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NSG210 Week 05 Summary: OB Lecture 2 - Complications of Pregnancy

The September 23 OB lecture (OB Lecture 2 on Canvas, syllabus Lecture 3, Durham Ch. 7) covers high-risk pregnancy: preterm labor, rupture of membranes, cervical insufficiency, multiple gestation, hyperemesis, diabetes, hypertensive disorders, bleeding and placental problems, pregnancy loss, Rh incompatibility, and teratogens. This content falls inside Exam 2 (content cutoff October 7).

Source: raw/nsg210_wk05_ComplicationsInPregnancy.md (lecture notes taken in class and expanded afterward). The “wk05” prefix matches the course week: September 23 is Week 05 on the Canvas layout. For the full textbook outline of the same material, see nsg210-exam-2-outline-durham-ch07; this page is the condensed lecture version.

Preterm Labor

Preterm labor is regular contractions with cervical change (dilation, effacement, or both) between 20 and 37 weeks. The single strongest predictor is a previous preterm birth; others include multiple gestation (overdistention), short cervix or cervical insufficiency, uterine anomalies, infection (UTI, bacterial vaginosis, chorioamnionitis, periodontal disease), polyhydramnios, placental problems, PPROM, a short interpregnancy interval, age under 17 or over 35, poor nutrition, substance use, chronic illness, stress, IPV, and little prenatal care. Black women have higher preterm birth rates independent of income, attributed to chronic stress and structural factors rather than biology.

Signs are often subtle: 4 or more contractions per hour (often painless early), a low dull backache, pelvic pressure, menstrual-like or abdominal cramping (with or without diarrhea), and a change in discharge (watery, mucoid, or bloody). Fetal fibronectin is most useful when negative - it strongly predicts that delivery will not happen within 2 weeks. A cervical length under 20 mm on transvaginal ultrasound is high risk.

Management has two goals: delay birth (tocolytics buy about 48 hours, plus treating causes such as infection or dehydration) and promote fetal maturity (antenatal corticosteroids - betamethasone or dexamethasone - to mature the lungs and reduce RDS, and magnesium sulfate for fetal neuroprotection against cerebral palsy when birth is expected before 32 weeks). A tocolytic is literally “labor-loosening” (Greek tokos, childbirth, plus lytikos, loosening); the same root gives tocodynamometer (“toco,” which measures contraction frequency and duration but not strength), dystocia (difficult labor), and oxytocin (“quick birth”).

Cervical Insufficiency

Cervical insufficiency (formerly “incompetent cervix”) is painless dilation and effacement in the second trimester without contractions, leading to loss or preterm birth. The key contrast with preterm labor: in preterm labor, contractions cause the cervical change; in cervical insufficiency, the cervix opens on its own. Losses cluster around 16-24 weeks and so straddle the 20-week line - before 20 weeks it is a late spontaneous abortion, at 20 weeks or later it is a preterm birth. The classic history is one or more painless second-trimester losses; other risks are cervical trauma or surgery (LEEP, cone biopsy, forceful dilation), connective tissue disorders, uterine anomalies, and DES exposure.

Treatment is a cerclage, a purse-string suture that holds the cervix closed, placed at 12-16 weeks and removed at 36-37 weeks. The early date is after first-trimester miscarriage risk has passed but before dilation starts; the late date is when the baby is near term, and removal prevents the cervix from tearing during labor. McDonald is the common transvaginal type; Shirodkar sits higher and may stay in with a cesarean birth. It is removed early for labor, ROM, or infection. Vaginal progesterone is used for a short cervix. Nursing watches for contractions, ROM, bleeding, and infection, and teaches the patient to report cramping, pressure, fluid leakage, bleeding, or fever.

Rupture of Membranes

SROM is spontaneous and AROM (amniotomy) is done by the provider. PROM is rupture before labor at term - “premature” means before labor, which is why many sources now say “prelabor rupture of membranes.” PPROM is rupture before labor and before 37 weeks, so it adds prematurity risks. Both carry infection (chorioamnionitis, rising past 18-24 hours), cord prolapse or compression, and abruption; PPROM adds RDS, IVH, NEC, oligohydramnios, and pulmonary hypoplasia if very early. PROM is usually induced; PPROM under 34 weeks is managed expectantly with latency antibiotics (ampicillin plus a macrolide), steroids, magnesium if under 32 weeks, and infection monitoring; at 34 weeks or later, delivery is recommended.

ROM is confirmed by nitrazine (alkaline amniotic fluid turns the paper blue; false positives with blood, semen, infection), the fern test (amniotic fluid dries into a fern-like crystal pattern from its salt and protein; more specific than nitrazine; false positives with cervical mucus or semen, false negatives with blood or too little fluid), pooling on speculum exam, and immunoassays such as AmniSure. After ROM, document the exact time, check fluid color (green or brown is meconium, cloudy or foul is infection), check the fetal heart rate right away for cord prolapse, watch maternal temperature and fetal tachycardia, and avoid digital cervical exams in PPROM.

Magnesium Sulfate and Deep Tendon Reflexes

Magnesium sulfate is a CNS depressant used for seizure prevention in preeclampsia, tocolysis, and fetal neuroprotection, with a narrow therapeutic range of about 4-8 mg/dL. Loss of DTRs is one of the earliest signs of toxicity, appearing before respiratory depression and cardiac changes, so DTRs are checked every 1-4 hours and before any rate increase (biceps instead of patellar if the patient has an epidural). Grading: 0 absent, 1+ diminished, 2+ normal, 3+ brisk, 4+ brisk with clonus. Hold the infusion and notify the provider for absent DTRs, RR under 12, urine output under 30 mL/hr, decreased LOC, or dysrhythmias. The antidote, calcium gluconate, stays at the bedside.

Newborn Urinary Output

The first void should occur within 24 hours of birth. Normal output is at least 1-2 mL/kg/hr; under 1 mL/kg/hr is oliguria. Pink or brick-dust urine (uric acid crystals) is normal in the first days. Wet diapers roughly match day of life (1 on day 1, 2 on day 2) and reach 6-8 per day by days 5-7. For precise measurement, weigh the diaper dry and wet: 1 g equals about 1 mL.

Multiple Gestation

Monozygotic (identical) twins come from one egg and one sperm that later split - same sex, about one-third of twins, a constant rate. Dizygotic (fraternal) twins come from two eggs and two sperm - two-thirds of twins, more common with maternal age, family history, fertility treatment, and higher parity. The clinically important question is chorionicity: the chorion forms the placenta and the amnion forms the sac. Di/di (two placentas, two sacs) is all dizygotic twins and monozygotic twins that split at days 0-3 - lowest risk. Mono/di (one placenta, two sacs; split at days 4-8, the most common monozygotic type) risks twin-to-twin transfusion syndrome, where shared vessels make one twin anemic and growth-restricted and the other volume-overloaded. Mono/mono (split at days 8-12) adds cord entanglement and is the highest risk; splitting after day 13 produces conjoined twins. Dichorionic monoamniotic is impossible because the amnion lies inside the chorion. On ultrasound, the lambda (twin peak) sign means dichorionic and the T sign means monochorionic diamniotic. All multiples raise the risk of preterm labor, preeclampsia, GDM, anemia, growth restriction, malpresentation, cesarean, and postpartum hemorrhage from uterine atony.

Hyperemesis Gravidarum

Hyperemesis gravidarum is vomiting severe enough to cause weight loss over 5% of pre-pregnancy weight, dehydration, electrolyte imbalance, and ketosis - unlike ordinary morning sickness (70-80% of pregnancies) it affects 0.3-3%. It peaks around 9-13 weeks and usually improves by 16-20 weeks, and is linked to high hCG, estrogen, and placental GDF15, so twins and molar pregnancy raise the risk. Classic labs: ketonuria, high urine specific gravity, low potassium, sodium, and chloride, metabolic alkalosis (lost stomach acid), and elevated hematocrit and BUN from hemoconcentration. The key complication is Wernicke encephalopathy from thiamine deficiency (confusion, ataxia, abnormal eye movements) - give thiamine before dextrose. Treatment steps from vitamin B6 with or without doxylamine to promethazine, metoclopramide, or ondansetron, then steroids, with IV fluids and potassium, and enteral feeding or TPN if needed. Nursing tracks I&O, daily weights, and urine ketones, and advances the diet slowly with small, dry, bland meals and fluids between (not with) meals.

Diabetes in Pregnancy

Pregestational diabetes (type 1 or 2 before pregnancy) exposes the embryo to high glucose during organogenesis, so it raises the risk of birth defects (heart, neural tube, caudal regression). Gestational diabetes (GDM) is glucose intolerance first recognized in pregnancy, screened at 24-28 weeks, and does not raise the anomaly rate because it starts after the organs form. GDMA1 is diet-controlled; GDMA2 needs medication, usually insulin.

The mechanism ties everything together: placental hormones (especially hPL) create insulin resistance; glucose crosses the placenta but maternal insulin does not; the fetal pancreas makes extra insulin, which acts as a growth hormone. That explains macrosomia and shoulder dystocia, neonatal hypoglycemia once the cord is cut, and delayed surfactant (RDS). In pregestational diabetes, insulin needs fall in the first trimester, rise steadily through the second and third (often doubling or tripling), and drop sharply once the placenta is delivered.

Two-step screening: a 1-hour 50 g challenge (positive at 130-140), then a 3-hour 100 g test with GDM diagnosed by two abnormal values (fasting 95, 1 hour 180, 2 hours 155, 3 hours 140). Targets: fasting under 95, 1 hour after meals under 140, 2 hours under 120. Nursing covers glucose self-monitoring, diet with a bedtime snack, walking after meals, insulin and hypoglycemia teaching (15 g carbohydrate, recheck in 15 minutes), third-trimester fetal surveillance, hourly glucose in labor (target about 70-110), newborn glucose checks, and a 75 g OGTT at 4-12 weeks postpartum because GDM carries a high lifetime risk of type 2 diabetes.

Hypertensive Disorders

All hypertensive disorders of pregnancy are defined by when the BP rises (140/90 or higher) and what comes with it. Chronic hypertension starts before pregnancy or before 20 weeks. Gestational hypertension is new high BP after 20 weeks alone - no proteinuria or organ damage - and resolves by 12 weeks postpartum; up to half progress. Preeclampsia is high BP after 20 weeks plus proteinuria (300 mg/24 hr or protein/creatinine 0.3) or signs of organ damage. Severe features are BP 160/110 or higher, platelets under 100,000, liver enzymes twice normal or RUQ/epigastric pain, creatinine over 1.1, pulmonary edema, a headache not relieved by medication, or visual changes. Eclampsia is preeclampsia plus new seizures, most often within 48 hours of delivery. Gestational hypertension with severe-range BP is managed like preeclampsia with severe features. Risk factors include nulliparity, prior preeclampsia (strongest), multiples, chronic hypertension, diabetes, kidney and autoimmune disease, obesity, and age over 35; low-dose aspirin started at 12-16 weeks prevents it in high-risk women.

The pathophysiology starts with abnormal placentation: the spiral arteries don’t widen, the underperfused placenta releases factors that damage the endothelium everywhere, and the result is vasospasm and leaky capillaries. Three lecture chains follow from that:

The only cure is delivering the placenta. Magnesium sulfate prevents seizures and continues for 24 hours after delivery. Severe-range BP (160/110 or higher for 15 minutes) is treated within 30-60 minutes with IV labetalol, IV hydralazine, or oral nifedipine, aiming for about 140-150/90-100 rather than normal, since dropping BP too far cuts placental flow. Seizure precautions: quiet dim room, padded rails, suction and oxygen at the bedside. In eclampsia, maternal health comes first - the fetus is best treated by stabilizing the mother (airway, side-lying position, safety, magnesium, BP), fetal bradycardia during a seizure usually recovers in 3-10 minutes, and delivery waits until the mother is stable. On exams, choose the maternal action over the fetal one.

HELLP, DIC, and IUGR

HELLP (Hemolysis, Elevated Liver enzymes, Low Platelets) is a severe form of preeclampsia. Lecture key points: it presents with RUQ or epigastric pain, malaise, and nausea and vomiting - easily mistaken for flu or heartburn - and BP may be only mildly high. Delivery is the treatment. Watch for liver hematoma or rupture (sudden severe RUQ or shoulder pain with hypotension), use bleeding precautions, and avoid pressure on the upper abdomen.

DIC (disseminated intravascular coagulation) is always secondary to another condition - abruption is the most common obstetric cause, followed by HELLP, amniotic fluid embolism, sepsis, and retained fetal demise. Widespread microclots use up platelets and clotting factors, so the patient oozes from IV sites, gums, and incisions. Labs: low platelets and fibrinogen, prolonged PT/aPTT, high D-dimer. Because fibrinogen is normally elevated in pregnancy (300-600), a value that looks normal may already be dangerously low. Treat the cause (usually delivery) and replace products: PRBCs, FFP, platelets, and cryoprecipitate.

IUGR (fetal growth restriction) is estimated fetal weight below the 10th percentile. Symmetric IUGR (whole body small) starts early from chromosomal problems or infection; asymmetric IUGR (normal head, small body) starts late from placental insufficiency as the fetus spares the brain. SGA is the newborn diagnosis and not every SGA baby had IUGR. Flags include fundal height lagging 2-3 cm or more behind weeks, oligohydramnios, and absent or reversed end-diastolic flow on umbilical artery Doppler. Newborns are at risk for hypoglycemia, hypothermia, and polycythemia.

Placental Abnormalities and Hemorrhage

Placenta previa is a placenta implanted over or near the cervical os. The exam cue: painless, bright red bleeding in the 2nd or 3rd trimester is previa, not abruption (“abruption aches, previa is painless”). The uterus is soft, malpresentation is common, and many low-lying placentas move up by the third trimester. Never do a digital vaginal exam; delivery is by cesarean; watch for postpartum hemorrhage.

Placental abruption is early separation of a normally placed placenta - sudden pain, dark red bleeding, a rigid board-like uterus, and fetal distress, with high DIC risk. Lecture risk factors: preeclampsia and hypertension (the most common - damaged spiral arteries), trauma (shearing between placenta and uterine wall; monitor at least 4 hours after trauma past 20 weeks), PPROM (the uterus shrinks under the placenta), and drug use (cocaine and methamphetamine vasoconstriction; smoking doubles the risk). Bleeding can be internal: in a concealed abruption, the pad can look nearly clean while the patient hemorrhages, so watch vital signs, pain, uterine tone, fundal height or girth, fetal status, and coagulation labs rather than the pad.

Placenta accreta spectrum is a placenta grown too deeply into the uterine wall - accreta “adheres” to the muscle (80%), increta goes “into” it (15%), percreta “penetrates” through it, sometimes into the bladder (5%). The biggest risk is a previa over a prior cesarean scar; with previa, the risk rises with each cesarean (about 3%, 11%, 40%, 61%, and 67%). Blood loss averages 3,000-5,000 mL. Management is a planned cesarean hysterectomy at 34-37 weeks with the placenta left in place, at a center with a large blood bank; never try to pull the placenta off. Vasa previa is unprotected fetal vessels over the os - painless bleeding at ROM with sudden fetal bradycardia, where the fetus (not the mother) can bleed to death in minutes.

Nursing for any bleeding: no vaginal exam until previa is ruled out; weigh pads (1 g = 1 mL); tachycardia is the earliest sign, and BP falls late because pregnancy raises blood volume 40-50%; continuous fetal monitoring (the fetus often shows distress first); side-lying position, two large-bore IVs, type and crossmatch, CBC, coagulation studies, fibrinogen, Kleihauer-Betke, Rh status and RhoGAM, oxygen, Foley (30 mL/hr or more), and preparation for cesarean.

Hemoglobin and hematocrit in hemorrhagic shock lag behind acute blood loss. Whole blood is lost, so the first H&H can look normal even after major bleeding; the drop appears hours later as fluid shifts and IV fluids dilute the blood. A normal H&H does not rule out hemorrhage - judge by vital signs, quantified blood loss, urine output, and fetal status, and trend serial values against the patient’s prenatal baseline (anemia in pregnancy is Hgb under 11 or Hct under 33%). Rough rules: a 1 g/dL drop in Hgb (about 3 points of Hct) is about 500 mL lost, and each unit of PRBCs raises Hgb about 1 g/dL. Conversely, hemoconcentration raises Hct in dehydration and preeclampsia, where a “normal” Hct can hide low blood volume.

Rh Incompatibility and RhoGAM

The Rh factor is the D antigen on red cells. The problem arises only when an Rh-negative mother carries an Rh-positive fetus. If fetal blood enters her circulation (most often at delivery, also with miscarriage, ectopic, amniocentesis, trauma, or bleeding), she makes anti-D antibodies and is permanently sensitized. The first baby is usually spared because the first response is slow IgM that doesn’t cross the placenta; in the next Rh-positive pregnancy, IgG antibodies cross and destroy fetal red cells, causing hemolytic disease of the newborn (erythroblastosis fetalis) - anemia, jaundice, kernicterus, and hydrops fetalis.

RhoGAM (Rho(D) immune globulin) is ready-made anti-D antibody from donor plasma. It clears any Rh-positive fetal cells from the mother’s blood before her immune system notices them, so she never makes her own antibodies. It is passive and temporary (about 12 weeks) and only works before sensitization. Give 300 mcg IM at 28 weeks and within 72 hours of delivery (if the baby is Rh-positive) or of any sensitizing event; 50 mcg may be used for first-trimester losses; Kleihauer-Betke guides extra doses after a large bleed. Candidates are Rh-negative mothers with a negative indirect Coombs (maternal antibody screen); the direct Coombs on cord blood checks for antibodies on the baby’s cells. It is a blood product (consent), never given to the baby or an Rh-positive mother. ABO incompatibility (type O mother, A or B baby) is usually milder, can affect a first pregnancy, and has no preventive injection.

Teratogens

A teratogen is any exposure during pregnancy that can cause a birth defect (Greek teras, “monster,” plus -genic). The first 2 weeks after conception are “all or none”; weeks 3-8 (organogenesis) are the most vulnerable for structural defects, often before the woman knows she is pregnant; after that, exposures more often cause growth or brain effects. Examples: isotretinoin, warfarin (use heparin instead), ACE inhibitors and ARBs, valproate and other antiepileptics, methotrexate, misoprostol, lithium, tetracyclines, radioactive iodine; alcohol (the leading preventable cause of birth defects), tobacco, cocaine; TORCH infections and Zika; maternal hyperglycemia, PKU, and fever; radiation, lead, and mercury. Prevention: preconception medication review, folic acid 0.4 mg daily, rubella and varicella immunity checked before pregnancy (live vaccines are not given during pregnancy), and tight glucose control.

Abortion Terminology

Abortion is any end of pregnancy before 20 weeks, spontaneous or induced; a loss at 20 weeks or later is fetal demise or preterm birth. Spontaneous abortion is the medical term for miscarriage - natural loss, about half from chromosomal abnormalities. Induced abortion is an intentional end by procedure or medication, described by reason: elective (at the woman’s request, not for health reasons) or therapeutic (for a serious maternal condition or fetal anomaly). Types of spontaneous abortion, sorted by bleeding and cervix: threatened (light bleeding, closed cervix, pregnancy may continue), inevitable (heavier bleeding, open cervix, loss cannot be stopped), incomplete (open cervix, some tissue retained, heavy bleeding), complete (all tissue passed, cervix closes), missed (fetal death with closed cervix and retained tissue, DIC risk if prolonged), septic (infected retained tissue), and recurrent (repeated consecutive losses). After any loss: bleeding precautions (call for soaking more than two pads an hour for 2 hours), RhoGAM if Rh-negative, pelvic rest, and grief support that makes clear early losses are usually chromosomal and not the woman’s fault.

nsg210-abortion-classification-diagrams

Memory aid: only threatened can still continue; an open cervix means the loss is happening (inevitable or incomplete); a closed cervix with a dead fetus is missed; a closed cervix after everything has passed is complete. Septic and recurrent are added descriptions that can apply on top of the others.

Memory Anchors