NLE High-Risk Pregnancy & Obstetric Complications — High-Risk Pregnancy & Bleeding DisordersDetailed Explanation

Classification of Obstetric Bleeding by Trimester

Obstetric bleeding is systematically classified by the trimester in which it occurs because the most likely causes differ dramatically depending on gestational age. This classification is the foundation of your clinical reasoning on the NLE. **First Trimester (Weeks 1–13):** The most common causes are spontaneous abortion (miscarriage) and ectopic pregnancy. Both involve the products of conception, but ectopic pregnancy is a surgical emergency due to the risk of tubal rupture and massive intraperitoneal hemorrhage. **Second Trimester (Weeks 14–27):** Less common for major bleeding; causes include late abortion, incompetent cervix (painless cervical dilation without contractions), and placenta previa beginning to manifest. Gestational trophoblastic disease (hydatidiform mole) typically presents in the first half of pregnancy. **Third Trimester (Weeks 28–40):** The two most critical and heavily tested causes are placenta previa and abruptio placentae. The classic NLE discriminator: PAINLESS bright-red bleeding = placenta previa; PAINFUL dark-red bleeding with a board-like uterus = abruptio placentae. This single distinction appears on virtually every NLE related to maternal nursing. Viability is a key threshold — generally 20 to 24 weeks or fetal weight above 500 g. Before viability, fetal loss is classified as abortion. After viability, premature delivery protocols apply. The nurse's immediate priority in any trimester is: assess maternal hemodynamic stability first (Maslow: physiological safety), then fetal status, then psychosocial support.

Spontaneous Abortion (Miscarriage) — Types and Nursing Management

Spontaneous abortion is the natural, unintended termination of pregnancy before viability (before 20–24 weeks or fetal weight <500 g). It is the most common complication of early pregnancy, with the majority caused by chromosomal abnormalities in the embryo. Other causes include maternal infection (e.g., TORCH infections), endocrine imbalances (hypothyroidism, uncontrolled diabetes), incompetent cervix, immunologic factors, and uterine structural abnormalities. The NLE frequently tests the ability to distinguish among the SIX types of abortion based on clinical findings: **1. THREATENED ABORTION:** Slight bleeding (spotting) + mild cramping + CLOSED CERVIX. Products of conception are still intact. Pregnancy MAY continue. Management: modified bed rest, avoid intercourse and strenuous activity, monitor beta-hCG and fetal heart tones. There is no proven benefit of strict bed rest, but activity restriction is advised. **2. INEVITABLE ABORTION:** Moderate to heavy bleeding + moderate cramping + OPEN (DILATED) CERVIX ± ruptured membranes. Loss CANNOT be stopped — it is inevitable. Management: prepare for D&C or suction evacuation, IV access, emotional support. **3. INCOMPLETE ABORTION:** Some products of conception (POC) expelled, some RETAINED. Heavy bleeding continues because the uterus cannot contract fully around retained tissue. Cervix is open. Management: URGENT D&C/suction curettage to remove retained products and control hemorrhage. **4. COMPLETE ABORTION:** ALL products of conception expelled. Bleeding and cramping SUBSIDE. Cervix closes. Uterus has returned toward its pre-pregnant state. Management: observation, confirm complete expulsion via ultrasound. **5. MISSED ABORTION:** Fetus dies but is RETAINED in utero. No active bleeding initially (which can mislead). Risk: if retained beyond 4–6 weeks, degrading POC release thromboplastin → DISSEMINATED INTRAVASCULAR COAGULATION (DIC). Management: D&C or medical induction; monitor coagulation studies (platelets, fibrinogen, PT/aPTT, D-dimer). **6. RECURRENT (HABITUAL) ABORTION:** Three or more consecutive spontaneous abortions. Warrants thorough investigation for chromosomal, anatomic, hormonal, or immunologic causes. **KEY nursing assessment:** Count and weigh perineal pads (1 g = 1 mL), save all tissue/clots for pathologic evaluation, monitor vital signs for hemorrhage, assess beta-hCG trends, and provide GRIEF CARE — never minimize the loss, even early in pregnancy. In the Philippine context, nurses must be sensitive to spiritual and cultural beliefs around pregnancy loss. **Rho(D) immune globulin (RhoGAM)** must be given to ALL Rh-negative unsensitized mothers after any pregnancy loss, regardless of gestational age.

Ectopic Pregnancy

An ectopic pregnancy occurs when the fertilized ovum implants OUTSIDE the uterine cavity. Over 95% occur in the FALLOPIAN TUBE, most commonly in the ampullary segment. The tube cannot accommodate a growing embryo and will eventually RUPTURE, causing massive intraperitoneal hemorrhage — a true obstetric emergency. **Risk factors (PPATID mnemonic for NLE):** - **P**elvic inflammatory disease (PID) — the #1 risk factor; causes scarring/adhesions in the tube - **P**rior tubal surgery or sterilization attempts - **A**dhesions from prior abdominal/pelvic surgery - **T**ubal anomalies (structural defects) - **I**ntrauterine device (IUD) use - **D**elayed transport from endometriosis or prior ectopic **Clinical Presentation — Three Phases:** **Phase 1 (Before Rupture):** Missed or abnormal menses + unilateral lower quadrant pain (dull to sharp) + scant dark vaginal spotting. The patient may not know she is pregnant. beta-hCG rises SLOWLY (fails to double every 48 hours, unlike normal pregnancy). **Phase 2 (Tubal Rupture — Emergency):** Sudden, SEVERE, knife-like unilateral abdominal pain → REFERRED SHOULDER PAIN (Kehr Sign) from blood irritating the diaphragm → signs of HYPOVOLEMIC SHOCK (tachycardia, hypotension, pallor, diaphoresis, cold clammy skin, restlessness, oliguria). **Cullen sign** (bluish periumbilical discoloration) may appear from retroperitoneal or intraperitoneal bleeding. This is a SURGICAL EMERGENCY. **Key Diagnostic Findings:** - Transvaginal ultrasound: empty uterus + adnexal mass (with or without free fluid in cul-de-sac) - beta-hCG: present but rising abnormally slowly (fails to double in 48 hours) - Culdocentesis: aspiration of non-clotting blood from the cul-de-sac confirms hemoperitoneum **Management:** 1. **UNRUPTURED ectopic (small, stable):** Medical management with **METHOTREXATE** IM — a folic acid antagonist that destroys trophoblastic tissue. The nurse teaches: avoid folic acid supplements, alcohol, NSAIDS, and prolonged sun exposure; report worsening abdominal pain (could indicate tubal rupture even during treatment); follow serial declining beta-hCG to confirm resolution. 2. **RUPTURED ectopic:** Surgical emergency — **salpingostomy** (conservative, preserves the tube) or **salpingectomy** (removal of the tube). PRIORITY nursing interventions: two large-bore IV lines, aggressive IV fluid/blood replacement, oxygen administration, continuous vital signs and urine output monitoring (goal >30 mL/hr), and preparation for emergency surgery. Give **Rho(D) immune globulin** to Rh-negative unsensitized women after ectopic pregnancy. Use the 50 mcg microdose if under 13 weeks; 300 mcg if ≥13 weeks.

Gestational Trophoblastic Disease — Hydatidiform Mole

A hydatidiform mole (molar pregnancy) is an abnormal proliferation of trophoblastic tissue where chorionic villi degenerate into grape-like, fluid-filled vesicles. It is a form of GESTATIONAL TROPHOBLASTIC DISEASE (GTD) and can progress to CHORIOCARCINOMA (malignant cancer) if not monitored. **Two Types — Both Tested on the NLE:** **COMPLETE MOLE:** - NO fetal tissue present - Karyotype: 46,XX (entirely paternal chromosomes — the egg nucleus was lost or inactivated) - HIGHER risk of progressing to choriocarcinoma (15–20%) - Uterus is markedly enlarged; extremely high beta-hCG **PARTIAL MOLE:** - SOME fetal/embryonic tissue present (usually non-viable) - Karyotype: TRIPLOID (69,XXX or 69,XXY — one set maternal, two sets paternal) - LOWER risk of malignancy - Uterus may be normal size or slightly enlarged **Classic Clinical Manifestations (HIGH-YIELD for NLE):** 1. Uterus **LARGER THAN EXPECTED** for gestational age (classic finding) 2. **Dark-brown ('prune juice') vaginal bleeding** ± passage of grape-like vesicles 3. **Excessively HIGH beta-hCG** (markedly elevated beyond expected for gestational age) 4. **Hyperemesis gravidarum** (severe nausea and vomiting from extremely high hCG stimulating the vomiting center) 5. **Signs of PREECLAMPSIA BEFORE 20 WEEKS** — this is pathognomonic. Normal preeclampsia NEVER occurs before 20 weeks, so early preeclampsia = red flag for molar pregnancy 6. **NO fetal heart tones** 7. Ultrasound shows a **'snowstorm' or 'cluster of grapes' pattern** — characteristic finding **Management:** 1. **Suction curettage** to evacuate the mole (treatment of choice) 2. **Serial beta-hCG monitoring** every 1–2 weeks until levels normalize, then monthly for 6–12 months 3. **Avoid pregnancy for at least 1 YEAR** (a new pregnancy increases hCG, which would mask a rising hCG from malignant transformation) 4. Use RELIABLE CONTRACEPTION (oral contraceptive pills are preferred — do NOT use IUD which could cause confusion with uterine bleeding) 5. If beta-hCG plateaus or rises = suspect **choriocarcinoma** → refer for CHEMOTHERAPY (methotrexate ± actinomycin D) **Why the NLE Loves This Topic:** The combination of preeclampsia before 20 weeks + uterus large for dates + NO FHT + snowstorm ultrasound is a textbook scenario. The post-treatment requirement of 'no pregnancy for 1 year' and serial hCG follow-up is a frequent patient teaching question.

Placenta Previa

Placenta previa occurs when the placenta implants in the LOWER UTERINE SEGMENT, partially or completely covering the INTERNAL CERVICAL OS. As the lower segment stretches and the cervix dilates (or even before labor), the placenta is disrupted, causing bleeding. **Types of Placenta Previa:** - **Total (Complete) Previa:** Placenta completely covers the internal os → MUST deliver by cesarean section - **Partial Previa:** Placenta partially covers the internal os - **Marginal Previa:** Placenta edge reaches the margin of the os - **Low-lying Placenta:** Placenta implants in the lower segment but does not reach the os (may resolve as the uterus grows upward) **Risk Factors (remember: multiplying, scarring factors):** - Multiparity (high parity) - Prior cesarean section or uterine surgery (scarred lower segment) - Advanced maternal age (>35 years) - Multiple gestation (large placental surface area) - Prior history of placenta previa - Smoking and cocaine use **Classic Manifestations — PAINLESS BRIGHT-RED BLEEDING:** - PAINLESS (no labor contractions, no uterine tenderness) - BRIGHT RED (fresh arterial blood) - SPONTANEOUS onset, often at rest or during sleep - SOFT, NON-TENDER UTERUS with NORMAL TONE - Fetal MALPRESENTATION (breech, transverse) — because the placenta blocks the lower pole - First episode is usually self-limiting (SENTINEL BLEED), but subsequent bleeds are heavier **Diagnostics:** - **TRANSABDOMINAL ULTRASOUND** — diagnostic test of choice; confirms placental location - AVOID vaginal examination — can perforate the placenta causing fatal hemorrhage **Nursing Management:** *Expectant Management (stable mother, preterm fetus):* 1. STRICT BED REST 2. Monitor amount of bleeding (count and weigh pads) 3. Monitor vital signs every 15–30 minutes 4. Continuous Electronic Fetal Monitoring (EFM) 5. Establish IV access; Type and Crossmatch blood (keep 2 units on standby) 6. **Betamethasone 12 mg IM every 24 hours × 2 doses** if <34 weeks (to accelerate fetal lung maturity — surfactant production) 7. Nothing per vagina — NO vaginal exams, NO sexual intercourse, NO tampons 8. Monitor for signs of preterm labor *Active Management (heavy bleeding, fetal distress, term fetus):* 9. **Cesarean section** for total previa; may attempt vaginal delivery for partial/marginal if bleeding controlled and cervix favorable 10. Prepare for **postpartum hemorrhage** — lower uterine segment contracts poorly → atony **Postpartum Risk:** The lower uterine segment has fewer smooth muscle fibers and contracts less effectively than the upper segment, predisposing to POSTPARTUM HEMORRHAGE (PPH) after delivery. The nurse must closely monitor uterine tone and lochia after birth.

Abruptio Placentae (Placental Abruption)

Abruptio placentae is the PREMATURE SEPARATION of a normally implanted placenta from the uterine wall AFTER 20 WEEKS of gestation. It is a life-threatening obstetric emergency for both mother and fetus. Unlike placenta previa (which is about WHERE the placenta is), abruption is about what HAPPENS to a normal placenta. **Risk Factors — the top three are critically tested:** 1. **MATERNAL HYPERTENSION** — the LEADING association (chronic hypertension, gestational hypertension, preeclampsia) 2. **COCAINE USE** — vasospasm causes placental separation 3. **ABDOMINAL TRAUMA** — motor vehicle accident, domestic violence (shear forces separate the placenta) 4. Other factors: smoking, short umbilical cord, rapid uterine decompression (after delivery of twins or amniotomy), prior abruption, thrombophilias **Types:** - **REVEALED (External) Abruption:** Blood escapes through the cervix → visible vaginal bleeding - **CONCEALED Abruption:** Blood is trapped behind the placenta → NO visible vaginal bleeding, but the uterus enlarges and hardens. DANGEROUS because visible blood loss underestimates true blood loss → shock may appear disproportionate to seen bleeding **Classic Manifestations — PAINFUL DARK-RED BLEEDING:** - **PAINFUL** — sudden, severe abdominal pain (constant, not just with contractions) - **DARK RED** blood (older/venous blood) - **RIGID, BOARD-LIKE, HYPERTONIC UTERUS** — the hallmark sign (Couvelaire uterus in severe cases) - **UTERINE TENDERNESS** on palpation - Signs of **FETAL DISTRESS** — late decelerations, bradycardia - Signs of **MATERNAL SHOCK** may EXCEED visible blood loss (especially in concealed) - Increasing **FUNDAL HEIGHT** (concealed hemorrhage expands the uterus) **Key Complications:** 1. **HYPOVOLEMIC SHOCK** — concealed hemorrhage is especially dangerous 2. **DISSEMINATED INTRAVASCULAR COAGULATION (DIC)** — placental separation releases tissue thromboplastin into the maternal circulation, triggering the coagulation cascade; fibrinogen is consumed → paradoxical bleeding from all sites. Monitor: platelets (↓), fibrinogen (↓), PT/aPTT (↑), D-dimer (↑) 3. **COUVELAIRE UTERUS** (uteroplacental apoplexy) — blood infiltrates the myometrium; the uterus appears purple-blue and fails to contract → may require hysterectomy 4. Fetal hypoxia and death **Nursing Management (Emergency Protocol):** 1. Position: LEFT LATERAL TILT (improves uteroplacental perfusion, relieves aortocaval compression) 2. OXYGEN: 10–15 L/min via non-rebreather mask 3. TWO LARGE-BORE IV LINES (14G or 16G) — rapid fluid resuscitation 4. Draw blood: CBC, type and crossmatch (4–6 units PRBCs), coagulation panel (PT, aPTT, platelets, fibrinogen, D-dimer) 5. CONTINUOUS EFM — watch for late decelerations (uteroplacental insufficiency) 6. MONITOR FUNDAL HEIGHT — increasing height = concealed hemorrhage 7. INSERT FOLEY CATHETER — monitor urine output hourly (goal >30 mL/hr) 8. PREPARE for EMERGENCY CESAREAN SECTION if significant abruption or fetal compromise 9. NEVER GIVE OXYTOCIN without physician order; DO NOT do vaginal exam until ultrasound rules out previa 10. Monitor for DIC — assess IV sites, gums, mucous membranes for oozing; check urine for hematuria

Rho(D) Immune Globulin (RhoGAM) — Priority Pharmacology

Rho(D) immune globulin (commonly called RhoGAM) is one of the most frequently tested pharmacologic topics in maternal nursing on the NLE. It prevents RH ISOIMMUNIZATION — the process by which an Rh-NEGATIVE mother develops antibodies against Rh-POSITIVE fetal red blood cells — protecting future pregnancies from HEMOLYTIC DISEASE OF THE NEWBORN (HDN). **The Physiologic Problem:** When an Rh-negative mother is exposed to Rh-positive fetal blood (fetomaternal hemorrhage), her immune system recognizes the Rh antigen as foreign and produces anti-D antibodies. In a SUBSEQUENT pregnancy with an Rh-positive fetus, these maternal anti-D antibodies cross the placenta and DESTROY fetal red blood cells → severe fetal/neonatal anemia, jaundice, hydrops fetalis, and potentially death. **How RhoGAM Works:** RhoGAM provides PASSIVE IMMUNITY — it contains pre-formed anti-D antibodies that DESTROY any Rh-positive fetal cells BEFORE the mother's immune system can recognize them and mount her own active immune response. Think of it as 'cleaning up' the evidence before the immune system sees it. **WHO receives RhoGAM:** - Mother must be: **Rh-NEGATIVE** AND **UNSENSITIZED** (indirect Coombs test NEGATIVE) - Baby must be: Rh-POSITIVE or unknown - It is given to the MOTHER — NEVER to the baby - It is USELESS if the mother is already sensitized (indirect Coombs positive) **WHEN to give RhoGAM (ALL situations where fetomaternal hemorrhage may occur):** 1. **28 WEEKS GESTATION** (antepartum prophylaxis) — standard prenatal care 2. **Within 72 HOURS after delivery** of an Rh-positive newborn (most critical window) 3. After SPONTANEOUS or INDUCED ABORTION 4. After ECTOPIC PREGNANCY (any gestational age) 5. After AMNIOCENTESIS or CHORIONIC VILLUS SAMPLING 6. After ABRUPTIO PLACENTAE 7. After ABDOMINAL TRAUMA in pregnancy 8. After EXTERNAL CEPHALIC VERSION **DOSING:** - **Standard dose: 300 mcg IM** — for events at ≥13 weeks gestation and postpartum - **Microdose: 50 mcg IM** — for FIRST TRIMESTER events (abortion or ectopic <13 weeks), as the fetal blood volume is much smaller **Route:** Intramuscular (IM injection) **ELIGIBILITY CHECKS (2 key tests):** 1. Mother's **INDIRECT COOMBS TEST** must be NEGATIVE (confirms she has NOT been sensitized — no pre-existing anti-D antibodies) 2. Newborn's **DIRECT COOMBS TEST** must be NEGATIVE (confirms the baby's cells are not already coated with maternal antibodies) **What the NLE asks about RhoGAM:** - When is it given? (28 weeks + 72 hours postpartum + after any bleeding event) - To whom? (Rh-negative, UNSENSITIZED mother only) - What test must be negative? (indirect Coombs for mother; direct Coombs for baby) - What does it protect against? (hemolytic disease of the newborn in future pregnancies) - Does it help a sensitized mother? (NO — it is PREVENTION only, not treatment)

Hypovolemic Shock and DIC — Complications of Obstetric Bleeding

Across all obstetric bleeding disorders, two complications account for the majority of maternal mortality: HYPOVOLEMIC SHOCK and DISSEMINATED INTRAVASCULAR COAGULATION (DIC). The nurse must recognize early warning signs and act BEFORE the patient deteriorates. **HYPOVOLEMIC SHOCK:** Shock results from INADEQUATE CIRCULATING BLOOD VOLUME to maintain tissue perfusion. In obstetric hemorrhage, the average blood volume at term is approximately 5 liters (increased by 40–50% over pre-pregnant baseline). This expanded volume means early signs of shock may be MASKED — a pregnant woman can lose 1–1.5 liters before clinical deterioration becomes obvious. **Three Stages (know these cold for NLE):** **Stage 1 — COMPENSATED:** - Blood loss: ~15–30% (approximately 750–1,500 mL) - Body COMPENSATES: catecholamine release → vasoconstriction and tachycardia - Signs: TACHYCARDIA (HR >100) is the EARLIEST sign; cool, pale skin; restlessness; NARROWING PULSE PRESSURE; normal to slightly decreased BP - KEY: Blood pressure is still NORMAL (the most dangerous misconception is 'BP is normal, patient is fine') **Stage 2 — DECOMPENSATED:** - Blood loss: ~30–40% (approximately 1,500–2,000 mL) - Compensation fails: BP drops significantly (hypotension) - Signs: falling BP, oliguria (urine output <30 mL/hr), altered mental status (confusion), tachycardia worsening, air hunger **Stage 3 — IRREVERSIBLE:** - Blood loss: >40% (>2,000 mL) - Organ failure; death may occur even with aggressive resuscitation **CRITICAL NLE PRINCIPLE:** Tachycardia is the EARLIEST sign of hypovolemic shock. Hypotension is a LATE sign. Do not wait for low blood pressure — act when you see tachycardia with other signs. **DISSEMINATED INTRAVASCULAR COAGULATION (DIC):** DIC is a CONSUMPTIVE COAGULOPATHY — the clotting system is activated systemically, consuming clotting factors and platelets, leading to paradoxical SIMULTANEOUS CLOTTING AND BLEEDING. **Obstetric triggers of DIC:** - Abruptio placentae (most common obstetric cause) - Missed abortion with prolonged retention - Amniotic fluid embolism - Severe preeclampsia/HELLP syndrome - Septic abortion **Mechanism:** These conditions release TISSUE THROMBOPLASTIN (factor III) into the maternal bloodstream → widespread activation of the coagulation cascade → microthrombi throughout the body → consumption of platelets, fibrinogen, factors V and VIII → fibrin degradation products (D-dimer) accumulate → SIMULTANEOUS BLEEDING FROM ALL SITES. **Clinical Signs of DIC:** - Oozing from IV sites, venipuncture sites - Petechiae and ecchymosis - Gum bleeding, epistaxis - Hematuria (blood in urine) - Prolonged bleeding from lacerations **Laboratory Values in DIC (memorize the DIRECTION of change):** - Platelets: ↓ DECREASED - Fibrinogen: ↓ DECREASED (normal in pregnancy is 400–600 mg/dL; DIC drops this) - PT (prothrombin time): ↑ PROLONGED - aPTT: ↑ PROLONGED - D-dimer: ↑ ELEVATED (fibrin degradation products) - Hemoglobin/Hematocrit: ↓ DECREASED **Management of DIC:** REMOVE THE TRIGGER (deliver the baby, evacuate the uterus) PLUS blood product replacement: - Packed Red Blood Cells (PRBCs) — for oxygen-carrying capacity - Fresh Frozen Plasma (FFP) — replaces clotting factors - Platelets — for hemostasis - CRYOPRECIPITATE — contains fibrinogen and factor VIII - Heparin is CONTROVERSIAL and rarely used in obstetric DIC

This scenario contains ALL the classic signs of ruptured ectopic: unilateral abdominal pain + Kehr sign + frank hypovolemic shock (BP 85/55, HR 136, restlessness, pallor, diaphoresis) with a positive pregnancy test. The PRIORITY follows ABCs and Maslow — circulation first. The 72-hour window for RhoGAM applies to delivery; for ectopic, it should be given as soon as the patient is stabilized. The microdose (50 mcg) applies because the event is under 13 weeks gestation.

Under RA 9173 (Philippine Nursing Act of 2002), the nurse has the professional and legal duty to question physician orders that are dangerous to the patient. A vaginal exam with suspected previa is life-threatening. The nurse must advocate for the patient by refusing the dangerous order, notifying the physician, and requesting the appropriate safe diagnostic test (ultrasound). Betamethasone is given because at 32 weeks, fetal lungs are immature — if delivery is required, preterm birth without corticosteroid cover risks neonatal respiratory distress syndrome.

This is a high-yield patient teaching scenario for the NLE. The emphasis on 'no pregnancy for 1 year' and serial hCG follow-up is the most frequently tested post-molar teaching. The nurse must explain the WHY behind each teaching point — patients are more compliant when they understand the reason (in this case, the serious malignancy risk). Under the Philippine health delivery context, the nurse should also refer the patient to the nearest DOH hospital or cancer center for follow-up if needed, and explain PhilHealth benefit coverage.

This is a complete DIC clinical scenario. The trigger was abruptio placentae releasing tissue thromboplastin. The delivery (removing the trigger) has been done, but the coagulation cascade has been activated. The treatment is now supportive — replacing what the body has consumed. The urine output of 15 mL/hr indicates renal hypoperfusion, which is a sign of organ compromise. The nurse must document all findings, report to the physician, and prepare for rapid blood product administration under physician orders, consistent with the nurse's scope of practice under RA 9173.

This is a critical distinction for the NLE. The paradox of missed abortion is that the absence of active bleeding can falsely reassure both the patient and health provider, allowing dangerous prolonged retention. The nurse must educate patients about missed abortion being a medical emergency requiring prompt intervention — NOT a 'wait and see' situation. DIC monitoring (platelets, fibrinogen, PT/aPTT, D-dimer) is essential if intervention is delayed.