• Gestational diabetes affects 2-10% of pregnancies; screened at 24-28 weeks with 50g glucose challenge test (GCT)
• Preeclampsia defined as BP ≥140/90 mmHg + proteinuria (≥0.3g/24h) or end-organ dysfunction after 20 weeks
• Placental abruption presents with vaginal bleeding, abdominal pain, and uterine tenderness; risk increases with trauma and cocaine use
• Hyperemesis gravidarum causes >5% pre-pregnancy weight loss and electrolyte abnormalities; peaks 4-8 weeks gestation
• Cholestasis of pregnancy presents with severe pruritus without rash; associated with increased fetal death risk

• Gestational diabetes: Asymptomatic; discovered on routine screening at 24-28 weeks
• Preeclampsia: Headache, visual disturbances, RUQ pain, edema after 20 weeks gestation in previously normotensive woman
• Placental abruption: Third-trimester bleeding with severe abdominal pain, rigid uterus, fetal bradycardia; "couvelaire uterus" if severe
• Hyperemesis gravidarum: Intractable vomiting in first trimester causing dehydration, hypokalemia, and metabolic alkalosis
• Cholestasis: Intense pruritus (especially palms/soles) in 2nd/3rd trimester; no primary skin lesions

1. 1.Confusing preeclampsia with gestational HTN: Gestational HTN lacks proteinuria/end-organ dysfunction and resolves postpartum; preeclampsia persists and carries eclampsia risk (seizures)
2. 2.Missing eclampsia: Don't wait for seizures—maternal headache + hypertension in third trimester IS preeclampsia requiring immediate management; eclampsia is seizure consequence
3. 3.Underestimating placental abruption severity: Concealed hemorrhage (blood trapped behind placenta) may show minimal vaginal bleeding but cause massive maternal-fetal blood loss and shock