NLE High-Risk Pregnancy & Obstetric Complications — Hypertensive & Metabolic Disorders of PregnancySummary

Abortion is the termination of pregnancy before viability (before 20–24 weeks or fetal weight < 500 g). The six clinical types are distinguished by cervical dilation, amount of retained products, and potential for continuation: threatened abortion presents with slight bleeding, mild cramping, and closed cervix—pregnancy may continue. Inevitable abortion shows moderate bleeding, cramping, and open cervix—loss cannot be stopped. Incomplete abortion has some products expelled, some retained, with heavy bleeding. Complete abortion has all products expelled, bleeding subsides, cervix closes. Missed abortion occurs when the fetus dies but is retained, posing DIC risk if retained > 4–6 weeks. Recurrent (habitual) abortion is three or more consecutive losses. The most common cause is chromosomal abnormality (50%), followed by maternal infection, endocrine imbalance (thyroid, diabetes), incompetent cervix, and immunologic factors. Assessment requires quantifying blood loss by counting and weighing perineal pads (1 g = 1 mL), evaluating for tissue passage (all tissue must be saved for products of conception evaluation), and serial monitoring of beta-human chorionic gonadotropin (beta-hCG) and hemoglobin. Nursing management includes recommending rest and avoiding strenuous activity and intercourse for threatened abortion (though no strong evidence supports strict bed rest), preparing the patient for dilation and curettage (D&C) or suction evacuation for inevitable/incomplete types, maintaining IV access, monitoring vital signs for hemorrhage, and providing compassionate grief care—never minimizing the loss.

Ectopic pregnancy is implantation of the fertilized ovum outside the uterine cavity; over 95% occur in the fallopian tube (ampulla is the most common site). Risk factors include pelvic inflammatory disease (from gonorrhea or chlamydia), prior tubal surgery, previous ectopic pregnancy, intrauterine device use, and endometriosis. As the embryo grows within the confines of the tube, the tube cannot expand; rupture occurs between 8–12 weeks, triggering a surgical emergency. Early manifestations include unilateral lower-quadrant abdominal pain, delayed or abnormal menstrual period, and scant dark vaginal spotting (vaginal bleeding in ectopic is typically scanty because the bleed is intraperitoneal, not intrauterine). Tubal rupture presents with sudden sharp, stabbing pain, referred shoulder-tip pain (Kehr sign—caused by diaphragmatic irritation from intraperitoneal blood), and rapid progression to hypovolemic shock: tachycardia, hypotension (late sign), pallor, cool clammy skin, and narrowing pulse pressure. Cullen sign (bluish periumbilical discoloration) may appear with significant intraperitoneal bleeding. Diagnostics include serial beta-hCG that rises abnormally slowly (fails to double every 48–72 hours), transvaginal ultrasound showing an empty uterus with an adnexal mass, and culdocentesis (aspiration of peritoneal fluid through the cul-de-sac) demonstrating intraperitoneal blood. Management depends on rupture status: for unruptured, small ectopic, methotrexate (a folic acid antagonist) 1 mg/kg IM is given to dissolve trophoblastic tissue; the patient must avoid folic acid supplements, alcohol, and sun exposure, and must report severe abdominal pain or dizziness. Follow-up requires serial beta-hCG every 3–7 days until undetectable (it should decline by at least 15% every 48 hours). For ruptured ectopic, emergency salpingostomy (tube-conserving surgery if possible) or salpingectomy is performed. Priority nursing care focuses on treating hypovolemic shock: two large-bore IV lines, aggressive fluid/blood replacement, supplemental oxygen, continuous vital sign monitoring, and assessment of urine output (target > 30 mL/hr).

Gestational trophoblastic disease (GTD) is abnormal proliferation of trophoblastic tissue; the most common type is hydatidiform mole (molar pregnancy). A complete mole contains only paternal chromosomes (46,XX or 46,XY; the ovum contributed no genetic material), has no fetal tissue, and carries the highest risk (15–20%) of malignant transformation to choriocarcinoma. A partial mole is triploid (usually 69,XXY), contains some fetal tissue, and has lower malignancy risk (1–5%). Pathophysiology involves abnormal chorionic villi that degenerate into grape-like fluid-filled vesicles rather than forming healthy placental tissue. Clinical manifestations are distinctive: the uterus is larger than expected for gestational age (because of the mass of vesicles and excessive fluid), dark-brown ('prune juice') or bright-red vaginal bleeding may occur with passage of vesicles (described as 'tissue like a bunch of grapes'), and beta-hCG is excessively elevated (often > 100,000 mIU/mL, much higher than normal early pregnancy). Hyperemesis gravidarum is severe because of extremely high hCG levels. A red-flag finding is early preeclampsia (hypertension, proteinuria, edema) before 20 weeks—normally preeclampsia appears after 20 weeks, so early preeclampsia strongly suggests molar pregnancy. Ultrasound shows a 'snowstorm' or 'bunch of grapes' appearance (no normal gestational sac, no fetus). There are no fetal heart tones. Management includes immediate evacuation of the uterus by suction curettage (D&C); the critical follow-up is serial beta-hCG monitoring for 6–12 months (or longer for complete mole) because a rising hCG after evacuation indicates malignant transformation (choriocarcinoma). The patient must avoid pregnancy for at least 1 year because a new pregnancy's rising hCG would mask malignant hCG elevation, making early detection of choriocarcinoma impossible. Reliable contraception (often oral contraceptives) is mandated. Any rising hCG prompts admission for chemotherapy (methotrexate or multi-agent regimens). In the Philippines, where molar pregnancy carries cultural significance and family planning services may be limited, nurses must sensitively explain why strict contraception and follow-up are essential for life preservation.

Third-trimester bleeding (after 20 weeks) requires rapid distinction between the two life-threatening placental abnormalities—placenta previa and abruptio placentae—because their management and risks differ fundamentally. The cardinal discrimination taught on every nursing exam is: painless bright-red vaginal bleeding = placenta previa; painful dark-red vaginal bleeding with a rigid board-like tender uterus = abruptio placentae. Placenta previa is implantation of the placenta in the lower uterine segment, partially or completely covering the internal cervical os. Types range from total (complete) previa covering the os to partial, marginal, and low-lying. Risk factors include multiparity, prior cesarean delivery or previa, advanced maternal age, and multiple gestation. Because the placenta is low-lying, it blocks fetal descent, so malpresentation (breech, transverse) is common. The bleeding is painless because there is no uterine irritation—the cervix dilates during late pregnancy and causes the previa to bleed from exposed maternal vessels. Bleeding may begin suddenly and can be massive. The uterus is soft, non-tender, with normal tone. Fetal heart rate is typically reassuring. Diagnosis is confirmed by transabdominal ultrasound (not transvaginal, which can increase bleeding). A critical nursing principle: never perform a vaginal or rectal examination with suspected previa because it can perforate low-lying placental tissue and trigger catastrophic hemorrhage. Management emphasizes bed rest (activity restrictions reduce bleeding), and for a stable preterm fetus, expectant management prolongs the pregnancy. Betamethasone (12 mg IM every 24 hours for 2 doses) is given to accelerate fetal lung maturity if delivery is anticipated before 34 weeks. Delivery is by planned cesarean section (scheduled before labor) for total or partial previa to avoid the risk of massive hemorrhage. Post-cesarean nursing care must watch for postpartum hemorrhage because the lower uterine segment contracts poorly, increasing risk of atony. Abruptio placentae (placental abruption) is premature separation of a normally implanted placenta after 20 weeks. It is the most common cause of maternal death from hemorrhage and represents a true obstetric catastrophe. Risk factors include maternal hypertension (the strongest association), cocaine and methamphetamine use, maternal trauma, and short umbilical cord. The pathophysiology involves rupture of maternal blood vessels at the placental interface; blood accumulates behind the placenta. Manifestations are opposite to previa: painful, dark-red (venous) vaginal bleeding with severe uterine pain and a rigid, board-like, tender uterus with increased tone (from irritation and tetanic contractions). Bleeding may be concealed (behind the placenta)—a hidden hemorrhage—so visible vaginal bleeding significantly underestimates true blood loss. The mother may be in shock from concealed loss despite minimal visible bleeding. Fetal distress and fetal loss are common because placental separation reduces oxygen delivery. A catastrophic complication is disseminated intravascular coagulation (DIC), triggered by release of tissue thromboplastin from the placental injury. Nursing management is emergent: position the mother in left lateral tilt to improve placental perfusion; administer oxygen; establish two large-bore IV lines with aggressive fluid and blood replacement; monitor continuous electronic fetal heart rate; measure fundal height every 15–30 minutes (an expanding girth indicates ongoing concealed bleeding); monitor coagulation studies (PT, aPTT, fibrinogen, D-dimer, platelet count) for DIC; and prepare for emergency cesarean delivery with significant abruption or fetal compromise. The mother's Rh status must be known for possible Rho(D) immune globulin administration.

Hemorrhage from any obstetric bleeding disorder threatens maternal life through hypovolemic shock—a pathologic state in which circulating blood volume is inadequate to perfuse vital organs. The body has compensatory mechanisms: initial sympathetic activation causes vasoconstriction, tachycardia, and shunting of blood to the heart, lungs, and brain at the expense of skin, kidneys, and gut. In compensated shock, the mother may be tachycardic and restless with cool, pale skin, but blood pressure remains normal-to-slightly-low (BP is a late sign of shock in young, healthy pregnant women). If hemorrhage continues, compensatory mechanisms fail and decompensated shock ensues: blood pressure falls, urine output drops below 30 mL/hr (oliguria), mental status changes (restlessness progresses to confusion, then unresponsiveness), and end-organ damage accelerates. Irreversible shock follows, with profound hypotension, organ failure, and death. The nursing imperative is to recognize early compensated shock and act immediately—do not wait for hypotension. Blood loss of 500 mL in the first 24 hours postpartum is defined as normal; 500–1000 mL is early hemorrhage; > 1500 mL is major hemorrhage. Obstetric hemorrhage can be massive and rapid: a rupture of a placental implantation site can bleed the entire maternal blood volume (4.5–5.5 liters) within minutes. Disseminated intravascular coagulation (DIC) is a consumptive coagulopathy triggered when thromboplastin from damaged tissue (placenta, amniotic fluid, fetal tissue) enters the maternal circulation. Triggers in obstetrics include missed abortion (retained fetus > 4–6 weeks), abruptio placentae, amniotic fluid embolism, septic abortion, and severe preeclampsia/eclampsia. DIC activates both coagulation and fibrinolysis simultaneously: platelets and clotting factors are consumed in widespread microthrombi, and fibrin is degraded, resulting in simultaneous clotting and bleeding—a paradox. Clinical signs of DIC include oozing from IV sites, gums, and surgical wounds; petechiae and ecchymoses; hematuria; GI bleeding; and continued bleeding despite transfusion. Laboratory findings show thrombocytopenia (< 100,000), prolonged PT and aPTT, decreased fibrinogen (< 100 mg/dL), and elevated D-dimer/fibrin degradation products. Management of shock and DIC is treatment of the underlying cause (delivery of the fetus, evacuation of retained products, antibiotics for infection) plus aggressive replacement of blood products: packed red blood cells (4 units for initial resuscitation), fresh frozen plasma (8 units to replace coagulation factors), platelets (6 units if count < 50,000), and cryoprecipitate (10 units to replace fibrinogen). Monitoring includes continuous vital signs, urine output via indwelling catheter, repeated coagulation studies, and assessment for new bleeding.

Rho(D) immune globulin (RhoGAM, WinRho) is a passive antibody preparation derived from human plasma that prevents Rh isoimmunization (sensitization) in an Rh-negative mother exposed to Rh-positive fetal red blood cells. The mechanism is immunosuppression: RhoGAM contains anti-D antibodies that bind to and destroy circulating fetal Rh-positive cells in the maternal circulation before the mother's immune system recognizes them as foreign. This prevents the mother from mounting her own immune response (which would produce IgG antibodies that cross the placenta and attack fetal RBCs in current and future pregnancies, causing hemolytic disease). It is passive immunity—temporary protection that must be repeated after each exposure. Standard dosing is 300 mcg (1500 IU) IM at 28 weeks of gestation (routine antenatal prophylaxis) and again within 72 hours after delivery of an Rh-positive infant (postpartum prophylaxis). A microdose of 50 mcg (250 IU) is used for first-trimester events (abortion, ectopic pregnancy, molar pregnancy, chorionic villus sampling before 13 weeks) because fetal-maternal hemorrhage is smaller early in pregnancy. After second or third-trimester events (amniocentesis, cordocentesis, antepartum hemorrhage, abdominal trauma, external cephalic version), a full 300 mcg dose or a higher dose (based on the Kleihauer-Betke test, which quantifies fetal RBCs in maternal circulation) is given—a rough rule is 100 mcg per mL of fetal whole blood or 20 mcg per fetal RBC. A critical eligibility check must be done: the mother must be Rh-negative (confirmed by type and screen), her indirect Coombs test must be negative (indicating she has not yet been sensitized), and the infant's direct Coombs test must be negative (confirming the infant is Rh-positive or D-positive). RhoGAM is given to the mother (never to the infant) and offers no benefit if the mother is already sensitized (indirect Coombs positive). The antibody has a half-life of about 3 weeks, so a new dose is needed with each sensitizing event. Timing is critical: it must be given within 72 hours of the sensitizing event (efficacy is higher if given within 24–48 hours). In the Philippine healthcare context, where many women deliver in rural or resource-limited settings with limited access to RhoGAM, nurses must coordinate with hospital laboratories and blood banks to ensure availability and proper administration. For Rh-negative women who cannot access RhoGAM or deliver outside hospital settings, postpartum testing of the infant's blood type and direct Coombs allows delayed administration if RhoGAM was missed, though efficacy decreases with time.

Accurate assessment of blood loss is essential to distinguish normal lochia from pathologic bleeding and to guide transfusion and intervention decisions. Visual estimates of blood loss are notoriously inaccurate—nurses typically underestimate loss by 30–50%. The gold standard is counting and weighing perineal pads: 1 gram of pad weight equals approximately 1 mL of blood. A scale sensitive to 0.5 g increments is used; the pre-weight of a dry pad is subtracted from the post-weight. All saturated pads are counted and saved (typically a completely soaked pad holds 5–10 mL). Clots are also assessed: large clots (> 2–3 cm) suggest more rapid bleeding and greater blood loss. Quantifying exact loss guides decisions: loss of 500 mL in the first 24 hours postpartum is normal; 500–1000 mL suggests early postpartum hemorrhage; > 1500 mL is major hemorrhage. In antepartum bleeding (third trimester), spotting (a few spots on underwear) is distinguished from light bleeding (< 5 pads per day), moderate bleeding (5–15 pads per day), and heavy bleeding (> 15 pads per day or saturated pad per hour). In first-trimester abortion, the nurse saves all tissue and clots passed—even a small amount should be sent for pathology to confirm products of conception and rule out ectopic pregnancy (if no chorionic villi are found, an ectopic must be ruled out). Hemoglobin and hematocrit should be checked at baseline and serially if bleeding continues; a drop of 2 g/dL hemoglobin represents approximately 500 mL blood loss. Clinical assessment of hypovolemia includes vital signs (tachycardia > 100 bpm, tachypnea, hypotension is a late sign), skin perfusion (cool, pale, clammy indicates vasoconstriction), mucous membrane color and moisture, capillary refill (normally < 2 seconds, delayed in shock), and urine output (target > 30 mL/hr; oliguria suggests inadequate renal perfusion). Mental status changes—restlessness progressing to confusion—indicate cerebral hypoperfusion.

According to NANDA-I nursing diagnosis classifications and the nursing process framework taught in BSN programs, bleeding disorders in pregnancy generate specific high-priority diagnoses aligned with Maslow's hierarchy of needs. At the physiologic safety level, the primary diagnoses are: (1) Deficient fluid volume related to excessive vaginal bleeding as evidenced by tachycardia, hypotension, oliguria—interventions include establishing large-bore IV access, administering isotonic crystalloids (0.9% normal saline or lactated Ringer's solution), and monitoring hemoglobin; (2) Ineffective tissue perfusion (renal, cerebral, peripheral) related to hypovolemic shock as evidenced by oliguria, confusion, cool extremities—interventions include oxygen therapy, fluid/blood replacement, continuous vital sign monitoring, and catheterization for accurate urine output; (3) Risk for disseminated intravascular coagulation related to release of tissue thromboplastin—interventions include monitoring PT, aPTT, fibrinogen, D-dimer, platelet count, and preparing blood products. At the security/safety level: (4) Risk for ineffective fetal tissue perfusion related to maternal hemorrhage—interventions include continuous electronic fetal monitoring, position changes (left lateral tilt), and prompt notification of obstetric team for intervention. (5) Fear related to threat to maternal and fetal life as evidenced by verbalization of anxiety—interventions include presence, explanation of procedures, and involving support persons. At the love/belonging level: (6) Anticipatory grieving related to potential fetal loss—interventions include allowing tissue viewing/holding, validating feelings, avoiding clichés, and referral to chaplaincy and counseling. The priority sequence follows Maslow: first stabilize circulation (large-bore IV, fluids, blood), then optimize fetal oxygenation (monitoring, positioning), then manage fear and grief. In the Philippine context where many nurses care for laboring women with limited physician availability, the nurse's priority interventions (fluid resuscitation, fetal monitoring, tissue specimen preservation, grief support) may be the difference between maternal survival and death.